Emergency Medicine 1st Edition - DR - Waleed (101 Papers)

Internal &
emergency medicine
for FRCophth exam
1 edition
st
Organized by
Dr.Waleed Badr
M.sc ophthalmology
Emergency medicine for the FRCophth exam
2011
INDEX
Cardiovascular
CPR for Cardiorespiratory arrest
Shock
Acute chest pain
Acute coronary syndrome (ACS)
Severe pulmonary oedema
Broad complex tachycardia
Narrow complex tachycardia
Venous thromboembolic diseases (DVT & PE)
Cardio-vascular drugs
Appendix : Basics & abnormalities of ECG
Chest
Bed side tests in chest medicine
Acute breathless patient
Acute severe asthma
Acute exacerbation of COPD
Pneumonia
Tension pneumothorax
Neurology
Headache D.D
Coma
Meningitis , Encephalitis & Cerebral abscess
Status epilepticus
Stroke
ICP
Endocrine
Coma in diabetic patients
Thyroid function tests
Thyroid emergencies
Addisonian crisis
Hypopituitary coma
Pheochromocytoma emergencies
GIT : Acute GIT bleeding
Haematology
An approach to bleeding disorders
Drugs affecting haemostasis
Hyperviscosity syndrome
Nephrology : Acute renal failure
Acute poisoning
Burns
Hypothermia
Needle-stick injuries
Perioperative care
Severe local anaesthetic toxicity
Choking in children
3
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Dr.Waleed Badr
2011
Cardiopulmonary Resuscitation (CPR) for cardiorespiratory arrest

Sudden cardiac arrest :
Sudden, unexpected loss of heart function, breathing & consciousness.
Usually results from an electrical disturbance in the heart e.g ventricular fibrillation, pulseless
ventricular tachycardia, Asystole or pulseless electrical activity that disrupts its pumping action &
causes blood to stop flowing to the rest of the body i.e loss of cardiac output.
Is different from a heart attack, which occurs when blood flow to a portion of the heart is blocked,
depriving the heart muscle of necessary oxygen. Like a heart attack, however, sudden cardiac arrest
almost always occurs in the context of other underlying heart problems, particularly coronary artery
disease.
Is a medical emergency. If not treated immediately, it is fatal, resulting in sudden cardiac death. With
fast, appropriate medical care, survival is possible. Administering cardiopulmonary resuscitation (CPR)
- or even just rapid compressions to the chest - can improve the chances of survival until emergency
personnel arrive.
Ventricular fibrillation (VF) :
These are the most common and most easily treatable cardiac arrest rhythms.
It produces rapid ineffective uncoordinated movement of the ventricles NO pulse.
ECG shows : rapid, bizarre & irregular ventricular complexes.
Pulseless (sustained) ventricular tachycardia (VT) :
Can cause cardiac arrest if the ventricular rate is so rapid that effective mechanical contraction &
relaxation cannot occur, especially if it occurs in the presence of severe LT ventricular impairment.
It may degenerate into VF.
Asystole :
This occurs when there is no electrical activity within the ventricles & is usually due to failure of the
conducting tissue or massive ventricular damage complicating MI.
When due to conducting tissue failure, permanent pacemaker implantation will be required if the
individual survives.
Pulseless electrical activity (PEA) :

[[
This occurs when there is no effective cardiac output despite the presence of organised electrical activity
i.e electromechanical dissociation (EMD) .
It may be caused by reversible conditions, such as hypovolaemia, cardiac tamponade or tension

pneumothorax, but is often due to a catastrophic event such as cardiac rupture or massive pulmonary
embolism, and therefore carries an extremely poor prognosis.
Dr.Waleed Badr
2011
Management of cardiorespiratory arrest
Chain of survival in cardiorespiratory arrest
e.g
semilateral
position
Adult BLS Algorithm (UK) 2005
Dr.Waleed Badr
2011
In a second, confirm the diagnosis (unconscious, absent carotid pulse, apnoeic), then:
Shout for help (HOW? Ask someone to call the cadiac arrest team and bring the defibrillator (AED).
Note the time)
Then do by yourself Basic
life support "BLS"
BLS aims to maintain a low level of circulation until more definitive treatment with advanced life support
"ALS" can be given.
BLS consists of ABC :
1. Prompt assessment & restoration of the airway.
2. Maintenance of breathing using rescue breathing ('mouth-to-mouth' breathing) .
3. Maintenance of the circulation using chest compressions
A: Establish a patent Airway

Protect cervical spine, if injury possible.
Assess: any signs of obstruction? Ascertain patency by:
Head tilt (if no spinal injury is suspected).
Chin lift.
Jaw thrust.
Clear the mouth.
B: Breathing
Assess by Look, listen and feel (10 sec max.) (look for chest movements,
listen to breath sounds & feel for the breath from the mouth).
If breathing is compromised, give high concentration O2 & manage
according to the findings e.g. relieve tension pneumothorax.
If no respiratory effort, treat as arrest, give 2 breaths after
1st
set of
compressions
-
Each inflation is 1s long.
Use Ambu system (specialized bag& mask system; in place by thumbs pressing downwards
either side of the mouth-piece, palms against cheeks) if available and 2 resuscitators present.
Otherwise, mouth-to-mouth breathing.
Dr.Waleed Badr
2011
C: Circulation (chest compressions)

Assess: check carotid pulse (in the next 10 seconds) if No pulse Start CPR immediately.
Check BP, capillary refill & look for evidence of haemorrhage. If shocked, treat accordingly.
Call for help again.
How to perform CPR ?
1. Start CPR on a firm surface.
2. Center over the lower 1/3 of the sternum.
3. Do 30 chest compressions to 2 breaths (30:2) .
4. Use the heels of hands placed one on top of the other with straight elbows
(directing the weight of your body through your vertical straight arms)
5. Aim for 4 cm chest depression at a rate of 100/min.
6. Allow the chest to recoil completely.
7. Interrupt infrequently as possible (only for DC and intubations).
8. Do 20 cycles (20 of 30:2) then recheck?
Then arrest team (not you except if you have the license) should have come to do:
Advanced life
support "ALS" ALS aims to :

1. Restore normal cardiac rhythm by Electrical defibrillation "DC shock" when the cause of cardiac
arrest is due to a tachyarrhythmia .
2. Restore cardiac output by correcting other reversible causes of cardiac arrest.
3. ALS can also involve administration of IV drugs to support the circulation,
4. Endotracheal intubation to ventilate the lungs.
D: Disability :
Assess level of consciousness by AVPU score or Glasgow coma scale if time allows (see P.53)
Check pupils (size, equality and reaction).
[
E: Exposure : Undress patient but cover to avoid hypothermia.

H: History from relatives and bystanders
Events surrounding onset of illness, evidence of overdose/suicide attempt, trauma .
Past medical history e.g. DM, asthma, COPD, drug abuse, epilepsy or recent head injury.
Medications.
Allergies.
Dr.Waleed Badr
2011
Advanced life support "ALS"

Place defibrillator (monophasic) paddles on chest (apex and under Rt. clavicle) as soon as possible
and set monitor to read through the paddles if delay in attaching leads.
Assess rhythm: is it VF/pulseless VT or Asystole/PEA ?
1- VF/VT :
Immediate defibrillation must occur without delay: 360J monophasic or 150-360 J biphasic .
Immediately Resume CPR 30:2 for 2 minutes without attempting to confirm restoration of a pulse
(because restoration of mechanical cardiac output rarely occurs immediately after successful defibrillation).
If still VF/VT, repeat defibrillation . All shocks are 360J. Thereafter, additional shocks are given
every 2 minutes after each cycle of CPR .
2- A systole/PEA:
Immediately resume CPR 30:2 for 2 minutes continue until the victim starts to breathe normally .
Transverse cardiac pacing may be tried .
Correct reversible causes "4H, 4T" (see Algorithm) .
During CPR
Oxygen 100% .
Adrenaline 1mg/ml IV, every 3 min .
Amiodarone 300 mg IV . a futher 150 mg may be given, followed by an infusion of 1mg/min for
6h, then 0.5 mg/min for 6h (in resistant VF/VT) .
Atropine 3 mg IV (once) (in Asystole/PEA) .
Treat acidosis with good ventilation. Sodium bicarbonate may worsen intracellular acidosis &
precipitate arrhythmias, so use only in severe acidosis after prolonged resuscitation (e.g. 50 ml of
8.4 % solution by IVI).
Dr.Waleed Badr
2011
Adult ALS Algorithm (UK) 2005
Dr.Waleed Badr
2011
NB :
Send someone to check patients notes & usual doctor, these may give clues to the cause of the
arrest .
If IV access fails, give drugs down tracheal tube (2-3 times the IV dose diluted in 10ml 0.9% saline
followed by 5 ventilations to assist absorption).
(Intracardiac injection in not recommended) (PLEASE)
When to stop CPR?

No general rule, as survival is influenced by the rhythm and the cause of the arrest. Stop only if:
Normal rhythm occurs, core temperature is > 33C and pH and K+ are normal.
There was significant delay in starting CPR (BLS started after 5 min or ALS started after 30 min).
After 20 minutes if there is refractory Asystole/PEA .
When to not resuscitate?

The patient's condition is such that resuscitation is unlikely to succeed .
Mentally competent patient stated or recorded that he does not want to be resuscitated OR If
resuscitation is not in the patients interest as it would lead to a poor quality of life.
NB. Ideally, involve patients and relatives in the decision before the emergency. When in doubt,
resuscitate.
After successful resuscitation What to do?

1. Transfer to CCU or ICU.
2. Monitor vital sign.
3. Consider ECG, CXR, glucose, blood gases, FBC, CK/troponin.
4. Seek expert advice from a cardiologist.
5. Explain to the patients relatives what has happened, whatever the outcome.
Dr.Waleed Badr
2011
Shock
Definition: Circulatory failure inadequate organ perfusion .

Causes:
1) Cardiogenic shock : either due to pump failure or 2ry to PE,tension pneumothorax & cardiac
tamponade i.e obstructive shock .
2) Hypovolaemic Shock : due to loss of blood volume
Bleeding: trauma, ruptured aortic aneurysm or ectopic pregnancy.
Fluid loss: vomiting (GIT obstruction), diarrhea (cholera), burns
Heat exhaustion.
3) Anaphylactic Shock.
4) Neurogenic shock : i.e related to a nervous system injury e.g. post spinal surgery.
5) Septic Shock : due to toxins or poisons released by an infection .
6) Iatrogenic : drugs e.g. anesthetics and antihypertensives.
7) Endocrine failure : e.g. Addisons ds or hypothyroidism.
Clinical picture :
1. Vital signs :
-
Temperature : commonly hypothermia .
Heart rate : commonly tachycardia >100 beats/min
Bl.P : in early stages of shock as COP but rapidly as shock progresses i.e hypotension .
Respiratory rate : (compensatory tachypnea) in an attempt to remove excess acids in the

form of CO2.
2. CNS: Early : change in personality & may progress to restlessness. Late : confusion & ultimately coma
may occur.
3. CVS : Chest pain. with profound acidosis, abnormal heart rhythms (cardiac dysrhythmias) are more
prevalent and are potentially fatal.
4. GIT problems : arise most often from the shunting of blood away from this system. Symptoms include :
abdominal pain, nausea, vomiting, or diarrhea + GIT bleeding with black/tarry stool .
5. Skin : cold, pale, clammy & cyanosed (if extreme low blood
O2
content) .
6. Renal problems : Oliguria & anuria (in severe cases) .
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Dr.Waleed Badr
2011
Management:
If BP unrecordable, call the cardiac arrest team
Call for help + make the patient lie on hard surface with raised legs.
A ensure patent airway (remove any obstruction, chin elevation, head tilt) & adequate
ventilation.
B O2 100%.
C Circulation (IV access x 2 wide bore, get help if this takes > 2 min).
Identify & treat underlying cause if clear ( e.g check abdomen for signs of trauma or aneurysm.
GIT bleeding and melena). If unclear, ttt as Hypovolaemic (most common cause).
Consider: arterial line, central venous line & Foley's catheter.
Infuse crystalloids: fast to raise BP (unless cardiogenic shock) as dictated by BP, CVP & urine output
(aim for a urine flow > 30 mL/h).
NB.Dont overload with fluids if cardiogenic shock (exclude PE & RV infarct 1st).
Vital sign monitoring: pulse, BP, temperature, respiration & peripheral perfusion.
Do some investigations: FBC, U&E, ABG, glucose, cross matching, ECG.
Treatment according to the cause
Cardiogenic shock: Cold & clammy patient.

Has a high mortality. Can occur suddenly or after progressively worsening heart failure.
Ask a senior physicians help both for exact diagnosis & treatment.
Causes:
1. MI, myocarditis or myocardial depression (drugs, hypoxia, acidosis, sepsis), endocarditis,
Arrhythmias .
2. 2ry to cardiac tamponade, tension pneumothorax &PE.
Management:
o If the cause is MI, prompt thrombolysis or acute angioplasty.
o Manage in CCU or ICU if possible.
o Oxygen.
o Morphine (2.5 5 mg IV) for pain and anxiety.
o Investigations: ECG (every hour until diagnosis is made), Cardiac enzymes/troponins, U&E, CXR,
echo, ABG.
o Close monitoring: CVP, BP, ABG, ECG & urine output.
o Correct arrhythmia, U&E and acid base imbalance.
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Dr.Waleed Badr
2011
o Consider a Swan Ganz catheter to assess pulmonary capillary wedge pressure (PCWP) and
cardiac output & an arterial line to monitor pressure.
PCWP < 15 mm Hg: give plasma expanders (100 mL every 15 min IV), aim for 15 20 mm Hg.
PCWP > 15 mm Hg: consider +ve inotropes e.g dopamine OR dobutamine (2.5 10 ug/kg/min
IVI), aim for systolic BP > 80 mm Hg.
o Look for and treat any reversible cause e.g. MI and PE (thrombolysis). Consider surgery for valvular
lesions.
Cardiac tamponade
Pericardial fluid collection intrapericardial pressure Heart cannot fill pumping stops.
Causes: trauma, lung or breast cancer, pericarditis and MI.
Signs:
BP, JVP & muffled heart sounds (Becks triad).
JVP on inspiration (Kussmauls sign) .
Pulsus paradoxus (pulse fades on inspiration).
Investigations:
ECG: electrical alternans.
CXR: globular heart, Lt. heart border convex or straight, Rt. costophrenic angle < 90.
Echo is diagnostic.
Management:
Very difficult. With actual senior help and luck, prompt pericardiocentesis brings swift
relief.
While awaiting, give oxygen, monitor ECG and set an IVI. Take blood for group & save.
Cardiothoracic surgery (e.g CABG, ventricular repair, or pericardial window) may have
a role
Hypovolaemic shock:
Treat underlying cause e.g. control obvious hemorrhage, urgent laparotomy or thoracotomy.
Fluid replacement: Saline 0.9% or colloid initially; if bleeding, use cross matched blood transfusion or
group O Rh ve blood via large bore cannula.Titrate against BP, CVP & urine output.
Correct electrolyte abnormalities and acidosis.
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Dr.Waleed Badr
2011
Anaphylactic shock:
More common in atopic individuals.
Pathophysiology: Type 1 IgE-mediated hypersensitivity reaction Release of histamine & other

mediators from mast cells increase in vascular permeability, vasodilatation & respiratory smooth
muscle contraction .
Causes: drugs e.g. penicillin and contrast mediators in radiology (e.g FA). Stings and some kinds of
food e.g. strawberries, eggs, fish .
NB. Anaphlactoid reaction involves direct release of mediators from inflammatory cells without involving
antibodies e.g. with drugs.
Clinical features : suggestive of anaphylaxis

-
H/O previous allergy or atopy .
Itching, sweating, erythema, urticaria .
Tachycardia, hypotension,
Wheezy chest, laryngeal obstruction (oedema), apnea & cyanosis.
Vomiting, diarrhea & urinary incontinence .
Syncope .
Differential diagnosis :
1. Causes of loss of consciousness :
Vasovagal attack (see below).
Hypoglycaemia .
MI .
2. Causes of respiratory distress : Acute asthma .

3. Causes of laryngeal obstruction : Idiopathic angioedema .
Treatment:
1. Remove cause, raise the feet + call for help .
2. ABC : Secure airway, 100% oxygen & Secure IV access.
3. Adrenaline 0.5 mg (0.5 mL of 1:1000) IM repeated every 5 min guided by BP, pulse and respiratory
function until better.
4. Antihistaminic e.g. chlorpheniramine 10 mg IV repeated every 6h if urticaria persists .
5. Hydrocortisone 200 mg IV (can be repeated if necessary) .
6.
If hypotensive : IVI 0.9 % saline 500 ml over 15 minutes (up to 2 L may be needed), titrated against BP.
7. If severe bronchospasm : Consider aminophylline & nebulized salbutamol 2.5 mg . titrated against
respiratory function .
8. if laryngeal edema is worsening (stridor) : refer to ICU & Intubation/ventilation.
NB: if patient is severely ill or has no pulse, consider IV adrenaline (1 mL of 1:10,000 solution per minute).
Stop as soon as a response has been obtained.
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Dr.Waleed Badr

9. After patient has come out of anaphylaxis
2011
patient is to be discharged only after 48hrs as
sometimes biphasic anaphylaxis reaction occurs which is even more severe.
Prophylaxis against anaphylactic shock :
Proper H/O atopy,drug allergy, hypersensitivity to insect bites or stings.
Family H/O anaphylaxis(AD inheritance) .
Skin- prick tests (showing specific IgE) helps in identifying which allergens to avoid.
Emergency tray equipped with Ambu bag with fascial fask, larnygyoscope, endotracheal tube,
oxygen cylinder
& medicines (Adrenaline,hydrocortisone,antihistaminics,aminophylline, IV
glucose) .
Educated and trained Staff to deal in emergency.
Suggest a Medic-alert bracelet naming the allergen.
Teach about self injected adrenaline in case no help is available .
Septic shock:
Endotoxin-induced vasodilatation with shock & coma but with no signs of infection (fever and
WCC).
Warm and well perfused with bounding pulse.
Antibiotics: is given (preferably after blood culture). if no clue to source IV cefuroxime 1.5 g / 8h or
gentamycin + antipseudomonal.
Give colloid or crystalloid by IVI.
Monitor in ICU (CVP and pulmonary artery wedge pressure).
Vasovagal attack:
Cause: generalized vasodilatation.
Clinical picture: bradycardia & hypotension.
Treatment: raise legs, IVI fluids, Atropine 1mg IV & hydrocortisone 200 mg I.V .
Heat exposure (exhaustion):
Tepid sponging and fanning.
Avoid ice and immersion.
IVI 0.9 % saline hydrocortisone 100 mg IV.
Chlorpromazine 25mg IM to stop shivering.
Stop cooling when core temperature < 39C.
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Dr.Waleed Badr
2011
Acute chest pain

Causes:
Life-threatening :
ACS (unstable angina & Acute MI) .
Pulmonary embolism.
Aortic dissection.
Tension pneumothorax.
Esophageal rupture.
Others :
Pericarditis.
Pneumonia, empyema & pleurisy.
Gastro-oesophageal reflux , oesophageal spasm .
Musculoskeletal : e.g. muscular, rib fractures, bony metastasis and costochondritis.
Cholecystitis, peptic ulceration & pancreatitis .
Cervical spondylosis .
Sickle-cell crises.
Management:
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Call for help.
ABC .
Level of consciousness.
Vital sign monitoring.
Dr.Waleed Badr
2011
Workup of chest pain
Site
Ischaemic
Aortic
Pericarditis/
cardiac
dissection
Pleurisy
Central,diffuse
Between
Retrosternal
Oesophageal
Musculoskeletal
shoulder
blades
Radiation
Jaw/neck/shoul
Back
der/arm/occasi
onally back
Character
Dull,constricting,
Sharp
choking,
tearing
&
Sharp
Can
mimic
anginal pain i.e
squeezing,
constricting
crushing
or
pressure
Precipitated
Exercise,
by
emotion,
cold,
coughing
after
large
lying flat
Breathing,
or
Food,lying flat,hot
Movement
drinks,alcohol
(bending,
stretching,
meal
Relieved by
turning)
Rest, nitrates
leaning
Nitrates,antacids
forwards
Associated
Autonomic
symptoms &
sweating, nausea & vomiting
over
signs
Breathlessness
costal cartilage
16
disturbance
e.g
Local tenderness
a
rib
or
Dr.Waleed Badr
2011
Acute coronary syndrome (ACS)

ACS includes :
Unstable angina
Non ST elevation MI (NSTEMI) = non Q wave or subendocardial MI.
ST elevation MI (STEMI) = acute MI .
[[
STEMI (Acute MI)

Risk factors: DM, HTN, atherosclerosis & smoking.
Clinical picture:
Heavy chest pain > 15min, radiating to the arm, neck and shoulder.
Dyspnea, sweating, palpitations, nausea, dizziness, collapse and shock.
Epigastric pain & vomiting (inferior MI) .
May present without chest pain (Silent MI) e.g in elderly or diabetics .
Investigations :
o
Bloods for FBC, U&Es, glucose, lipids and cardiac enzymes.

