CARDIAC EMERGENCY

PROBLEMS
Prof. Dr. dr. Ali Aspar Mappahya, Sp.PD, Sp,JP
Bagian Ilmu Penyakit Dalam
Fakultas Kedokteran Universitas Hasanuddin

CONGESTIVE HEART FAILURE

ACUTE PULMONARY EDEMA : Dyspnea, orthopnea, rales,
and wheezing. X-ray : perihilar congestion, hypoxemia.
CARDIOGENIC SHOCK ; Hypotension; abnormal renal,
hepatic and CNS function due to decreased perfusion and
lactic acidosis.
Cardiomegaly, decreased VEF/abnormal ventricular wall
motion, elevated PAWP, low cardiac output.
May have a previously known cause such as valvular heart
disease/cardiomyopathy but may present also as a result
of ischemia or secondary to severe systemic hypertension.

 Pneumonia, ARDS, fluid overload, COPD, asthma.

Pericardial effusion,

Cor pulmonale, pulmonary arteriopathy/PPH. Pulmonary

emboli
Volume depletion, sepsis, pulmonary embolism

1. Systolic dysfunction without hypotension.

Digoxin, diuretics, ACEI
Metolazone/HCT
Nesiritide ( a recombinant human BNP)
Spironolactone
Nitrate/hydralazine
Ultrafiltration
Mechanical ventilation

2. Severe CHF with hypotension (Cardiogenic shock)

BP < 90 mmHg :
Intravenous dopamine (titrated)
Intravenous dobutamine/milrinone
BP = 90-100/>100 mmHg:
Nitroprusside-drips (titrated)
Intravenous Diuretics (Furosemide)
Intravenous NTG
Nesiritide (with caution)
IABP (Intra aortic balloon pumping)
PTCA/CABG/transplantation
After optimizing hemodynamic variables:
ACEI, ARB, BB, hydralazine

3. CHF with severe systemic hypertension

Initial therapy : Control of BP
Intravenous nitroprusside/ NTG
Intravenous enalaprilat
Continued treatment
BB/ CCB (with caution)
4. High output or volume overload CHF
Treatment should be directed at the cause of high
cardiac output (eg, anemia, B1 defficiency, sepsis,
hyperthyroidism
Volume overload state (renal failure, excessive Na intake)
---- ultrafiltration

5. CHF with diastolic dysfunction

Beta adrenergic blockade
Attention : aggressive diuretic therapy is
counterproductive
6. Isolated right heart failure with pulmonary
hypertension

Diuretics
Oxygen therapy
Digoxin
NO/intravenous prostacyclin

CARDIAC TAMPONADE
Evidence of elevated pericardial pressure manifested
as elevated systemic venous pressure .
Decreased cardiac output and hypotension;
evidence of decreased peripheral perfusion.
Echocardiography : large pericardial effusion;
RV early diastolic collapse, RA diastolic collapse,
LA diastolic collapse; etc.
Right heart catheterization: Equalization of RA pressure,
LA pressure, PCWP, and Ventricular EDP.

 Initial treatment / Medical therapy :

Rapid intravenous fluid loading and dopamine
Avoidance diuretics or vasodilators.
Priority of therapy (percutaneous or surgical therapy) :
Drainage (Tapping)--- needle pericardiocentesis
Surgical drainage : subxiphoid pericardioectomy,
pericardial window, and subtotal pericardiectomy
Percutaneous balloon pericardiotomy

HYPERTENSIVE CRISIS AND

MALIGNANT HYPERTENSION
Hypertensive crisis : Systemic BP > 240/130 mmHg
without symptoms, or elevated BP with chest pain,
headache, or heart failure. May have intracranial
hemorrhage, aortic dissection, pulmonary edema,
myocardial infarction, or unstable angina.
Hypertensive crisis traditionally has been classified as:
- Emergency and
- Urgency
Malignant hypertension : Severe hypertension

associated with encephalopathy, renal failure, or

papiledema.

(Rapid decompensation of vital organ function)

In general, diastolic BP >120 mmHg

Malignant HTN with papiledema
Hypertensive encephalopathy
Severe HTN in the setting of stroke, subarachnoid
hemorrhage, head trauma
Acute aortic dissection
HTN and LV failure
HTN and myocardial ischemia/infarction
HTN after CABG operation
Pheocromocytoma crisis
Food and drug interactions with MAO inhibitors
Cocain abuse
Rebound HTN after sudden drug withdrawal (clonidine)
Idiosyncratic drug reactions ( atropin)
Eclampsia

(Marked elevations of BP without acute or progressive target organ)

Diastolic BP > 120 mmHg, but no symptoms and sign of

tissue damage

Severe HTN, accelerated HTN

Pheochromocytoma crisis
Food and drug interactions with MAO inhibitors
Rebound HTN after sudden drug withdrawal
Idiosyncratic drug reactions
Preoperative HTN
Postoperative HTN

 The goal therapy : immediate, controlled reduction in BP.

BP initially be reduced by no more than 25% of MAP
(diastolic pressure + 1/3 pulse pressure) over minutes to
hours. (exception : aortic dissection, LV failure, and
pulmonary edema.
Medical therapy :
Nitroprusside (drug of choice), Glyceryl trinitrate,
Labetalol ( contraindicated for patients with CHF,
bradycardia, heart block, reactive airway disease),
Nicardipine, Enalapril, Phentolamine, Hydralazine,
Fenoldopam.

 Captopril (Fastest-acting oral ACEI)

caution : marked renal insufficiency/ volume depletion
Clonidine
Labetalol
Nifedipine (Sublingual nifedipine should not be used
in the treatment of patients with HTN).

