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34 Cards in this Set
- Front
- Back
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CHF causes (4)
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1. cardiac valve abnormalities
2.impaired myocardial contraction (ischemic heart disease, cardiomyopathy) 3.systemic HTN 4.pulm HTN (cor pulmonale) |
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are CHF symptoms closely r/t severity of LV dysfunction?
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no. only mildly
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is LV dysfunction closely r/t mortality?
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yes
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decreased ventricular systolic wall motion represents diastolic or systolic dysfunction?
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systolic dysfunction
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increased end diastolic pressure in a normal sized chamber represents diastolic or systolic dysfunction? why?
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diastolic dysfunction
cannot fill at normal diastolic pressures |
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how is diastolic CHF diagnosed?
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absence of cardiomegaly w/ pulmonary/systemic congestion
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diastolic CHF s/s
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pulmonary/systemic venous congestion w/ normal Left ventricular chamber
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some diastolic CHF tx (4)*
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1.avoid Na intake
2.cautious diuretics 3.restoration & maintenance of NSR 4.correction of precipitating factors |
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what is CO?
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cardiac output = stroke volume X heart rate
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CO for severe CHF?
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decreased CO < 2.5 L/min/m2
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what is the relationship of SV and LVEDP in CHF?
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lower SV for any given LVEDP
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what is Vmax?
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maximum velocity of myocardial contraction representing inotrope state of heart
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what happens to Vmax in CHF?
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decreased
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what happens to catechols in CHF?
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depleted
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what is afterload?
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tension ventricle has to develop to open aortic & pulmonic valves
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what is the rate-treppe phenomenon?
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increases in myocardial contractility w/ increase HR
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what is increased CO in CHF dependent on?
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increases in HR b/c the SV is fixed
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what effect does CHF have on the heart?
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-myocardial hypertrophy & dilation
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how is BP maintained in CHF eventhough CO is decreases?
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1.increased HR - increases CO
2.arteriolar & venous constriction - shift blood from periphery to central circulation, increases venous return, and maintains CO |
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what is the CHF vicious cycle?
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a.the vasoconstictive compensatory responses to maintain central circulation volume constricts blood from kidneys, splanchnic organs, etc.
b.this decrease BF to kidneys causes increased tubular Na & H2O absorption to increase blood volume & CO c.increased fluid retension, increases venous return & afterload increasing work on the heart and further decreases in CO |
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what medication can break the CHF vicious cycle?
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peripheral vasodilators
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what are 3 ways EF can be decreased?
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1.decreased contractility
2.increased afterload 3.asynchrony of LV contraction |
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normal LV ejections
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56-78%
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What happens to EDP and EDV in CHF?
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both increased b/c parallel each other
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normal LVEDP
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< 12 mmHg
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normal RVEDP
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< 5 mmHg
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hallmark sign of CHF
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fatigue at rest or with minimal exertion
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hallmark findings of CHF (5)
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1.decreased CO
2.increased VEDP 3.peripheral vasoconstriction 4.metabolic acidiosis 5.tachycardia |
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signs of LV failure (5)*
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1.pulmonary edema
2.paroxysmal nocturnal 3.hilar peripheral haze (cxr) 4.butterfly pattern (cxr) 5.pleural effusion (cxr) |
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signs of RV failure (3)*
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1.peripheral edema
2.systemic HTN 3.organomegaly (liver) |
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name 4 traditional pharm tx for CHF and what they do
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1.ACE inhibitors = conserve K & excretes Na
2.diuretics = excretes fluid volume from body 3.vasodilators = decrease resistance to LV ejection & increased venous capacitance 4.digitalis = enhances inotropy & decreases activation of SNS |
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treatment of dig toxicity (5)
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1.correct low K
2.lidocaine 3.phenytoin 4.atropine 5.temporary pacer for complete block |
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name 2 non-pharm tx of CHF
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1.ventricular assist devices
2.mechanical pump |
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name 2 newer pharm tx for CHF
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1.beta-adrenergic antagonists (metoprolol)
2.Ca2+ channel blocking durgs (felodipine, amiodipine) |
