CARDIAC1 A AND P Flashcards
HOW MUCH BLOOD IS LEFT ATRIUM RESPONSIBLE FOR CONTRIBUTING TO LVEDV VIA ATRIAL KICK?
20-30%
FLUID IN WHAT AREA OF THE HEART CAUSES CARDIAC TAMPONADE?
A THIN POTENTIAL SPACE BETWEEN THE VISCERAL AND PARIETAL PERICARDIUM. IT NORMALLY CONTAINS 10-25 ML OF SEROUS FLUID.
WHAT PART OF THE MYOCARDIUM IS AT GREATEST RISK FOR MI AND WHY?
SUBENDOCARDIUM BECAUSE IT IS SUPPLIED DURING DIASTOLE.
WHAT DOES THE A, C, AND V WAVE REPRESENT?
A= CONTRACTION OF THE RIGHT ATRIUM C = CLOSURE OF THE TRICUSPID VALVE V= PASSIVE FILLING OF THE RIGHT ATRIUM.
WHAT IS THE ONLY WAY TO INCREASE O2 DELIVERY TO THE MYOCARDIUM?
INCREASE BLOOD FLOW TO THE MYOCARDIUM
IF THE HEART RATE IS INCREASED WHAT IS HAPPENING TO THE DIASTOLIC FILLING TIME?
ITS DECREASED.
WHEN IS THE LEFT VENTRICLE PERFUSED?…HOW ABOUT THE RIGHT VENT?
LEFT V =75% PERFUSION DURING DIASTOLE
RV=PERFUSED BOTH SYSTOLE AND DIASTOLE.
WHAT IS THE BLOOD FLOW (CO) TO VARIOUS PARTS OF THE BODY?
BRAIN 12 LIVER 24 KIDNEY 20 MUSCLE 23 INTESTINES 8 SKIN 6 HEART 5
CORONARY BLOOD FLOW IS ? CC/MIN TO HEART?
225-250
CPP=?
DP-LVEDP
WHAT ARE THE EFFECTS OF VA ON CBF?
DIRECT VASODILATION, REDUCE MYOCARDIAL METABOLIC DEMANDS, REDUCE BLOOD PRESSURE (PRELOAD AND AFTERLOAD),
NO EVIDENCE VA CAUSE CORONARY STEAL
ARE SARCOMERES INVOLVED IN BOTH SKELETAL AND MYOCARDIAL MUSCLE?
YES
WHAT IS THE CHEMICAL AND MECHANICAL PROCESS FOR SARCOMERE INTERDIGITATION….THUS CONTRACTION?
CALCIUM IS RELEASED FROM SARCOPLASMIC RET. WHICH BINDS TO TROPONIN/TROPOMYOCIN, SITES ON MYOCIN HEADS ARE UNCOVERED AND ALLOWS ACTIN AND MYOCIN TO BIND. ATP IS NEEDED FOR THIS. TROPONIN C’S AFFINITY FOR CALCIUM DETERMINES FORCE OF CONTRACTION. AND CONSEQUENTLY CARDIAC OUTPUT.
WHAT IS OPTIMAL SARCOMERE LEGTH FOR GOOD CARDIAC OUTPUT?
2-2.4 UM.
ARE CARDIAC CELLS AEROBIC OR ANAROBIC?
AEROBIC. THEY DONT STORE OXYGEN.
WHAT ARE THE PHASES OF THE ACTION POTENTIAL AND WHAT HAPPENS AT EACH PHASE?
PHASE0=DEPOLARIZATION NA INFLUX, GATES OPEN AT -70
PHASE 1=INITIAL REPOLARIZATION. OVERSHOOT 2-30
P 2=PLATEAU. SLOW CA CHANNELS OPEN . ALLOWS VENTRICULAR FILLING. GET A QRS. LASTS .2-.3 SEC.
P3= REPOLARIZATION. RAPID. K LEAVES, CALCIUM CHANNEL INACTIVATED. CELLS ARE REFRACTORY TO SUBSEQUENT DEPOLARIZATION UNTIL PHASE 4.
P4= COMPLETION OF REPOLARIZATION. RETURN TO RESTING POT AND READY FOR NEXT AP. NA/K PUMP REESTABLISHED. RELAXATION OCCURS AS CALCIUM IS ACTIVELY PUMPED BACK INTO THE SR BY CA MG ATPASE.
WHY IS THE SA NODE CAPABLE OF SPONTANEOUSLY DEPOLARIZING?
LEAKEY CALCIUM CHANNELS.
WHY DO THE ATRIA AND AV NODE CONTRACT?
DUE TO THE CA ENTERING THE CELLS DURING PHASE 2
WHAT IS THE FORCE OF CONTRACTION DIRECTLY RELATED TO?
THE AMOUNT OF INITIAL CALCIUM INFLUX.
HOW DOES CA LEAVE THE CELL AFTER CONTRACTION?
BY EXCHANGE WITH MAGNESIUM VIA ATP-ASE IN THE CELL MEMBRANE.