-
CK : 8 12 h till 72 h.
Lactate dehydrogenase : 1 - 2 days till 7 days.
Cardiac troponin & Aspartate transaminase.
Chest x ray: in cardiac size.
ECG: normal or elevated ST segment & pathological Q.
Echocardiography and coronary angiography.
Management :
Arrange for an emergency ambulance.

Attach ECG monitor and record a 12 lead ECG.
High flow oxygen 100% by face mask.
IV access.
Brief assessment :
Brief history: previous attack & risk factors for IHD or any contraindications for thrombolysis.
Examination: vital signs.
Medications :
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Morphine 5 -10 mg IV + antiemetic e.g Metoclopramide 10 mg IV.
Sublingual nitrate (2 puffs or 1 tablet) unless hypotensive.
Aspirin 300 mg PO chewed (unless clear contraindication).
Dr.Waleed Badr

B-blocker e.g. atenolol 5 mg IV (unless asthma or Lt. ventricular failure).
2011
Restore coronary perfusion either primary percutaneous coronary intervention (PCI) e.g angioplasty
(if available) or thrombolysis .
Primary PCI:
The treatment of choice if ongoing ischaemia & presentation is within 12h.
More effective than thrombolysis, with a greater reduction in the risk of death, recurrent MI or
stroke .
Not available in all locations .
Thrombolysis:
Greatest benefit if given < 12 h of onset, up to 24 h. thrombolysis is contraindicated beyond 24h
from the time of onset of symptoms .
Indications: ECG criteria for thrombolysis
1. ST elevation > 1 mm in 2 or more limb leads OR > 2 mm in 2 or more chest leads.
2. LBBB (unless known to have LBBB previously) .
3. Posterior changes : deep ST depression & tall R waves in leads V1 to V3 .
NB. Dont thrombolyze ST depression alone, T-wave inversion alone or normal ECG .
Contraindications: Internal bleeding, suspected aortic dissection, esophageal varices, active
peptic ulcer, recent surgery, trauma or hemorrhagic stroke. severe hypertension, pregnancy .
Choice of agent :
-
Streptokinase (SK): 1.5 million units in 100 mL 0.9 % saline IVI over 1h.
In cases of allergy to SK (rare) : Tissue plasminogen activator might be used e.g Alteplase
(human tPA), Tenecteplase & Reteplase ( tPA analogues) .
Complications:
-
Recurrent ischaemia or Failure to reperfuse (persistent pain with continuing ST-segment

elevation) consider re-thrombolysis or rescue angioplasty
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Stroke .
Pericarditis, cardiogenic shock & heart failure.
Dr.Waleed Badr
2011
NSTEMI
Patients should be managed medically until symptoms settle and then investigated by angiography
with a view to possible angioplasty or surgery (CABG).
Assessment: brief history (previous attack, relief with rest/nitrates, risk factors for IHD, history of
cardiovascular diseases), examination (vital signs, signs of heart failure).
Investigations: ECG (ST depression, flat or inverted T or normal), cardiac enzymes, CXR, glucose,
lipids, U&E, FBC.
NB: measurement of cardiac troponin helps predict which patients are at risk of a cardiac event and
who can be discharged early (2 different forms: troponin T and troponin I).
Management:
Admit to CCU and monitor closely.
High flow O2.
Analgesia: Morphine (5 10 mg IV) + metoclopramide (10 mg IV).
Nitrates: GTN spray or sublingual tablets as required.
Aspirin 300 mg PO followed by 75mg/d (unless contraindicated) .
BBlockers e.g. metoprolol 50-100 mg/8h . If contraindicated (asthma, COPD, LVF, bradycardia &
coronary artery spasm), give calcium channel antagonist e.g verapamil 80-120 mg/8h .
Low molecular weight (LMW) heparin SC with monitoring APTT.
IV nitrate if pain continues e.g GTN 50 mg in 50mL 0.9% saline .
If symptoms fail to improve, refer to a cardiologist for urgent angiography angioplasty or CABG.
If improving (no further pain, normal ECG and negative troponin), treat medically, address risk factors
(DM, HTN, smoking), gentle mobilization and arrange further investigations (stress test & angiogram).
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Dr.Waleed Badr
2011
Severe pulmonary edema

Causes:
Cardiovascular (LV failure post MI or IHD, mitral stenosis, arrhythmias & malignant hypertension).
ARDS from trauma, post-op, sepsis.
Fluid overload.
Neurogenic e.g. head trauma.
Symptoms: Dyspnea, orthopnea, pink frothy sputum.

Signs: distressed, pale, sweaty, pulse, tachypnea, pink frothy sputum, fine lung basal crackles &
wheeze. Usually sitting up and leaning forward.
DD:
1. asthma/COPD.
2. Pneumonia & pulmonary edema are often hard to distinguish especially in the elderly where they
may co-exist. Do not hesitate to treat all three simultaneously.
Investigations: begin treatment before investigations.
CXR: cardiomegaly, signs of pulmonary edema (bilateral shadowing, small effusions at

Costophrenic angles, fluid in lung fissures and Kerley B lines linear opacities).
ECG (MI), U&E, cardiac enzymes, ABG, consider echo.
Treatment:
Sit the patient upright.
Oxygen 100%.
IV access and monitor ECG, treat arrhythmias (AF).
Diamorphine (2.5 5 mg IV slowly).
Diuretics e.g. frusemide 40-80 mg IV slowly.
GTN spray or SL.
Start nitrate infusion e.g isosorbide dinitrate 2-10 mg/h IVI if systolic BP 100 mmHg.
If patient is worsening, give further dose of frusemide.
Consider ventilation or venesection (get help).
If systolic BP < 100 mmHg, treat as cardiogenic shock (inotropes support).
Once stable and improving, do all investigations again and treat permanently accordingly.
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Dr.Waleed Badr
2011
Broad complex tachycardia

ECG shows rate of > 100bpm and QRS complexes > 120 ms (> 3 small squares done at the standard UK rate
of 25 mm/s).
Management :
If in doubt, treat as ventricular tachycardia (the commonest cause).
Identify the underlying rhythm and treat accordingly.
If No pulse, treat as arrest.
Treatment of ventricular tachycardia:
Oxygen,
IV
access,
hypomagnesaemia,
if
unstable
amiodarone
(sedation,
or
lidocaine),
DC
shock,
correct
hypokalaemia
and
if
stable
(correct
hypokalaemia
and
hypomagnesaemia, amiodarone or lidocaine, sedation, DC shock).
After correction of VT: find the cause, anti-arrhythmic therapy, surgical isolation of arrythmogenic
area or implantable cardioverter defibrillator (ICD) may help.
Treatment of ventricular fibrillation: use non-synchronized DC shock (no R wave to trigger

defibrillation).
Treatment of ventricular extrasystoles (ectopics): common after MI, seen in healthy, no need for antidysrhythmic drugs, seek expert advice.
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Dr.Waleed Badr
2011
Narrow complex tachycardia

ECG shows rate > 100 bpm and QRS complex duration of < 120 ms (< 3 small squares on ECGs done at the
standard UK rate of 25 mm/s).
DD:
Sinus tachycardia (normal P wave followed by normal QRS)
Atrial fibrillation (absent P wave, irregular QRS complexes)
Atrial flutter: (rate 300 bpm, sawtooth baseline, ventricular rate 150 bpm (2:1 block)) .
Multifocal Atrial tachycardia
Junctional tachycardia
Atrial fibrillation (AF)

Causes:
Cardiac :
-
Coronary artery disease (including acute MI) .
Valvular heart disease (especially Mitral valve disease) .
Hypertension .
Non-cardiac : Pneumonia, pulmonary embolism & Hyperthyroidism .
Idiopathic (lone AF) .
Symptoms : may be asymptomatic or present with chest pain, palpitations & dysnea.
Signs :
Pulse : irregularly irregular* ( apical pulse rate (300-600 bpm) is greater than the radial rate) .
First heart sound is of variable intensity.
hypotension & pulmonary embolism.
Complications: embolic stroke, CRAO.

Investigations:
U&E, cardiac enzymes , thyroid function tests , D-dimer (if the patient has risk factors to pulmonary embolism)
ECG : absent P wave, irregular QRS complexes .
ECHO : (LA enlargement, mitral valve disease, poor LV function).
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Treatment: of Acute AF (< 72h)

Goals of treatment :
1. Hemodynamic stabilization
2. Ventricular rate control
3. Prevention of embolic complications .
Treat any associated acute illness e.g. MI.
Control ventricular rate with B-blocker (Esmolol) or digoxin PO or IV.
-
PO : Loading dose 0.5mg 6-hourly for 2 doses, then 0.125-0.25 mg daily .
IV : 0.75-1 mg in 0.9% NACL over 1 hr .
If AF does not resolve, consider drug or electrical cardioversion.

-
Drug cardioversion: Amiodarone IVI 5 mg/kg over 1hr then up to 15 mg/kg/24h .
DC cardioversion: indicated in electively following a first attack with an identifiable cause

OR as an emergency if patient is compromised. Protocol: 200J, 360J, 360J (DO ECHO FIRST; is
heart structurally normal?).
Anticoagulation is not required if AF of recent onset with normal echo but aspirin 300 mg PO
maybe given. Otherwise, give warfarin 3 wks before and 4 wks after DC cardioversion.
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Venous thromboembolic disease (VTE)

The most common presentation is Deep vein thrombosis (DVT) of the leg and/or pulmonary embolism (PE) .
Deep vein thrombosis (DVT)

DVTs occur in 25-50% of surgical patients, and many non-surgical patients.
Risk factors (of DVT/PE) :

1. Patient factors : Age,obesity,varicose veins, previous DVT/PE, family history, pregnancy, oestrogencontaining oral contraceptives & HRT.
2. Immobility : especially long flights (> 4hours) or associated with illness / hospital admission) .
3. Surgical conditions : recent major surgery (especially pelvic or orthopaedic) .
4. Medical conditions : MI/heart failure, inflammatory bowel disease, pneumonia & malignancy .
5. Haematological disorders : thrombophilic states, hyperviscosity syndromes & Myeloproliferative
disease
Signs :
Calf warmth/tenderness/swelling/erythema
Pitting oedema.
Mild fever .
Homans' sign ( resistance/pain on forced foot dorsiflexion) : should not be tested for as it may
dislodge thrombus.
Differential diagnosis :
Ruptured knee (Bakers Cyst) : Usually occur in patients with rheumatoid arthritis .
Cellulitis : Infective cellulitis is usually distinguished by marked skin erythema & heat which is localised
within a well-demarcated area of the leg and may be associated with an obvious source of entry of
infection (e.g. an insect bite or leg ulcer).
NB.Both may coexist with a DVT .
Investigations :
1. FBC (WCC to help find infection; Hb to look for polycythaemia; platelet count look for
thrombocytosis) .
2. D-dimer blood tests (evidence of clot lysis) : High sensitivity but low specificity ( if thrombosis,
infection, malignancy & post-op) .
3. Compression U/S of calf & leg (ideally doppler U/S) : if ve, repeat at 1wK to catch those with
early but propagating DVTs ; this should also rule out ruptured knee
4. ECG; CXR; ABG; V/Q scan & CT pulmonary angiography (If pulmonary embolus a serious
concern).
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5. Thrombophilia tests : before commencing anticoagulant therapy if there are no predisposing

factors, in recurrent DVT, or if there is a family history of DVT.
Complications :
1. Pulmonary embolism : range of severity from asymptomatic, to symptomatic, to sudden death
2. Chronic post-phlebitic leg problems (10-30%) :
due to damage of venous valves by the
thrombus . it results in pain, swelling, eczema, itch & ulceration .

3. Stroke or other arterial embolus : via mechanism of paradoxical embolus through cardiac defect
4. Complications of anticoagulants e.g haemorrhage (intra-cranial, ocular, GI & other)
Prophylaxis : (against DVT/PE)
Early post-op mobilization (the simplest method) .
Compression stockings (to prevent further thrombosis) .
Low M.W heparin e.g enoxaparin 20 mg/24h SC .
Aspirin .
Avoid contraceptive pill if at risk e.g major or orthopaedic surgery.
Vena caval filters (of limited use) .
Management :
Graded support stocking .
Treatment of any underlying risk factors .
Anti-coagulants :
Assessment of risk factors for haemorrhage .
Initially with heparin e.g LMWH (enoxaparin 1.5mg/kg/24h SC) .
Start warfarin simultaneously with LMWH (as it is prothrombotic for the first 48h) .
Stop heparin when INR is 2-3
Treat for 3 months if post-op; 6 moths if no cause is found;malignancy or recurrent DVT.
Vena caval filters : may be used in active bleeding, or when anticoagulants fails, to minimize risk
of pulmonary embolus.
When is there a high probability of a DVT ? (WELLS Score)
Calf swelling > 3cm compared to the other leg (measured 10cm below tibial tuberosity)
Immobile (e.g in bed, in plaster or paralysed) .
Local tenderness over deep venous system .
Active malignancy .
Family history of DVT ( 2 close relatives).
Others : pitting edema & dilated superficial veins .
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Pulmonary embolism (PE)

Always suspect PE in sudden collapse 1-2 wks after surgery.
Mechanism: Venous thrombi, usually from DVT, pass into the pulmonary circulation and block blood
flow to lungs. The source is often occult.
Risk factors: malignancy, long immobilization following surgery (especially pelvic), venous disease,
obesity, the PILL & HRT.
Signs and symptoms:
Acute dyspnea , tachypnea , pleuritic chest pain .
Hypotension, tachycardia, gallop rhythm, loud P2, JVP .
Haemoptysis, syncope, Cyanosis, AF and DVT (swollen leg).
Investigations:
U&E, FBC, baseline clotting.
ECG:
-
Normal or sinus tachycardia (the commonest)
Rt. ventricular strain pattern (V1 3), Rt. Axis deviation, RBBB .
AF.
Rarely, SI,QIII,TIIII pattern occurs : deep S waves in I, pathological Q waves in III, inverted T waves
in III.
CXR: often normal, vascular markings, small pleural effusion, wedge shaped area of infarction.
ABG: O2, CO2 and PH.
D-dimer blood test:

-
if thrombosis is present as it indicates plasma level of fibrin product, so it helps to exclude PE if

Normal.
High sensitivity but low specificity as it also in infection, malignancy & post-op .
CT pulmonary angiography (CTPA): Better with helical (spiral) CT. It is sensitive & specific in
determining if emboli are in pulmonary artery. If unavailable, a ventilation-perfusion (V/Q) scan can
aid diagnosis. If equivocal, pulmonary angiography or bilateral venograms may help.
Doppler U/S for leg veins.
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Management
Prevention: see DVT prophylaxis P.25

Immediate management :
Oxygen 100 %.
Morphine 10 mg IV (if pain) + antiemetic.
If critically ill, consider immediate thrombolysis or surgery.
IV access and start LMWH or Unfractioned heparin (faster onset & rapid reversal of anticoagulation)
10,000 U IV bolus then 15 25 U/Kg/h IVI as guided by APTT.
If systolic BP > 90 mm Hg, start warfarin 10 mg/24h PO and confirm diagnosis.
If systolic BP < 90 mm Hg, start rapid colloid infusion.
If still BP after 500 mL colloid, give dobutamine 2.5 10 ug/kg/min IV (aim for BP > 90 mmHg).
If still BP, consider noradrenaline.
If still BP after 30 60 min of standard treatment with clinically definite PE and clinical
improvement, consider thrombolysis with streptokinase (loading dose 250,000 U IVI over 30 min,
maintenance 100,000 U/h for 12 72 h according to response).
TTT of underlying risk factors .
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Cardiovascular drugs
1. B-blockers :
Classification :
1. 1st generation
(Non-selective blockers)
2. 2nd generation
(selective B1 blockers)
(cardioselective)
3. 3rd generation
(blockers with V.D action)
Propranolol
Sotalol
Timolol
Levobunolol
Metipranolol
Atenolol
Metapralol
Bisoprolol
Betaxolol
Dilevalol
Nebivolol
Mechanism of action : Block B-adrenoceptors, thus antagonizing the sympathetic nervous system. Blocking
B1-receptors is negatively inotropic and chronotropic (Pulse by firing of sinoatrial node), and B2receptors induce peripheral vasoconstriction and bronchoconstriction.
Indications :
1. Hypertension (2nd line).
2. Ischaemic heart diseases : Angina, post MI (mortality).
3. Cardiac arrythmias (antidysrhythmic).
4. Hyperthyroidism .
5. Prophylaxis of migraine .
6. Anxiety & tremors .
7. Glaucoma .
Side effects :
1. Bronchospasm (in susceptible patients) .
2. Hypotension & bradycardia (antidote to bradycardia is Atropine up to 3mg IV. Give glucagon 210mg IV bolus + 5% dextrose if atropine fails ( an atropine infusion of 50g/kg/h). If unresponsive,
consider pacing or an aortic balloon pump).
3. Peripheral ischaemia, intermittent claudication & cold extremities .
blood flow to liver & kidney metabolism & excretion of drugs .
4. Potentiation of the hypoglycaemic effect of insulin & oral hypoglycaemic drugs & masking of the
hypoglycaemic symptoms .
5. Hyperkalaemia in diabetic & uraemic patients .
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6. Miscellaneous S/E : night mares, depression, headache, nausea, vomiting, lipido & possible of
plasma HDL level .
Contraindications :
Congestive heart failure .
heart Block
Asthma/COPD .
Hypotension & bradycardia .
Prinzmetal's angina (angina due to coronary spasm caused by hyperactivity of receptors in the
coronaries) .
Peripheral vascular disease .
2. Diuretics :
Mechanism
of action
Indications
Side effects
Loop diuretics
Thiazide diurectics
K+ sparing diuretics
(Furosemide)
(hydrochlorothiazide)
(Spironolactone)
Act mainly at limb of Act mainly at proximal Act mainly at distal part of
loop of henle .
part of DCT.
DCT & upper part of
Inhibit
Na+/K+/2CL- Inhibit Nacl cotransport collecting tubules .
cotransport Na+ &
Na+ & CL- reabsorption. Competitive inhibition with
CL- reabsorption .
aldosterone .
Acute pulmonary edema Congestive heart failure
Given
with
other
Hypertensive
Essential hypertension .
diuretics (to balance K+
emergencies .
Diabetes insipidus .
loss) .
Hyper Ca2+ & Hyper K+ .
Hyperaldosteronism
Hypokalaemia .
Hyperkalaemia .
Hypomagnesaemia .
Gynecomastia
&
Hyponatraemia .
impotence in males .
Hypocalcaemia .
Menstrual disorders &
Hyperuricaemia .
hirsutism in females
Ototoxicity .
3. Calcium channel blockers :

