Chapter 24: Treatment of CHF Flashcards
Preload is proportional to the end-diastolic ventricular volume,
or the amount of blood in the ventricles immediately before systole.; the
amount of fluid the heart must pump
Preload
afterload can be related to the amount of systemic resistance
the ventricles must overcome to eject blood into the vasculature.; the
pressure that the heart must work against in the peripheral vessels
Afterload
increasing or decreasing the force of muscular contractions
Inotropic
influencing the rate especially of the heartbeat
Chronotropic
affecting the conductivity of cardiac muscle —used of the
influence of cardiac nerves
Dromotropic
Chronic condition in which the heart is unable to pump sufficient quantity
of blood to meet the needs of peripheral tissues
Congestive Heart Failure
Arises from the tendency of fluid to accumulate in the lungs and peripheral tissues
Congestion
CHF symptoms (PDD)
○ Peripheral edema
○ Decreased tolerance for physical activity
○ Dyspnea, SOB in pulmonary congestion
CHF Prognosis
approximately 50% of patients die within 5 years after they are
diagnosed with heart failure
CHF Pathophysiology
Mechanisms underlying chronic heart failure:
● Disturbances in the cardiac cell
● Altered genetic expression of myocardial cells
● Systemic changes in hemodynamics and
● Humoral factors
● Self-perpetuating - initiates a vicious cycle that leads to
further decrements in cardiac function
Primary problem: the heart is unable to push blood forward through the circulatory system -> pressure to build up in the veins returning to the heart→ blood begins to back up in the venous system → increase pressure gradient for fluid to move out of the capillaries → edema or congestion
Congestion in Left and Right Heart Failure
- The left atrium and ventricle are unable to pump the blood coming from the lungs
- Pressure build up in the pulmonary veins, fluid accumulates in the lungs
- Pulmonary edema
Left HF
- The right atrium and ventricle are unable to
handle blood returning from the systemic
circulation - Fluid accumulate in the peripheral tissues
- Ankle edema and organ congestion
Right HF
- Usually caused by hypertension, CAD, and valvular diesease
- Divided into two subtypes: Systolic (reduced ED), Diastolic (preserved ventricular function)
Symptoms:
- cough
- crackles
- pink sputum
- tachycardia
- fatigue
- cyanosis
- exertional dyspnea
Left HF
- Can be caused by left ventricular failure, right MI, or pulmonary hyptertension
- Right ventricle cannot empty completely
- May be secondary to pulmonary problems (COPD)
Symptoms:
- peripheral edema
- ascites
- enlarged liver and spleen
- JVD
- weight gain
- increased peripheral venous pressure
Right HF
- Digitalis
- Phosphodiesterase (PDE) inhibitors
- Dopamine, Dobutamine
(DPD - PIA)
Agents That Increase Myocardial Contraction Force (Positive Inotropic
Agents)
○ ACE inhibitors (-pril)
○ ARBs (-sartan)
○ Direct renin inhibitor - Aliskiren
○ Beta blockers (-olol)
○ Diuretics
○ Vasodilators
Agents That Decrease Cardiac Workload
● Digoxin, digitoxin
● Benefits: Improves cardiac pumping ability; increases CO at rest and during exercise; increased exercise tolerance; decrease symptoms of HF and decrease hospitalization
Digitalis
(Positive Inotropic Agent)
Effects:
○ direct inhibitory effect on SNS activity; reflex stimulation of Vagus nerve
○ stabilize HR, slow impulse conduction
● Indications: systolic heart failure (heart failure with reduced ejection fraction
(HFrEF)); Ejection fraction <40% and Atrial Fibrillation, Atrial Tachycardia
● AE: GI distress, CNS disturbance (drowsiness, fatigue, confusion, visual
disturbances), arrhythmias: (PACs, PVCs, VTach, high degree AV block,
paroxysmal atrial tachycardia)
Digitalis
(Positive Inotropic Agent)
Increases myocardial
contractility by elevating
intracellular calcium levels and facilitating actin-myosin
interaction in cardiac cells; may also help normalize autonomic
effects on the heart
Digitalis
(Positive Inotropic Agent)
● Inamrinone, milrinone
● Cause a cAMP-mediated increase in intracellular calcium ->
increases force of contraction
● Phosphodiesterase enzyme breaks down cAMP in cardiac cells
● cAMP is a common second messenger
○ acts on membrane calcium channels to allow more calcium
to enter the cell
Phosphodiesterase (PDE) inhibitors
● Dopamine, Dobutamine
● Indications: Acute or severe HF (not used to control chronic HF)
● MOA: stimulate beta 1 receptors on the myocardium
● Effect: positive inotropic effect
Drugs used to stimulate the heart
Drugs affecting RAAS
- ACE inhibitors (-pril)
- ARBs (-sartan)
- Direct renin inhibitor (Aliskiren)
Agents That Decrease Cardiac Workload
○ Angiotensin II:
■ promotes abnormal growth and remodeling of the heart
■ growth and hypertrophy and thickening of peripheral blood vessels -
> reducing lumen size
■ Angiotensin III (by product): Promotes aldosterone secretion ->
increase water reabsorption
○ ACEi prevent angiotensinogen II-induced cardiac remodeling
○ Increases bradykinin(a vasodilator) levels in the bloodstream
○ AE: skin rashes, GI discomfort, dizziness, persistent dry cough
ACE inhibitors (-pril)
