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68 Cards in this Set
- Front
- Back
WHY IS 2/3 OF HEART LEFT OF MIDLINE?
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HEART IS ROTATED LEFT AND TILTED FORWARD
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ATRIAL KICK
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WHEN BOTH ATRIA CONTRACT AT THE END OF DIASTOLE
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CORRELATES WITH THE S4 HEART SOUND IN A PATHOLOGIC HEART
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ATRIAL KICK
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WHEN DO SEMILUNAR VALVES OPEN AND CLOSE?
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OPEN DURING SYSTOLE AND CLOSE DURING DIASTOLE
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CLOSURE OF SEMILUNAR VALVES CORRESPONDS WITH WHAT HEART SOUND?
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S2 HEART SOUND
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WHEN DO THE A-V VALVES OPEN AND CLOSE?
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OPEN DURING DIASTOLE AND CLOSE DURING SYSTOLE
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CLOSURE OF A-V VALVES CORRESPONDS TO WHAT HEART SOUND?
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S1 HEART SOUND
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WHAT DO PAPILLARY MUSCLES DO AND WHEN?
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PULLS THE LEAFLETS OF MV AND TV TOGETHER (TO KEEP CLOSED DURING SYSTOLE) AND DOWNWARD AT ONSET OF ISOVOLUMETRIC VENTRICULAR CONTRACTION
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WHERE SYMPATHETIC INNERVATION ORIGINATES FROM?
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THORACIC GANGLIA 1-5
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WHERE DO SYM. BRANCHES MEET AND INNERVATE?
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MEET AT THE CARDIAC PLEXUS NEAR THE ARCH OF THE AORTA AND INNERVATE B1 RECEPTORS IN HEART
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PARASYMPATHETIC INNERVATION TO THE HEART IS TRANSMITTED VIA WHAT NERVE?
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VAGUS NERVE
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WHEN DO THE CORONARY ARTERIES FILL?
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DURING DIASTOLE (LOW PRESSURE BACKWASH)
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CORONARY ARTERY THAT FEEDS THE INFERIOR WALL OF THE LV, RA, RV, PART OF SEPTUM, SA NODE IN 70%, AV NODE, AND PDA IN 85%
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RCA
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CORONARY ARTERY THAT FEEDS PART OF THE SEPTUM AND BUNDLE BRANCHES, AS WELL AS MOST OF THE LEFT VENTRICLE
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LAD
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CORONARY ARTERY THAT FEEDS SA NODE IN 25%, LATERAL/PART OF POSTERIOR WALL OF LV, LA, PDA IN 10%
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CIRCUMFLEX
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CORONARY ARTERY THAT FEEDS PART OF SEPTUM
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PDA
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HOW DO YOU MEASURE CO IN HOSPITALIZED PATIENT?
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WITH A SWAN-GANZ CATHETER USING THERMODILUTION TECHNIQUE
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VOLUME OF BLOOD EXITING THE LEFT VENTRICLE INTO THE AORTA WITH EACH CONTRACTION
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STROKE VOLUME
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THE LOAD THAT STRETCHES THE HEART PRIOR TO CONTRACTION
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PRELOAD
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HOW IS PRELOAD MEASURED?
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BY: VENTRICULAR END DIASTOLIC VOLUME; VENTRICULAR END DIASTOLIC PRESSURE
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HOW DO WE DIRECTLY MEASURE PRELOAD?
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LEFT HEART CATHETERIZATION
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HOW DO WE ESTIMATED PRELOAD?
