Heart failure

cgeorge's version from 2016-02-27 11:43


Question Answer
In a healthy heart how is a decreased arterial blood pressure brought back upItsd detected by baroreceptors, sends to CNS, Increase sympaethetic activty, decrease vagal. Vasoconstriction to increase TPR. TPR X CO = Increased BP
Describe frank starling mechanismIncreased force of contraction due to heart muscle fibers responding to stretch by increasing sensitivty to Ca and therefore increasin force of contraction
Why does left ventricular wall thicken in response to elevanted blood pressureTo compensate to minimize wall stress
Cardiac physiology of heart failure;1)Decreased SV & CO 2) Increased EDV pressure 3) Ventricular hypertrophy 4) Reduced ejection fraction
Vascular physiology of heart failure1) Increased systemic resistance 2) Decreased arterial pressure 3) Decreased venous compliance 4) Increased blood pressure
In heart failure you get increased activation of the Renin angiotensin aldoserone system pathway which causesIncreased release of BNP and ANP which leads to vasoconstriction
Renin is released by... & stimulates the formation of ... in blood which stimulates release of ... from adrenal cortexKidneys, stimulates formation of angiotensin, which stimulates release of aldosterone
4 Effects of angiotensin (on blood vessels,cardiac muscle, other hormones)1) Vasoconstriction 2) Stimulates cardiac hypertrophy 3) Stimualtes release of vasopressin, increasing fluid retention by kidneys 4)Cause release of aldosterone
Cardiac compensatory mechanisms of heart failure 1) Tacycardia 2)Ventricular hypertrophy 3) Frank starling mechanism - Increased pre load and cardiac force also increases by increasing EDV
Autonomic compensatory mechanisms of heart failureReduce BP initiates baroreceptor reflex - Increase sympathetic , reduce vagal
Hormonal compensatory mechanisms of heart failure1) Renin angiotensin aldosteron system 2) Vasopressin (antidiuretic hormone) 3) Circulating catecholamines 4) Natriuretic peptides (BNP, ANP)
Troponin I normally increasesIncreased rate of cardiac muscle relaxation, therefore increasing contractility
4 mechanisms as to how Ca homeostasis is affected in heart failure1) Decrease in intracellular [Ca]. 2) Increased threshold for Ca release from SER 3)Decreased Ca reuptake of SER 4) Upregulation of Na/Ca exchanger to promote removal of Ca from cell
What is the effect of decreased number of b-adrenoceptors on the heart in heart failure?Decrease camp levels > Decreased PKA > Decreased phosphorylation of troponin I > Decreased contractility
Phosphorylation of troponin I causesMuscle relaxation quicker
What happens to the RyR receptors to act as a compensatory mechanism for reduced Ca levels in the cellPKA causes Ryr malfunction, therefore causes depletion of SER Calcium and release of Ca during diastole
Dopamine is a drug to activateB-adrenoreceptors
Mercarbil is a drug to activatieFormation of actin-myosin cross bridges
Nitroxyl donor is a drug to activateSERCA
Milrinone is a Phosphodiesterase 3 inhibitor
Inhibiting camp phosphodiesterase, whats the effect?Increase camp =Increased pka pathway = Phosphorylates things like troponin I/PLB/L type channels = increase contracility = increase heart rate and vasodilates vessels
Inotropic agents work on what receptorsb-ADRENOCEPTORS
Whats the benefit of PKA phosphorylatiing L type channelsIncrease ca influx and increases RyR stimulation
Whats the benefit of PKA phosphorlyating PLBAccelerates SER accumulation of Ca & relaxation

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