Classification :
1. Dihydropyridines
2. Nondihydropyridines
29
Drugs
Nifedipine
Amlodipine
Lacidipine
Nimodipine
Nicardipine
Felodipine
Verapamil
Diltiazem
CVS pharmacological effects

Peripheral V.D .
Coronary V.D .
Tachycardia (can be used with
B-blockers) .
Bl.P lowering effect
Indications
Hypertension
angina
A-V & S-A conduction delay

Bradycardia (Don't give with Bblockers " risk of bradycardia
LVF").
Peripheral & Coronary V.D .
Bl.P lowering effect .
Hypertension, angina
& arrhythmias .
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Dr.Waleed Badr
2011
Mechanism of action : Work by blocking voltage-gated ca2+ channels in cardiac muscle & blood vessels. This
intracellular Ca2+ leading to a reduction in muscle contraction, thereby promoting coronary & peripheral
vasodilatation & reducing cardiac contractility and myocardial oxygen consumption (Bl.P ) .
Side effects :
1.
2.
3.
4.
5.
6.
Aggravation of congestive heart failure .

A-V block in patients with pre-existing disease .
Dizziness, fatigue, headache & flushing .
Ankle oedema .
Gigival hyperplasia .
Nausea, vomiting & constipation
Contraindications: heart failure & heart block.
4. Digitalis (Digoxin) :
Mechanism of action :
1. +ve inotropic action (Blocks the Na+/K+ pump free intracellular ca2+) improves myocardial
contractility & COP .
2. Slow the heart rate (used in fast AF to control ventricular rate. aim for pulse <100).
3. Conduction velocity : in small doses & in large doses .
Indications :
1. the major indication is CHG associated with atrial fibrillation .
2. other indications : heart failure not responding to diuretics, atrial fibrillation, atrial flutter & paroxysmal
atrial tachycardia .
Dosage :
PO:
-
loading dose : 0.5 mg PO twice daily (in AF, we give a large intial loading dose in 3-4 divided
doses at 6-hours intervals. A total dose of 1.25-1.5 mg is often necessary)
Maintenace dose : 0.125 mg 0.25 mg PO daily
IV : 0.75-1mg in 0.9% NaCl over 2h.
CI:
1. Possibility of digitalis toxicity .
2. Heart block .
3. Hypertrophic obstructive cardiomyopathy .
4. WPW syndrome .
5. Paroxysmal ventricular tachycardia .
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Precautions for digitalis therapy :
Never give I.V digitalizing dose before being sure that the patient has not received any digitalis
during previous 14 days to avoid digitalis toxicity .
Make sure that K+ level is normal .
Use lower digitalizing dose with elderly people , since toxic effects may be pronounced after
administration of the normal adult dose of digitalis .
If on digoxin, Avoid/or use less energy in cardioversion.
If on amiodarone , halve the dose of digoxin.
SE (digitalis toxicity)
Cardiac : Any arrhythmia (particularly AV block & ventricular tachycardia/fibrillation) .
Ocular : white halos, yellow/green chromatopsia, diplopia .
Nausea , vomiting & appetite .
Hypokalaemia .
Headache, confusion , delirium & hallucinations (digitalis delirium) .
Gynaecomastia & galactorrhea .
Management of digitalis toxicity :
Stop digitalis administration .
Check & correct hypokalaemia .
Treat any arrhythmia .
Digoxin-specific antibody fragments IVI (Digibind) : specific antibodies that permits high renal
clearance of digitalis complex by glomerular filteration .
5. Antiarrhythmic drugs
Classification :
1. Class I
Ia : Quinidine, Disopyramide, Procainamide

Ib : Lidocaine
Ic :Flecainide
2. Class II
B blockers
3. Class III
Amiodarone *
4. Class IV
Calcium channel blockers (Verapamil & diltiazem)
5. Class V
Adenosine .
Digoxin
* S/E of amiodarone : vortex keratopathy ,cataract, optic neuropathy, peripheral neuropathy, myopathy,
alteration of thyroid function & hepatotoxicity .
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Appendix1 : Basics & abnormalities of ECG
ECG: A methodical approach

First confirm the patient's name and age, and the ECG date. Then:
Rate:
-
At usual speed (25mm/s) each "big square" is 0.2s; each "small square" is 0.04s.
To calculate the rate, divide 300 by the number of big squares per R-R interval .
Rhythm:
-
If the cycles are not clearly regular, use the "card method": lay a card along ECG, marking
positions of 3 successive R waves. Slide the card to and fro to check that all intervals are equal. If
not, note if different rates are multiples of each other (i.e varying block), or is it 100% irregular (AF
or VF)?
Sinus rhythm is characterized by a P wave (upright in II, III, & aVF; inverted in aVR) followed by a
QRS complex.
AF has no discernible P waves and the QRS complexes are irregularly irregular.
Atrial flutter has a "sawtooth" baseline of atrial depolarization (~300/min) and regular QRS
complexes.
Nodal rhythm has a normal QRS complex but P waves are absent or occur just before or within
the QRS complex.
Ventricular rhythm has QRS complexes >0.12s with P waves following them.
Axis:
-
The mean frontal axis is the sum of all the ventricular forces during ventricular depolarization.
The axis lies at 90 to the isoelectric complex (ie the one in which positive and negative
deflections are equal).
Normal axis is between -30 and +90 .
As a simple rule of thumb, if the complexes in leads I and II are both "positive", the axis is normal.
Left axis deviation (LAD) is -30 and -90. Causes: left anterior hemiblock, inferior MI, VT from LV
focus, Wolff- Parkinson-White (WPW) syndrome (some types).
Right axis deviation (RAD) is +90 and +180 . Causes: RVH, PE, anterolateral MI, left posterior
hemiblock (rare), WPW syndrome (some types).
P wave:
-
Normally precedes each QRS complex.

Absent P wave: AF, sinoatrial block, junctional (AV nodal) rhythm.
Dissociation between P waves and QRS complexes indicates complete heart block.
P mitrale: bifid P wave, indicates left atrial hypertrophy.
P pulmonale: peaked P wave, indicates right atrial hypertrophy (Pseudo-P-pulmonale seen if K+ ) .
P-R interval:
-
32
Measure from start of P wave to start of QRS.

Normal range: 0.12- 0.2s (3-5 small squares).
A prolonged P-R interval implies delayed AV conduction (1st degree heart block).
A short P-R interval implies unusually fast AV conduction down an accessory pathway e.g WPW .
Dr.Waleed Badr
2011
QRS complex:
-
Normal duration: <0.12s (less than 3 small squares) .

If >0.12s suggests ventricular conduction defects, e.g a bundle branch block .
Large QRS complexes suggest ventricular hypertrophy.
Normal Q wave <0.04s wide and <2mm deep. They are often seen in leads V5 and V6, aVL and I,
and reflect normal septal depolarization, which usually occurs from left to right. Pathological Q
waves may occur within a few hours of an acute MI.
QT interval:
-
Measure from start of QRS to end of T wave. It varies with rate. Calculate corrected QT interval
(QTc) by dividing the measured QT interval by the square root of the cycle length, i.e
. Normal QTc: 0.38-0.42s
Prolonged QT interval: acute myocardial ischaemia, myocarditis, bradycardia (eg AV block),

head injury, hypothermia, U&E imbalance (K+, Ca2+, Mg2+), drugs(quinidine, antihistamines,
macrolides (eg erythromycin), amiodarone, phenothiazines, tricyclics).
ST segment:
-
Usually isoelectric.
elevated (>1mm) in infarction .
depressed (>0.5mm) in ischaemia .
T wave:
-
Normally inverted in aVR, V1 and occasionally V2.

Abnormal if inverted in I, II, and V4-V6.
Peaked in hyperkalaemia & flattened in hypokalaemia.
ECG additional points

Where to place the chest leads ?
V1: right sternal edge, 4th intercostal space
V2: left sternal edge, 4th intercostal space
V3: half-way between V2 and V4
V4: the patient's apex beat (p64); all subsequent leads are in the same horizontal plane as V4
V5: anterior axillary line
V6: mid-axillary line (V7: posterior axillary line)
Finish 12-lead ECGs with a long rhythm strip in lead II.
Disorders of ventricular conduction

Bundle branch block
Delayed conduction is evidenced by prolongation of QRS >0.12s. Abnormal conduction patterns

lasting <0.12s are incomplete blocks. The area that would have been reached by the blocked
bundle depolarizes slowly and late. Taking V 1 as an example, right ventricular depolarization is
normally +ve and left ventricular depolarization is normally -ve.
In RBBB, the following pattern is seen: QRS >0.12s, "RSR" pattern in V1, dominant R in V1, inverted T
waves in V1-V3 or V4, deep wide S wave in V6. Causes: normal variant (isolated RBBB), pulmonary
embolism, cor pulmonale.
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In LBBB, the following pattern is seen: QRS >0.12s, "M pattern" in V5, no septal Q waves, inverted T
waves in I, aVL, V5-V6. Causes: IHD, hypertension, cardiomyopathy, idiopathic fibrosis. NB: If there is
LBBB, no comment can be made on the ST segment or T wave.
Bifascicular block : is the combination of RBBB and left bundle hemiblock, manifest as an axis
deviation, eg LAD in the case of left anterior hemiblock.
Trifascicular block : is the combination of bifascicular block and 1st degree heart block.
Ventricular hypertrophy
There is no single marker of ventricular hypertrophy: electrical axis, voltage, and ST wave changes
should all be taken into consideration. Relying on a single marker such as voltage may be unreliable
as a thin chest wall may result in large voltage whereas a thick chest wall may mask it.
Suspect left ventricular hypertrophy (LVH) if the R wave in V6 >25mm or the sum of the S wave in V 1
and the R wave in V6 is >35mm .
Suspect right ventricular hypertrophy (RVH) if dominant R wave in V1, T wave inversion in V1-V3 or V4,
deep S wave in V6, RAD.
Other causes of dominant R wave in V1: RBBB, posterior MI, some types of WPW syndrome .
Causes of low voltage QRS complex: (QRS <5mm in all limb leads) Hypothyroidism, chronic
obstructive pulmonary disease (COPD), haematocrit (intra-cardiac blood resistivity is related to
haematocrit), changes in chest wall impedance (eg in renal failure, subcutaneous emphysema but
not obesity), pulmonary embolism, bundle branch block, carcinoid heart disease, myocarditis,
cardiac amyloid, adriamycin cardiotoxicity, and other heart muscle diseases, pericardial effusion,
pericarditis.
ECG abnormalities
Sinus tachycardia (Rate >100) : Causes: Anaemia, anxiety, exercise, pain, fever, sepsis, hypovolaemia,
heart failure, pulmonary embolism, pregnancy, thyrotoxicosis, beri beri, CO 2 retention, autonomic
neuropathy, sympathomimetics, e.g caffeine, adrenaline, and nicotine (may produce abrupt changes
in sinus rate, or other arrhythmia).
Sinus bradycardia (Rate <60) : Causes: Physical fitness, vasovagal attacks, sick sinus syndrome, acute MI
(esp. inferior), drugs (B-blockers, digoxin, amiodarone, verapamil), hypothyroidism, hypothermia,
intracranial pressure, cholestasis.
AF: Common causes: IHD, thyrotoxicosis, hypertension. (See before) .
A-V block :
-
1st degree : AV conduction is delayed so the PR interval is prolonged (> 0.20s). It rarely causes
symptoms.
2nd degree: In this condition dropped beats occur because some impulses from the atria fail to
conduct to the ventricles.
Mobitz type I : there is progressive lengthening of successive PR intervals, culminating in a
dropped beat. The cycle then repeats itself. It is usually due to impaired conduction in the
AV node itself.
Mobitz type II : the PR interval of the conducted impulses remains constant but some P
waves are not conducted (2:1or 3:1). it is usually caused by disease of the His-Purkinje
system and carries a risk of asystole.
Causes of 1st & 2nd degree: Normal variant, athletes, sick sinus syndrome, IHD, acute
carditis, drugs (digoxin, B-blockers).
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2011
3rd degree (complete): When AV conduction fails completely, the atria and ventricles beat
independently (AV dissociation). Ventricular activity is maintained by an escape rhythm arising in
the AV node or bundle of His (narrow QRS complexes) or the distal Purkinje tissues (broad QRS
complexes).
Causes of 3rd degree: Idiopathic (fibrosis), congenital, IHD, aortic valve calcification,
cardiac surgery/trauma, digoxin toxicity, infiltration (abscesses, granulomas, tumours,
parasites).
Q waves: Pathological Q waves are usually >0.04s wide and >2mm deep. Usually as sign of infarction,
and may occur within a few hours of an acute MI.
ST elevation: Normal variant (high take-off), acute MI, Prinzmetal's angina , acute pericarditis (saddleshaped), left ventricular aneurysm.
ST depression: Normal variant (upward sloping), digoxin (downward sloping), ischaemic (horizontal).
T inversion: In V1-V3: normal (Blacks and children), right bundle branch block (RBBB), pulmonary
embolism. In V2-V5: subendocardial MI, HOCM, subarachnoid haemorrhage, lithium. In V 4-V6 and aVL:
ischaemia, LVH, associated with left bundle branch block (LBBB).
NB: ST and T wave changes are often non-specific, and must be interpreted in the light of the clinical
context.
MI:
-
Within hours, the T wave may become peaked and ST segments may begin to rise.
Within 24h, the T wave inverts, as ST segment elevation begins to resolve. ST elevation rarely
persists, unless a left ventricular aneurysm develops. T wave inversion may or may not persist.
Within a few days, pathological Q waves begin to form. Q waves usually persist, but may resolve
in 10%.
The leads affected reflect the site of the infarct: inferior (II, III, aVF), anteroseptal (V 1-4),
anterolateral (V4-6, I, aVL), posterior (tall R and ST in V1-2).
"Non Qwave infarcts" (formerly called subendocardial infarcts) have ST and T changes without Q
waves.
Pulmonary embolism:
- Sinus tachycardia is commonest.
- There may be RAD, RBBB , right ventricular strain pattern (R-axis deviation. Dominant R wave and T
wave inversion/ST depression in V1 and V2. Leads II, III and aVF may show similar changes).
- Rarely, the SIQIIITIII pattern occurs: deep S waves in I, pathological Q waves in III, inverted T waves
in III.
Metabolic abnormalities:
-
Digoxin effect: ST depression and inverted T wave in V 5-6 (reversed tick). In digoxin toxicity, any
arrhythmia may occur (ventricular ectopics and nodal bradycardia are common).
Hyperkalaemia: Tall, tented T wave, widened QRS, absent P waves, "sine wave" appearance .
Hypokalaemia: Small T waves, prominent U waves.
Hypercalcaemia: Short QT interval.
Hypocalcaemia: Long QT interval, small T waves.
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Exercise ECG testing

The patient undergoes a graduated, treadmill exercise test, with continuous 12- lead ECG and blood
pressure monitoring.
Indications:
To help confirm a suspected diagnosis of IHD.

Assessment of cardiac function & exercise tolerance.
Prognosis following MI. Often done pre-discharge (if +ve, worse outcome).
Evaluation of response to treatment (drugs, angioplasty, coronary artery bypass grafting, CABG).
Assessment of exercise-induced arrhythmias.
Contraindications:
Unstable angina
Recent Q wave MI (<5 days ago)
Severe AS
Uncontrolled arrhythmia, hypertension, or heart failure.
Be cautious about arranging tests that will be hard to perform or interpret:

Complete heart block, LBBB
Pacemaker patients
Osteoarthritis, COPD, stroke, or other limitations to exercise.
Stop the test if:
Chest pain or dyspnoea occurs.

The patient feels faint, exhausted, or is in danger of falling.
ST segment elevation/depression >2mm (with or without chest pain).
Atrial or ventricular arrhythmia (not just ectopics).
Fall in blood pressure, failure of heart rate or blood pressure to rise with effort, or excessive rise in
blood pressure (systolic >230mmHg).
Development of AV block or LBBB.
Maximal or 90% maximal heart rate for age is achieved.
Interpreting the test:

A positive test only allows one to assess the probability that the patient has IHD. 75% with significant coronary
artery disease have a positive test, but so do 5% of people with normal arteries (the false positive rate is even
higher in middle-aged women, eg 20%). The more positive the result, the higher the predictive accuracy.
Down-sloping ST depression is much more significant than up-sloping, e.g 1mm J-point depression with downsloping ST segment is 99% predictive of 2-3 vessel disease.
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Bed side tests in chest medicine

Peak expiratory flow rate (PEFR) : is measured by a maximal forced expiration through a peak flow meter.
It correlates well with the forced expiratory volume in 1 second (FEV1) and is used as an estimate of
airway calibre. Peak flow rates should be measured regularly in asthmatics to monitor response to
therapy and disease control.
Pulse oximetry : allows non-invasive assessment of peripheral O2 saturation . It provides a useful tool for
monitoring those who are acutely ill or at risk of deterioration. On most pulse oximeters, the alarm is set at
90%. A PaO2 80% is clearly abnormal and action is required (unless this is normal for the patient e.g in
COPD).
Arterial blood gas (ABG) analysis :

Heparinized blood is taken from the radial, brachial, or femoral artery & pH, PaO2, and PaCO2 are
measured using an automated analyser.
Normal pH is 7.40 0.05.
A pH < 7.35 indicates acidosis & a pH > 7.45 indicates alkalosis.
What is the difference between metabolic & respiratory acidosis & alkalosis ? SIMPLE RULES
-
CO2 is an acidic gas (N: 4.5-6.0 kPa).
HCO-3 alkaline (N: 22-28 mmol/L).
1 changes in HCO-3 are termed metabolic, and of CO2 respiratory.
1 Look at the pH: is there an acidosis or alkalosis?

