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Cardiology- physio

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drnieves's version from 2017-06-18 02:37

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Question Answer
IV fluidsIncrease intravascular and ventricular preload= increases end diastolic sarcomere length= increase SV and cardiac output
CHFDecreased CO
Pulmonary veinsIncreased AT II
LV afterloadmajor determinant of the forward to regurgitant flow ratio in pots with MR.
Decreasing afterload on MVincrease forward flow while reducing regurgitant flow.
Increase in LV preload in MRCan contribute or worsen MR when the degree of regurgitation is dependent on LV size.
RV MIHypotension, elevated jugular venous P and clear lungs. Setting of acute LV inferior wall MI due to right coronary a occlusion.
Elevated RA and central venous P, reduced PCWP, and reduced CORV MI
Phase 0 of pacemaker APOpening of Ca ch.
Phase 3 of pacemaker APInactivation of Ca ch, increase in K efflux.
Phase 4 of pacemaker APK efflux. Automaticity of nodes, determines HR.
ACh/ adneosinedecrease rate of diastolic depolarisation and HR
CatecholaminesIncrease depolarisation and HR.
AfibIrregularly irregular. Short QRS. HTN, CAD, rheumatic heart disease, binge drinking, HF, valvular disease, hyperthyroidism.
Can lead to cardioembolic eventsafib
Afib txwarfarin, B-blocker, non-dihydropyrimidines, digoxin, IC or III, cardioversion.
Mitral/tricuspid regurgitationHolosystolic high pitched.
MRRadiates to axilla. Often due to ischemic heart, post MI, MVP, LV dilation
TRRadiates to R sterna border. RV dilation.
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