Lecture 14: Cardiac Failure, Heart Sounds, And Circulatory Shock Flashcards Preview

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Flashcards in Lecture 14: Cardiac Failure, Heart Sounds, And Circulatory Shock Deck (26):

Define Cardiac Failure

Failure of the heart to pump enough blood to satisfy the needs of the body


How does the body compensate for acute cardiac failure?

* Note that a number of circulatory reflexes are activated in order to increase activation of the sympathetic innervation to the heart and decrease parasympathetic innervation.
* Effects of sympathetic innervation:
- Strengthens muscle contraction (both undamaged and damaged)
- Increases tone of most vessels, especially veins: Increases mean systemic filling pressure
- See Slides 6-8


What are compensations taken by the ANS during acute cardiac failure

- Baroreceptor reflex
- Chemoreceptor reflex
- CNS ischemic response


Describe the strong sympathetic stimulation compensatory mechanism

- If all the ventricular musculature is diffusely damaged but is still functional, sympathetic system strengthens this damaged musculature.
- If part of the musculature is nonfunctional and part is still normal, the normal muscle is strongly stimulated.
- 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.

- See Slide 10


What are the acute effect changes in circulatory dynamics following an acute heart attack

- Reduced cardiac output
- Damming of blood in the veins → increased venous pressure


Follow acute heart attack and subsequent compensation by the sympathetic nervous system, what are more long-term changes to circulatory dynamics?

- Result from partial heart recovery and renal retention of fluid;
- Maximum pumping ability of the partly recovered heart is still depressed to less than one-half normal.
- When a person is in compensated heart failure, any attempt to perform heavy exercise usually causes immediate return of the symptoms of acute failure because the heart is not able to increase its pumping capacity to the levels required for the exercise.
- An increase in right atrial pressure can maintain the cardiac output at a near normal level despite continued weakness of the heart.
- See Slide 13


Describe circulatory pressure changes following acute heart failure

See Slide 15-17


Describe what occurs during pulmonary edema and left heart failure

- Left side of the heart fails without concomitant failure of the right side.
- Blood continues to be pumped into the lungs, but it is not pumped adequately out of the lungs.
- Therefore, the mean pulmonary filing pressure rises because of the shift of large volumes of blood from the systemic circulation into the pulmonary circulation.
- The pulmonary capillary pressure increases.
- If this rises above a value approximately equal to the colloid osmotic pressure of the plasma (≈ 28 mm Hg) fluid begins to filter out of the capillaries into the lung interstitial spaces and alveoli, resulting in pulmonary edema.


What are the two major problems of left heart failure?

- Pulmonary vascular congestion
- Pulmonary edema.

--In severe acute left heart failure, pulmonary edema may occur so rapidly that it can cause death by suffocation in 2030 minutes.


See Slides 21-33. Thoroughly.



What are 2 examples of high output cardiac failure?

- Arteriovenous fistula
- Beriberi


Describe an arteriovenous fistula

- Overloads heart because of excessive venous return.
- Venous return curve (red curve in Figure 22-8) rotates upward (Slide 35)


Describe Beriberi

- Thiamin deficiency
- Weakening of heart
- Decreased blood flow to kidney → fluid retention
- Increased mean filling pressure
- Shift of venous return curve to right
- Slide 35-37


Explain what the first and second heart sounds refer to

First sound: AV valves close at the onset of ventricular systole.
Second sound: Semilunar valves close at the end of systole.

- See Slides 40-41


Give examples of valvular defects

- Valvular lesions
- Rheumatic valvular lesions
- Heart murmurs
- Aortic stenosis
- Aortic regurgitation
- Mitral regurgitation
- Mitral stenosis

** Review Textbook Pages 285, 286


Describe Congenital Defects

Congenital Defects:
- Distinguish between left-right and right-left shunts:
- Left-to-right:
- Blood flows backward and fails to flow through systemic circulation.
- Right-to-left:
- Blood flows from right to left side of heart, bypassing lungs.
- Patent ductus arteriosus (Left-to-right shunt)
- Tetralogy of Fallot (Right-to-left shunt)
- See Slides 45, 46


Give the definition of circulatory shock

Circulatory shock means 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.


List 5 cardiac abnormalities that can decrease the ability of the heart to pump blood

1. Myocardial infarction
2. Toxic state of the heart
3. Severe heart valve dysfunction
4. Heart arrhythmias
5. Circulatory shock that results from diminished cardiac pumping ability is called cardiogenic shock


List 3 cardiac abnormality factors that may decrease venous return

1. Diminished blood volume
2. Decreased vascular tone (especially of venous reservoirs)
3. Obstruction of blood flow


Describe negative feedback mechanisms for blood loss

* Powerful sympathetic reflexes:
- Initiated mainly by the arterial baroreceptors and other vascular stretch receptors)
- Result from:
-- Decrease in arterial pressure after hemorrhage
-- Decreases in pressures in the pulmonary arteries and veins in the thorax
* These reflexes result in three important effects:
- Arterioles constrict in most parts of the systemic circulation.
- The veins and venous reservoirs constrict.
- Heart activity increases markedly (up to 160-180 bpm).
* Autoregulation in cerebral and cardiac vessels maintains more-or-less normal pressure as long as the arterial pressure does not fall below 70 mm Hg.


List 6 factors that can help assist in recovery from shock

* Factors that cause a person to recover from moderate degrees of shock:
- Baroreceptor reflexes → elicit powerful sympathec smulaon of the circulation.
- Central nervous system ischemic response → elicits even more powerful sympathetic stimulation throughout the body but is not activated significantly until arterial pressure falls below 50 mm Hg.
- Reverse stress-relaxaon of the circulatory system → causes blood vessels to contract around the diminished blood volume so that the blood volume that is available more adequately fills the circulation.
- Increased secretion of renin by the kidneys and formation of angiotensin II → constricts the peripheral arteries and also causes decreased outputs of water and salt by the kidneys.
- Increased secretion by the posterior pituitary gland of vasopressin (ADH) → constricts the peripheral arteries and veins and greatly increases water retention by the kidneys.
- Increased secretion by the adrenal medullae of epinephrine and norepinephrine → constricts the peripheral arteries and veins and increases heart rate.


Following shock, describe mechanisms that help 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
- Increased thirst and increased appetite for salt
- See Slide 57


What is a non-progressive shock?

- Sympathetic reflexes and other factors compensate enough to prevent further deterioration of the circulation.

- All these factors are negative feedback mechanisms that attempt to return cardiac output and arterial pressure back to normal.


What is progressive shock?

- Positive feedbacks
- When the 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.
- One of the important features of progressive shock is whether or not it is hemorrhagic in origin.
- See Slide 61


What are factors in the final lethal progression of shock

* Vasomotor failure
* Blockage of small vessels (sludged blood)
* Increased vascular permeability
* Release of toxins by necrotic tissue
* Cardiac depression caused by endotoxin
* Generalized cellular deterioration
- Diminished active transport of sodium and potassium through cell membrane
- Depressed mitochondrial activity
- Breakdown of lysosomes
- Depression of cellular metabolism of nutrients

* See Slide 62 and 63


Define Neurogenic Shock

* Shock may occur without any loss of blood volume.
* The vascular capacity increases so much that even the normal amount of blood becomes incapable of filling the circulatory system adequately.
* One of the major causes of the above is sudden 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
- Brain damage: Causes vasomotor paralysis