2 Is the CO2 abnormal? If so, is the change in keeping with the pH ( i.e if there is an acidosis, is
CO2 raised)? If so it is a respiratory problem. If there is no change, or an OPPOSITE one, then
the change is compensatory.
3 Is the HCO-3 abnormal, and if so, is the change in keeping with the pH? If so the problem is a
metabolic one.
An example
pH 7.05, CO2 2.0 kPa, HCO-3 8.0 mmol/L.
There is an acidosis, and the CO2 is low, and so is a compensatory change. The HCO-3 is low,
and is thus the cause; ie a metabolic acidosis.
37
Dr.Waleed Badr
2011
Acidosis
Metabolic
Alkalosis
HCO-3
Respiratory
pH
Lactic
acid
(shock,infection,hypoxia) .
Urate (renal failure) .
Ketones (D.M, alcohol) .
Salicylate poisoning .
pH CO2
Respiratory failure
pH HCO-3
Vomiting .
Burns .
K+ depletion (Diurectics) .
Ingestion of base .
pH CO2
A result of hyperventilation
CNS : stroke, subarachnoid
hge,meningitis.
Others
:
anxiety,
fever,
pregnancy, salicylate poisoning.
Normal PaO2 is 10.5-13.5 kPa.
Causes
of
Hypoxia
ventilation/perfusion
(V/Q)
mismatch
"the
commonest
cause",
hypoventilation, abnormal diffusion, right to left cardiac shunts.
Severe hypoxia is defined as a PaO2 < 8kPa .
Normal PaCO2 is 4.5-6.0 kPa.
PaCO2 is directly related to alveolar ventilation.
A PaCO2 < 4.5 kPa indicates hyperventilation and a PaCO2 > 6.0kPa indicates hypoventilation.
Type 1 respiratory failure is defined as PaO2 < 8 kPa and PaCO2 < 6.0 kPa, whereas type II respiratory
failure is defined as PaO2 < 8 kPa and PaCO2 > 6.0 kPa.
When to consider arterial blood gas (ABG) measurement

In these clinical scenarios:
Any unexpected deterioration in an ill patient.
Anyone with an acute exacerbation of a chronic chest condition.
Anyone with impaired consciousness.
Anyone with impaired respiratory effort.
Or if any of these signs or symptoms are present:
Signs of CO2 retention : bounding pulse, drowsy, tremor (flapping), headache, pink palms,
papilloedema .
Signs of hypoxia : cyanosis, confusion, visual hallucinations .
Or to monitor the progress of a critically ill patient:
Monitoring the treatment of known respiratory failure.
Anyone ventilated on ITU.
After major surgery.
After major trauma.
To validate measurements from transcutaneous pulse oximetry:
38
Pulse oximetry sometimes suffices when it is not critical to know PaCO2.
Dr.Waleed Badr
2011
Acute breathless (dyspnea) patient

Causes:
Wheezy:
Acute asthma.
Acute exacerbation of COPD.
Heart failure.
Anaphylaxis.
Stridor (upper air way obstruction):
Tumor or FB.
Acute epiglottitis.
Trauma e.g Laryngeal fracture.
Crepitations:
Heart failure.
Pneumonia.
Bronchiectasis.
Clear chest:
PE.
Metabolic acidosis e.g DKA.
Anemia.
Shock.
CNS causes.
Drugs e.g salicylates
Others:
Pneumothorax.
Pleural effusion.
Workup:
History
Rate of onset & severity of the breathlessness
H/O Associated cardiovascular symptoms (chest pain, palpitations, sweating and nausea) or
respiratory symptoms (cough, wheeze, haemoptysis, stridor) .
A previous history of repeated episodes of left ventricular failure, asthma or exacerbations of

COPD.
39
In the severely ill patient it may be necessary to obtain the history from accompanying relatives.
Dr.Waleed Badr
2011
In children, the possibility of inhalation of a foreign body or acute epiglottitis should always be
considered.
Clinical assessment :
Level of consciousness
Degree of central cyanosis
Evidence of anaphylaxis (urticaria or angioedema)
Patency of the upper airway
Ability to speak (in single words or sentences)
Cardiovascular status (heart rate and rhythm, BP and degree of peripheral perfusion).
NB.Pulmonary oedema is suggested by pink frothy sputum and bi-basal crackles, asthma or COPD by
wheeze and prolonged expiration, pneumothorax by a silent resonant hemithorax, and pulmonary
embolus by severe breathlessness with normal breath sounds. The peak expiratory flow should be
measured whenever possible. Leg swelling may suggest cardiac failure or, if asymmetrical, venous
thrombosis.
Investigations : ABG, CXR & ECG ( to confirm the clinical diagnosis).
Management : look chest pain
40
Dr.Waleed Badr
2011
Differential diagnosis of acute breathlessness

Condition
History
C/P
CXR
ABG
ECG
Pulmonary
oedema
Chest
pain,
palpitations,
orthopnoea,
cardiac history*
Central
cyanosis, JVP,
sweating, cool
extremities, pink
frothy
sputum
,basal crackles*
Cardiomegaly,
oedema/pleural
effusions*
PaO2
PaCO2
Sinus
tachycardia,
ischaemia*,
arrhythmia
pulmonary
embolism
Risk
factors,
chest
pain,
pleurisy,
syncope*,
dizziness*
Central
cyanosis, JVP*,
absence of signs
in
the
lung*,
shock
(tachycardia,
hypotension)
Often
normal
Prominent
hilar
vessels,
oligaemic
lung
fields*
PaO2
PaCO2
Sinus
tachycardia,
RBBB, S1Q3T3
pattern
T (V1-V4)
Acute severe
asthma
History
of
asthma,
asthma
medications,
wheeze*
Tachycardia,
pulsus
paradoxus,
cyanosis (late),
JVP *, peak
flow, wheeze*
Hyperinflation
only
(unless
complicated by
pneumothorax)*
PaO2
PaCO2
(PaCO2
extremis)
Sinus
tachycardia
(bradycardia in
extremis)
Acute
exacerbation
of COPD
Previous
episodes*,
smoker. If in
type
II
respiratory
failure may be
drowsy
Cyanosis,
hyperinflation*,
signs of CO2
retention
(flapping tremor,
bounding
pulses)*
Hyperinflation*,
bullae,
complicating
pneumothorax
or
PaO2
PaCO2 in type
II failure H+,
HCO3
in
chronic type II
failure
Normal, or signs
of right
ventricular
strain
Pneumonia
Prodromal
illness*, fever*,
rigors*, pleurisy*
Fever, confusion,
pleural
rub*,
consolidation*,
cyanosis
(if
severe)
Pneumonic
consolidation*
PaO2
PaCO2 (
extremis)
Tachycardia
Metabolic
acidosis
Evidence
of
DM or renal
disease, aspirin
or
ethylene
glycol
overdose
Fetor (ketones),
hyperventilation
without heart or
lung
signs*,
dehydration*, air
hunger
Normal
PaO2
normal
PaCO2, H+
Psychogenic
Previous
episodes,
digital or perioral
dysaesthesia
No cyanosis, no
heart or lung
signs,
carpopedal
spasm
Normal
PaO2 normal*
PaCO2, H+*
41
in
in
Dr.Waleed Badr
2011
Acute severe asthma
Presentation: acute breathlessness and wheeze.

History: Ask about usual treatment, previous attacks, if admitted to ICU.
Clinical picture:
Severe attack: Unable to complete sentences, respiratory rate > 25/min, pulse >110 beats/min, PEFR <
50% of predicted.
Life threatening attack: PEFR < 33% of predicted, silent chest, sweating, panic, speechless, using
accessory muscles, cyanosis, bradycardia, hypotension, confusion, coma.
Investigations: Peak expiratory flow rate (PEFR), ABG (high CO2, low O2 (<90%) + low pH), CXR, FBC & U&E.
Treatment:
Call for help .
Sit patient up & do not sedate.
ABC : Ensure patent airway, Give oxygen 100% & secure IV line .
Salbutamol (B2-agonist) 5 mg (or terbutaline 10 mg) plus ipratropium bromide 0.5 mg nebulized with
oxygen.
Hydrocortisone 100 mg IV or prednisolone 30 mg PO or both if very ill.
Monitor oxygen saturation (pulse oximeter), heart rate and respiratory rate. CXR to exclude
pneumothorax.
If still not improving (after 30 min), repeat salbutamol every 15min or 10mg continuously per hour &
give Hydrocortisone 100 mg IV or prednisolone 30 mg PO if not already given.
If still not improving, consider aminophylline (5 mg/kg IVI over 20 min) or give salbutamol IVI (3 20
ug/min).
NB.Dose of aminophylline is adjusted according to the individual patient e.g :
-
dose in : cardiac or liver failure, drugs that life of aminophylline e.g cimetidine, ciprofloxacin,
erythromycin & contraceptive steroids .
dose in : smoking, drugs that life e.g phenytoin, carbamazepine, barbiturates & rifampicin.
42
Dr.Waleed Badr
2011
If still not improving, consider transfer to ICU to intubate, give adrenaline and 500 mL colloid IVI.
Once patient is improving:
-
Wean and stop aminophylline over 12 24h.
Switch to inhaled B-agonist bronchodilator and steroids.
Continue to monitor PEFR with the above for 24h with rate > 75% of predicted or best with diurnal
variability < 25% (beware of early morning dips in PEFR).
Look for cause of acute exacerbation.
Acute exacerbation of COPD
Common in winter & triggered by viral or bacterial infections.

Presentations: cough, breathlessness or wheeze with exercise capacity.
History: ask about usual treatment (home oxygen), smoking and exercise capacity.
Investigations: PEFR, ABG, CXR, ECG, blood culture (if pyrexial) & sputum culture.
Management:
Look for the cause e.g. infection or pneumothorax.
Controlled oxygen
-
therapy :
Dont leave patients hypoxic. However,in some patients, who rely on their hypoxic drive to
breathe; too much oxygen may lead to a reduced respiratory rate and hypercapnia with a
consequent fall in conscious level.
In case of evidence of CO2 retention, start with 24 28 % O2. Reassess after 30 min.
Monitor the patient carefully.
Aim to raise O2 above 8.0KPa with a rise in CO2 < 1.5KPa.
In case there is no retention, use 28-40% O2 but still monitor and repeat ABG.
Nebulized bronchodilator (salbutamol 5mg/4h & ipratropium 500ug/6h).

Hydrocortisone 200mg IV & oral prednisolone 30-40mg.
Antibiotics if evidence of infection.
Physiotherapy to aid sputum expectoration.
If no response, consider IV aminophylline.
If no response, consider nasal intermittent positive pressure ventilation (NIPPV) delivered by a nasal
mask and a flow generator.
Consider intubation and ventilation if pH and CO2 .
43
Dr.Waleed Badr
2011
Consider respiratory stimulant drug e.g. doxapram (only for patients not suitable for mechanical
ventilation and as a short term measure only).
TTT of Stable COPD: Stop smoking, encourage exercise, proper nutrition, weight reduction and
influenza vaccination. Give short acting B2-agonist, ipratropium and corticosteroid inhalations
according to severity.
Consider long term oxygen therapy.
Surgery is indicated in selected cases e.g. recurrent pneumothorax or isolated bullous disease.
Assess social circumstances and support required. Identify and treat depression.
Air travel is hazards if O2 saturation is low, check availability of O2.
44
Dr.Waleed Badr
2011
Pneumonia
Definition: an infection of the lung parenchyma.

Incidence: 12 per 1000 adults & mortality rate is 10% .
Causative organisms:
Strept. pneumoniae (the commonest) 60-75% .
Mycoplasma pneumoniae 5-18% .
Others : staph.aureus, haemophilus influenza, legionella & chlamydia psittaci, G-ve bacilli e.g
pseudomonas (often hospital-acquired or immunocompromised) .
Symptoms : fever, rigors, malaise, anorexia, dyspnea, cough, purulent sputum, haemoptysis & pleuritic
chest pain.
Signs :
Fever, cyanosis, herpes labialis, confusion .
Tachypnoea, tachycardia, hypotension .
Signs of consolidation (diminished expansion, dull percussion note, tactile vocal fremitus/vocal
resonance, bronchial breathing) .
Pleural rub .
Severity :
Calculate the core adverse features CURB-65
score
Confusion .
Urea > 7mmol/L .
Respiratory rate 30/min .
BP < 90/60 .
Age 65 .
45
Score : 0-1 home treatment if possible; 2 hospital therapy; 3 severe pneumonia.
Dr.Waleed Badr
2011
Management :
A Adequate ventilation (may need intubation) .
B Oxygenation.
C Circulation IV line. Treat hypotension & shock
Investigations : CXR, ABG, FBC, U&E, LFT, CRP, blood culture, aspiration of pleural fluid for culture
& bronchoscopy (if immunocompromised)
Empirical antibiotics :
o
Cefuroxime 1.5g/8h IV + clarithromycin 500 mg/12h IVI .
If atypical :
Legionella : add levofloxacin + rifampicin .
Chlamydia : add tetracycline .
If hospital acquired/immunocompromised : gentamicin IV + antipseudomonal penicillin .
Intravenous fluids : may be required .
Analgesics : for pleuritic chest pain .
Some patients may need intubation & a period of ventilatory support .
Complications : Pleural effusion, empyema, lung abscess, respiratory failure, septicaemia, pericarditis,
myocarditis, cholestatic jaundice & renal failure .
46
Dr.Waleed Badr
2011
Tension pneumothorax
This is a medical emergency, requires immediate relief. Do not delay management for obtaining a CXR.
Causes:
1ry (Spontaneous) : esp.in young thin men.
2ry : to underlying lung disease e.g asthma, COPD, TB, pneumonia, lung abscess, lung fibrosis &
carcinoma .
Trauma, iatrogenic (subclavian CVP line insertion, pleural aspiration or biopsy, percutaneous liver
biopsy & +ve pressure ventilation).
Pathophysiology : Air drawn inside the pleural space with each inspiration has no route to escape
during expiration, pushing the mediastinum to the opposite side, kinking and compressing great veins.
Unless the air is rapidly removed, cardio respiratory arrest will occur.
Clinical picture:
Symptoms : may be asymptomatic or sudden onset of dyspnea and/or pleuritic chest pain.
Signs:
-
Tachycardia & hypotension .
Distended neck veins .
Reduced expansion, Hyper-resonance on percussion and diminished breath sounds on the

affected side.
Trachea deviated away from the affected side.
Investigations: CXR, ABG.
47
Dr.Waleed Badr
2011
Management: depends on whether it is 1ry or 2ry, size & symptoms
Aspiration of pneumothorax :
After infilterative anaesthesia, Insert a large bore (14 - 16 G) cannula (venflon) into the 2nd
intercostal space in the mid-clavicular line on the side of the suspected pneumothorax.
Connect the cannula to a 3-way tap and 50mL 0.9% saline. Aspirate up to 2.5 litres of air.
Request CXR to confirm resolution.if successful repeat CXR after 24h to exclude recurrence .
Advice to avoid air travel for 6 weeks after normal CXR. Diving should be permanently avoided.
If unsuccessful, insert an intercostal drain.
Chest (intercostal) drain :
Inserted in 4th 6th intercostal space, anterior to mid-axillary line .
Use a small tube unless blood/pus is also present.
May be removed 24h after the lung has re-expanded & air leak has stopped (i.e the tube stops
bubbling). This is done during expiration or a Valsalva manoeuvre.
If failed to re-expand lung (within 48h), suction or surgical intervention may be required
Arrange for surgical advice if :

Bilateral .
Lung fails to expand after intercostal drain insertion .
2 or more previous episodes on the same side.

History of pneumothorax on the opposite side.
48
Dr.Waleed Badr
2011
Headache D.D
A. Life- or Vision-Threatening
1. Subarachnoid hemorrhage : Extremely severe headache, stiff neck, conscious level; rarely, subhyaloid
hemorrhages seen on fundus examination, usually from a ruptured aneurysm.
2. Structural abnormality of the brain e.g tumor, aneurysm, AV malformation ( conscious level, signs of
ICT, or neurologic signs during, and often after, the headache episode).
3. Epidural or subdural hematoma (follows head trauma; altered level of consciousness; may produce
anisocoria.).
4. Infectious CNS disorder e.g meningitis, encephalitis, brain abscess (fever, stiff neck, conscious level,
photophobia, neurologic signs).
5. Giant cell arteritis (GCA) : Age >50 years, ESR & CRP, scalp tenderness, ..etc
6. Acute angle-closure glaucoma
7. Ocular ischemic syndrome
8. Malignant hypertension
9. ICT e.g Papilloedema & ICH (headaches usually worse in the morning & worsened by Valsalva) .
B. Others
Migraine
Cluster headache
Tension headache
Herpes zoster ophthalmicus : headache or periocular pain may precede the herpetic vesicles .
Sinus headache : may be a serious headache in diabetic patients and immunocompromised hosts
because mucormycosis may be responsible .
Vertebral artery dissection (neck pain & cerebellar/medullary signs) .
Cervical spine disease .
Pagets disease ( Alk phos)
Trigeminal neuralgia :
-
Brief attacks of severe paroxysmal & sharp pain (like an electric shock) lasting a few seconds that
start in the distribution of one of the divisions of the trigeminal nerve
Normal facial sensation
49
Dr.Waleed Badr
2011
Raeder paratrigeminal neuralgia :

-
Occurs in middle aged men
Severe unilateral headache with periocular pain in the distribution of the 1 st division of trigeminal
nerve .
Lasts from hours to weeks before it resolves spontaneously .
Associated with ipsilateral postganglionic horner syndrome .
Tolosa-Hunt syndrome .
Convergence insufficiency & Accomodative spasm .
Drugs e.g nitrates, CCB & Carbon monoxide poisoning .
50
Dr.Waleed Badr
2011
Coma
Definition: unarousable, unresponsiveness.

