Part C

14. (Part B) the forgotten one….heheh

How and when are defibrillation and synchronized cardioversion done?
- Synchronized Cardioversion – may be done if meds ineffective or in emergency
with rapid rate and serious signs/symptoms; used as tx foratrial fibrillation, supra
ventricular tachycardia, ventricular tachycardia
- Procedure: (ensure patent IV access for ER drug admin)
o Use standard precautions
o Turn on the cardioverter-defibrillator and ECG monitor
o Connect client’s ECG cable to the cardioverter. Select a lead w/prominent
R waves for monitoring
o Cardioverter set to “synchronize” mode. Observe the ECG waveform on
the monitor for indications of synchronization, such as a flashing bold line
or a blip. (may also send message “synchronized mode”
o Conductive pads placed on chest below the right clavicle to the right of the
sternum and in the midaxillary line on the left. If using conductive paste,
spread it evenly on pads
o Turn on ECG recording strip for continuous printout
o Charge the paddles to the prescribed energy dose. Machine will beep to
dindicate selected energy level has been reached and are ready for
discharge
o Firmly apply paddles over conductive pads (done by physician)
o Oxygen off and removed
o Ensure no one is touching client or bed prior to d/c of electrical shock
(sometimes there is a slight delay in shock delivery as machine
synchronizes with the R wave)
o Repeat if not successful
o Remove conductive pads. Use a dry gauze pad to clean paste from chest
and paddles
o Post: assess return of consciousness from sedative or cardioversion/Eval:
neuro; cardio; & respiratory status
o Complication: emboli (esp. cerebral), resp. dep, dysrhythmias
-
Defibrillation – is used at 200,300,360 joules followed by CPR & alternating
drug & shock for no measurable waveforms, soarse or fine wavy baseline, no
pulse treatment for ventricular fibrillation

1. What is atherosclerosis and what are the risk factors for it?
- accumulation of lipids in intimal layer of arteries
- progressive disease charachterized by plaque (atheroma)
- plaque obstructs blood flow plaque can rupture vessel, bleed or form thrombus
- begins w/injury to or inflammation of endothelial cells lining the artery
- atherogenic lipoproteins collect in the intimal lining
Risk Factors:
Non-modifiable: age (50% are older than 65); sex (Male); family hx; race: African
American
Modifiable: hypertension (greater than 140/90)
Diabetes
Hyperlipidemia: total cholesterol/LDL/HDL/triglycerides
Homocysteine levels
Metabolic Syndrome:
 abdominal obesity; hyperlipidemia; hypertension;
 insulin resistance
 increased tendency toward clotting & inflammation
 women- premature menopause; oral contraceptions; HRT
Lifestyle factors:
 smoking, obesity (body wt greater than 30% over ideal wt)
 increased BMI, physical inactivity, diet (fat & cholesterol intake)

2. What should you teach patients about their diet to lower their risk for heart disease?
- Reduce saturated fat & cholesterol intake (whole milk products, red meats, coconut oil)
- recommend increased intake of nonfat dairy products & recommend increased intake
of fish, poultry as primary protein sources (TUNA, SALMON, MACKREL-OMEGA 3)
-use soft margarines & vegetable oils
- monosaturated fats in olive, canola & peanut oils reduces LDL & cholesterol levels
- increased fiber (oats, psyllium, fruit (pectin) & beans
- leafy green vegetables & legumes (folate)
- moderate alcohol intake (no more than 2 drinks/day for men/1 for women= 5oz
wine/12oz beer/1.5oz whiskey
- obese= reduce carloric intake

3. How does the drug class “statins” lower cholesterol and what are the side effects?
Mevacor (lovastatin), Prevachol (pravestatin), Zocor (simvastatin)= 1st line drugs
- inhibit the enzyme HMG-COA reductase in liver; reducing LDL synthesis &
serum levels