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DURING RIGHT HEART CATHETERIZATION VIA PULMONARY CAPILLARY WEDGE PRESSURE
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FOUR MAJOR COMPONENTS OF PRELOAD
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TOTAL BLOOD VOLUME, DISTRIBUTION OF BLOOD VOLUME, ATRIAL CONTRACTION, COMPLIANCE
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THE TENSION DEVELOPED IN THE WALL OF THE VENTRICLE DURING CONTRACTION
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AFTERLOAD
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2 FACTORS THAT DETERMINE AFTERLOAD
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AORTIC PRESSURE (MEAN BP) AND THE VOLUME OF THE VENTRICULAR CAVITY AND TE THICKNESS OF THE VENTRICULAR WALL
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THIS IS A USEFUL MEANS FOR ASSESSING PRIMARY CARDIAC FUNCTION
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EJECTION FRACTION
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FRACTION OF END DIASTOLIC VOLUME EJECTED FROM THE VENTRICLE DURING EACH SYSTOLIC CONTRACTION
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EJECTION FRACTION
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EF IS NOT MEASURED DIRECTLY, BUT RATHER ESTIMATED BY WHAT?
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NUCLEAR VENTRICULOGRAPHY (MUGA), ECHOCARDIOGRAPHY, OR THE GOLD STANDARD- CARDIAC CATHETERIZATION (INVASIVE)
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WHAT IS MYOCARDIAL CONTRACTILITY?
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FORCE OF CONTRACTION GENERATED BY THE VENTRICLES
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THE LAW OF LAPLACE DEALS WITH WAT?
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VENTRICULAR WALL TENSION IN TERMS OF COLUME OF TEH VENTRICULAR CAVITY AND THE THICKNESS OF THE VENTRICULAR WALL
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STATE THE LAW OF LAPLACE
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WALL TENSION= VENTRICULAR PRESSURE TIMES VENTRICULAR CHAMBER RADIUS/ 2 (VENTRICULAR WALL THICKNESS
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NORAML EJECTION FRACTION
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BETWEEN 55 AND 75%
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FORMULA FOR STROKE VOLUME
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SV= EDV- ESV
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FORMULA FOR EF
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SV/ EDV
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WHAT PROCESS ALLOWS FOR BEAT TO BEAT COMPENSATION?
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FRANK STARLING MECHANISM- ACUTELY, AN INCREASE IN THE LEFT VEDV PRODUCES AN INCREASE IN CONTRACTILITY BY INCREASING THE LENGTH AND STRETCH OF THE CARDIAC MUSCLE FIBERS
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WHAT CAN CHRONIC SYMPATHETIC STIMULATION LEAD TO?
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DOWN REGULATION OF ADRENERGIC RECEPTORS (A GIVEN STIMULATION RESULTS IN LESS THAN USUALL EFFECT)
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DESCRIBE VENTRICULAR HYPERTROPHY AS A COMPENSATION MECHANISM.
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CHRONIC; CHRONIC CONTRACTION AGAINST HIGH AFTERLOAD; MUSCLE WALL THICKENS OVER TIME---LONNG TERM DISADVANTAGES BECAUSE IT DECREASES COMPLIANCE AND INCREASES MYOCARDIAL OXYGEN DEMAND
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DESCRIBE VENTRICULAR DILATION AS A COMPENSATION MECHANISM.
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CHRONIC; RESPONSE TO PROLONGED INCREASE IN LEFT EDV/EDP (DUE TO HIGH PRELOAD AS OPOSED TO INCREASED AFTERLOAD); THIN WALL ENLARGED VENTRICLE THAT INITIALLY INCREASES CO BUT EVENTUALLY DECREASES CO; INCREASED WALL STRESS AND MYOCARDIAL OXYGEN DEMAND ARE DISADVANTAGES
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CHRONIC PROCESS ASSOCIATED WITH HIGH AFTERLOAD
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VENTRICULAR HYPERTROPHY
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CHRONIC PROCESS ASSOCIATED WITH HIGH PRELOAD
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VENTRICULAR DILATATION
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TWO ACUTE COMPENSATORY MECHANISMS
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FRANK STARLING AND SYMPATHETIC STIMULATION
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TWO CHRONIC COMPENSATORY MECHANISMS
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VENTRICULAR HYPERTROPHY AND DILITATION
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WHERE DOES THE RIGHT VENTRICLE LAY?
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UNDER THE STERNUM
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IF YOU HAVE A DISPLACED PMI?
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DILATED LEFT VENTRICLE
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IF THERE IS A DILATED LEFT ATRIUM, WHAT SYMPTOM MIGHT THE PATIENT HAVE?