Causes:
Metabolic
Neurological
Drugs, poisoning e.g CO1, alcohol
Trauma .
Hypoglycaemia, Hyperglycaemia .
Infection
Hypoxia, CO2 narcosis (COPD)
Septicaemia .
Tumours .
Hypothermia .
Stroke .
Myxoedema, Addisonian crisis .
Epilepsy .
Hepatic/uraemic encephalopathy .
e.g
meningitis,
encephalitis .
Management of coma
Call for help.
ABC .
Consider intubation if GCS < 8.
Stabilize cervical spine.
Vital signs monitoring.
Level of consciousness (document).
Blood glucose in all patients; give 50 mL 50% dextrose IV immediately if presumed hypoglycemia.
Control seizures.
Consider IV glucose, IV thiamine (alcohol, Wernickes encephalopathy), IV naloxone (opiate
intoxication) and IV flumazenil (benzodiazepine intoxication if airway compromised).
Brief examination:
Signs of trauma e.g haematoma, laceration, fracture .
Signs of other diseases e.g. liver disease, DM .
Skin : for needle marks, cyanosis, pallor, .etc
Smell breath alcohol, hepatic fetor, ketosis, uremia .
Meningism, heart and lung, abdomen and rectum exam .
Eye examination (see below) .
Foci of infection e.g abscesses .
Examine for CNS asymmetry e.g tone, spontaneous movements, reflexes.
51
Dr.Waleed Badr
2011
Quick history from family, ambulance staff and bystanders.

Investigations: ABG, FBC, CXR, U&E, LFT, toxin screen, ethanol and drug levels, CT and lumbar
puncture, urine analysis: save the first few for drug levels, monitor the outflow and check for glucose
and ketones.
Mannitol 20% hydrocortisone in case of cerebral edema.
Monitor the neurological signs and coma scale.
General care of comatosed patients.
Eye examination in coma (don't dilate)

1. Eye opening (see glasgow coma score)
2. Blinking reflex in light coma, test fields with visual threat. No blink in 1 field suggests hemianopia &
contralateral hemisphere lesion .
3. Eye movements & Vestibulo-ocular reflex (dolls head maneuver or ice water calorics .
4. Pupil size: checked every few minutes during the early stages, particularly if trauma is the likely cause
localizing sign.
a) Fixed, dilated pupil :
Unilateral 3rd nerve palsy with transtentorial herniation.
Bilateral atropine or barbiturate poisoning .
b) Marcus Gunn pupil ON or chiasm damage, pit. Apoplexy

c) Pin point
Unilateral Horners syndrome.
Bilateral pontine haemorrhage, opiate poisoning
5. Fundus:
Papilloedma ICT.
Hemorrhage: subhyaloid & subarachnoid in Tersons syndrome.
Signs of other disease e.g HTN and DM.
52
Dr.Waleed Badr
2011
Glasgow coma scale
This gives a reliable, objective way of recording the conscious state of a person. It is used for initial
and continuing assessment. It also has value in predicting ultimate outcome. 3 types of response are
assessed
1) Best motor response:(6 grades) Obeying commands(6), Localizing response to pain (5), Withdrawal
to pain* (4), Flexor response to pain (decorticate posture)** (3), Extensor response to pain
(decerebrate posture)*** (2), No response to pain (1). Note that it is the best response of any limb
which should be recorded.
* omitted in some centers so GCS is 14 not 15 .
** Damage above the level of red nucleus in midbrain
*** damage below the level of red nucleus in midbrain
2) Best verbal response (5 grades): Oriented (5), Confused Conversation (4), Inappropriate speech (3),
Incomprehensive speech (2), None (1). Record level of best speech.
3) Eye opening (4 grades) : Spontaneous eye opening (4), Eye opening in response to speech (3), Eye
opening in response to pain (2), No eye opening (1).
An overall score is made by summing the score in the 3 areas assessed:
Severe injury (GCS 8).
Moderate injury (GCS 9 - 12).
Minor injury (GCS 13 - 15).
Primary scale (AVPU): is sometimes used in the initial assessment primary survey
53
A alert.
V responds to vocal stimuli (voice) .
P responds to pain.
U unresponsive.
Dr.Waleed Badr
2011
Meningitis
Organisms: Meningococcus or pneumococcus. Less commonly Haemophilus influenza; listeria; CMV;

cryptococcus or TB .
Clinical features :
Early : headache, leg pains, cold hands and feet, abnormal skin colour .
Later :
Signs of Meningism : neck stiffness, photophobia, kernigs sign (pain + resistance on passive knee
extension with hip flexed) .
conscious level & coma .
Seizures focal CNS signs opisthotonus .
Petechial rash (non blanching) .
Signs of septicaemia (capillary refill; DIC; BP) .
Investigations :
U&E, FBC, LFT, glucose, coagulation screen .
Blood culture & serology .
Lumbar puncture(LP): for opening pressure ( in meningitis) & CSF sample for microscopic
examination .
CSF PCR (in aseptic meningitis) .
CXR (for TB meningitis) .
Management :
A Adequate ventilation.
B Oxygenation.
C Circulation IV line.
Start antibiotics immediately :
54
< 55Y : Cefotaxime 2g/6h slow IV .
> 55Y : Cefotaxime + ampicillin 2g/4h IV (for listeria).
Aciclovir (if viral encephalitis suspected) .
If septicaemic signs :
o
Dont attempt LP .
Get help from critical care team .
Treat shock (if present) & careful monitoring .
If meningitic signs :
o
Dexamethasone 4-10 mg/6h IV (avoid if immunocompromised) .
If signs of ICP take to ITU & dont do LP .
Dr.Waleed Badr
2011
If no shock or ICP signs do LP .
If not sure , get senior help .
Subsequent therapy :
o
Cefotaxime 2g/8h IVI for 10 days ( dose in renal failure) .
Maintenance fluids .
Isolation for the 1st 24h.
If poor response, consider intubation & ventilation inotropic/vasopressor support .
Encephalitis
Organisms:
Viral : HSV-1&2, arboviruses, CMV, EBV, VZV, HIV, measles, mumps,rabies, japanese B encephalitis,
west nile virus, tick-borne encepahlitis .
Non-viral : any bacterial meningitis, TB, malaria, listeria, lyme disease, legionella, leptospirosis,
aspergillosis, cryptococcus, schistosomiasis .
Signs & symptoms: Confusion, coma, seizures, fever, headache, focal neurological signs history of
travel or animal bite .
Investigations:
U&E, FBC, LFT, glucose, coagulation screen .
Blood culture & serology .
CT (contrast-enhanced) or MRI :
-
Focal bilateral temporal lobe involvement HSV encephalitis
Meningeal enhancement meningoencephalitis .
Lumbar puncture (LP) & CSF PCR : CSF protein & lymphocytes and glucose
EEG
Management: mortality in untreated viral encephalitis is 70%
Symptomatic ttt e.g phenytoin for seizure .
Aciclovir 10 mg/kg/8h IV over 1h for 14 days .
Cerebral abscess
Causes: it may follows ear, sinus, dental of periodontal infection; skull fracture; congenital heart disease;
endocarditis; bronchiectasis .
Signs & symptoms: seizures, fever, signs of ICP & signs of sepsis elsewhere
Investigations: CT/MRI, WBC, ESR .
Management: referral to neurosurgery treat the source infection + treat ICP .
55
Dr.Waleed Badr
2011
Status epilepticus
Definition: Seizures lasting > 30min or repeated without intervening consciousness. Mortality & risk of
permanent brain damage with the length of attack.
Causes of seizures:
1. Idiopathic .
2. Genetic : e.g tuberous sclerosis .
3. Cerebrovascular disease : stroke, SOL, AV malformation .
4. Infections : encephalitis, cysticerosis, AIDS .
5. Inflammatory : sarcoidosis, SLE, PAN .
6. Metabolic : hyperglycaemia, hypoglycaemia, hyponatraemia, hypocalcaemia, liver failure, renal
failure .
7. Drugs : phenothiazines, tricyclics, benzodiazepines (withdrawal), alcohol (withdrawal), inadequate
anticonvulsant dose .
Management
Call for help.

A Adequate ventilation. Open & maintain the airway. Remove false teeth. Insert oral/nasal airway.
Intubate if necessary.
B 100% O2 + suction, as required
Protect from injury.
C Circulation. IV access and take blood sample for investigations .
Admit in ICU with vital signs monitoring.

Investigations: U&E, LFT, glucose, ABG, ECG, LP, EEG, CT, pulse oximeter, cardiac monitor, calcium,
toxicology screening if indicated & anticonvulsant levels.
Treatment:
Give thiamine 250 mg IV if alcoholism & malnourishment suspected.
IVI glucose 50% 50 mL if low glucose level .
IVI fluids (saline) if hypotensive .
56
Dr.Waleed Badr
2011
Control of seizures : Aim to terminate seizures in < 20min
Lorazepam :
-
2- 4 mg as a slow bolus ( 2 min) into a large vein.
if no response within 10min give a second dose.
Beware of respiratory arrest during the last part of the injection & Have full resuscitation
facilities around.
Alternatively use diazepam 10 mg IV over 2min;if needed, repeat at 5 mg/min, until seizures
stop or 20 mg given.
While waiting for this to work, prepare other drugs. If fits continue
Phenytoin infusion (18mg/Kg IVI at a rate of 50mg/min). Beware of hypotension and dont use in
case of bradycardia and heart block. Requires BP and ECG monitoring. If fits continue
Diazepam infusion (100mg in 500mL of 5% dextrose at about 40 mL/h). Monitor respiratory

function.
Dexamethasone 10 mg IV if vasculitis or cerebral edema possible.
General anesthesia.
As soon as seizures are controlled :
57
Start oral drugs .
Search for the cause .
Dr.Waleed Badr
2011
Stroke
Definition : ischemic infarction (or bleeding into) any part of the brain. It manifests by rapid onset (over
minutes) of focal CNS signs and symptoms (contralateral hemiplegia & sensory loss + homonymous
hemianopia) .
Causes:
1. Atherothromboembolism (e.g from carotid) .
2. Heart emboli (AF;IE;MI) .
3. CNS bleed (hypertension, trauma and aneurysm rupture).
Risk
factors:
hypertension,
smoking,
DM,
heart
disease
(AF,
valvular,
ischaemic)
&
hypercholesterolemia.
Management
Call for help.
Level of consciousness (document).
B Oxygenation.
Vital sign monitoring for hypertension, admit and control over days not hours.
Admission to stroke units for nursing/physio saves lives and is a great motivation.
Investigations:
Urgent CT/ MRI within a few days of stroke to differentiate hemorrhagic from ischemic if
considering anticoagulation.
Pointers to hemorrhagic strokes are meningism, severe headache, and coma within hours.
Pointers to ischemic strokes are carotid bruit, AF and past TIA.
NB1. TIA : sudden onset of focal CNS signs (resolve within few minutes) due to temporary occlusion, usually
by emboli, of part of cerebral circulation .
NB2 : carotid bruit may signify stenosis (>30%), often near the internal carotid origin. It is heared best behind
the angle of jaw .
Other investigations: FBC, CXR, ECG, ESR, U&E, lipids, blood glucose, clotting tests, echo, carotid
doppler & carotid angiography .
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Dr.Waleed Badr
2011
Treatment:
Unless there is strong suspicion of CNS bleeding, acute aspirin (300mg/24h PO) has a worthwhile
effect.
Nil by mouth if swallowing is a problem.
Maintain hydration. Dont over hydrate (cerebral edema).
Monitor and treat BP.
If cerebellar hemorrhage possible, refer for immediate evacuation.
Turn regularly and keep dry (consider catheterization) to stop bed sores.
Passive limb movements, subcutaneous heparin and compressing stocking (DVT prophylaxis).
Emotional support and rehabilitation.
NB. some randomized trials suggest thrombolysis with alteplase within 3h of onset of symptoms might
decrease risk of adverse outcome. These hospitals have CNS thrombolysis teams with a dedicated
imaging service on 24h call. Howerever, this is still not recommended yet in the UK.
Prevention of stroke :
1. Control risk factors .
2. Exercise ( HDL) .
3. Life long anticoagulants " for those with rheumatic or prosthetic heart valves on lt side" .
4. Aspirin 75 mg/day for life .
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Dr.Waleed Badr
2011
Intracranial pressure (ICP)
Normal ICT : 0-10 mmHg.

Causes :
Tumours (1ry or metastatic) .
Hydrocephalus .
Head injury .
Cerebral oedema .
Brain haemorrhage (any type) .
Status epilepticus .
Infection : meningitis, encephalitis,brain abscess .
Signs & symptoms :
Headache, vomiting nausea .
Deterioration of consciousness : drowsiness; irritability;seizures; coma
pulse , BP (cushings response) & Cheyne-Stokes respiration .
Ophthalmic signs :
-
VA & peripheral visual field loss .
Pupil changes (constriction 1st, later dilatation) .DONT DILATE .
Papilloedema (NB. There is loss of previous spontaneous venous pulsation,if preserved exclude
papilloedema ) .
Investigations :
U&E, FBC, LFT, glucose, serum osmolarity, clotting, blood culture, CXR .
CT head & Lumbar pucture (opening pressure) .
Management :
A Adequate ventilation (intubate if needed)
B Oxygenation.
Correct hypotension & treat seizures .
Brief history & examination .
Elevate the head of the bed 30- 40.
Osmotic agents e.g mannitol 20% 1-2g/kg IV over 10-20 min (5mL/kg) .clinical effect is seen after
20 min and lasts for 2-6h (Aim for serum osmolarity 300 mosmol/kg) .
Corticosteroids e.g dexamethasone 10 mg IV then 4 mg/6h IV/PO (if cerebral oedema) .
Fluid restriction to < 1.5L/d .
Close monitoring & monitor ICP .
Search for a cause and treat exacerbating factors e.g hyperglycaemia, hyponatraemia .
Refer to neurosurgeon for definitive treatment if possible .
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Dr.Waleed Badr
2011
Hypoglycemic coma
Glucose level < 3.6 mmol/L sympathetic activity cold & sweaty skin.
Glucose level < 2.6mmol/L neuroglycopenia confusion & slurred speak.
Glucose level < 1.5mmol/L Coma.
Management :
Call for help .

ABC .
Level of consciousness .
Vital sign monitoring (sweating, pulse , seizures).
Blood sample (gluco-sticks) "glucose oxidase strips".
Treatment:
Give 200 300 mL of 10% dextrose IV (20-30g) OR
Glucagon 1mg IM (if no IV access). It will not work in drunk patients.
Once conscious, give sugary drinks & a meal.
Give IV Thiamine 1-2 mg/kg if there is malnutrition or suspicion of alcohol.
If history of oral hypoglycemic ttt is +ve admission to the hospital to give 10% glucose over 1-2
hour to overcome another attack.
Diabetic ketoacidosis (DKA)

DKA coma only occurs in type I D.M (IDDM) ; it may be the mode of presentation.
Signs and symptoms: Gradual drowsiness, vomiting, dehydration, abdominal pain, polyuria,
polydepsia, lethargy, anorexia, ketotic breath, coma .
Precipitating factors: infection, surgery, MI, chemotherapy, non-compliance, or wrong insulin dose.
Investigations: The diagnosis requires hyperglycaemia + ketosis + metabolic acidosis (pH < 7.3)
Blood : blood sample (gluco-sticks) "glucose oxidase strip", lab glucose , U&E, HCO3, osmolarity,
ABG, FBC .
61
Urine for ketones . ECG to exclude silent MI.
Dr.Waleed Badr
2011
Management:
Call for help.
ABC .
Level of consciousness.
Vital sign monitoring.
Fluid replacement for correction of Dehydration : dehydation is more lethal than hyperglycemia, so
its correction takes precedence.
-
IV access and start fluid (0.9% saline IVI) replacement immediately.
Give 1L stat, then 1L over the next hour, 1L over 2h, 1L over 4h, then 1L over 6h.
Use dextrose 5% when blood glucose is < 10 mmol/L.
Use saline more cautiously in elderly and heart failure patients.
Monitor CVP (to guide fluid therapy) .
NG tube only if nauseated/vomiting/unconscious.
Insulin sliding scale via IVI pump :

Add 50 U soluble insulin to 50 ml saline in a syringe (1U/ml)
-
Check plasma glucose: usually > 20mmmol/L ; if so give 4 8 U soluble insulin IV / h .
Aim for a fall in glucose of 5 mmol /L per h.
Dont stop the pump before routine SC insulin has been started .
If No pump, load with 20U IM, then give 4-6 U/h IM while glucose is > 10mmol/L (then to 2hourly) .
K+ replacement (KCL 20 - 40mmol/L of IV fluid) N K+ : 3.5-5 mmol/L

-
During DKA, the total body K+ is low because of osmotic diuresis, but the serum K + conc. is
raised because of the lack of insulin action, which allows K+ to shift out of the cells to
extracellular fluid, so hyperkalaemia.
During insulin treatment, K+ is shifted into the cells, which may lead to profound hypokalaemia
& dangerous irregularities in heart rate if not treated, therefore, continuous observation of the
heart rate is recommended, as well as repeated measurement of K + levels & addition of Kcl to
IV fluids depending on blood K+ levels .
Dont add K+ to the first bag .
Monitor urine output hourly;start adding K+ when urine flows at > 30ml/h .
Check U&Es hourly initially and replace as required.
NB : less K+ will be needed in renal failure or oliguria .
Monitor potassium, glucose and HCO3 hourly initially.
Urinary catheter if no urine passed for > 4h.
Treat infection if present.
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Dr.Waleed Badr
2011
Give LMW heparin 5000U/8h SC until mobile.
Change to SC insulin when ketones are 1+ and eating.
If acidosis is severe (pH < 7), give IV bicarbonate after discussing with your senior because of its
effects on Hb -dissociation and cerebral circulation.
If cerebral edema occurs, consider giving mannitol and hydrocortisone.
Hyperglycemic hyperosmolar non ketotic coma (HONK)
Typically those with type II DM (NIDDM) are at risk of this.