EVALUATION OF CHEST PAIN

IN THE EMERGENCY DEPARTMENT
Chest pain : substernal pressure, squeezing, or sensation
of suffocation. Some patients describe aching, burning,
tigHTNess. The pain radiate to the shoulder, neck, jaw,
left or right arm and the fingertips. Occasionally the pain
predominantly epigastric or intrascapular.
Dyspnea may also be the only major presenting symptom
in about 10% patients wit AMI (atypical presentation)
Other atypical : fatigue, syncope, altered sensorium, stroke,

nausea, vomiting and lethargy

Atypical presentations:
More common in elderly, diabetics, women

Cardiac causes:
ACS
Syndrome X
Pericarditis
MVP
Aortic stenosis
Hypertrophic cardiomypathy
Aortic causes:
Aortic dissection
Penetrating ulcer of aorta
Pulmonary causes :
Embolism
Gastrointestinal causes:
Esophageal spasm, reflux
Gastritis, gastric ulcer
Cholecystitis

Costochondritis :
Tietzes syndrome

Neurologic causes :
Cervical spondylosis
Other compression neuropathy
Herpes

Psychological causes :
Panic disorder
Anxiety
Depression
Hysteria

 ECG
Biochemical markers : CK/CKMB, Myoglobin, Troponins
BNP, hsCRP

Imaging studies : Echocardiography, Radionuclide

perfusion imaging (Thalium/Technetium)
Early exercise stress testing (Treadmill)

 Depend on the causes of the chest pain

ACS
Pericarditis
Aortic dissection
Pulmonary embolism

ACUTE CORONARY SYNDROME ;

UNSTABLE ANGINA PECTORIS (UAP) &

NON ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION (NSTEMI)

Upon diagnosis of UAP or NSTEMI, level of risk for death

& nonfatal cardiac ischemic events must be assessed.
Treatment is based on this risk level.
Patients considered HIGH RISK if one or more of the
following are present:
1. Recurrent ischemia (ST-depression/ST elevation).
2. Ongoing chest pain at rest >20 min.
3. Elevated cardiac marker levels (CK-MB, Troponin T, CRP).
4. Developing hemodynamic instability.
5. Major arrhythmias (VF, VT) or LV dysfunction.
6. Early post-infarction UAP
7. Thrombus on angiography.

 LOW RISK PATIENTS :

1. No recurrent chest pain
2. No evidence of angina at rest
3. No elevation of troponin or other biochemical markers
4. Norma or unchanged ECG during chest discomfort

Aspirin & clopidogrel/ticlopidine

Nitrates (sublingual/spray or IV)
Oral beta-blocker (if not contraindicated)
Calcium antagonists (diltiazem)
Lipid lowering agent (statin/ fibrate/niacin)
Heparin (Low molecular weight heparin-LMWH)
Stress test (Treadmill test) recommended either during hospitalization
or within 72 hr.

 Bed rest with continuous ECG monitoring

Supplemental O2 to maintain O2 saturation>90%
Treatment of ischemic pain
Nitrates (sublingual/spray/IV) :
- contraindicated in patients who have taken sildenafil within
the past 24 hr
- Use with caution in patients with RV failure

Beta-blockers
Morphine sulfate
- May be administered with nitrates.

- may need concomitant administration of anti emetic

Calcium antagonists (CCB)

ACE inhibitors

 Antiplatelet & anticoagulant therapy :

Aspirin & Clopidogrel (should be initiated promptly)
Heparin (LMWH) sc / UFH
GP IIIa/IIb receptor antagonist.
Risk modification:
Lipid lowering agents: statin/ fibrate/ niacin
Invasive procedures :
Intra aortic balloon counterpulsation (IABP).
Percutaneous coronary intervention (PCI) or
Coronary artery bypass graft (CABG)

CARDIOGENIC SHOCK
Diagnosis :
Decreased urine output(<30 mL/h)
Impaired mental function
Cool extremities
Distended neck vein (jugular vein)
Hypotension with evidence of peripheral and

pulmonary venous congestion.(Syst.BP <80 mmHg,

or syst.BP <90 mmHg with medication/IABP)
Cardiac index <2,2 L/min/m2
Pulmonary artery wedge pressure (PCWP) >18 mmHg

When more than 45% of the LV myocardium is NECROTIC,

cardiogenic shock becomes evident clinically.
Bradycardia and arrhythmias may underlie cardiogenic
shock

 Non-mechanical causes of cardiogenic shock:

1. AMI (ACS-STEMI)
2. Low CO syndrome
3. RV infarction
4. End-stage cardiomyopathy
Mechanical causes of cardiogenic shock :
1. Rupture of septum or free wall
2. Mitral or aortic insufficiency
3. Papillary muscle rupture or dysfunction
4. Critical aortic stenosis
5. Pericardial tamponade

A. Stage I (Compensated hypotension)

B. Stage II (Decompensated hypotension)
C. Stage III (Irreversible shock)

If the the cause CS is AMI, controlling the infarct size.

Oxygen ( 4 L - 6 L/min) / Intubation may be required

Fluid resuscitation (monitoring CO and PCWP)
Pharmacologic support :
1. Inotropes:
Dobutamine,
Dopamine ,
Digoxin
Isoproterenol ,
Norepinephrine , Amrinone
Glucagon
2. Vasodilators : Nitroprusside , Nitroglycerin
Other modalities : Thrombolytic therapy, PCI, IABP, etc.