Lecture 13 Cardiac Failure, Heart Sounds, and Circulatory Shock Flashcards
Define Cardiac Failure
Failure of the heart to pump enough blood to satisfy the needs of the body
Compensation for acute cardiac failure, effects of sympathetic innervation:
Strengthens muscle contraction (both undamaged and damaged)
Increases tone of most vessels, especially veins–> increases mean systemic filling pressure
Compensatory mechanisms by ANS for acute cardiac failure:
Baroreceptor reflex
Chemoreceptor reflex
CNS ischemic response
Strong Sympathetic Stimulation - If all the ventricular musculature is diffusely damaged but is still functional then:
Sympathetic system strengthens this damaged musculature
Strong Sympathetic Stimulation - If part of the musculature is nonfunctional and part is still normal then:
The normal muscle is strongly stimulated
Strong Sympathetic Stimulation - Increases tone of most of the blood vessels of the circulation and, therefore, increases venous return:
Raises mean systemic filling pressure to 12 to 14 mm Hg, increasing the tendency for blood to flow from the veins back into the heart
Circulatory Change Dynamics (Following Acute Heart Attach) - Acute effects:
Reduced cardiac output
Damming of blood in the veins –> increased venous pressure
Pulmonary Edema and Left Heart Failure (wordy)
Left side of heart fails w/o failure of right side
Blood continues to be pumped into lungs, bt it is not pumped adequately out of lungs.
Mean pulmonary filing pressure rises b/c of the shift of large vol. of blood from systemic circ. into the pulmonary circ.
Pulm. capillary pressure increases
If rises above value approx. equal to the colloid osmotic press. of the plasma, fluid begins to filter out of the caps. into the lung interstitial spaces & alveoli, = pulmonary edema.
Two major problems of left heart failure:
Pulmonary vascular congestion
Pulmonary edema
Conditions that result in High Output Cardiac Failure
Arteriovenous Fistula
Beriberi
Arteriovenous Fistula
Overloads heart because of excessive venous return
Venous return curve rotates upward (Fig. 22-8)
Beriberi
Thiamin deficiency
Weakening of heart
Decreased blood flow to kidney –> fluid retention
Increased mean filling pressure
Shift of venous return curve to right (Fig. 22-8)
First Heart Sound
AV valves close at the onset of ventricular systole
Second Heart Sound
Semilunar valves close at the end of systole
Valvular Defects
Valvular lesions Rheumatic valvular lesions Heart murmurs Aortic stenosis Aortic regurgitation Mitral regurgitation Mitral stenosis