Rehab Test #2 - Cardiac, Pulmonary

Question 1

Atherosclerosis

Answer 1

Narrowing of arteries
Endothelial lining altered as a result of inflammation and injury
Injury allows deposit of cholesterol and lipid within the intimal wall of the artery
Begins as soft deposits of fat that harden with age
Plaque becomes unstable, ruptures, platelets aggregate leads to thrombus formation

Question 2

Angina

Answer 2

When the heart’s supply of oxygen rich blood is insufficient to meet the heart muscle’s metabolic demands the heart muscle “aches” - this is called angina pectoris, or chest pain.

Question 3

Classifications of Angina

Answer 3

Class I
Ordinary physical activity does not cause angina strenuous activity only.
Class II
Angina occurs with walking or climbing stairs rapidly or up hill.
Class III
Marked limitation in ordinary daily activity
Class IV
Anginal symptoms may be present at rest

Question 4

Myocardial Infarction

Answer 4

Myocardial infarction (MI) occurs when there is sustained ischemia to heart muscle which results in myocardial cell death (necrosis).

Question 5

Heart Failure

Answer 5

Heart failure (HF) is a pathologic state in which the heart is unable to pump blood in sufficient amounts to meet the body’s metabolic needs (decreased CO).
Systolic
Diastolic

As blood flow out of the heart slows, blood returning to the heart through the veins backs up, causing congestion in the tissues

Major causes:
Chronic hypertension 
Myocardial infarction
Other causes
Valve deficiency
Atrial fibrillation/flutter
Aging of the myocardium
Diabetes

Question 6

Left-sided heart failure

Answer 6

Pulmonary edema
Coughing
Dyspnea

Question 7

Right-sided heart failure

Answer 7

Jugular vein distention
Ascites - abnormal accumulation fluid in the abdominal (peritoneal) cavity.
Pedal edema

Question 8

Patient Education for Heart Failure

Answer 8

Daily weights
Acronym FACES
F - fatigue
A - limitation of activities
C - chest congestion/ cough
E - dependent edema
S - shortness of breath
According to the American Heart Association and the American College of Cardiology (2005) treatment of chronic heart failure should be directed at reducing the effects of the:
Renin-angiotensin-aldosterone system (RAAS)
Sympathetic nervous system (SNS)

Question 9

Medications Used for HF

Answer 9

Diuretics
Agents that inhibit the RAAS
ACE inhibitors (ACEI)
Angiotensin II receptor blockers (ARBs)
Aldosterone antagonists
Agents that inhibit the SNS
Beta-blockers
Others
Cardiac glycosides, B-type natriuretic peptides, vasodilators (BiDil)

Question 10

ER management of HF

Answer 10

Start IV
Administer O2 2-4 liters via NC
Nitrogylcerin SL and ASA
Morphine for pain
Continous ECG, BP and O2 sat monitoring
Emergent PCI 
Treatment of choice for confirmed MI
Balloon angioplasty + stent(s) placement

Question 11

Statins - prevent heart attack

Answer 11

Mechanism of action: Decrease the rate of cholesterol production in the liver by inhibiting hydroxymethylglutaryl coenzyme A reductase (HMG-CoA reductase). May also decrease inflammation as well.

Drug effects: Decrease LDL cholesterol by 25-63%
Examples: atorvastatin (Lipitor), rosuvastatin (Crestor), simvastatin (Zocor), pravastatin (Pravachol)

Adverse effects:
GI disturbance such as dyspepsia, cramps, flatulence, constipation, abdominal pain  (mild and transient)
Hepatotoxicity (0.5-2%)
Myopathy (5-10%)
Rhabdomylosis (rare)
Contraindication
Pregnancy category X

Nursing implications:
Initial effects 2 weeks, maximal effects 4 to 6 weeks, reversal of effects upon withdrawal.
Monitor LFT, CPK levels
Assess for C/O weakness, muscle aches

Patient education
Most effective when taken at bedtime
Educate patient to immediately report muscle pain/weakness
Keep follow up appointments

Question 12

Antianginal Drugs Controller drugs

Answer 12

Beta-blockers, calcium channel blockers, and long-acting nitrates provide baseline prophylaxis or protection against acute angina attacks

Question 13

Antianginal Drugs Rescue drugs

Answer 13

Sublingual (SL), translingual spray, and intravenous (IV) nitroglycerin is used to treat acute anginal pain

Question 14

Nitrates

Answer 14

Mechanism of action/drug effects:
Dilates vessels, especially veins, by relaxing vascular smooth muscle. Reduces preload. Also, dilates coronary arteries which improves blood flow through coronary vasculature.
Examples:
nitroglycerin (Nitro-Bid, Nitrostat)
isosorbide dinitrate (Isordil)
isosorbide mononitrate (Imdur)

Indications:
Stable, unstable, and vasospastic angina
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Contraindications:
Hypotension, erectile dysfunction drugs (e.g. Viagra)

Adverse effects:
Headache
Orthostatic hypotension
Reflex tachycardia

Do NOT Combine ED Drugs and NTG!