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PROBLEMS SWALLOWING
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THIS MURMUR RADIATES TO THE MIDAXILLARY/BACK
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MITRAL REGURGITATION
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THIS MURMUR RADIATES TO THE NECK
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MITRAL STENOSIS
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WHAT DOES AN XRAY TELL YOU ABOUT THE HEART?
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SIZE (BUT NOT WHETHER HYPERTROPHIC OR DILATATION) AND WHETHER THE PATIENT IS IN HF
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IF THERE IS DECREASED INTRATHORACIC PRESSURE, WHAT HAPPENS TO FILLING OF THE RIGHT VENTRICLE?
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THERE IS MORE FILLING
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WHAT HEART SOUND DO YOU HEAR WITH ALL ISCHEMIC PATIENTS?
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S4
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JUGULAR VENOUS DISTENTION REPRESENTS PRESSURE IN WHAT PART OF THE HEART? WHAT TYPES OF CONDITIONS CAN CAUSE THIS?
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RIGHT ATRIUM; PULMONARY HTN, ACUTE PE, AND COPD
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WHAT COMMONLY CAUSES MITRAL VALVE REGURGITATION?
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AN MI IN WHICH THE PAPILLARY MUSCLES BECOME ISCHEMIC AND CANNOT CONTRACT ADEQUATELY
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WHY IS THE RIGHT ATRIUM MOST AFFECTED BY FLUID AROUND THE HEART?
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B/CIT HAS THE LOWEST NORMAL PRESSURE
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WHAT IS SOMETIMES THE FIRST SIGN OF PERICARDIAL EFFUSION?
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RIGHT ATRIAL COLLAPSE- JVD
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WHAT PART OF THE HEART CYCLE- DIASTOLE OR SYSTOLE- ALLOWS FOR PERFUSION OF CORONARY ARTERIES?
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DIASTOLE---SO IF LOW DIASTOLIC PRESSURE---ISCHEMIA
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WALL TENSION IS ESSENTIALLY?
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AFTERLOAD
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WHICH HAS A GREATER EFFECT ON THE FUNCTION OF THE HEART---VENTRICULAR WALL THICKNESS OR VENTRICULAR CHAMBER RADIUS?
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VENTRICULAR WALL THICKNESS
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IF AFTERLOAD IS INCREASED, WHAT DOES THAT SAY ABOUT STROKE VOLUME?
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IT IS DECREASED
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IF PRELOAD AND CONTRACTILITY INCREASE, WHAT HAPPENS TO STROKE VOLUME?
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IT INCREASES
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IF YOU DEPLETE THE TOTAL BLOOD VOLUME, WHAT HAPPENS TO PRELOAD?
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IT DECREASED
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IF YOU GIVE SALINE, WHAT HAPPENS TO PRELOAD?
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IT INCREASES
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IN A FIB, THE ATRIA STOP CONTRACTING...WHAT HAPPENS TO PRELOAD?
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IT DECREASES
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LESS COMPLIANCE IN VENTRICLES CAN BE CAUSED BY WHAT CONDITIONS?
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TAMPONADE, LVH, PERICARDIAL EFFUSION, PREVIOUS MI
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WHAT IS A NONINVASIVE METHOD TO ESTIMATE EF?
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ECHOCARDIOGRAM
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TO INCREASE EJECTION FRACTION, WHAT MUST INCREASE?
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CONTRACTILITY AND PUMPING
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IF THERE IS MORE VOLUME IN LV, WHAT HAPPENS TO CONTRACTILITY?
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THE LEFT VENTRICLE SQUEEZES MORE FORCEFULLY AND CONTRACTILITY IS INCREASED
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IF THE HEART IS HAVING A PUMPING ISSUE THAT LEADS TO POOR CARDIAC OUTPUT, WHAT IS THE CAUSE?
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DILATION
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IF THE HEART IS HAVING A FILLING ISSUE THAT LEADS TO POOR CARDIAC OUTPUT, WHAT IS THE CAUSE?
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HYPERTROPHY
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