Congestive Heart Failure: Guided Practice Set #1

Myocardial Performance Factors

For any given inotropic state, ventricular performance will be significantly affected by the degree of ventricular stretch as determined by ventricular end-diastolic volumes (EDV).
The general relationship, as shown above, is the Frank-Starling mechanism. Several factors influence end diastolic volumes, beginning with total blood volume.
- Significant volume depletion leads to decreased cardiac output with preload and end-diastolic volumes declining.
- Venous tone
- Skeletal muscle activity
Atrial contraction:
- Atrial contraction (atrial kick) enhances ventricular filling.
- In the hypertrophic ventricle (with reduced compliance) appropriately time atrial contraction may be especially important in achieving adequate levels of ventricular filling.
Inotropic state (myocardial contractility): Factors that influence the inotropic state affect ventricular performance at a given ventricular end-diastolic volume. These factors change the concentration of Ca²⁺ at the myofilaments and include in part
- Adrenergic nerve activity
- Circulating catecholamines
- Exogenously administered agents:
  - Cardiac glycosides
  - Dopamine/dobutamine
  - Caffeine
  - Isoproterenol
  - Theophylline
  - Calcium
Exogenously administered agents: Drugs that decrease ventricular performance:
- Procainamide
- Disopyramide
- Calcium channel blockers
- Alcohol
- Barbiturates
- Local and general anesthetics
Physiological Depressants: hypoxia, hypercapnia, ischemia, and acidosis.
Loss of ventricular muscle mass:
Ventricular afterload:
- Afterload is the stress developed in the wall of the ventricle during ejection and depends on aortic pressure and ventricular dimensions.
- Myocardial fiber tension is determined by the product of the intracavity ventricular pressure and radius divided by wall thickness (Laplace's law).
- Therefore, for the same level of aortic pressure, afterload increases with ventricular dilation.
- Left ventricular stroke volume is inversely proportional to afterload.
- In the failing heart with limited or no preload reserve (increasing preload in a normal heart increase contractility), afterload determines ventricular performance.
- When afterload increases (increase in vasoconstriction) in the failing heart, cardiac output may be reduced further even while oxygen demand increases.
- Vasodilators may improve myocardial performance by reducing ventricular afterload
Exercise:
- With exercise, venous return is significantly increased and results in enhanced ventricular filling and preload.
  Increases in cardiac adrenergic activity and increases in circulating levels of catecholamines increase heart rate and enhance the myocardial contractility.
- Arterial pressure does not increase substantially since vasodilatation in exercising muscles offset the increase in cardiac output.

This drug should probably not be administered to a patient with congestive heart failure because the drug may further reduce contractility; the drug should probably also not be prescribed to an asmatic since the drug may increase bronchiolar smooth muscle tone.
1. digoxin (Lanoxin, Lanoxicaps)
2. terbutaline (Brethine)
3. metoprolol (Lopressor)
4. atropine
In congestive heart failure, decreased cardiac output and changes in ANS activity produce:
1. increased blood volume
2. increased GFR
3. decreased renin levels
4. A & B
Factors that affect cardiac performance:
1. circulating epinephrine
2. digoxin (Lanoxin, Lanoxicaps)
3. rhythm of cardiac contraction
4. A, B & C
Most important in acutely altering the position of the force velocity and left ventricular function curve:
1. circulating catecholamine
2. dopamine levels
3. norepinephrine released from adrenergic nerves
4. total blood volume.
Drug(s) that affect left ventricular stroke volume:
1. furosemide (Lasix)
2. dobutamine (Dobutrex)
3. metoprolol (Lopressor)
4. all of the above
At any given preload and myocardial inotropic state, cardiac output would be significantly affected by afterload. Which drug(s) would reduce afterload soon after administration.
1. diazoxide (Hyperstat)
2. minoxidil (Loniten)
3. phentolamine (Regitine)
4. all of the above
Reduces preload
1. minoxidil (Loniten)
2. isosorbide dinitrate (Isordil, Sorbitrate)
3. hydralazine (Apresoline)
4. phentolamine (Regitine)
Reduces afterload in a CHF patient
1. minoxidil (Loniten)
2. captopril (Capoten)
3. phentolamine (Regitine)
4. all of the above
Reduces preload AND afterload
1. nitroprusside sodium (Nipride)
2. phentolamine (Regitine)
3. captopril (Capoten)
4. A & C
Cardiac physiological affects associated with the action of digoxin:
1. increases force developed during myocardial muscle fiber shortening at a given preload for a CHF patient
2. increases the force developed during myocardial muscle fiber shortening at a given preload for a normal individual
3. decreases the AV nodal effective refractory period.
4. A & B
Effect of norepinephrine on cardiac force-velocity curves in normal individuals and those with CHF:
1. shift upward (CHF patient)
2. shift upward (Normal)
3. both
4. neither
Mechanism for a decrease in heart rate by digoxin (Lanoxin, Lanoxicaps) in a congestive heart failure patient:
1. competive blocade of norepinephrine effects at the SA node
2. improvement of cardiac function decrease sympathetic drive and thus heart rate is decreased.
3. decrease in AV conduction
4. digoxin (Lanoxin, Lanoxicaps) directly decreases phase-4 depolarization
Associated with chlorthalidone (Hygroton) use in CHF management.
1. hyperuricemia
2. hypoglycemia
3. hypocalcemia
4. hypolipdemia
In severe congestive heart failure with significant pulmonary and peripheral edema and compromised renal function, furosemide (Lasix) may be more appropriate than hydrochlorothiazide (HCTZ, Esidrix, HydroDIURIL) because:
1. thiazides are less effective when renal blood flow is reduced
2. furosemide (Lasix) causes a larger excreted fraction of filtered sodium than hydrochlorothiazide
3. furosemide (Lasix) reduces preload by venous dilation
4. A, B & C
Useful in pharmacological management of congestive heart failure:
1. prazosin (Minipress)
2. captopril (Capoten)
3. hydralazine (Apresoline)
4. all of the above
Diuretic used in CHF that is most likely to cause hypokalemia
1. triamterene (Dyrenium)
2. amiloride (Midamor)
3. spironolactone (Aldactone)
4. furosemide (Lasix)
H. M. is a 63 year old male with a long history of hypertension and coronary vascular disease.
He has had two myocardial infarctions over the past three years and complains of arthritic pain.
He has been taking atenolol and chlorothalidone for his hypertension and verapamil to prevent
recurrence of paroxysmal supraventricular tachycardia. He also takes large doses of
non-steroidal anti-inflammatory drugs (high dose ibuprofen) for his arthritis. He presents with
severe systemic edema as a result of congestive heart failure which had been gradually
worsening over the past six months. His serum potassium is 2.9 mEq/L (3.5-5.3). What
medications may have contributed to heart failure in this patient?
H. M. is a 63 year old male with a long history of hypertension and coronary vascular disease.
He has had two myocardial infarctions over the past three years and complains of arthritic pain
1. atenolol (Tenormin)
2. ibuprofen
3. verapamil (Isoptin, Calan)
4. all of the above