Question 15

Sublingual Nitroglycerin - for angina

Answer 15

Tablet should be held under tongue until dissolved. Avoid eating, drinking, or smoking until tablet is dissolved.
Acute anginal attacks:
Advise patient to sit down
Relief should occur within 5 minutes
If no relief after first dose call 911
May be repeated every 5 minutes for 3 doses

Question 16

Beta-Blockers - for angina and heart failure

Answer 16

Mechanism of action:
Prevent stimulation of beta receptors in the heart whichdecreases heart rate and contractility. Also prevents release of renin.

Drug effects:
Decreased myocardial oxygen demand

Examples:
propranolol (Inderal)
metoprolol (Lopressor)

Indications:
Prevention/prophylaxis of stable angina

Contraindications:
Bradycardia, AV block, asthma
Adverse effects:
Dizziness (10%)
Bradycardia (3%), heart block
Mask signs/symptoms of hypogylcemia in diabetics
Bronchoconstriction (3%)
Constipation

Nursing implications:
Assess for contraindications
Assess vital signs – hold and notify MD for HR less than 60

Patient education:
Inform patient they are for long-term prevention, not immediate relief
Change positions slowly, avoid time in hot tubs, saunas which result in vasodilation
Monitor glucose closely if diabetic
Do not abruptly stop (rebound angina)

Question 17

Calcium Channel Blockers (CCB) - for angina

Answer 17

Mechanism of action:
Prevents influx of calcium ion across cell membrane of vascular smooth muscle. Dilation of peripheral and coronary arteries.

Drug effects:
Decreased afterload decreases workload of the heart and therefore, myocardial oxygen demand.

Examples:
diltiazem (Cardizem), verapamil (Calan)

Indications:
Prevention/ prophylaxis of stable, variant angina

Adverse effects:
Dizziness (4%)
Hypotension (4%)
Constipation (9%)
Peripheral edema (2%)

Nursing implications:
Monitor vital signs

Patient education:
Avoid hazardous activities while dizzy
Change positions slowly
Increase fluid and fiber intake to prevent constipation unless otherwise instructed by provider.

Question 18

Diuretics (Loop Diuretics) - for heart failure

Answer 18

Mechanism of action:
Decreases Na, Cl, and K reasborption in thick ascending limb of the loop of Henle in the nephron which results in profound diuresis.

Drug effects:
Reduced blood volume decreases venous pressure (preload) and atrial pressure (afterload). Reduce cardiac dilation. Reduced pulmonary and peripheral edema.

Examples:
furosemide (Lasix)

Indications:
Acute and chronic HF

Dosages and Routes:
Oral: 20-80 mg/daily or BID

Adverse effects:
Hypokalemia (↑ risk of Digoxin toxicity)
Severe hypotension

Nursing implications:
Assess patient’s fluid volume status, vital signs, labs
Patient education:
Avoid taking late in the afternoon due to nocturia.
Eat foods rich in potassium (bananas, oranges, potatoes, tomatoes, meats, fish, wheat bread, legumes). K+ supplement may be necessary
Signs of hypokalemia include weakness, leg cramps.

Question 19

ACE inhibitor - for heart failure

Answer 19

Mechanism of action:
Inhibits ACE which prevents the conversion of angiotensin I to angiotensin II (a powerful vasoconstrictor). Also reduces aldosterone secretion. Suppress degradation of kinins (vasodilator).

Drug effects:
Arteriolar and venous dilation results in reduced preload, afterload, pulmonary congestion/pedal, and increased cardiac output. ↑ kinins reduces cardiac remodeling. 
Examples:
lisinopril (Prinvil), captopril (Capoten), enalapril (Vasotec) 
Indications: 
Cornerstone of HF therapy
Adverse effects:
Hypotension (0.9-6.7%)
Cough (9%)
Hyperkalemia
Angioedema

Question 20

Beta Blocker - for heart failure

Answer 20

Mechanism of action:
Protect heart from excessive sympathetic stimulation

Drug effects:
Improve LV ejection fraction (1-3 months), slow the progression of HF, reduce need for hospitalization, and prolong survivial.

Examples:
Carvedilol (Coreg), bisoprolol, sustained-release metoprolol (Toprol XL)

Dosages and routes:
Start low and go slow. Excessive beta blockade can reduce contractility.

Contraindications:
Heart block

Adverse effects:
Fluid retention/ worsening HF
Bradycardia/ heart block
Hypotension

Question 21

Cardiac Glycosides

Answer 21

Oldest group of cardiac drugs
Comes from the foxglove plant
Digoxin (Lanoxin) is the only cardiac glycoside available in the U.S.
No longer used as first-line treatment

Mechanism of action:
Inhibits the sodium-potassium adenosine triphosphatase pump. This causes an accumulation of calcium within the myocytes. ↑Ca++ augments contractile force by facilitating the interaction of myocardial actin and myosin.