4. What is the difference between stable and unstable angina?

- Stable Angina:
o Most common & predictable form
o Occurs w/predictable amt of activity or stress & is a common
manifestation of CHD
o Usually occurs when the work of the heart is increased by physical
exertion, exposure to cold, or stress
o Relieved by rest & nitrates
- Unstable Angina:
o Occurs w/ increased frequency, severity, & duration
 o Pain is unpredictable & occurs w/decreasing levels of activity or stress &
may occur at rest
o Clients are at risk for MI
5. How do you tell the difference between angina pectoris, MI, pericarditis, GI or
musculoskeletal causes of chest pain?
Angina Pectoris:
- P- exertion, stress, eating, cold or hot weather; relieved w/rest & nitrates
- Q- tightness, pressure, squeezing
- R- substernal or precordial; may radiate to neck, arm, shoulders or jaw
- S- severity 2-4 on scale of 10
- T- lasts less than 15 mins, sudden or gradual
- Other: dyspnea, pallor, tachycardia, anxiety, indigestion, pale, SOB

MI:
- P- exertion, stress, eating, may occur at rest; may or may not be relieved with
NTG or narcotics
- Q- severe pressure, crushing, heaviness
- R-substernal or precordial, may radiate to neck, arm, jaw, or shoulders
- S- severity 6 or higher on scale of 10
- T- lasts longer than 15-20mins; sudden onset
- Other: EKG changes, dyspnea, increased HR, increased RR, increase or decrease
in BP, diaphoresis, N/V, dysrhythmias, CHF, hx

Pericarditis:
- P-Hx MI, trauma, uremia, upper resp. infection; relieved by NSAIDS or leaning
forward (reduces pressure off the heart)
- Q- main difference from angina is pain may be aching, or sharp & stabbing.
Worse w/deep inspiration, coughing or supine position
- R-similar to angina
- S-severity could be 1-10 (depends on pain tolerance)
- T-association w/fever, pericardial friction rub (fever=infection)

GI or GERD:
- P-precipitated by alcohol, foods, meds, recumbent position; usually relieved by
antacids but may be relieved by NTG if esophageal spasm (smooth muscle)
- Q-main difference from angina is pain is burning or gnawing

Musculoskeletal:
- Dull, sore if touched, hurts w/movement or coughing
- Hx of muscle strain or surgery
- Usually relieved by analgesics or NSAIDS & rest
- Past CABG pts: important to differentiate musculoskeletal pain from angina

6. What is the primary goal in management of angina or MI and what interventions

should you do to meet this goal?
Primary goal is to relieve pain by increasing oxygen supply & decrease oxygen demand
**Nursing DX – “Ineffective Tissue Perfusion: Cardiac**

-MONA:
- M – morphine – if unrelieved by NTG (vasodilates; reducing pain & anxiety)
- O - oxygen – 2-5L; nasal cannula
- N - nitroglycerin – lie down, give NTG; sub-x3 every 5mins
- A - aspirin – decreases platelet aggregation (clumping) by inhibiting
prostaglandins

Mgmt of MI: MOVE TINA

- M- morphine O- oxygen V- venous access E- EKG
- T – thrombolytics (tPa,rRA)- may be contraindicated if recent CPR, stroke,
surgery)
- I - isoenzymes (CK MB, Troponin)
- N- nitro
- A- aspirin, antiarrhythmias

7. Name some drugs that are called thrombolytics and their primary side effect
Streptokinase, t-PA(alteplase), r-PA (reteplase), t NKase (tenectaplase)
s/e – bleeding; give w/I 12hrs onset of chest pain w/at least 1mm ST elevation

8. What are the side effect to Nitroglyerin and the nursing implications for sublingual
and topical forms?

Nitropaste, Transderm-Nitro, Nitro-Dur, NitroBid, Isordil

S/E- headache, hypotension, syncope
Nursing:
- Keep sublingual tabs in dark bottle; replace every 6mos
- Topical ointment/patches – wear gloves; apply to hairless area; no rubbing or
massaging; apply in AM, remove in HS

9. What are names of some Beta Blockers, how do they work, and what are some side
effects?
Atenolol (Tenormin)- metoprolol (Lopressor)

Actions: block beta adrenergic response

- O- output decreases (decreasing contractility)
- L – lowers BP (decreased afterload)
- O- decreased oxygen demand (decreases workload)
- L – lessens HR & arrhythmias

**asthmatic will not tolerate BB

S/E:
- Bradycardia (hold if HR less than 50)
- Hypotension (hold if BP less than 90-100 systolic)
 - Bronchospasms, fatigue, CHF, impotence, rebound hypertension if d/c abruptly

