L22: Compensatory mechanisms in disease states Flashcards Preview

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Flashcards in L22: Compensatory mechanisms in disease states Deck (24)
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1
Q

What is heart failure

A

any condition reducing the efficacy of myocardium through damage or overloading

2
Q

What is eccentric hypertrophy

A

reduced contractility or force of contraction, due to overloading of the ventricle

3
Q

How does eccentric hypertrophy occur

A

sarcomeres are added in series so myocytes become longer, chamber larger and thin walled due to VOLUME OVERLOAD

4
Q

how does concentric hypertrophy occur

A

sarcomeres are added in parallel so wall is thicker and chamber smaller due to PRESSURE OVERLOAD

5
Q

What pathological heart changes does concentric hypertrophy result in?

A

Greater force can be generated but DEC filling, thus DEC EDV.

6
Q

How does the heart attempt to compensate for heart failure (early, compensated heart failure)

A
Vasoconstriction 
INC HR 
INC SV 
Renal effects to maintain BP 
Frank Starling forces INC EDV and thus CO 
Cardiac hypertrophy
7
Q

How does vasodilation compensate for heart failure

A

Increasing TPR to maintain BP

8
Q

What is the “undesired effect” of vasoconstriction during compensated heart failure?

A

INC after load

9
Q

What cardiac effects occur to compensate for heart failure

A

Heart works harder,
INC HR
INC SV

10
Q

What is the “undesired effect” of INC HR and INC SV in compensatory heart failure

A

Inc CO and INC work, “flogging a failing heart”

11
Q

How do renal effects attempt to compensate for heart failure

A

Na+ and H20 rentention to INC BP.

INC TPR to maintain BP (Angiotensin is a powerful vasoconstrictor)

12
Q

What are the “undesired effects” of the kidney’s attempt to compensate for heart failure ? (3-4)

A

INC blood volume INC preload and after load
So does persistent vasoconstriction (angiotensin is a very powerful vasoconstrictor!!)
Chronic INC angiotensin DEC baroreceptor sensitivity
AND angiotensin has a direct role in causing myocardial toxicity

13
Q

Describe two ways in which baroreceptors decrease in sensitivity during heart failure

A

Can’t cope with chronic INC in pressure so both high and low baroreceptors change their set point.
Persistent INC angiotensin DEC baroreceptor sensitivity

14
Q

How do Frank Starling forces act to attempt to compensate for heart failure?

A

Increasing EDV and thus INC CO

15
Q

What is the “undesired effect” of the kidney’s attempt to compensate for heart failure?

A

Vessels only have a finite capacity to dilate

16
Q

How does Cardiac hypertrophy attempt to compensate for heart failure?

A

increasing SV

17
Q

What is the “undesired effect” of the heart undergoing hypertrophy to compensate for heart failure?

A

INC work of contraction

18
Q

what eventually leads to decompensated heart failure?

A

System becomes exhausted and preload becomes diminished so that an increase in EDV doesn’t correlate to an increase in CO.

19
Q

Which two adverse effects arise from chronic activation of the sympathetic NS during heart failure?

A
  • Reduction in baroreceptor sensitivity due to chronic pressure activation, so will keep firing even when MAP is appropriate. Will change their set point.
  • Down regulation of B receptors in heart, which reduces its capacity to respond to sympathetic NS stimulation. Requires higher volumes of Na+ to get response
20
Q

What adverse effects arise from the chronic activation of RAAS during compensated heart failure?

A

Persistent vasoconstriction will lead to an INC preload (also inc BV) and after load, because angiotensin is a very potent vasoconstriction.

INC angiotensin DEC baroreceptor sensitivity

Angiotensin can be toxic to the myocardium

21
Q

What is the effect of a positive inotrope

A

increases SV by increasing intracellular Ca++

22
Q

What is the effect of a negative inotrope

A

Decreases contractility of heart. pretty risqué

23
Q

How might you use diuretics to treat heart failure

A

Will reduce BV and thus reduce preload to enable actin and myosin to better overlap and contract

24
Q

How might you use vasodilators to treat heart failure

A

Reduce afterload to ultimately increase the ejection fraction (therefore reducing volume in arteries that were preventing the valves from opening!)