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NURS 350 Patho cardi

Pathophys cardiovascular #1 through HF

simple version Frank-Starling Laws the heart pumps that which is returned to it. increasing venous return (r. vent) and (left)ventricular preload-->increase in stroke volume. important fole in blancing output of 2 ventricles
essence of Frank-Starling graph with respect to sarcomere length x axis = SV----------y axis = LVEDP. Basically, the amount of pressure exerted against ventricle will increase SV ---BUT ONLY TO A CERTAIN POINT----this will avail more actin/myosin binding sites, increase contractility
What happens in Frank-Starling if there is too much ESV or ESP there will be too much pressure, causing sarcomeres to be too far apart to cross-bridge and contract.
What factors effect the Family of Frank-starling curves afterload and inotrophy affect these curves. increased length-tension curve is hyperactive state. Lower length-tension curve is decreased contractility like HF
four factors affecting cardiac performance preload, afterload, HR, contractility
preload is pressure generated in left ventricle at end of diastole. what does it depend upon depends upon LVEDP (relates to LVEDV as well)
afterload is the resistance by aorta for ejection. what do we use as its index? aortic systemic pressure is estimated by bp
heart rate is characteristic of cardiac tissue (SA/AV, conduction system). what influences HR HR influenced by neuronal (SNS/PSNS) and hormonal factors
contractility is characterist of cardiac tissue. what is it influenced by neuronal (symp/psymp) and hormonal --- any changest that allow Ca++ into cell, such as epi/nor. ALL FACTORS THAT CAUSE AN INCREASE IN CONTRACTILITY WORK BY INCREASING INTRACELLULAR Ca++
2 factors that affect preload r. vent venous return ---l.vent ESV
2 factors that affect afterload aortic valve function --- aortic pressure
3 factors that affect contractility myocardial oxygen supply --- symp stimulation (epi/nor increase Ca intracell, inc contractility) ---EDV/EDP
5 factors affecting Heart Rate hormones---atrial receptors---natural reflexes---symp/psymp NS----CNS
just for fun - define contractility and its synonym inotrophy and contractility - the inherent capacity of myocardial contraction INDEPENDEND of changes in pre/afterload
name 6 factors that affect the inotropic/contractile state psymp---symp---catecholamines---HR---systolic failure---afterload
positive inotropic agents affect contracility - they are catecholamines --- TH ---isoproterenol
what do chronotropic agents affect they affect conduction/speed of contraction
negative inotropic agents ETOH---propanolol---procainamide---quinidine
cardiac output amount of blood pumped into aorta/min. CO=SVxHR
ejection fraction amount actually ejected, usually 60-75%
what are the factors regulating blood flow blood pressure---CO----peripheral resistance
factors effecting blood pressure/HTN fluid volume & venous constriction ---both of which affect preload
factors affecting CO contractility as it is affected by EDV, SNS & O2 demands
factors affecting peripheral resistance PR vessel diameter, blood viscosity (and vessel length)
HTN definition consisent elevation of systemic arterial bp
primary/secondary HTN primariy (most)---secondary is altered hemodynamics bwo of disease like atherosclerosis
isolated systolic HTN where systolic # is HIGH and diastolic # is LOW---manifestation of increased CO and/or rigid aorta
primary HTN risk factors genetics/env/lifestyle---altered Na/Ca/neurogenic mechanisms----high dietary Na----smoking/nicotine is vasoCON
chronic HTN definition prolonged vasocon/inc bp thickens arteries---arterial sm musc hypertrophy/hyperplasia---injury stim inflamm mediators---contributes to atherosclerosis
take home message chronic HTN sustained pressure causes vascular damage, non-compliance and atherosclerosis ---EVEN IN KIDS.
normal bp systolic <120
normal bp diastolic <80
preHTN bp systolic 123-130
preHTN bp diastolic 80-90
stage 1 HTN systolic 140-160
stage 1 HTN diastolic 90-100
stage 2 HTN systolic >160
stage 2 HTN diastolic >100
how would we classify a bp = 170/78 isolated systolic HTN
orthostatic HTN - normal compensation gravitational changes compensated by reflex arteriolar constriction ---inc HR---venous valve/sk milking-----------------------------also volume shifts initiate baroceptor reflex-->SNS-->vasocon/inc HR
MOA of orthostatic HTN uncompensated state-->dec cerebral perfusion-->dizz/vison loss/syncope(fainting)
acute orthostatic HNT contributing factors (most common in elderly, prolonged immobility) drug rxns---starvation---exhaustion---hypovolemic conditions---altered blood chemisty
Heart failure is classified as left HF (CHF) and right side HF. what are 2 sub-classes of LHF/CHF diastolic LHF/CHF,systolic LHF/CHF
MOA LHF/CHF-diastolic chronic HTN renders L. vent non-compliant---pressure increases and is reflected to L. atrium---reflects back into pulm circ---can ALSO be reflected to right side of heart ---to cause Right-side HF
is LEDV or contractility affected in LHF/CHF-diastolic HF no - No - NO! has to do with pressures and non-compliance--> . nothing to do with contractility
s/s of diastolic-LHF/CHF dyspnea with exertion, S4 gallop (sound of atrial filling KNOCKING against non-compliant l.ventricle wall
so . . .in diastolic LHF/CHF, bottom line pulmonary congestion DESPITE normal SV/CO
in what type of HF does heart start to fail as a pump in SYSTOLIC CHF/LHF . . .heart cannot generate sufficient CO to perfuse tissues
in systolic-LHF/CHF how is contractility affected (primary MOA) an increased preload/LVEDV surpasses Frank-Starling threshold---dec. contractility---dec ejection fraction
secondary MOA systolic LHF/CHF the increased preload---underperfusion detected by kidney---RAAS activated to vasoCON---which increases periph resistance---INCREASES AFTER LOAD---which also DECREASES contractility.
so, in short, do we have a viscious cycle with systolic-LHF/CHF yes, Yes, YES it is a visous cycle that is also influenced by inflam abns/neurohormonal factors such as---catacholamines/RAAS/ANP-BNP in response to atrial stretching
how does the body compensate for systolic-LHF we get hypertrophy and dilation of the myocardium
what causes systolic LHF any condition that affects contractility. For example ---RF, hypervolemia affect preload which indicrectly affects contractility. ----directly affecting contractility is----myocardial fx, ischemic dx, cardiomyopathy, vascular dx, dysryth
short version of what causes systolic LHF MI---myocarditis---cardiomyopathies (deteriorating myocardium)
RHF causes hypoxic pulmonary disease (cor pulmonale)---diastolic-LHF reflecting to right side
so in RHF we have a pulmonary dx that creates vasuclar resistance and hypoxia . . .then what heart cant pump against increased pulmonary pressure, so it fails. thiss increased ventricular/atrial pressure is reflected back into systemic venous circulation and results in peripheral edeman
what causes RHF again severe CHF---lung disiase---R. ventricular contracility disorders
high output HF where the body can deliver oxygenated blood (normal Bvolume, contractility), but the body can't use the 02
why can't the body use the O2 in high output HF there is generally a disease state that requires EXCESS 02 beyond what the heart can deliver
what are examples of diseases involved with high output cardiac failure anemia---septicemia---hyperthyroidism---Beriberi/thiamine deficiency. all these states result in increased cellular metabolism that requires extra 02
Created by: lorrelaws