Heart Failure Flashcards
Changes in Acute HF
A = normal heart before damage
B = instantaneous effect of cardiac damage (MI)
C = effect of sympathetic stimulation ~30s after cardiac damage
D = compensated HF due to partial cardiac recovery and renal retention of fluid over a period of days to weeks
**Note: heart is functioning close to normal in compensated HF due to high RAPs while person is at rest. Any attempts at heavy exercise, however, will bring the person back to acute HF because the heart is not able to increase its pumping as required by the exercise ( = reduced cardiac reserve)
Features of Compensated HF
- Relatively normal CO as long as the person remains at rest
- ⇡ Right atrial pressure → JVD (key in diagnosis)
- ⇣ Cardiac reserve
- ⇡ HR
- Pale or clammy skin (normalizes after recovery)
- Sweating and nausea (normalizes after recovery)
- Dyspnea
- Weight gain from fluid retention
Why is RAP increased in compensated HF?
- Blood from the damaged heart backs up into the right atrium
- Venous return increases due to sympathetic stimulation
- Blood volume and venous return increase due to sodium and water retention by the kidneys
Main Causes of Decompensated HF
Due to a failure of the heart to pump sufficient blood to make the kidneys excrete daily the necessary amounts of fluid (fluid retention continues).
- Longitudinal tubules of SR fail to accumulate enough calcium → myocardial weakness
- Myocardial weakness → excess fluid retention → overstretching of sarcomeres → ⇣contractility
- Excess fluid retention → edema of heart m. → stiffened ventricular wall → ⇣diastolic filling (⇣PL)
- ⇣NE content at sympathetic cardiac nerve endings → ⇣contractility
Treatments for Decompensated HF
- Cardiotonic drug like digitalis → ⇡Ca2+ in cardiac cell → ⇡contractility
- Rapid-acting diuretics like furosemide → ⇣fluid retention and venodilation → ⇣preload on heart
- ⇣Sodium and water intake: allows a balance between fluid intake and output despite low CO
Causes of Sodium and Water Retention by the Kidneys during HF
- ⇣arterial P → ⇣GFR
- Sympathetic constriction of afferent arterioles → ⇣GFR
- Increase in renin release (due to above & ⇡sympathetic output) → ⇡ANGII formation and concentration → efferent arteriole constriction → ⇣peritubular capillary pressure → promotion of sodium and water retention
- ⇡Aldosterone release due to stimulation of adrenal gland by ⇡ANGII in blood and ⇡plasma K+
- ⇡ADH release due to ⇡renal sodium retention (water must follow sodium and ADH helps with the water retention)
Detrimental Effects of Excess Fluid Retention in Severe HF
- Increases the workload on an already damaged heart
- Overstretching of the heart → weakens the heart further
- Filtration of fluid into the lungs → PE and deoygenation of blood
- Extensive edema throughout the body
“Greatly depressed cardiac output that indicates decompensated heart disease. Progressive fluid retention raises the right atrial pressure over a period of days, and the cardiac output progresses from point A to point F, until death occurs.” – Guyton & Hall
How Left-sided acute HF can lead to pulmonary vascular congestion and pulmonary edema
- In left-sided HF w/o concomitant right HF, blood keeps flowing into the R heart and lungs with the usual vigor, but pumped out of the lungs and the L heart and into systemic circulation in the normal manner
- This leads to a rise in mean pulmonary filling pressure (due to a shift in blood volume from systemic circulation to pulmonary circulation)
- As blood volume in the lungs rises, pulmonary capillary pressure (PCP) rises
- If PCP rise above colloid osmotic P of plasma → fluid filtering out of the capillaries, into lunginterstitial spaces and alveoli → pulmonary vascular congestion and pulmonary edema
Treatment of cardiogenic shock due to HF
- Drug that ⇡cardiac strength (e.g., digitalis)
- Infusion of whole blood or plasma to ⇡ arterial P
- A vasopressor to ⇡ arterial P
- tPA infusion to dissolve the clot (< 1 hour of CP)
Goal is too maintain coronary blood flow to prevent the viscious cycle of deterioration (compromised flow → deterioration → further heart weakness → further decreases in flow → further deterioration)
Chronic Responses to HF
HF → ⇣CO → ⇣ arterial P → ⇣ urine output → sodium and water retention → ⇡ blood volume → ⇡ mean systemic filling P and vein distention, ⇣ venous resistance → ⇡ venous return
Features of L-sided HF
- Increased LAP
- Pulmonary congestion
- Pulmonary edema if pulmonary capillary pressure exceeds 28 mmHg
- Arterial P and CO remain normal as long as patient remains at rest
- Intolerance to exercise, which if attempted may worsen pulmonary edema
Features of R-sided HF
- Increased RAP
- Peripheral edema
- Arterial P and CO remain normal as long as patient remains at rest
- Intolerance to exercise, which if attempted may worsen pulmonary edema