10. What are names of some Calcium Channel blockers, how do they work, and what
are some side effects?
Narcardipine (Cardene)- diltiazem (Cardizem)-verapamil (Calan)

Actions:
- Dilate coronary arteries, lowers BP
- Slows HR
- Reduces contractility
- Decreases workload & O2 demand
- **3 Amigos – MAKE THE CORONARIES GROW, HEART RATE SLOW,
& BP LOW**
S/E:
- bradycardia (hold if HR less than 50)
- hypotension (hold if systolic BP less than 90-100)
- signs of CHF or AV Block

11. How should a patient with MI be managed medically in the first 12-24hrs (i.e.
activity and diet)?
- bed rest 1st 12 hrs w/bedside commode
- than advance to chair & ambulation as ordered
- clear liquid diet for 1st 12hrs,
- than advance as tolerated (lowfat, low cholesterol, low sodium)
- stool softeners – to avoid straining

12. list the potential complications of an MI and the related signs and symptoms
dysrhythmias – PVC’s, VT/VF (v tach & v fib – most common)
CHF/cardiogenic shock
Infarct extension (reinfarction 10-14 days after MI = early intervention
Pericarditis or dresslers syndrome (hypersensitivity response to necrotic tissue or an
autoimmune disorder (days to weeks later) after AMI)

Structural defects: ventricular aneurysm; valve regurgitation

Emotional issues: encourage verbalization of feelings; cardiac rehab- increases
activity; teach family CPR, use 911

13. What is the purpose of the Intra Aortic Balloon Pump?

- Mechanical circulatory support device that may be used after cardiac surgery or to
treat cardiogenic shock following AMI
- Temporary supports cardiac function, allowing the heart gradually to recover by
decreasing myocardial workload & O2 demand & increasing perfusion of the
coronary arteries
- Inflated during dystole, balloon supports cerebral, renal & coronary artery
perfusion
- Deflates during systole, so CO is unimpeded
14. Describe the nursing diagnoses and interventions for a patient pre and post CABG
Preop:
- Stop antiplatelets & anticoagulants 5-7 days before
- Verify diagnostic test results in chart: CBC, coagulation profile, urinalysis, chest
x-ray & coronary angiogram
- Correct any electrolyte imbalances or anemia
- Type & crossmatch blood (4 or more units)
- Skin & bowel preps
- Pt. education: - ventilator, chest tubes, pacing wires, foley, IVs, cardiac monitor,
pulmonary artery monitoring, medications
Postop:
- “Decreased Cardiac Output” - # 1 PRIORITY IMMEDIATE PO – 1ST 24 HRS

- monitor VS, O2 sat, hemodynamic parameters every 15mins

(initial hypothermia & bradycardia are expected, HR should return to norm
w/rewarming)
- bp may fall w/rewarming as vasodilation occurs (hypotension & tachycardia may
indicate low CO, PAP, PAWP, CO & O2 sat are monitored to evaluate fluid
volume, cardiac function & gas exchange)
- assess skin color
- measure I&O – report if less than 30ml/h for 2 consecutive hours
- record chest tube output=greater than 70ml/hr (warm, red, and free flowing
indicates hemorrhage; may need to return to surgery)
- monitor H&H & serum electrolytes
- admin. IV fluids, boluses & blood transfusions as ordered ; ensure blood volume
& O2 (carrying capacity)
- administer meds to maintain CO= inotropicdopamine, dobutamine to increase
contractions
- administer meds nitro- to reduce vascular resistance & afterload///antidysrythmias
to correct dysrhythmias
- keep temporary pacemaker at bedside, initiate pacing as indicated
- assess for signs of tamponade:
o increased HR
o decreased BP
o decreased urine
o increased CVP
o sudden decrease in chest tub output (muffles/distal heart sounds, decreased
peripheral pulses

- DX: Hypothermia
o Maintain to decrease metabolic rate & protect vital organs from ischemic
damage

- DX: Acute Pain

 o Frequently assess for pain using standard pain scale
o Admin. Analgesics on scheduled basis, by PCA, or continuous infusion
for 1st 24 -48 hrs
o Pre-medicate 30mins before activities or planned procedures

