Cardiac Glycosides: Digoxin

Use: Increases contractility of cardiac muscle fibers
Indications: heart failure; heart rate control in atrial fibrillation
Desired results: Slows heart rate; decreases rate of cardiac electrical conduction; increases strength of cardiac muscle contraction. Improves heart failure symptoms by improving peripheral circulation, which increases fluid excretion.

Prototype drug: Digoxin (Lanoxin)—long half-life

• Narrow Therapeutic Window: therapeutic range = 0.5 (to treat HF) - 2.0 (best for atrial flutter or fibrillation) ng/ml
• Low serum potassium level (<3.5) can result in drug toxicity
• Bradycardia, N/V, visual “halos”, confusion
• Antidote: Digoxin immune Fab (Digibind)

Maintenance dose: 0.125 - 0.5 mg/dl. For older adults, dose is usually 0.125 mg/dl
Pulse rate should be above 60 beats/min.
Does not convert atrial fibrillation to normal heart rhythm. For mngmt. of atrial fibrillation, a calcium channel blocker, such as Calan may be prescribed. To prevent thromboemboli resulting from atrial fibrillation, Warfarin is prescribed concurrently w/ other drugs.
In clients w/ failing heart, cardiac glycosides increases myocardial contraction, w/c increases cardiac output and improves circulation and tissue perfusion. Because it decrease conduction through the AV node, the heart rate decreases.
Phenytoin and lidocaine are effective in treating digoxin induced ventricular dyshrythmias.
Lasix, HCTZ and systemic cortisone can cause hypokalemia. Patient should consume potassium rich foods or take potassium supplements.
Antacid can reduce Digoxin absorption so avoid taking it on the same time.

PHOSPHODIESTERASE INHIBITORS - Positive inotropic drug used for acute heart failure treatment
Promotes increase in cardiac muscle contraction, vasodilation

• IV drugs: inamrinone (Inocor), milrinone (Primacor) - increase stroke volume and cardiac output and promote vasodilation. Administered for no longer than 48-72 hours.

Used for short-term acute management of heart failure, requires cardiac monitoring during therapy for severe dysrhythmias can occur.

ATRIAL NATIURETIC PEPTIDE HORMONE
Nesiritide (Natrecor)— diuresis for heart failure treatment
Inhibits  ADH by increasing urine sodium loss. Promote vasodilation, diuresis and natriuresis. Useful for treating clients who have acute decompensated HF w/ dyspnea at rest or who have dyspnea w/ little exertion.

Heart failure

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.
Renin is secreted by the juxtaglomulerus of the kidney in response to the request of the baroreceptors in the aortic arch. Renin 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 Renin. 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

Symptom	heart	kidney	liver
Ascitesedema	ADH, renin, Aldosterone secretion, venous congestion into right ventricleIncreased hydrostatic pressure	ADH, renin, Aldosterone secretion, venous congestionLack of output	Decreased albuminPortal hypertension, increased capillary pressure, obstruction of venous flow
hypertension	ADH, renin, Aldosterone secretion, arterial congestion, edema, arterial constriction	ADH, renin, Aldosterone secretion, fluid retention	Liver does not metabolize aldosterone
breath		acetone	Fetor hepaticus
Change sensorium	Decreased circulation and oxygen	Increased nitrogen and acidosis	Ammonia and nitrogen
hepatomegaly	Venous engorgement		Scar tissue, inflammation
puritis		Uric acid crystals, uremic frost	Bile salts and jaundice
anemia	Low hemoglobin and oxygen carrying power	Lack of erythropoietin	Inability to metabolize hemoglobin and clotting factors
Diagnostic labs	H &H, BNP, Aldosterone	BUN, creatinine, electrolytes Creatinine clearance	AST, ALT, PT, BUN, A/G ratio
acidosis	Decrease CO, inadequate tissue perfusion, decrease oxygen exchange in cells, lactic acidosis	Hydrogen retention
anorexia	Venous stasis in the abdominal organs, ascites	Toxins, ammonia	Ascites, toxins
diet	DASH, low sodium, cholesterol, low triglycerides, and fluid restriction	Low sodium, potassium, protein, fluid restriction, high carbohydrate	High carbohydrate, low protein, low sodium
hepatomegaly	venous engorgement		Inflammation, scar tissue
Treatments	diuretics	dialysis	Diuretics, SPA

Heart Failure

Heart failure develops when the heart cannot effectively fill or contract w/ adequate strength to function as a pump to meet the needs of the body. As a result, cardiac output falls, leading to decreased tissue perfusion. The body initially adjusts to reduced cardiac output by activating compensatory mechanisms to restore tissue perfusion. These normal mechanisms may result in vascular congestion -- hence, the commonly used term congestive heart failure. As these mechanisms are exhausted, heart failure ensues, w/ increased morbidity and mortality.

Depending upon the cause, HF presents initially as right sided heart failure or left sided heart failure; as it progresses, the other side becomes affected

Left heart failure:

• the left ventricle has reduced capacity to pump blood into systemic circulation causing decreased cardiac output and stasis or backup of blood into the pulmonary circulation
• due to coronary artery disease, hypertension, cardiomyopathy, rheumatic heart disease
• Presenting symptoms: dyspnea on exertion (1st sign), orthopnea, PND, new s3, crackles; pulmonary edema.

Right heart failure:

•  the right ventricle has reduced capacity to pump blood into pulmonary circulation causing stasis or back up of blood into the venous circulation
• due to COPD, pulmonary embolism, rv infarct
• usually called cor pulmonale
• Presenting symptoms: edema of lower extremities, jugular venous distention, abdominal discomfort and nausea occur from fluid congestion in the abdominal organs

Both sides:

•  Presenting symptoms are unexplained fatigue, decrease exercise tolerance, unexplained altered mental status

Further clarification:

• Fall in cardiac output activates mechanisms that cause increased salt and water retention which causes weight gain and further increases pressures in the capillaries, resulting in edema
• Nocturia develops as edema fluid from dependent tissues is reabsorbed when the patient is supine
• Paroxysal nocturnal dyspnea, a frightening condition in w/c the pt. awakens at night acutely short of breath. It occurs when edema fluid that has accumulated during the day is reabsorbed into the circulation at night, causing fluid overload and pulmonary congestion
• Congestive hepatomegaly and splenomegaly caused by engorgement of the portal venous system results in increased abdominal pressure, ascites and GI problems. 
• Prolonged RHF may lead to impaired liver function

Main goals for care:

• slow progression
• reduce cardiac workload
• improve cardiac function
• control fluid retention