The history is longer (e.g. 1wk), old patient, presenting for the 1 st time .
There is marked dehydration and glucose > 35 mmol/L.
Acidosis is absent (no switch to ketone metabolism).
Occlusive events may occur e.g focal CNS signs, DIC, DVT (so fully heparinize).
Treatment:
63
Rehydration with 0.9% saline IVI over 48h at 1/2 the rate used on DKA.
Wait an hour before giving insulin, it may not be needed. If needed, give 1U/h .
K+ replacement (when urine starts to flow) .
Heparin administration risk for thrombosis.
Look for the cause e.g. MI or infection.
Dr.Waleed Badr
2011
Thyroid emergencies
Thyroid function tests (TFTs)

The hypothalamus secretes thyrotrophin releasing hormone (TRH which stimulates production of
thyroid stimulating hormone (TSH) from the anterior pituitary. TSH production and release of
thyroxine (T4) and triiodothyronine (T3) from the thyroid, which exert negative feedback on TSH
production.
The thyroid produces mainly T4, which is 5-fold less active than T3. 85% of T3 is formed from peripheral
conversion of T4.
Most T3 and T4 in plasma is protein bound, mainly to thyroxine-binding globulin (TBG). The unbound
portion is the active part. T3 and T4 cell metabolism, via nuclear receptors, and are thus vital for
growth and mental development. They also catecholamine effects.
Thyroid hormone abnormalities are usually due to problems in the thyroid gland itself, and rarely
caused by the hypothalamus or the anterior pituitary.
Basic tests
Measurement of free T4 and T3 levels is more useful than total T4 and T3 levels as the latter are
affected by TBG. Total T4 and T3 are when TBG is and vice versa. Free T3 and T4 levels are
unaffected.
TBG is in pregnancy, oestrogen therapy (HRT, oral contraceptive pill) and hepatitis. TBG is in
nephrotic syndrome and malnutrition (protein loss), drugs (e.g androgens, corticosteroids, phenytoin),
chronic liver disease and acromegaly.
Hyperthyroidism suspected: Ask for T3, T4, and TSH. In hyperthyroidism, all will have TSH (except for
the rare phenomenon of a TSH-secreting pituitary adenoma). Most have T4, but ~1% have only
T3.
Hypothyroidism suspected or monitoring replacement treatment: Ask for only T4, and TSH. Measuring
T3 does not add any extra information.
Interpretation of tests :
If TSH & T4
If TSH & normal T4
If TSH & T4
If TSH & T4 or T3
If TSH & normal T4 & T3
If TSH & T4 & T3
If normal TSH & T4 abnormal
64
:Primary hypothyroidism
:Subclinical hypothyroidism
: TSH secreting tumour, or thyroid hormone resistance
:Hyperthyroidism
:Subclinical Hyperthyroidism
:Pituitary disease
:Hormone-binding problems e.g prgnancy; thyroidbinding globulin; amiodarone; pituitary TSH tumour .
Dr.Waleed Badr
2011
Hyperthyroid crisis (thyrotoxic storm)

Definition : uncommon medical emergency more often seen in patients with Graves' disease caused
by an exacerbation of hyperthyroidism
Signs & symptoms :
More in females (4:1) .
Hyperpyrexia (>41oC) & dehydration .
Tachycardia (>140bpm AF or other arrythmia), hypotension & congestive heart failure .
Diarrhea, vomiting, Abdominal pain (exclude surgical causes) .
Agitation, confusion & coma .
Precipitated by : infection, recent trauma, MI or stroke, withdrawal of or non-compliance with antithyroid medication, recent thyroid surgery or radioiodine .
Investigations :
Investigations for any underlying precipitant .
Thyroid function tests : T3, T4, TSH "Don't wait for test results if urgent treatment is needed"
ECG , CXR & ABG .
Management : aimed at counteract peripheral effects of thyroid hormones, inhibit thyroid hormone
synthesis & treat systemic complications .
Treatment of precipitating cause e.g any suspected infection .
Resuscitation : IVI 0.9% saline, 500ml/4h (Adjust IV fluids as necessary;ideally guided by CVP). NG
tube if vomiting .
Beta blockers (propranolol 40 mg/8h PO or 1 mg over 1min IV ) unless contraindicated e.g

asthma & poor cardiac output. Use ultra-short acting B-blockers e.g IV esmolol if propranolol is
contraindicated .
Antithyroid drugs :
Carbimazole 15-25 mg/6h PO; after 4h give Lugols solution 0.3 mL/8h PO well-diluted in
water for 1wK to block thyroid .
Hydrocortisone Na succinate 100 mg/6h IV or dexamethasone 4 mg/6h PO (blocks T4 to T3

conversion) .
For severe agitation, Sedate with chlorpromazine 50mg PO/IM. Monitor BP .
Cool with tepid sponging paracetamol .Avoid aspirin which can T4 .
High-dose digoxin e.g 1mg over 2h IVI : may be needed to slow the heart . Cardioversion will not
be effective for AF until the patient is euthyroid .
Further thyroid management will depend on the progress of each individual patient & must be
under the care of an endocrinologist.
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Dr.Waleed Badr
2011
Myxoedema coma
Signs & symptoms :
Hypothyroid, > 65yrs, hypothermia, hyporeflexia, glucose, bradycardia.
Coma & seizures (may have been psychotic myxoedema madness just before the coma) .
May be associated with radioiodine, thyroidectomy or signs of hypopituitarism .
Goitre, cyanosis, BP (cardiogenic), Heart failure.
Management : (preferably on intensive care)
Take blood for T3, T4, TSH, FBC, U&E .
High flow O2 if cyanosed.
Correct any hypoglycaemia .
T3 5-20 ug/12h IV slowly with caution; you may precipitate manifestations of ischaemic heart
disease. Alternatively give Levothyroxine .
Hydrocortisone 100 mg/8h IV, if pituitary hypothyroidism is suspected .
IVI 0.9% saline. Be sure to avoid precipitating LVF .
Treat any suspected infection, heart failure & hypothermia .
Addisonian crisis
Signs & symptoms :
Endocrinal shock & Hypoglycaemia .
Precipitated by infection, trauma, surgery .
Management : if suspected, treat before biochemical results
Take blood for cortisol & ACTH if possible .
Hydrocortisone Na succinate 100mg/6h IV .
IV fluids e.g 0.9% saline (as guided by clinical state)
Monitor blood glucose : Glucose IV may be needed if hypoglycaemia .
Treat any infection present .
Change to oral steroids after 72h if patients condition good .
Search for & treat the underlying cause .
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2011
Hypopituitary coma
Signs & symptoms :
Hypothermia , refractory hypotension septic signs without fever associated with short stature or
loss of axillary/pubic hair gondal atrophy.
Headache, ophthalmoplegia, consciousness, hypoglycaemia .
Investigations :
Take blood for cortisol, T4, TSH, ACTH & glucose dont wait for results & start ttt .
Pituitary fossa CT/MRI
Management :
Hydrocortisone Na succinate 100 mg IV/6h .
Only after hydrocortisone begun, liothyronine 10 ug/12h PO or 5-20 ug/12h .
Prompt surgery is needed if the cause is pituitary apoplexy .
Pheochromocytoma
Pheochromocytoma is a rare catecholamine-producing tumour of the adrenal medulla.
Signs & symptoms :
Pallor, pulsating headache, malignant hypertension.
LVF, ST segment, VT & cardiogenic shock .
Management :
Phentolamine 2-5 mg IV .repeat to maintain safe BP .
When BP controlled, give phenoxybenzamine 10 mg/24h PO ( by 10 mg/d as needed, up to 30

mg) .
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Surgery is usually done electively after 4-6 wks .
Dr.Waleed Badr
2011
Acute GIT bleeding

GIT bleeding can be divided into:
1. Upper GI bleeding (above the ligament of Treitz)
2. Lower GI bleeding (below the ligament of Treitz)
Upper GIT bleeding

Causes:
1. Esophagus
2. Stomach
3. Duodenum
4. Coagulopathy
Esophagitis
Esophageal varices
Esophageal cancer
Mallory Weiss tear (mucosal tear at gastro-esophageal junction due to retching)
Gastric ulcer (40%)
Gastritis
Gastric cancer
Duodenal ulcer
Aortoenteric fistula (if previous aortic graft)
Drugs (alcohol, aspirin, NSAIDS, thrombolytics & anticoagulants)
Renal disease
Liver disease
Symptoms:
Hematemesis (vomiting of blood) : frequency, volume of blood
Melena (black tarry stool) : usually due to upper GI bleeding. Occurs when blood comes in contact
with hydrochloric acid in the gut. Only need > 50 ml of blood loss .
Hematochezia (bright red or maroon rectal bleeding) : Usually a sign of a lower GI bleed & rarely
seen unless the patient is having a very large, brisk upper GI bleed ( > 1000 ml) .
Postural dizziness, fainting, abdominal pain, dysphagia.
Chest pain, dyspnea & syncope .
Signs:
Cool & clammy skin
Vital signs :
Pulse : tachycardia .
Bl.P : hypotension & postural changes
Urine output & JVP :
Jaundice (biliary colic + jaundice + melaena suggests haemobilia) .
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2011
Management:
Assess whether patient is in shock
Cool and clammy.
Pulse > 100 bpm.
Systolic BP < 100mm Hg.
JVP < 1cm H2O.
Urine output < 30mL/h.
If not shocked:
Insert 2 big cannulae (14-16G), start slow saline IVI (to keep lines patent), check bloods & monitor vital
signs + urine output.
If shocked:
Protect airway : endotracheal intubation to prevent aspiration in massive bleeding or mental status
change .
High flow oxygen.
Insert 2 big cannulae.
Draw bloods for laboratory investigations & Cross match 6 units.
Rapid IV crystalloid infusion (normal saline or ringer lactate) up to 1L.
If still shocked, give group specific blood or group O Rh ve until cross matching is done (transfuse
as dictated by haemodynamics) .
NB.Avoid saline in patients with decompensated liver disease (ascites, peripheral oedema)
Correct clotting abnormalities (Vit k, FFP, platelet concentrates).
Set up CVP line to guide fluid replacement.
Catheterize and monitor urine output (aim for > 30 mL/h).
Vital signs monitoring every 15min until stable,then every 1h.
Notify surgeons of all severe bleeds.
Keep NPO .
Nasogastric tube placement (Sengstaken-Blakemore tube) : if massive or continuous bleeding for

aspiration of stomach contents & lavage (may be useful in assessing the activity and severity of
upper GI bleeding and in clearing the blood and clots of stomach before endoscopic examination)
ECG : looking for signs of ischemia or infarct (inferior MI) .
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2011
Endoscopy :
Can identify the source of bleeding, estimate the risk of rebleeding +/- therapeutic intervention to
achieve hemostasis ( e.g varices ligation therapy, varices injection therapy, injection therapy for
ulcer bleeding, destroying visible vessel by heat probe thermocoagulation, hemoclip or laser) .
Should be performed early after volume resuscitation has been achieved
Risks for rebelling include spurting or oozing, visible vessel or fibrin clot
NB. If site of bleeding is not identified on endoscopy; bleeding site has healed; nose bleed
(swallowed blood); site distal to 3rd part of duodenum
NB. UGI barium studies are contraindicated in the setting of an acute UGI bleed as it will interfere with
subsequent endoscopy or surgery if needed .
Proton pump inhibitors e.g omeprazole 40 mg PO to prevent stress ulcers .
Eradicate Helicobacter pylori if +ve .
Prognosis :
80% of UGIB stop spontaneously. Mortality is approximately 10%
Care for rebleeds: very serious event. 40 % of those patients will die.
Poor prognostic signs : Rockall scoring system
70
Age > 60 .
Signs of shock ( pulse > 100 bpm, SBP < 100 mmhg) .
Significant co-morbidity e.g renal/liver failure or malignancy .
Bleeding diathesis .
Dr.Waleed Badr
2011
Lower GIT bleeding

Causes:
1. Small Bowel
2. Colon
3. Perianal
4. Coagulopathy
Neoplasm
Mockers diverticulum
Crohns disease
Aortoenteric fistula
Vascular problems
Diverticuli
Angiodysplasia
Inflammatory bowel disease (ulcerative colitis & crohn's disease) .
Ischemic gut
Neoplasm
Infectious
Hemorrhoids
Fissure
Fistula
Drugs, renal disease, liver disease
History:
1. Volume:
Occult blood loss is associated with colon cancer
Small amounts on the tissue or surface of stool associated with hemorrhoids or fissures
Hematochezia
Massive blood loss likely due to either diverticulosis, angiodysplasia, or occasionally aortoenteric
fistula
Must always rule out a massive UGIB! Usually site is distal to the pylorus
2. Symptoms associated with inflammatory bowel disease or any other systemic disease
3. Constitutional symptoms or recent change in bowel habits suggesting a malignancy
4. Food intake which may give a false impression of rectal bleeding beets or iron
5. Infectious symptoms or recent ingestion of any poorly cooked meat
Signs: (look UGIT bleeding)

Management
Volume resuscitation and management of ABCs should be the first priority for these patients. If the patient is
hemodynamically stable with low volume blood loss then the patient can be followed clinically with volume
resuscitation and blood as needed. Once the bleeding has settled, the patient can be prepped for
colonoscopy and the cause of bleeding determined.
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2011
If patients are hemodynamically unstable with rapid rates of blood loss other investigations can be
arranged.
1. Tagged red blood cell scan (TRBC scan)
RBCs labeled with 99mTc remain in circulation for as long as 48 hours and extravasate into the bowel
lumen with active bleeding
Non-invasive, but only localized bleeding to areas of the abdomen.
It is accurate in identification of the location of the bleeding in 80% of cases
Bleeding rates as low as 0.1 ml/minute can be detected
Could be used as screening before arteriography
2. Angiography
Allows rapid localization and potential therapy of GI bleeding when bleeding rates exceed 0.5
ml/minute .
Identifies site in 60% of bleeds, 50-80% are a result of bleeding from the superior mesenteric artery
Allows for therapeutic intervention (When bleeding lesion is found, intra-arterial infusion of
vasopression or embolization of bleeding artery can stop bleeding)
3. Colonoscopy
Is not useful in the setting of ongoing bleeding so there is no urgent indication.
Best performed in patients whose condition has clinically stabilized and who can tolerate an
adequate bowel purge
Barium enemas may detect proximal lesions not detected by colonoscopy, but interferes with
subsequent angiography and colonoscopy, thus there is no indication for urgent use.
4. Surgery : Consider in patients with ongoing bleeding and hemodynamic instability but with failure of
other therapeutic maneuvers.
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2011
An approach to bleeding disorders

There are 3 sets of questions to be answered:
1) Is there an emergency? needing immediate resuscitation or senior help?

Is the patient about to exsanguinate (shock, coma)?
Is there hypovolaemia (postural hypotension, oliguria)?
Is there CNS bleeding (meningism, CNS, and retinal signs)?
2) Why is the patient bleeding?

Is bleeding normal, given the circumstances (e.g surgery, trauma, parturition), or does the patient
have a bleeding disorder?
Is there a secondary cause e.g drugs (warfarin), alcohol, liver disease, sepsis?
Is there unexplained bleeding, bruising, or purpura?
Past or family history of excess bleeding e.g during trauma, dentistry, surgery?
Is the pattern of bleeding indicative of vascular, platelet, or coagulation problems ? Are
venepuncture or old cannula sites bleeding (DIC)? Look for associated conditions (e.g with DIC).
Is a clotting screen abnormal? Check FBC, platelets, PT, APTT and thrombin time. Consider D-dimers,
bleeding time, and a factor VIII assay.
3) In the case of a bleeding disorder, what is the mechanism?

Coagulation tests (Sodium citrate tube; false results if under-filled or over-filled)
1. Prothrombin time (PT) & International normalized ratio (INR):
PT is the time it takes plasma to clot after addition of tissue factor (obtained from animals) . this
measures the quality of
of the extrinsic pathway (as well as the common pathway) of
coagulation i.e PT tests for abnormalities in factors I,II,V,VII,X . Normal range for PT is usually 11-16
seconds
INR : is the ratio of a patient's prothrombin time to a normal (control) sample. (INR was devised to
standardize the results, as The result (in seconds) for a prothrombin time performed on a normal
individual will vary according to the type of analytical system employed. This is due to the
variations between different batches of manufacturer's tissue factor used in the reagent to
perform the test) .
They are used to determine the clotting tendency of blood, in the measure of warfarin dosage,
liver damage & vitamin K status .
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The speed of the extrinsic pathway is greatly affected by levels of factor VII in the body. Factor VII
has a short half-life and its synthesis requires vitamin K. The prothrombin time can be prolonged as
a result of deficiencies in vitamin K, which can be caused by warfarin, poor factor VII synthesis
(due to liver disease) or increased consumption (in disseminated intravascular coagulation) .
A high INR level such as INR=5 indicates that there is a high chance of bleeding, whereas if the
INR=0.5 then there is a high chance of having a clot. Normal range for a healthy person is 0.91.3
and for people on warfarin therapy, 2.03.0, although the target INR may be higher in particular
situations, such as for those with a mechanical heart valve, or bridging warfarin with a lowmolecular weight heparin (such as enoxaparin) perioperatively.
2. Activated partial thromboplastin time (aPTT) :
aPPT measures the quality of
of the intrinsic pathway (as well as the common pathway) of
coagulation i.e aPPT tests for abnormalities in factors I,II,V,VIII,IX,X,XI,XII . Normal range for aPPT is
usually 35-45 seconds .
Prolonged by: heparin treatment, haemophilia, DIC, liver disease.
3. Thrombin time (TT) :
TT is the time it takes a clot to form in the plasma of a blood sample to which an excess thrombin
has been added. This measures abnormality in the conversion of fibrinogen to fibrin . Normal
range for TT is usually 10-15 seconds .
Prolonged by : heparin treatment, DIC, fibrinogen deficiency /abnormality (dysfibrinogenaemia) .
D-dimers:
These are a fibrin degradation product (FDP), released from cross-linked fibrin during fibrinolysis i.e
tests the fibrinolytic system .
in DIC, or in the presence of venous thromboembolism : deep vein thrombosis (DVT) or

pulmonary embolism (PE).
D-dimers may also be in inflammatory states e.g with infection or malignancy.
Bleeding time:
This is a test to assess platelet function (N platelet count : 150.000 400.000)
Carried out by making two small incisions into the skin of the forearm. The time it takes for
bleeding to stop (as thus the time it takes for a platelet plug to form) is measured.
Normal time <7 minutes.
Prolonged bleeding time occurs in thrombocytopenia, disseminated intravascular coagulation

(DIC) .
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Antiplatelets e.g Aspirin and other cyclooxygenase inhibitors can prolong bleeding time
significantly. While warfarin and heparin have their major effects on coagulation factors .
NB: This test is seldom performed now, as results are very operator dependent.
Disorder
Heparin
DIC
Liver disease
Platelet defect
Vit K deficiency
Haemophilia
Von willebrand's
INR
--
-----
aPTT
--
TT
---------
Platelet count
--
---------
Bleeding time
--
----
Management :
depends on the degree of bleeding. If shocked, resuscitate. If bleeding continues, in the presence of a
clotting disorder, or a massive transfusion, discuss the need for fresh frozen plasma (FFP) and platelets with a
haematologist. In ITP , steroids IV immunoglobulin may be used. Especially in pregnancy , consult an
expert. Is there overdose with anticoagulants? In haemophiliac bleeds, consult early for coagulation factor
replacement. Never give IM injections.
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Drugs that affect haemostasis
1)
2)
3)
4)
5)
Coagulants & haemostatics : e.g Vit.K , Ethamsylate (Dicynone)

Anticoagulants : heaprin & warfarin (Marevan) see below
Antiplatelets (antithrombotics) : Aspirin, Clopidogrel .
Fibrinolytics : streptokinase & tissue plasminogen activator (tPA) .
Antifibrinolytics : Tranexamic acid & Aminocaproic acid
Anticoagulants
Indications :
1. Therapeutic: Venous thromboembolic disease: DVT and PE.
2. Prophylactic:
Prevention of DVT/PE in high-risk patients e.g post-op.
Prevention of stroke e.g in chronic AF or prosthetic heart valve.
Preparations :
Heparin
Route & dosage

Examples
Mechanism
Characteristics
1. Low molecular weight heparin

(LMWH)
SC
Dalteparin, enoxaparin, tinzaparin
Inactivates factor Xa (but not
thrombin) .
It
has
replaced
unfractionated
heparin (UFH) as the preferred option
in the prevention and treatment of
venous thromboembolism and in
acute coronary syndrome (longer T1/2 ,
2. Standard (Unfractionated heparin)

(UFH)
IV or SC
Binds antithrombin III (an endogenous
inhibitor of coagulation) . increasing its
ability to inhibit thrombin, factor Xa,
and Ixa
Rapid onset and has a short T1/2.
Monitor and adjust dose with APTT .
more
predictable
response
&
no
laboratory monitoring is usually required)
S/E
Bleeding (e.g at operative site, gastrointestinal, intracranial),

Heparin induced thrombocytopenia (HIT),
Osteoporosis with long-term use.
NB. HIT and osteoporosis are less common with LMWH than UFH. Beware hyperkalaemia.
C/I
Antidote
76
Bleeding disorders, previous HIT, peptic ulcer, cerebral haemorrhage, severe

hypertension, neurosurgery.
Protamine sulphate IV (usually 1 mg IVI is required to counteract 100 units heparin)
Dr.Waleed Badr
2011
Warfarin
Route & dosage
Mechanism
CI
Antidote
Oral once daily as long-term anticoagulation.