- DX: Ineffective Airway Clearance/Impaired Gas Exchange- #1 PRIORITY

AFTER EXTUBATION, USUALLY AFTER 24HRS

- Evaluate RR, depth, effort, symmetry of chest expansion & breath sounds
- Note ETT (endo tube) placement on x-ray/mark tube position & secure
- Maintain ventilator settings as ordered – monitor ABGs
- Suction as needed
- After extubation:
o Teach use of spirometer & encourage use every 2hrs
o Encourage DB- advise against vigorous coughing
o Teach use of “cough pillow” to splint chest incision & reduce pain
o Frequently turn & encourage movement
o Postop Day 1 – dangle, DB, controlled coughing & position changes

- DX: Risk for Infection

o Assess sternal wound every shift – document redness, warmth, etc
o Maintain sterile dressing for 1st 48hrs; then leave incision open to air. Use
steri strips as needed to maintain approximation of wound edges
o Report signs of wound infection
o Culture wound drainage as necessary
o Collaborate w/dietitian to promote nutrition & fluid intake

- DX: Distrubed Thought Processes

o Frequently reorient during initial recovery period
o Explain all procedures before performing them
o Secure all IV lines & invasive catheters/tubes
o Note verbal responses to questions. Correct misconceptions immediately
o Maintain a calendar & clock within client’s view
o Involve family members in providing reorientation
o Promote client participation in care
o Adm. sedatives cautiously
o Reevaluate neuro status every shift

- DX: Activity Intolerance

o Out of bed to chair 1st PO day
o Ambulate room 2nd PO day

- DX: Knowledge Deficit

o Postop & D/C instructions
15. What are the causes of Congestive Heart Failure?
Frequently due to impaired myocardial contraction from coronary heart disease &
myocardial ischemia or infarction from a primary muscle disorder: cardiomyopathy or
myocarditis
- Valve disorders or congential heart defects (structural cardiac disorders)
- Hypertension (hypertension & CHD are leading causes)

16. Describe the neuroendocrine responses and compensatory mechanisms that occur
during CHF
Neuroendocrine responses:
- Decreased CO stimulates the sympathetic nervous system & catecholamine
release
o Increased HR, BP & contractility
o Increased vascular resistance
o Increased venous return
- Decreased CO & decreased renal perfusion stimulate rennin/angiotensin system
o Vasoconstriction & increased BP
- Angiotensin stimulates aldosterone release from adrenal cortex
o Na & H2O retention by kidneys
o Increased vascular volume
- ADH is released from posterior pituitary
o H2O excretion inhibited
- Atrial natriuretic factor is released
o Increased Na excretion
o Diuresis
- Blood flow is redistributed to vital organs (Heart & Brain)
o Decreased perfusion of other organ systems
o Decreased perfusion of skin & muscles

17. How are the symptoms of left sided CHF different from right sided CHF?

Right Sided CHF (often caused by conditions that restrict blood flow to the lungs (ex.
chronic pulmonary disease)
- Increased pressures in the pulmonary vasculature of (rt. Ventricular muscle)
damage impair the right ventricle’s ability to pump blood into the pulmonary
circulation
o Rt. Ventricle & atrium become distended
o Blood accumulates in systemic venous system
o Increased venous pressures cause abdominal organs to become congested
& peripheral tissue edema to develop (feet & legs; if bedridden edema in
sacrum)
o Hepatic enlargement; ascites – rt. Upper quadrant pain
o Lethargy, fatigue
 o Jugular vein distension – increased venous pressure
o Increased rt. Heart pressures, CVP elevated
o Can have RSF alone w/RV heart attack
o Congestion of GI tract (anorexia & nausea)

Left Sided Failure of CHF = coronary heart disease & hypertension are common
causes
o Left sided can lead to rt. Sided failure as pressures in the pulmonary
vascular system increase with congestion behind the failing left ventricle
o As ventricular pressure fails, CO fails
o Pressure in left ventricle & atrium increase as the amt of blood remaining
in the ventricle after systole increase
o These increase pressures impair filling, causing congestion & increase
pressures in the pulmonary vascular system (which is normally low-
pressure system)
o leading to increased fluid movement from blood vessels into interstial
tissues & the alveoli (decreased O2 to cells; blood pools in left side of
heart & backs up into lungs)
o Signs:
- Inspiratory crackles & wheezes
- Orthopnea, SOB, cyanosis (impaired gas exchange)
- Paroxysmal nocturnal dyspnea, (diff. breathing while lying down)
- Dizziness, syncope= decreased CO
- Cough
o Pulmonary Edema – (severest form of CHF)
- Severe left sided CHF
• Cough w/blood tinged sputum, JVD
• Restlessness, tachycardia
• PCWP more than 25-30mmHg (norm 15-20)
- Tx: EMERGENCY
• Decrease excess fluid
• Pt upright; pulse ox; ABGs
• Give O2
• Morphine – vasodilator
• Diuretics – lasix – IV PUSH- response 20 mins
• NTG – vasodilator

