L22: Compensatory mechanisms in disease states Flashcards
What is heart failure
any condition reducing the efficacy of myocardium through damage or overloading
What is eccentric hypertrophy
reduced contractility or force of contraction, due to overloading of the ventricle
How does eccentric hypertrophy occur
sarcomeres are added in series so myocytes become longer, chamber larger and thin walled due to VOLUME OVERLOAD
how does concentric hypertrophy occur
sarcomeres are added in parallel so wall is thicker and chamber smaller due to PRESSURE OVERLOAD
What pathological heart changes does concentric hypertrophy result in?
Greater force can be generated but DEC filling, thus DEC EDV.
How does the heart attempt to compensate for heart failure (early, compensated heart failure)
Vasoconstriction INC HR INC SV Renal effects to maintain BP Frank Starling forces INC EDV and thus CO Cardiac hypertrophy
How does vasodilation compensate for heart failure
Increasing TPR to maintain BP
What is the “undesired effect” of vasoconstriction during compensated heart failure?
INC after load
What cardiac effects occur to compensate for heart failure
Heart works harder,
INC HR
INC SV
What is the “undesired effect” of INC HR and INC SV in compensatory heart failure
Inc CO and INC work, “flogging a failing heart”
How do renal effects attempt to compensate for heart failure
Na+ and H20 rentention to INC BP.
INC TPR to maintain BP (Angiotensin is a powerful vasoconstrictor)
What are the “undesired effects” of the kidney’s attempt to compensate for heart failure ? (3-4)
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
Describe two ways in which baroreceptors decrease in sensitivity during heart failure
Can’t cope with chronic INC in pressure so both high and low baroreceptors change their set point.
Persistent INC angiotensin DEC baroreceptor sensitivity
How do Frank Starling forces act to attempt to compensate for heart failure?
Increasing EDV and thus INC CO
What is the “undesired effect” of the kidney’s attempt to compensate for heart failure?
Vessels only have a finite capacity to dilate
How does Cardiac hypertrophy attempt to compensate for heart failure?
increasing SV
What is the “undesired effect” of the heart undergoing hypertrophy to compensate for heart failure?
INC work of contraction
what eventually leads to decompensated heart failure?
System becomes exhausted and preload becomes diminished so that an increase in EDV doesn’t correlate to an increase in CO.
Which two adverse effects arise from chronic activation of the sympathetic NS during heart failure?
- 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
What adverse effects arise from the chronic activation of RAAS during compensated heart failure?
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
What is the effect of a positive inotrope
increases SV by increasing intracellular Ca++
What is the effect of a negative inotrope
Decreases contractility of heart. pretty risqué
How might you use diuretics to treat heart failure
Will reduce BV and thus reduce preload to enable actin and myosin to better overlap and contract
How might you use vasodilators to treat heart failure
Reduce afterload to ultimately increase the ejection fraction (therefore reducing volume in arteries that were preventing the valves from opening!)