The therapeutic range is narrow, varying with the condition being treated
& is measured as a ratio compared with the standard INR.
Inhibits the reductase enzyme responsible for regenerating the active form of
vitamin K (utilized in formation of clotting factors by the liver), producing a state
analogous to vit K deficiency.
Peptic ulcer, bleeding disorders, severe hypertension, pregnancy
(teratogenic). Use with caution in the elderly and those with past GI bleeds.
Vitamin K " 5-10 mg I.V" .
Prothrombin complex concentrate (50 units/kg) or fresh frozen plasma (FFP)
Vitamin K may take several hours to work, and can cause prolonged resistance when
restarting warfarin, so should be avoided if possible when long-term anticoagulation is
needed. Prothrombin complex concentrate contains a concentrate of Factor IX, and
provides a more complete and rapid reversal of warfarin than FFP.
Beginning therapeutic anticoagulation

For treatment of venous thromboembolism, LMWH or UFH are used initially, and warfarin is given in
combination usually from day 1. Heparin should be continued until INR has reached target therapeutic
range and until day 5, as warfarin has an initial prothrombotic effect.
Give UFH 5000iu IV bolus over 30min. (10.000iu in severe PE).
Then Add 25,000iu to 50mL 0.9% saline (=500iu/mL) in a syringe pump .
Start infusion at 1000-2000iu/h IVI (2.8mL/h=1400iu/h). Check APTT at 6h, aim for aPTT ratio 1-2 (see
table) . Measure APTT 10h after dose change.
>5
APTT
4-5
3-4
2-3
1-2
1.2-1.4
Change rate (iu/h) by Stop* - 500 - 300
-100
-50
0
+ 200
*Stop for 1 hour then recheck APTT. Reduce dose by 500iu/h and restart if <5
<1.2
+400
Alternatively , use LMWH. Continue for 6 days & until adequately anticoagulated with warfarin.
Start warfarin 10mg PO at 18.00 on day 1. Do INR 16h later.
If INR <1.8 (as is likely) the 2nd dose of warfarin is 5 or 10mg at 18.00 (24h after first dose). Give the
lower dose if >60yrs, liver disease, or cardiac failure. But if INR >1.8 (warfarin sensitivity; rare) give just
0.5mg.
Do INR daily for 5d and adjust dose (see table) (use 5mg, not 10mg dose3 if over 60, or liver disease,
or cardiac failure).
Measure INR on alternate days until stable, then weekly or less often.
Stop heparin after 5d and when INR >2 for 2d. Tell lab when stopped.
<2
INR
2
2.5
2.9
10mg
3rd dose
5mg
4mg
3mg
6mg
Maintenance
5.5mg
4.5mg
4mg
*Miss a dose; give 1-2mg the next day (if INR >4.5, miss 2 doses).
Lower doses are given in certain groups of patients .
77
3.3
2mg
3.5mg
3.6
0.5mg
3mg
4.1
0mg
*
Dr.Waleed Badr
Target INR levels :
2011
Prophylaxis of DVT
DVT or PE treatment .
Atrial fibrillation .
Recurrent DVT or PE .
Prosthetic heart valves
INR 2.0 2.5

INR 2.5
INR 3.5
Duration of anticoagulation in DVT/PE

-
If the cause will go away (eg post-op immobility):

o
At least 6 weeks for below knee DVT.
At least 3 months for above knee DVT or PE.
At least 6 months if no cause found.
Indefinitely for identified, enduring causes, e.g thrombophilia .
Surgery in those on anticoagulants
Contact your lab, and inform the surgeon and anaesthetist.
Very minor surgery has been undertaken without stopping warfarin (do INR within 24h: it may be safe to
proceed if <3.5).
In major surgery, drugs may be stopped for 2-5d pre-op. Risks and benefits are individual to each patient,
so exact rules are impossible. Discuss these issues when arranging consent.
Vitamin K (e.g 10mg IV) FFP may be needed in emergency surgery.
Monitor clotting meticulously.
One elective option is conversion to heparin (stop 6h prior to surgery, and monitor APTT perioperatively):
unfractionated heparin's short t1/2 allows swift reversal with protamine .When rewarfarinizing, don't stop
heparin cover until the INR is therapeutic, as warfarin is prothrombotic in the early stages.
The bleeding tendency effects of aspirin are reversed by 5d after stopping. but check with local policy to
see if cessation is required.
Antiplatelet drugs
Mechanism of action :
Aspirin (Acetylsalicylic acid) irreversibly acetylates & thus inactivates cyclo-oxygenase, preventing
production of thromboxane A2 & prostacyclin, thereby inhibiting platelet aggregation.
Aspirin also liberation of ADP & serotonin from the platelets .
Indications : Used in low dose (e.g 75mg/24h PO) for secondary prevention following MI, TIA/stroke, and
for patients with angina or peripheral vascular disease. May have a role in primary prevention.
NB. Clopidogrel also block platelet aggregation, but may cause less gastric irritation. They have a role if truly
intolerant of aspirin, and post-coronary stent insertion
78
Dr.Waleed Badr
2011
Hyperviscosity syndrome
Definition : This occurs if the viscosity of blood rises enough to impair the microcirculation. It affects patients
with a very high RBCs count, WBCs count or plasma components (usually immunoglobulins).
Causes:
Polycythaemia rubra vera
Acute or chronic leukaemia
Multiple myeloma : malignant proliferation of plasma cells with production of monoclonal

immunoglobulins, IgG (55%), IgA (25%) .
Waldenstorm's macroglobulinaemia (as IgM is larger and so viscosity more than the same amount
of IgG).
Presentation:
Lethargy & confusion .
Spontaneous bleeding: GU or GI .
Retinopathy : characterized by venous dilatation, segmentation & tortuosity with retinal

haemorrhages & exudates .
Treatment: depends on the cause.
Venesection is done in polycythaemia.
Leucopheresis in leukaemias to remove white cells.
Plasmapheresis in myeloma & Waldenstorm's: blood is withdrawn via a plasma exchange machine,
the supernatant plasma from this is discarded, and the RBCs returned to the patient after being resuspended in a suitable medium.
79
Dr.Waleed Badr
2011
Acute renal failure (ARF)
Definition : Acute (over hours or days) deterioration in renal function, characterized by in serum
creatinine & urea, often with oliguria or anuria .
Causes :
Hypovolaemia , low COP , drugs .
Glomerulonephritis , sepsis , vasculitis .
Obstruction & Hepatorenal syndrome .
Management :
Catheterize to assess hourly urine output & establish fluid charts .
Assess intravascular volume BP, JVP, skin turgor, fluid balance sheet, weight, CVP, attach to
cardiac monitor. Consider inserting a central venous cannula .
Investigations :
o
U&E, Ca2+, PO-34, FBC, ESR, CRP, INR, LFT, CK, LDH, protein electrophoresis, hepatitis
serology, autoantibodies (ANA,ANCA, complement, anti-GBM, ASOT), blood cultures
Urgent urine microscopy & cultures.
WBCs infection & interstitial nephritis .
RBCs inflammatory glomerular condition .
USS of the renal tract : to exclude obstruction .
ECG, CXR .
Treat the precipitating cause :

o
Acute blood loss blood transfusion .
Sepsis antibiotics .
Identify & treat life-threatening hyperkalaemia (if K+ > 6mmol/L)
Causes : oliguric renal failure, metabolic acidosis (DM) & K+ sparing diuretics) .s
ECG changes in hyperkalaemia (use a cardiac monitor).
Tall T waves flat P waves PR interval .
Widening of QRS complex VF/VT .
How to treat ?
-
10 mL Ca gluconate (10%) IV over 2min, repeated as necessary. This provides cardioprotection ( threshold potential); it does not change serum K+ levels .
Insulin + glucose (unless hyperglycaemic) e.g 50mL of 50% glucose + 10U of rapidly
acting insulin IV over 30 minutes, repeat if needed. (Insulin moves K+ into cells) .
80
Nebulized salbutamol (2.5 mg) also makes K+ enter cells
Dr.Waleed Badr
2011
Polystyrene sulfonate resin (e.g Ca Resonium 15 g/6-8h in water PO or 30g enema

followed by colonic irrigation "if vomiting", to remove K+ from colon) .
Dialysis .
Treatment of dehydration :
-
Give 250-500 mL of colloid or saline over 30min . Repeat if still dehydrated. Aim for a CVP
of 5-10 cm
Once fluid replete, continue fluids at 20 mL + previous hours urine output per hour .
If volume overloaded, consider urgent dialysis. A nitrate infusion, furosemide or renal

dose dopamine may help in the short term, especially
to make space for blood
transfusion etc. but does not alter outcome .
Correct acidosis with sodium bicarbonate e.g 50 mL of 8.4% IV .
Diet : high in calorics with adequate high-quality protein. Consider nasogastric or parentral
feeding if too ill .
Avoid nephrotoxic drugs e.g NSAIDS & aminoglycosides
Urgent diaysis if :
81
Persistent hyperkalaemia ( > 6 mmol/L)
Acidosis (pH < 7.2) .
Hypercatabolic renal failure .
Pulmonary edema & no substantial diuresis .
Pericarditis (in tamponade, only dialyse after pressure on the heart is relieved) .
Dr.Waleed Badr
2011
Acute poisoning
B Oxygenation.
C Circulation IV line (if required) .
Level of consciousness (consider naloxone if conscious level) .
Vital signs monitoring.
Assess the patient : take history from patient, friends or family + examination .
Investigations :
Glucose, U&E, FBC, LFT, INR, ABG, ECG, paracetamol & salicylate levels .
Urine/serum toxicology.
General supportive measures e.g
Gastric lavage (rarely used) :
Lavage after 30-60 min may make matters worse.
Dont empty stomach if petroleum products or corrosives e.g acids or alkalis have
been ingested OR if the patient is unconscious OR unable to protect their airway
(unless intubated).
NEVER induce vomiting .
Oral activated charcoal :
the absorption of many drugs from the gut when given as a single dose of 50g with
water e.g salicylates, paracetamol.
Dont use with petroleum products, corrosives,alcohols or metal salts .
Specific measures i.e antidotes (see below)

Psychiatric assessment
Some specific poisons & their antidotes

Drug
Benzodiazepines
B-Blockers
Cyanide
CO1
Digoxin
Iron
Oral anticoagulants
Opiates
Phenothiazine poisoning e.g chlorpromazine
Carbon tetrachloride poisoning
Organophosphorus insecticides
Paraquat poisoning (weed-killers)
Ecstasy poisoning
Snakes
82
Antidote
Flumazenil
Atropine
Hydroxycobalamin
100% O2
Digoxin-specific antibody fragments (Digibind)
Desferrioxamine
Vit K + prothrombin
Naloxone
No specific antidote
N-acetylcysteine
Atropine (full atropinization)
Activated charcoal
Activated charcoal
Antivenom (IgG from venom-immunized sheep
Dr.Waleed Badr
2011
Salicylate poisoning
Dose-related
Mild : 150 mg/kg .
Moderate : 250 mg/kg .
Severe : > 500 mg/kg .
Signs & symptoms :
Vomiting, dehydration, hyperventilation, tinnitus, vertigo & sweating .
Rarely: lethargy or coma, seizures, BP and Heart block, pulmonary oedema, hyperthermia .
Respiratory alkalosis initially due to a direct stimulation of central respiratory centres then
metabolic acidosis .
Hyper- or hypoglycaemia may occur .
Management :
Correct dehydration .
Gastric lavage if within 1h + activated charcoal .
Serum glucose, urine output, U&E, LFT, INR, HCO3, FBC & salicylate level (repeated after 2h,
due to continuing absorption if a potentially toxic dose has been taken) .
83
Correct any metabolic acidosis with HCO3 . Aim to make the uring pH 7.5-8.5 .
Dialysis may be needed if salicylate level > 700 mg/L.
Dr.Waleed Badr
2011
Paracetamol poisoning
150 mg/kg, or 12g in adults may be fatal.
Signs & symptoms :
Vomiting + pain at right upper quadrant .
Later, jaundice and encephalopathy from liver damage renal failure .
Management :
Gastric lavage + activated charcoal (if 1h since ingestion) .
Serum glucose, urine output, U&E, LFT, INR, HCO3, FBC & paracetamol level (at 4h post
ingestion) .
If < 8h since overdose & plasma paracetamol concentrations above normal treatment line
start N-acetylcysteine .
If > 8h & suspicion of large overdose start N-acetylcysteine, stopping it if level below
treatment line.
Dose of N-acetylcysteine :
150 mg/kg IVI in 200 mL of 5% dextrose over 15 min.
Then 50 mg/kg in 500 mL of 5% dextrose over 4h.
Then 100 mg/kg every 16h in 1L of 5% dextrose .
Methionine 2.5g/4h PO for 16h is an alternative if acetylcysteine is unavailable .
Criteria for transfer to a specialist unit :
Encephalopathy or ICT .
INR > 2 at <48h OR > 3.5 at <72h (so measure INR every 12h). if INR is normal at 48h, the
patient may go home .
84
Renal impairment (creatinine > 200 umol/L) .
Blood pH < 7.3 (lactic acidosis tissue hypoxia)
Systolic BP < 80mmHg .
Dr.Waleed Badr
2011
Burns
Assessment : Assess burn extent, depth & site

1. Extent :
The most important as it influences the size of the inflammatory response (vasodilatation, vascular
permeability) & thus fluid shift from the intravascular volume .
Burns are classified according to the extent into :

a) Minor burn : < 15% in adults & < 10% in children
b) Intermediate burn : 15-25 % in adults & 10-20% in children
c) Major burn : > 25% in adults & > 20% in children.
Estimation of the extent of burns by :

a) Rule of 9 : Easy & rapid method but generally overestimates burn area (better than
underestimating)
b) Lund & Browder charts : more accurate in all age groups. It correlates between age, area
involved & depth of burn
85
Dr.Waleed Badr
2011
Rule of 9 in adults :
-
Head & Neck .9%
Each upper limb .9%
Each lower limb .18%
Front of turnk. 18%
Back of trunk.18%
Perineum & genitalia.1%
Modified rule of 9 in children :

-
From birth to 1Y : head & neck is 18% and each leg is 14% .
For each year after, the head loses 1% & each leg gains 0.5%, so adult proportions are
reached by the age 10Y.
86
Dr.Waleed Badr
2.
2011
Depth : This determines healing time/scarring

a) Partial thickness
Involves
the epidermis & superficial part of
b) Full thickness
the whole skin
dermis
Appearance
Blisters surrounded by erythema + wet
White or black eschar (burn slough) + dry
Pain
Very painful
Painless (loss of terminal nerve endings)
3. Site :
87
Burns in face & neck are serious oedema of glottis & disfigurement .
Burns of perineum difficult to nurse .
Dr.Waleed Badr
2011
Management :
A Endotracheal intubation is indicated if there is evidence of airway obstruction or smoke

inhalation.
B 100% O2 , exclude life-threatening chest injuries e.g tension pneumothorax & suspect CO 1
poisoning (history, cherry-red skin & carboxyhaemaglobin "CoHB" level) .
C Circulation put up 2 large-bore (14 or 16G) IV lines.

Start fluid resuscitation using a burns calculator formula e.g
Parkland formula (popular) : 4 X wight (kg) X % burn = mL crystalloid solution in 24h, half
given in 1st 8h .
Muir & Barclay formula : [wight (kg) X % burn]/2 = mL colloid (albumin) per unit time .time
periods are 4h,4h,4h,6h,6h, and 12h.
Adjust IVI according to clinical response & urine output. Aim for 0.5mL/kg/h (1mL/kg/h in
children) .
Beware of over-resuscitation abdominal compartment syndrome .
Cooling the burnt area using saline or tap water & warm the patient : Dont apply cold water to
extensive burns for long periods intensify shock .
Give antitetanic serum, Anti gas gangrene serum, antibiotics & morphine 10 mg.
Definitive dressings:
Partial thickness either biological (e.g pigskin, cadaveric skin) or synthetic (Mepitel,
Duoderm) + sulfadiazine cream .
Full thickness tangential excision & split-skin grafts .
88
Dr.Waleed Badr
2011
Hypothermia
Definition: a core (rectal) temperature < 35 C .

Causes :
o
In the young : usually from cold exposure e.g near-drowning or 2ry to impaired consciousness e.g
following excess alcohol or drug overdose .
In the elderly : due to
Age-related impaired homostatic mechanisms .
room temperature due to poverty & poor housing .
Impaired thermoregulation due to pneumonia,MI & heart failure .
metabolism due to immobility, hypothyroidism,D.M .
Autonomic neuropathy e.g DM & parkinsons .
Excess heat loss due to psoriasis .
cold awareness due to dementia & confusion .
exposure to cold .
Drugs : major tranquilizers, antidepressants, diuretics & alcohol
Investigations : U&E, plasma glucose, thyroid function tests, FBC & ECG (show J-waves)
Management :
A Adequate ventilation (if comatosed or respiratory insufficiency) .
B Oxygenation.
C Circulation warm IVI.
Antibiotics for prevention of pneumonia (given routinely in patients > 65Y with T< 32C .
Urinary catheter to monitor renal function .
Slowly rewarm if too quickly V.D shock & death. Aim for a rise of 1/2 C/h. the 1st sign of
too rapid warming is BP.
Vital sign monitoring (every hour )
Complications : Arrhythmias, pneumonia, pancreatitis, acute renal failure & intravascular coagulation
Prognosis : depends on age & degree of hypothermia. If age > 70Y & T<32 C then mortality > 50% .
89
Dr.Waleed Badr
2011
Needle-stick injuries
Needle-stick transmission rates from infected patients are :
0.5% for HIV .
10-15% for hepatitis C .
20% for hepatitis B .
Immediate management :
Encourage the injury to bleed & wash under running water; if body fluids splashed onto eyes irrigate
them copiously .
Report to the occupational health dept.(within 1h) OR accident & emergency dept. (if out-of-hours) .
If high risk of HIV transmission start post-exposure prophylaxis; this should be started within 1h by the
occupational health/A&E physician (see below)
Store blood from the donor & the recipient. Screening for hepatitis B & HIV where appropriate
generally arranged by the occupational health physician .
Post-exposure prophylaxis (PEP) where exposure to HIV
The Occupational Health/A&E physician will assess risk of HIV transmission based on patient history,
nature of body fluid & route of transmission .
The decision of whether to start post-exposure prophylaxis is made according to risk.

o
High risk :
-
This
includes
exposure
to
blood/high-risk
body
fluids
(from
patient
with
known/suspected HIV) through sharps injury.