THE PRESSURE VOLUME LOOPS ARE REFERRING TO WHAT/
LEFT VENTRICLE.
WHAT RELATIONSHIP DOES VENTRICULAR COMPLIANCE EXAMINE?
REL BTW VOL AND PRESSURE IN VENT
WHAT IS STROKE VOL?
AREA WITHIN V/P CURVE. VOL EJECTED WITH CONTRACTION. SV=EDV-ESV
WHAT IS EF?
EF=EDV-ESV/EDV. SO…..THE % OF TOTAL VOL IN HEART THAT WAS EJECTED. NORM IS 60% ITS NEVER 100% SICK PEOPLE IS AROUND 40%.
WHATS THE MOST IMPORTANT DETERMINANT OF PRELOAD?
VENOUS RETURN
WHAT PARTS OF THE SMP/PARASYMP NS INNERVATE THE HEART?
SNS: T1-T4 TO SA NODE. INCR IN HR SV. SNS HAS GREATER EFFECT ON CONTRACTILITY.
PNS: VAGUS. DECR HR AND CONTRACTILITY. THIS PNS TONE PREDOMINATES…NORMAL RESTING HR IS 72BPM
R VAGUS INNERVATES SA
L VAGUS INNERVATES AV
WHAT ARE THE 3 FACTORS THAT AFFECT HR AND CONTRACTILITY?
CARDIAC INNERVATION (ANS), HUMORAL CONTROL, CARDIAC REFLEXES.
WHAT IS THE BARORECEPTOR REFLEX?
THESE MECHANORECEPTORS IN CAROTID SINUSES AND AORTIC ARCH SENSE STRETCH FROM INCREASED PRESSURE AND RESPOND BY MODIFYING (DECREASE) HR. THESE ARE NOT AS SENSITIVE AS PEOPLE AGE.
WHAT IS THE BAINBRIDGE REFLEX?
RECEPTORS IN ATRIA. INCREASED STRETCH IN SA NODE CAUSES SA TO INCREASE RATE. INCREASE HR. (IF HR IS LOW) IF THERE ALREADY IS A HIGH HR, THEN ADDITION STRETCH ON TOP THE HR DECREASES.
A TRUE REFLEX IE: VALSAVA.
WHAT IS THE RESPIRATORY REFLEX?
A NORMAL ARRYTHMIA SOMEWHAT COMMON IN YOUNG HEALTHY MEN….RECEPTORS IN MEDULLA……UPON INSPIRATION GET AND INCREASED HR AND VICE VERSA.
WHAT IS A CHEMORECEPTOR REFLEX?
RECEPTOR IN AORTIC ARCH AND CAROTID SINUS….ACTIVATED BY HYPOXIA AND HYPERCAPNEA STIMULATED DURING ASPHYXIA AND SEVERE HYPOTENSION….CAUSING A STIMULATION IN BREATHING AND CV EFFECTS INCLUDING SYMP CONSTRICTION OF SKEL MUSC ARTERIOLES, SPLANCHINIC VENOCONSTRICTION, AND INCR HR. THIS HELPS MAINTIAN BLOODFLOW TO THE BRAIN AT ART PRESSURE TOO LOW TO ACTIVATE THE BARORECEPTORS. BUT EVENTUALLY THIS WILL CRAP OUT AND A DECR O2 SAT =DECR. HR/ASYSTOLE.
WHAT IS THE FRANK STARLING CURVE AND WHAT DOES IT SHOW?
PLOTS LVEDP AGAINST STROKE VOLUME. IT LOOKS AT THE ABILITY OF THE HEART TO CHANGES ITS FORCE OF CONTRACTION (STROKE VOL) IN RESPONSE TO CHANGES IN VENOUS RETURN (LVEDP). THEY DO NOT SHOW HOW CHANES IN VENOUS RETURN AFFECT DIASTOLIC VOL.
WHAT DOES EF EVALUATE?
THE INOTROPIC STATE OF THE HEART. (HOW HARD THE HEART CAN CONTRACT) NORM IS 60% INCR. INOTROPY INCREASES THE EF.
WHAT ARE THE DETERMINANTS OF MYOCARDIAL O2 SUPPLY?
CORONARY ARTERY ANATOMY
DIASTOLIC PRESSURE
DIASTOLIC TIME
ART O2 CONTENT/ O2 EXTRACTION (HGB SAO2)
WHAT ARE DETERMINANTS OF O2 DEMAND (CONSUMPTION) ? AKA CO
HR MYOCARDIAL CONTRACTILITY MYOCARDIAL WALL TENSION (PRELOAD-MYOCARDIAL WALL TENSION, AFTERLOAD-MAP) VENTRICULAR COMPLIANCE NORMAL CO IS 4-8L/MIN CO=SV X HR
HOW DO YOU CALC. MAP?
MAP= [SBP + (DBP X 2)] / 3
WHAT IS THE FORM FOR SVR?
SVR= [(MAP-RAP) X 80] / CO
FORMULA FOR CPP?
CPP=DIASTOLIC BP - PAWP
FORMULA FOR EF?
EF= SV/EDV
