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NURS 350 Patho cardi
Pathophys cardiovascular #1 through HF
| Question | Answer |
|---|---|
| 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
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