18. What are non-pharmacologic nursing interventions for CHF?

Nursing:
- Decrease fluid intake
- Lower salt in diet
- Semi-fowlers to ease breathing
- TEDs/SCDs – to decrease thrombus in legs
- Weight daily & report more than 2#
- Report SOB, cough
 - Record pulse
- Report decrease in activity tolerance which is 1st sign of declining CHF

19. What are names, actions, and side effects of ACE inhibitors and diuretics?
Enalapril (Vasotic)-captopril (Capoten)

Actions:
- Inhibit angiotensin II resulting in vasodilation & less aldosterone
o (decrease BP & reduces blood volume)
S/E:
- hypotension
- impaired renal failure (over time)
- hyperkalemia
- neutopenia
- persistent dry cough

Diuretics: - furosemide (Lasix)- Hydrochlorothiazide (HCTZ)- spironolactone

(Aldactone) – K+ sparing

Actions:
- act on kidney tubules to inhibit reabsorption of sodium and water, promote K
excretion
S/E:
- hypokalemia **
- dehydration
- ototoxicity (Lasix) (give 20mg/min IV)----do not give any faster!!! TOXICITY
- need t worry about decrease in Potassium/ give supplement

Nesiritide (Natrecor)

New IV drip for decompensated CHF

Action: increases human b-type natriuretic peptide (BNP)
Improves dyspena by reducing PWCP, vasodilator, mild diuretic
S/E:
- hypotension; dysrhythmias (V tach); monitor cardiac rhythm and VS frequently

20. What are the signs and symptoms of Digoxin toxicity and what should you do?
Digotoxin toxicity :
- early signs: anorexia, N/V
- extreme bradycardia , diarrhea, yellow green halos, hypotension, AV block
o hypokalemia potentiates toxicity because it increases myocardial uptake of
digoxin-- monitor potassium level if >2 may be dig toxic
o administer digoxin immune tab (digibind)
o apical pulse for 1 full minute
o don’t give with antacids/ hold if hr <60
 - is a positive inotropic= & a (-) chronotropic, enhjances contractility and slows HR

Not one of the questions but FYI: Dopamine and Dobutamine are also (+) Inotropics
- sympathomimetic agents that increase contractility and CO
- Dopamine increases renal blood flow at lower doses and increases BP at higher
doses
- S/E
o Tachycardia, dysrhythmias (PVC, VT), tissue necrosis if extravasation
(tissue gets sloughly)

21. What are important items to include in discharge teaching for CHF patient?
- Perform as many activities as independently as you can
- Space your meals & activities
o Eat 6 small meals a day
o Allow time during day for periods of rest & relaxation
- Perform all activities at a comfortable pace
o If you get tired during any activity, STOP & rest for 15mins
o Resume only if you are up to it
- Stop any activity that causes chest pain, SOB, dizziness, faintness, excessive
weakness, or sweating Rest – Notify physician if activity tolerance changes & if
symptoms continue after rest
- Avoid straining. DO NOT lift heavy objects
o Eat a high fiber diet & drink plenty of water to prevent constipation
o Use laxative or stool softeners as approved by physician
- Begin a graded exercise program. Walking is good exercise that does not require
any special equipment
o Plan to walk 2x a day, at a comfortable slow pace for 1st couple of weeks
at home & gradually increasing
o Progress at own rate – take your time
o Aim for walking 3x per week (every other day
- Low sodium diet