Drug effects:
Positive inotropic effect on the heart increases the force of ventricular contraction which increases cardiac output. Increased CO, can reverse all the overt manifestations of HF.

The sodium-potassium-adenosine triphosphate pump keeps the kids (K+) in the house (cell)……
The sodium-potassium-adenosine triphosphate pump keeps the neighbors (Na+) and their cats (Ca++) out of the house (cell)
Digoxin inhibits the sodium-potassium adenosine triphosphate pump…this allows the neighbors (Na+) and their cats (Ca++) into the house (cell) and the kids (K+) out on the streets (vessels)

Indications:
Second-line heart failure, atrial fibrillation
Precautions:
Lasix (secondary to risk of hypokalemia)

Adverse effects:
Digoxin toxicity
Cardiac dysrhythmia

Question 22

Digoxin (Lanoxin)

Answer 22

Signs of dig toxicity include anorexia, nausea, vomiting, yellow tinge to vision, halos

Very narrow therapeutic window.
Drug levels must be monitored
0.5 to 0.8 ng/mL (old upper limit 2 ng/mL)

Low potassium levels increase its toxicity. Electrolyte (serum K) levels must be monitored (normal range 3.5 – 5 mEq / L)

Question 23

Identify diagnoses appropriate for cardiac rehabilitation

Answer 23

Chronic, stable angina
Stable heart failure
Post angioplasty
Post MI
Post CABG
Post heart transplant
Not had a cardiac event but are at risk because of unfavorable risk factor
Stable heart disease, deconditioned by another serious illness

Question 24

Delineate the phases of cardiac rehabilitation

Answer 24

Phase 1:
Initiated while the patient is still in the hospital
Phase 2:
A supervised ambulatory outpatient program spanning 3–6 months
Phase 3:
A lifetime maintenance phase in which physical fitness and additional risk-factor reduction are emphasized.

Question 25

Coronary artery bypass grafting (CABG)

Answer 25

is a type of surgery that improves blood flow to the heart. Surgeons use CABG to treat people who have severe coronary heart disease (CHD).

Question 26

Describe the components of a cardiac rehabilitation program

Answer 26

Medical evaluation
Prescribed exercise
Education on nutrition
Counseling of patients with cardiac disease
Emotional support

Question 27

Discuss the goals of cardiac rehabilitation

Answer 27

Prevent progression of disease/ disability
Improve physical functioning
Improve quality of life

Question 28

Define Chronic Obstructive Pulmonary Disease (COPD)

Answer 28

Two lung diseases: chronic bronchitis and emphysema. Both characterized by irreversible airflow obstruction that interferes with normal breathing and gas exchange. Airflow limitation is progressive and associated with an abnormal inflammatory response.

Question 29

Chronic Bronchitis

Answer 29

Defined as a cough and sputum production for at least 3 months in each of 2 consecutive years with inflammation and eventual scarring of the bronchial tube lining

Question 30

Emphysema

Answer 30

Air spaces enlarge as a result of the destruction of alveolar walls
The surface area where gas exchange takes place is reduced

Question 31

A “pink puffer”

Answer 31

emphysema - destruction of the airways distal to the terminal bronchiole–which also includes the gradual destruction of the pulmonary capillary bed and thus decreased inability to oxygenate the blood.

less surface area for gas exchange
less vascular bed for gas exchange-
but less ventilation-perfusion mismatch than blue bloaters

The body then has to compensate by hyperventilation (the “puffer” part).
Their arterial blood gases (ABGs) actually are relatively normal because of this compensatory hyperventilation.

Eventually, because of the low cardiac output, people afflicted with this disease develop muscle wasting and weight loss.
They actually have less hypoxemia (compared to blue bloaters) and appear to have a “pink” complexion and hence “pink puffer”. Some of the pink appearance may also be due to the work (use of neck and chest muscles) these folks put into just drawing a breath.

Question 32

A “blue bloater”

Answer 32

chronic bronchitis - excessive mucus production with airway obstruction resulting from hyperplasia of mucus-producing glands, goblet cell metaplasia, and chronic inflammation around bronchi.
Unlike emphysema, the pulmonary capillary bed is undamaged.

Instead, the body responds to the increased obstruction by decreasing ventilation and increasing cardiac output.

There is a dreadful ventilation to perfusion mismatch leading to hypoxemia and polycythemia.

In addition, they also have increased carbon dioxide retention (hypercapnia).

Because of increasing obstruction, their residual lung volume gradually increases (the “bloating” part). They are hypoxemic/cyanotic because they actually have worse hypoxemia than pink puffers and this manifests as bluish lips and faces–the “blue” part.