Cardiac Review- Dr E ppt Flashcards

Question

What happens during diastole?

Answer 1

* Isovolumetric relaxation * Blood returns from the periphery * Aortic valve closes * Ventricular pressure still exceeds atrial pressure for about 0.02-0.04 secs, as the ventricular pressure continues to drop and equalizes and then gets lower than atrial pressure * Ventricular filling * AV Valve begins to open * Then opens completely * Ventricular volume rises rapidly, and then slower as pressure rises slightly until the ventricle is filled and the AV valve closes

Answer 2

SYSTOLE: * Isovolumetric contraction * The AV valve is closed (atrial diastole) * Ventricular pressure continues to rise * The semilunar valve opens * Ventricular systole occurs * Ventricular action * Atrial pressure decreases, due to blood now entering the pulmonary artery & aorta * Rapid ejection occurs

Answer 3

From pressure-volume loop picture- 1. closing of mitral valve 2. aortic valve opening 3. aortic valve closure 4. mitral valve opening a. diastolic filling b isovolumetric contraction c. ventricular ejection d. isovolumetric relaxation Volume for 1-4= SV * SV= EDV-ESV

Answer 4

CO= Volume of blood pumped by the heart each minute Determined by: 1. Preload 2. Afterload 3. Heart rate 4. Contractility 5. Ventricular compliance

Answer 5

* relationship between SV and LVEDP * afterload increases or CO decreases---\> frank startling curve downward * afterload decreases or increase in CO--\> frank starling curve upward

Answer 6

* Supply * Can be raised only by increasing coronary blood flow * Diastolic time * HR * CPP * Coronary vasc. tone * Intramural obstruction * Arterial O2 content/extraction * Demand * Wall tension * Preload * Afterload * Contractility * HR * More important to address-easier

Answer 7

* Preload * Reduce wall tension, increase perf. press * Afterload * Maintain afterload, hypotension is Undesirable * Contractility * Depression is desired when LV function is adequate * HR * Maintain a slow HR, this is of utmost importance * Rhythm * Usually sinus rhythm * Myocardial O2 balance * Control of demand is not enough, must monitor for ischemia and increase supply

Answer 8

* Supply * •Decreased BP * •Increased PCWP * ACTIONS: * Vasoconstrictors * Decrease depth of anesthesia * Phenylephrine + NTG, Inotropes, CCB * Demand * •Increased BP * •Increased PCWP * •Increased HR * ACTIONS: * NTG * Increase depth of anesthesia * Treat cause * β blockers

Answer 9

* Narrowing of the valve * At **0.8cm2 s**ymptoms are truly evident * Chronic obstruction to LV ejection * Increased systolic pressure * Increased wall tension * **_Concentric hypetrophy_** * Decreased diastolic compliance * Myocardial O2 supply&demand **compromised** * Characteristic triad of * syncope * angina * dyspnea on exertion (SAD)

Answer 10

* Narrowing of aortic valve causes obstruciton to forward flow * *typically due to rheumatic fever, valve calficiation, or bicuspid valve* * this causes pressure overload (stenosis is always pressure overload) * pressure overload always causes concentric hypertrophy * increase LV mass * compensated * normal wall tension, normal afterload * normal contractility * decreased LV compliance * decrease early filling, increase in late filling of ventricle--\> SV nromal * decompensated * fibrosis caues * increase wall tension: afterload excess * decrease contractility * decrease LV compliance * leads to LV dilation * decreased SV

Answer 11

* Sensitivity to volume depletion * Depend heavily on atrial “kick” for adequate ventricular filling pressure * Wide swings in ventricular filling pressure * PCWP underestimates LVEDP * **Increase LVEDP reduces CPP**

Answer 12

**_Slow, tight, full_** * Preload * Full, maintain adequate preload * Afterload * Maintain CPP, already somewhat elevated * Contractility * In end stage AS might need inotropes especially on induction * HR * Maintain nml, too slow will DECREASE CO, * too fast will cause ischemia * Rhythm * Must maintain NSR, SVTs will cause hymodynamic instability * Myocardial O2 Balance * Ischemia is a big risk, must avoid tachycardia and hypotension **ADEQUATE Diastolic TIME and Perfusion Pressure are KEY!**

Answer 13

* Dilation of aortic root * *Pathophys-* * *acute-* * *infective endocarditis* * *trauma* * *dissection of thoracic aneurysm* * *chronic* * *prior rheumatic fever* * *persistent systemic hypertension* * Leads to chronic **volume overload** * ******Eccentric** hypertrophy (chamber enlargement, increased wall thickness) * Chamber size increased gradually * Increased wall stress * Decrease in forward left ventricular SV * Increase in chamber diastolic compliance thus maintenance of LVEDP * Can be acute or chronic

Answer 14

**_Fast, Normal, Forward_** * Preload * Normal to slightly INCREASEd * Afterload * Reduction will benefit forward flow * Contractility * Usually adequate * Rate * Modest tachycardia will reduce ventricular volume, raises aortic diastolic pressure * Rhythm * Usually sinus, not a problem * Myocardial Oxygen Balance * Usually not a problem **¨INCREASE PRELOAD AND DECREASE AFTERLOAD-Key** *

Answer 15

* -LV is not subject to pressure or volume overload**, actually underloaded** * -Instead, LA pressures rise * -Leads to LA enlargement * -Predisposes the pt to have Afib * -DOE occurs when CO is increased * -Severe MS leads to CHF * *_Pathophys-_* *typically due to rheumatic fever* Pathophys summary * obstruction to LA emptying * increase LA Pressure, size--\> afib * increase in pulm venous pressure * increase PA pressure * decrease CO * Severe pulm HTN * RV overload--\> TR * Perivascular edema * reversal pulmonary blood flow * decrease pulmonary compliance * increase WOB

Answer 16

**_Slow, Tight, Full_** * Preload * Enough to maintain flow across stenosis * Afterload * Avoid RV afterload, inotropes for hypotenstion * Contractility * LV is okay, RV may be impaired * Rate * Slow to allow time for ventricular filling * Rhythm * Often have Afib, control ventricular response * Myocardial Oxygen Balance * Usually not a problem * **_¨ SLOW heart rate-key_**

Answer 17

* -Portion of systolic ventricular flow regurgitates back to the LA * *pathophys- usually due to rheumatic fever and associated with mitral stenosis* * -Regurgitant fraction depends on * •Size of the regurgitant valve orifice * •Pressure gradient b/w LA & LV * Inotropic state of Lv-peak systolic BP * Compliance of the LA * Compliance of pulmonary veins * Time available for regurgitation to occur (systole) * Aortic outflow impedence * SVR * Regurgitation can be significantly influenced by changes in impedance to aortic flow

Answer 18

Fa**_st, Full, Forward_** * Preload * Pretty full, although reduction may reduce regurgitant flow * Afterload * Decreases are beneficial, increases augment regurgitant flow * Contractility * Unrecognized myocardial depression * Rate * Faster rate decreases LV volume * Rhythm * Usually Afib, control ventricular response, this rhythm is usually a problem * Myocardial Oxygen Balance * Problematic only if regurge is due to MI * **¨REDUCE AFTERLOAD-KEY**

Cardiac Review- Dr E ppt Flashcards

(42 cards)