Heart Failure – Answers

In the latest textbooks, the terminology has changed. It used to be called Congestive Heart Failure (CHF), but the new term is just Heart Failure (HF). In this study guide we will use the term heart failure.


Review and define the terms:

Preload is the amount of blood returning to the heart from the body via the Vena Cava.

 After load is the amount of resistance the heart must pump against to eject blood from the heart into the body.

Cardiac output = SV X R stroke volume times rate is the amount of blood circulated through the body in a minute.

Stroke volume is the amount of blood pump from each ventricle during contraction

Starling’s Law of the Heart reflects the elasticity creating force of cardiac cells to contract. As heart goes into failure the cells are stretch and dilated and so loose the ability to contract with efficient force. Think of a rubber band, the more it is stretch and dilated the weaker it is and loses its recoil ability. This is the same physiology seen in heart failure.


How do the baroreceptors in the carotid arch influence hormone secretion in heart failure?

Baroreceptors sense the pressure with which the blood as ejected and fills the aorta. This is reflected in the blood pressure. If the pressure is low, word is sent out to secrete hormones of the body to contract the arteries, and retain fluid to fill the arteries thus raising the blood pressure.


Explain the role of these hormones in heart failure:

Adrenalin – causes vasoconstriction of blood vessels leading to hypertension

Aldosterone – binds with sodium to retain water and cause the symptom of edema

Antidiuretic Hormone closes the epithelial cells in the distal kidney tubule and thereby retains water that adds to the symptoms of hypertension and edema.

Rennin is secreted by the juxtaglomulerus of the kidney in response to the request of the baroreceptors in the aortic arch. Rennin then goes to the lungs to initiate the formation of Angiotensin I and II that will add to hypertension.

Angiotensin II goes to the cardiac cells to stimulate remodeling or the formation of immature cardiac cells that are not able to contract with the force necessary to eject the volume of blood necessary for adequate stroke volume, thus the cardiac output remains low and the heart continues into failure.


What is the physiology that causes the primary symptoms of dyspnea, edema, and fatigue in heart failure?

Dyspnea comes from lungs trying to compensate for decrease perfusion in alveoli.

Fatigue results from lack of oxygen and build up of carbon dioxide in cells as sluggish circulation cause tissues to not have normal cleaning and perfusion.

Edema is a safety mechanism to third space fluid and decrease the work load of the heart pumping blood.


Why does PND paroxysmal nocturnal dyspnea occur primarily at night?

Edema fluid held in the legs during the day while a person is sitting, returns to the general circulation when the person is horizontal in bed. This fluid causes overload and drowning sensation leading to symptoms of severe dyspnea, air hunger and pulmonary edema.


Contrast the etiology of left and right sided heart failure.

Left sided heart failure occurs after MI, hypertension, or other causes that weaken the pumping ability of the left ventricle. Occurs in response to resistance of blood pumping in afterload. Low blood flow over the carotid baroreceptors triggers the compensatory hormone mechanisms or Adrenalin, Aldosterone, ADH and Rennin. Treatment is medication to reduce afterload or intraortic balloon pump is person goes into shock.

Right sided heart failure deals with preload. The edema fluid is trying to return to the already full distended right ventricle.

Think about it … blood can’t be pumped out to the body or lungs so ventricles are full of blood. Where is new blood trying to ender the heart going to go? It backs up so jugular veins distend and A/V waves can be seen when the heart contracts. The body employs safety measure of third spacing reducing the flow of blood back to the heart by pushing it into the tissues by increased hydrostatic pressure. This is similar to when a river is full of water; the water overflows the banks and seeps into the ground. Same thing in heart failure, the ground is the tissues of the body (pulmonary edema of lungs, ascites from the liver, and pitting edema in the legs.


Differentiate Cor Pulmonale from right sided heart failure.

Right sided heart failure occurs with MI, Cor Pulmonale occurs from COPD as heart has to pump against the resistance of lung tissue pathology.


Comparison of heart, kidney, and liver failure symptoms

AscitesedemaADH, rennin, Aldosterone secretion, venous congestion into right ventricleIncreased hydrostatic pressureADH, rennin, Aldosterone secretion, venous congestionLack of outputDecreased albuminPortal hypertension, increased capillary pressure, obstruction of venous flow
hypertensionADH, rennin, Aldosterone secretion, arterial congestion, edema, arterial constrictionADH, rennin, Aldosterone secretion, fluid retentionLiver does not metabolize aldosterone
breathacetoneFetor hepaticus
Change sensoriumDecreased circulation and oxygenIncreased nitrogen and acidosisAmmonia and nitrogen
hepatomegalyVenous engorgementScar tissue, inflammation
puritisUric acid crystals, uremic frostBile salts and jaundice
anemiaLow hemoglobin and oxygen carrying powerLack of erythropoietinInability to metabolize hemoglobin and clotting factors
Diagnostic labsH &H, BNPAldosteroneBUN, creatinine, electrolytesCreatinine clearanceAST, ALT, PT, BUN, A/G ratio
acidosisDecrease CO, inadequate tissue perfusion, decrease oxygen exchange in cells, lactic acidosisHydrogen retention
anorexiaVenous stasis in the abdominal organs, ascitesToxins, ammoniaAscites, toxins
dietDASH, low sodium, cholesterol, low triglycerides, and fluid restrictionLow sodium, potassium, protein, Giovanetti diet, fluid restriction, high carbohydrateHigh carbohydrate, low protein, low sodium
hepatomegalyvenous engorgementInflammation, scar tissue
TreatmentsdiureticsdialysisDiuretics, SPA