22. What is the purpose of monitoring pressure in the pulmonary artery with a Swan
Ganz catheter?
- Inserted into a central vein (internal jugular/subclavical) and threaded into the rt.
Atrium
- Catheter is used to evaluate left ventricular & overall cardiac function
o Norm PA pressure is around 25/10mmHg (increased in LS failure)
o Norm mean pulmonary artery pressure is 15mmHg
o PAWP or PWP – (pulmonary artery wedge) – assesses left ventricular
function
o Norm 8-12mmHg (increased in left ventricular failure & pericardial
tamponade) (decreased in hypovolemia)
23. Why do some types of artificial heart valves require anticoagulation therapy for
the rest of the patient’s life?
Used to prevent the development of clots on the valve

24. What are signs and symptoms of pericarditis and cardiac tamponade?
Pericarditis:
- Chest pain – sharp, pleuretic – abrupt onset; most common symptom/ may radiate
front to back ; aggravated by respiratory movements (cough, DB)
- Pericardial friction rub
- Dyspnea
- Pericardial effusion-abnormal (sit up right & lean forward; moves heart away
from diaphragmatic side of lung pleura)
- Collection of fluid (pus, blood, serum, lymph)

Tamponade:
- Paradoxical pulse – markedly decrease in amplitude during inspiration (lg drop in
BP on inspiration)
- Hypotension, JVD, muffled heart sounds
- Fever, chills, fatigue (Increased WBC)

25. what are risk factors and signs/symptoms of abdominal aortic aneurysms?
- Abdominal aortic aneurysms – dilation of artery/weakness in wall
- (over 70) increases with age
- smoking
- most are asymptomatic- pulsating mass in the mid & upper abdomen & a bruit
over the mass aorta & illac arteries (these are classical signs)
- S/S
o Abdominal pain – radiates to back
o Different BP in arms & thigh, BP higher in thigh (shock ,systolic bruits)

26. How would you recognize complications after AAA surgery, such as infection,
graft leakage, pneumonia, lower extremity embolism,bowel ischemia, and impaired
renal function?

Graft Leakage:
- Ecchymoses of scrotum, perineum or penis: new or expanding hematoma
- Increased abdominal girth
- Weak/absent peripheral pulses/tachycardia, hypotension
- Decreased motor function or sensation in the extremities
- Fall in H&H
- Increasing abdominal, pelvic, back or groin pain
- Decrease in urinary output (less than 30ml/hr)
- Decreasing CVP, pulmonary artery pressure or pulmonary artery wedge pressure
Bowel Ischemia – pain & distention occult or fresh blood in stools or diarrhea – may
result from embolism

Lower Extremity embolism

- Pain & numbness in lower extremity
- Decreasing pulses (may be absent 4-12 hrs postop due to vasospasm
- Pale, cool, cyanotic skin

Renal Impairment
- Reduced urine output
- Fixed specific gravity
- Increasing BUN/Creatinine levels
- Hypovolemia or clamping of aorta during surgery

27. Define Hypertensive Crisis (Hypertensive Emergency) and the causes of it

- Rapid, significant elevations in systolic and/or diastolic pressures
- Systolic greater than 240mmHg
- Diastolic greater than 130 mmHg
- Most often occur when pts stop their meds suddenly or hypertension is poorly
controlled
S/S:
- Rapid onset
- Blurred vision, papilledema
- Headache
- Confusion
- Motor & sensory deficits
- Sys >240mmHg/dia>130mmHg

28. What are the goals for reducing BP in the first 2 hours and then the next 2-6hours
of hypertensive crisis?

- Reduce BP by no more than 25% in 2 hrs, then 160/100 in 2-6hrs

- Decreasing too quickly = rebound hypertension/causes stroke
- Immediate tx (w/I 1hr) vital to prevent cardiac, renal & vascular damage & reduce
morbidity & mortality
- BP monitored frequently (every 5-30mins)
- Carefully monitor BUN/Creatinine, CA & total protein levels  to determine
prognosis for recovery

29. What fast acting vasodilators are prescribed for hypertensive crisis and what are
the side effects?

Niprides – onset in secs – DRUG OF CHOICE (sodium nitroprusside)

- s/e: headache (thiocynate poisoning: absent reflexes; disorientation, muscle
spasms)dizziness, restlessness; blurred vision, tinnitus, abdominal pain, dyspnea
Nitro (NTG) – headaches, hypotension, syncope

Diazoxide (Hyperstat) – orthostatic hypotension

Apresoline – dizziness, drowsiness, headache, tachycardia, sodium retention, arrhythmia,

orthostatic hypotension