Lecture 15 Flashcards
Cardiac Failure
Failure of the heart to pump enough blood to satisfy the needs of the body
How Does the Heart Compensate for Acute Cardiac Failure
Increases sympathetic innervation and decreases parasympathetic innervation; increased sympathetic innervation strengthens muscle contractions in damaged and undamaged areas and increases the tone of vessels (especially veins) which increases mean systemic filling pressure
Compensatory Mechanisms by ANS for Acute Cardiac Failure
Baroreceptor Reflex
Chemoreceptor Reflex
CNS Ischemic Response
Acute Effects following Acute Heart Attack
Reduced cardiac output and damming of blood in the veins which increases venous pressure
Chronic Compensations following Acute Heart Attack (Compensated Heart Failure)
Partial heart recovery and renal retention of fluid; maximum pumping ability of the partly recovered heart is still depressed to less than 1/2 normal; any attempt to perform heavy exercise usually causes immediate return of symptoms of acute failure because heart can’t increase its pumping capacity to the levels required for exercise; an increase in right atrial pressure can maintain the cardiac output at a near normal level despite continued weakness of the heart
Pulmonary Edema
Left side of the heart fails without concomitant failure of the right side; blood continues to be pumped into the lungs but is NOT pumped adequately out of the lungs; this causes the mean pulmonary filling pressure to rise because of the shift of large volumes of blood from the systemic circulation into pulmonary circulation; pulmonary capillary pressure then increases; if this rises above colloid osmotic pressure, fluid begins to filter out of the capillaries into the lung interstitial spaces and alveoli
2 Major Problems of Left Heart Failure
Pulmonary Vascular Congestion and Pulmonary Edema
Arteriovenous Fistula
Overloads heart because of excessive venous return
Beriberi
Thiamin deficiency and weakening of the heart; decreased blood flow to the kidney results in fluid retention; this increases mean filling pressure
First Sound of a Heart
AV valves close at the onset of ventricular systole
Second Sound of a Heart
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
Left-to-Right Shunt
Blood flows backward and fails to flow through systemic circulation (Patent Ductus Arteriosus)
Right-to-Left Shunt
Blood flows from right to left side of the heart, bypassing the lungs (Tetralogy of Fallot)
Circulatory Shock
Generalized inadequate blood flow through the body, to the extent that the body tissues are damaged, especially because of too little oxygen and other nutrients delivered to the tissue cells
Cardiac Abnormalities that Decrease the Ability of the Heart to Pump Blood
Myocardial infarction Toxic state of the heart Severe heart valve dysfunction Heart arrhythmias Cardiogenic shock
Cardiogenic Shock
Circulatory shock that results from diminished cardiac pumping ability
Factors that Decrease Venous Return
Diminished blood volume
Decreased vascular tone (especially of venous reservoirs)
Obstruction of blood flow
What causes powerful sympathetic reflexes?
Decrease in arterial pressure after a hemorrhage and decreases in pressures in the pulmonary arteries and veins in the thorax
What do sympathetic reflexes result in?
Arterioles to constrict in most parts of the systemic circulation, veins and venous reservoirs constrict, and heart activity increases markedly
After a shock, what compensatory mechanisms return blood volume back to normal?
Absorption of large quantities of fluid from the intestinal tract, absorption of fluids into the blood capillaries from the interstitial spaces of the body, conservation of water and salt by the kidneys, and increased thirst and increased appetite for salt
Non-Progressive Shock
Sympathetic reflexes and other factors compensate enough to prevent further deterioration of the circulation; all of these factors are negative feedback mechanisms that attempt to return cardiac output and arterial pressure back to normal
Progressive Shock
Positive feedbacks; when arterial pressure falls low enough, coronary blood flow decreases below that required for adequate nutrition of the myocardium; this weakens the heart muscle and decreases cardiac output even more
Important factor in progressive shock is whether it is hemorrhagic in origin or not
Factors in the Final Lethal Progression of Shock
Vasomotor failure, blockage of small vessels, increased vascular permeability, release of toxins by necrotic tissue, cardiac depression caused by endotoxin, and generalized cellular deterioration
Neurogenic Shock
May occur with/without any loss of blood volume; vascular capacity increases so much that even the normal amount of blood becomes incapable of filling circulatory system adequately; loss of vasomotor tone resulting in massive dilation of the veins
Causes of Neurogenic Shock
Deep general anesthesia (depresses vasomotor center enough to cause vasomotor paralysis), spinal anesthesia (blocks sympathetic nervous outflow), and brain damage (causes vasomotor paralysis)