-
PEP drugs starting within 1h (e.g zidovudine PO 250mg 2x/d + lamivudine PO 150mg
2x/d + indinavir PO 800mg 3x/d) .
If donor is HIV+
(already known or discovered on testing)
- Continue PEP for 4wKs.
- Test recipient for HIV seroconversion at
6wKs, 3mths & 6mths .
- Follow up with occupational health.
90
If donor is HIV-
Discontinue PEP .
Test
recipient
for
HIV
seroconversion at 3mths & 6mths .
Follow up with occupational
health .
Low risk :
-
This applies to non-blood-stained lolw-risk material .
PEP is not offered .
Dr.Waleed Badr
2011
Perioperative care (OHO)

Specific systemic contraindications to ophthalmic surgery
Uncontrolled BP (e.g., >180/100 mmHg)
Myocardial ischemia (unstable ischemic heart disease or myocardial
Infarction (MI) in the last 3 months)
Uncontrolled hyperglycemia
Uncontrolled arrhythmias
Excessive INR
Acute systemic illness
Preoperative management
Patients
for
general
anesthesia
Patients with diabetes
nothing by mouth (e.g., from 8 hours before).
Patients with hypertension
continue antihypertensives (including day of surgery); for example,

consider postponing surgery if BP >180/100 mmHg.
Patients with IHD
continue usual antianginal medication and ensure their usual prn

medication (e.g., sublingual nitroglycerin) is available in the operating
room; postpone surgery if unstable angina or within 3 months of MI.
Patients
with
valvular
heart disease
Patients on aspirin
antibiotic prophylaxis is not required for intraocular procedures.
Patients on anticoagulants
ideally the INR should be <3 for intraocular and strabismus surgery but
<2 for orbital and oculoplastic surgery . This should be checked within
48 hours of surgery. If this is not compatible with their therapeutic
target, coordinate care with their hematologist or PCP. They may
consider changing to heparin in the perioperative period.
91
normal (or near-normal) regime can be continued in most patients

having local anesthesia; a sliding scale may be required in poorly
controlled patients or some insulin requiring patients having general
anesthesia (coordinate care with anesthesiologist). See below
continue for intraocular and strabismus surgery; for orbital &

oculoplastic surgery, it would ideally be discontinued for 2 weeks prior
to surgery. However, this must be discussed with their PCP.
Dr.Waleed Badr
2011
Diabetic patients undergoing surgery

IDDM (Type 1 D.M)
Stress or intercurrent illness increases basal insulin needs .
Always try to put the patient first on the list (surgery, endoscopy, bronchoscopy, etc.). Inform the surgeon
and anaesthetist early.
Stop all long-acting insulin the night before. Get IV access before you need it urgently. If surgery is in the
morning, stop all SC morning insulin. If surgery is in the afternoon, have the usual short-acting insulin in the
morning at breakfast. No medium- or long-acting insulin.
Check U&E pre-op. Start an IVI of 1L of 5% dextrose with 20mmol KCl/8h. Dextrose saline can be given if
Na+ low, but do not give only saline; dextrose may need constant infusion to maintain blood glucose.
Start an infusion pump with 50U short-acting insulin (eg Actrapid) in 50mL 0.9% saline. Give according to a
sliding scale (see table) adjusted in the light of blood glucose.
Check blood glucose hourly. Aim for 7-11mmol/L during surgery.
Post-op, continue IV insulin + dextrose until patient tolerating food. Check fingerprick glucose every 2h.
Switch to usual SC insulin regimen .
IV insulin sliding scale (This is only a guide; values are in mmol/L)

Fingerprick glucose
<2
2-5
5-10
10-15
15-20
>20
IV soluble insulin*
None (50% glucose IV)
No insulin
1u/h
2u/h
3u/h
6u/h: get urgent diabetic review
Alternative SC insulin**
None (50% glucose IV)
No insulin
2u/h
5u/h
7u/h
* Check glucose hourly & adjust insulin accordingly .

** Only use SC route if IV route is problematic as it is associated with much variability; check finger prick glucose
every 2-4h if NBM, or pre-meals if using SC insulin to supplement other hypoglycaemics
NIDDM (Type 2 D.M)
These patients are usually controlled on oral hypoglycaemics . If diabetes poorly controlled (e.g fasting
glucose >10mmol/L), treat as for type 1 diabetes.
Do not give long-acting sulphonylureas (eg glibenclamide) on the morning of surgery, as they can cause
prolonged hypoglycaemia on fasting.
Beware lactic acidosis in patients on biguanides (eg metformin), especially if using IV contrast agents
and/or renal function poor (creatinine >150mol/L).
If the patient can eat post-operatively, simply omit tablets on the morning of surgery and give post-op with
a meal.
If the patient is having major surgery with restrictions to eating post-op, check fasting glucose on the
morning of surgery and start IV or SC insulin given according to sliding scale. Post-op, consult the diabetic
team as the patient may need a phase of insulin to supplement their oral hypoglycaemics.
92
Dr.Waleed Badr
2011
Severe local anaesthetic toxicity

"from The Association of Anaesthetists of Great Britain & Ireland" (AAGBI)
1) Recognition "Signs of severe toxicity"
Sudden loss of consciousness tonic-clonic convulsions
Cardiovascular
collapse:
sinus
bradycardia,
conduction
blocks,
asystole
and
ventricular
tachyarrhythmias may all occur
Local anaesthetic (LA) toxicity may occur some time after the initial injection
2) Immediate management
Stop injecting the LA
Call for help
Maintain the airway and, if necessary, secure it with a tracheal tube
Give 100% oxygen and ensure adequate lung ventilation (hyperventilation may help by increasing pH
in the presence of metabolic acidosis)
Confirm or establish intravenous access
Control seizures: give a benzodiazepine e.g midazolam, thiopental or propofol in small incremental
doses
Assess cardiovascular status throughout
3) Treatment
Management of cardiac arrest associated with LA injection:
Start cardiopulmonary resuscitation (CPR) using standard protocols
Manage arrhythmias using the same protocols, recognising that they may be very refractory to
treatment
Prolonged resuscitation may be necessary; it may be appropriate to consider other options:

o
Consider the use of cardiopulmonary bypass if available
Consider treatment with lipid emulsion (see below)
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Dr.Waleed Badr
2011
Treatment of cardiac arrest with lipid emulsion:

o approximate doses are given in red for a 70-kg patient
Give an intravenous bolus injection of Intralipid 20% 1.5 ml.kg-1 over 1 min
o
Give a bolus of 100 ml
Continue CPR
Start an intravenous infusion of Intralipid 20% at 0.25 ml.kg-1.min-1

o
Repeat the bolus injection twice at 5 min intervals if an adequate circulation has not been restored
o
Give at a rate of 400 ml over 20 min

Give two further boluses of 100 ml at 5 min intervals
After another 5 min, increase the rate to 0.5 ml.kg-1.min-1 if an adequate circulation has not been
restored
o
Give at a rate of 400 ml over 10 min
Continue infusion until a stable and adequate circulation has been restored
Remember:
Continue CPR throughout treatment with lipid emulsion
Recovery from LA-induced cardiac arrest may take >1 h
Propofol is not a suitable substitute for Intralipid
Replace your supply of Intralipid 20% after use
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Dr.Waleed Badr
2011
Choking in children
Recognition of choking :
When a foreign body enters the airway the child reacts immediately by coughing in an attempt to
expel it. A spontaneous cough is likely to be more effective and safer than any manoeuvre a rescuer
might perform. However, if coughing is absent or ineffective, and the object completely obstructs the
airway, the child will become asphyxiated rapidly. Active interventions to relieve choking are
therefore required only when coughing becomes ineffective, but they then must be commenced
rapidly and confidently.
The majority of choking events in children occur during play or whilst eating, when a carer is usually
present. Events are therefore frequently witnessed, and interventions are usually initiated when the
child is conscious.
Choking is characterised by the sudden onset of respiratory distress associated with coughing,
gagging, or stridor. Similar signs and symptoms may also be associated with other causes of airway
obstruction, such as laryngitis or epiglottitis, which require different management. Suspect choking
caused by a foreign body if:
1. the onset was very sudden;
2. there are no other signs of illness;
3. there are clues to alert the rescuer, for example a history of eating or playing with small items
immediately prior to the onset of symptoms.
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Dr.Waleed Badr
2011
Pediatric choking treatment Algorithm (UK) 2010
Relief of choking :
If the child is coughing effectively, then no external manoeuvre is necessary. Encourage the child to
cough, and monitor continuously.
If the childs coughing is, or is becoming, ineffective, shout for help immediately and determine the
childs conscious level.
1. Conscious child with choking
If the child is still conscious but has absent or ineffective coughing, give back blows.
If back blows do not relieve choking, give chest thrusts to infants or abdominal thrusts to children.
These manoeuvres create an artificial cough to increase intrathoracic pressure and dislodge the
foreign body.
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Dr.Waleed Badr
2011
Back blows
In an infant:
Support the infant in a head-downwards, prone

position, to enable gravity to assist removal of the
foreign body.
A seated or kneeling rescuer should be able to support

the infant safely across his lap.
Support the infants head by placing the thumb of one

hand at the angle of the lower jaw, and one or two
fingers from the same hand at the same point on the
other side of the jaw.
Do not compress the soft tissues under the infants jaw,

as this will exacerbate the airway obstruction.
Deliver up to 5 sharp back blows with the heel of one

hand in the middle of the back between the shoulder
blades.
The aim is to relieve the obstruction with each blow

rather than to give all 5.
In a child over 1 year:
Back blows are more effective if the child is positioned head down.
A small child may be placed across the rescuers lap as with an infant.
If this is not possible, support the child in a forward-leaning position and deliver the back blows
from behind.
If back blows fail to dislodge the object, and the child is still conscious, use chest thrusts for infants or
abdominal thrusts for children. Do not use abdominal thrusts (Heimlich manoeuvre) for infants.
Chest thrusts for infants:
Turn the infant into a head-downwards supine position.

This is achieved safely by placing your free arm along
the infants back and encircling the occiput with your
hand.
Support the infant down your arm, which is placed

down (or across) your thigh.
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Dr.Waleed Badr
2011
Identify the landmark for chest compression (lower sternum approximately a fingers breadth
above the xiphisternum).
Deliver up to 5 chest thrusts. These are similar to chest compressions, but sharper in nature and
delivered at a slower rate.
The aim is to relieve the obstruction with each thrust rather than to give all 5.
Abdominal thrusts for children over 1 year:
Stand or kneel behind the child. Place your arms under

the childs arms and encircle his torso.
Clench your fist and place it between the umbilicus

and xiphisternum.
Grasp this hand with your other hand and pull sharply
inwards and upwards.
Repeat up to 4 more times.
Ensure that pressure is not applied to the xiphoid

process or the lower rib cage as this may cause
abdominal trauma.
The aim is to relieve the obstruction with each thrust

rather than to give all 5.
Following chest or abdominal thrusts, reassess the child:
If the object has not been expelled and the victim is still conscious, continue the sequence of back blows
and chest (for infant) or abdominal (for children) thrusts.
Call out, or send, for help if it is still not available.
Do not leave the child at this stage.
If the object is expelled successfully, assess the childs clinical condition. It is possible that part of the object
may remain in the respiratory tract and cause complications. If there is any doubt, seek medical assistance.
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2011
2. Unconscious child with choking
If the choking child is, or becomes, unconscious place him on a firm, flat surface.
Call out, or send, for help if it is still not available.
Do not leave the child at this stage.
Airway opening:
Open the mouth and look for any obvious object.
If one is seen, make an attempt to remove it with a single

finger sweep.
Do not attempt blind or repeated finger sweeps these

can impact the object more deeply into the pharynx and cause
injury.
Rescue breaths:
Open the airway and attempt 5 rescue breaths.
Assess the effectiveness of each breath: if a breath does not make the chest rise, reposition
the head before making the next attempt.
Chest compression and CPR:
Attempt 5 rescue breaths and if there is no response, proceed immediately to chest

compression regardless of whether the breaths are successful.
Follow the sequence for single rescuer CPR (step 7B) for approximately 1 min before
summoning the EMS (if this has not already been done by someone else).
When the airway is opened for attempted delivery of rescue breaths, look to see if the foreign
body can be seen in the mouth.
If an object is seen, attempt to remove it with a single finger sweep.
If it appears that the obstruction has been relieved, open and check the airway as above.
Deliver rescue breaths if the child is not breathing and then assess for signs of life. If there are
none, commence chest compressions and perform CPR (step 7B).
If the child regains consciousness and is breathing effectively, place him in a safe side-lying
(recovery) position and monitor breathing and conscious level whilst awaiting the arrival of the
EMS.
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2011
Step.7B
If there are no signs of life, unless you are CERTAIN that you can feela definite pulse of greater than 60
min-1 within 10 s
Start chest compression.
Combine rescue breathing and chest compression.
For all children, compress the lower half of the sternum:
To avoid compressing the upper abdomen, locate the xiphisternum by finding the angle where
the lowest ribs join in the middle. Compress the sternum one fingers breadth above this.
Compression should be sufficient to depress the sternum by at least onethird of the depth of the
chest.
Dont be afraid to push too hard. Push hard and fast.
Release the pressure completely, then repeat at a rate of 100 - 120 min-1
After 15 compressions, tilt the head, lift the chin, and give two effective breaths.
Continue compressions and breaths in a ratio of 15:2.
The best method for compression varies slightly between infants and children.
Chest compression in infants:
The lone rescuer should compress the sternum with the tips of two fingers.
If there are two or more rescuers, use the encircling technique:

o
Place both thumbs flat, side by side, on the lower half of the sternum (as above), with the tips
pointing towards the infants head.
Spread the rest of both hands, with the fingers together, to encircle the lower part of the
infants rib cage with the tips of the fingers supporting the infants back.
Press down on the lower sternum with your two thumbs to depress it at least one-third of the
depth of the infants chest.
Chest compression in children aged over 1 year:
Place the heel of one hand over the lower half of the sternum (as above).
Lift the fingers to ensure that pressure is not applied over the childs ribs.
Position yourself vertically above the victims chest and, with your arm straight, compress the
sternum to depress it by at least one-third of the depth of the chest.
In larger children, or for small rescuers, this may be achieved most easily by using both hands with
the fingers interlocked.
------------------------------------------------------------------------------------------
GOOD LUCK
31/12/2011
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Dr.Waleed Badr
2011
Other important topics in Internal medicine

1. ECG (OHCM)
2. Hypertension : causes , complications & treatment (AAO & OHCM) .
3. Infective endocarditis (OHCM & AAO) .
4. Effects of cardiovascular disease on the eye (collections)
5. Diagnosis & Treatment of osteoporosis (OHCM, AAO).
6. Hyperthyroidism (symptoms & clinical manifestations) (OHCM, AAO & Kanski) .
7. D.M : complications & treatment (AAO,OHCM & Pharma) .
8. Surgical considerations in Diabetic patient? (AAO, OHCM & OHO)
9. Surgical considerations in a patient on anticoagulants (OHCM & OHO).
10. Steroids & immunosuppressants (OHO) .
11. Blood transfusion & blood products (OHCM & Surgery notes).
12. Choking in children (pediatric BLS) .
13. Workup for headache (WILLS) .
14. Needle-stick injuries & hepatitis virus immunization (OHO, AAO, OHCM)
15. Blackouts (OHCM) .
NB. Review perioperative care chapter in both AAO & OHO .
101
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Emergency Medicine 1st Edition - DR - Waleed (101 Papers)

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Internal &

Emergency medicine for the FRCophth exam

Emergency medicine for the FRCophth exam

Cardiopulmonary Resuscitation (CPR) for cardiorespiratory arrest

Sudden, unexpected loss of heart function, breathing & consciousness.

Ventricular fibrillation (VF) :

It produces rapid ineffective uncoordinated movement of the ventricles NO pulse.

ECG shows : rapid, bizarre & irregular ventricular complexes.

Pulseless (sustained) ventricular tachycardia (VT) :

It may degenerate into VF.

Pulseless electrical activity (PEA) :

It may be caused by reversible conditions, such as hypovolaemia, cardiac tamponade or tension

Emergency medicine for the FRCophth exam

Management of cardiorespiratory arrest

Chain of survival in cardiorespiratory arrest

Adult BLS Algorithm (UK) 2005

Emergency medicine for the FRCophth exam

Note the time)

Then do by yourself Basic

life support "BLS"

A: Establish a patent Airway

Head tilt (if no spinal injury is suspected).

Clear the mouth.

Each inflation is 1s long.

Emergency medicine for the FRCophth exam

C: Circulation (chest compressions)

support "ALS" ALS aims to :

E: Exposure : Undress patient but cover to avoid hypothermia.

Emergency medicine for the FRCophth exam

Advanced life support "ALS"

Emergency medicine for the FRCophth exam

Adult ALS Algorithm (UK) 2005

Emergency medicine for the FRCophth exam

(Intracardiac injection in not recommended) (PLEASE)

When to stop CPR?

When to not resuscitate?

After successful resuscitation What to do?

Emergency medicine for the FRCophth exam

Definition: Circulatory failure inadequate organ perfusion .

Bleeding: trauma, ruptured aortic aneurysm or ectopic pregnancy.

Fluid loss: vomiting (GIT obstruction), diarrhea (cholera), burns

Temperature : commonly hypothermia .

Heart rate : commonly tachycardia >100 beats/min

Respiratory rate : (compensatory tachypnea) in an attempt to remove excess acids in the

6. Renal problems : Oliguria & anuria (in severe cases) .

Emergency medicine for the FRCophth exam

Treatment according to the cause

Cardiogenic shock: Cold & clammy patient.

Emergency medicine for the FRCophth exam

Causes: trauma, lung or breast cancer, pericarditis and MI.

BP, JVP & muffled heart sounds (Becks triad).

JVP on inspiration (Kussmauls sign) .

Pulsus paradoxus (pulse fades on inspiration).

ECG: electrical alternans.

Correct electrolyte abnormalities and acidosis.

Emergency medicine for the FRCophth exam

More common in atopic individuals.

Pathophysiology: Type 1 IgE-mediated hypersensitivity reaction Release of histamine & other

Clinical features : suggestive of anaphylaxis

H/O previous allergy or atopy .

Itching, sweating, erythema, urticaria .

Wheezy chest, laryngeal obstruction (oedema), apnea & cyanosis.

Vomiting, diarrhea & urinary incontinence .