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191 Cards in this Set
- Front
- Back
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What is the cardiac cycle? (in very basic terms)
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a period of systole followed by diastole
-the sequence of electrical and mechanical events that repeats with each heartbeat |
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What percent of coronary blood flow happens in diastole/systole?
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diastole-70%
systole-30% |
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What determines the cardiac cycle length?
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Duration (sec/beat)=60 (sec/min) / heart rate (beats/min)
ie. for a HR of 75 the cardiac cycle lasts 0.8 s = (60/75) |
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What are the 7 phases of the cardiac cycle?
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Atrial systole
Isovolumetric contraction rapid ejection reduced ejection isovolumetric relaxation rapid filling reduced filling |
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When in ventricular volume at its maximum?
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at the end of atrial systole
-this is called end diastolic volume |
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What is a normal EDV?
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120 mL
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What is the EDV in endurance athletes or during heart failure?
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180-240 mL (it is greatly increased)
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What happens to contractility during sympathetic stimulation?
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rates of pressure development and dissipation are increased
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What is the mathematical basis for contractility?
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it shows the rate in pressure change over time
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What is responsible for the S1 heart sound?
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closing of the AV valves
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What is normal ESV?
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50 mL
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What produces the S2 heart sound?
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closing of the Semilunar valves during isovolumic relaxation
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How is stroke volume calculated?
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EDV-ESV
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During isovolumic relaxation, which valves closes first?
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the aortic valve closes slightly before the pulmonary valve
=splitting of S2 |
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What causes splitting of S2?
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inspiration b/c it delays closing of the pulmonic valve
-inspiration causes intrathoracic pressure to decrease and increases venous return to the RV, increases preload in the RV and stroke volume, prolongs RV ejection time, delays closure of P2 |
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What is the a wave?
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it is the venous pulse created during atrial systole, an increase in right atrial pressure is reflected back to the veins
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What effect would a dialated R. atrium have on the a wave?
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it would cause a larger a wave b/c the atrium would have to build more pressure to contract
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What is the c wave?
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it is the venous pulse detected during RV systole (rapid ejection) and is caused by the bulging of the tricuspid valve into the R. atrium, the peak then drops reflecting downward displacement of the tricuspid during RV emptying
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What is the v wave?
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the venous pulse measured during isovolumic relaxation due to filling of central veins and R. atrium behind a closed tricuspid
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Which atrium contracts first?
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right
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Which ventricle contracts first?
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the left
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Which valve opens first: aortic or pulmonary?
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pulmonary b/c the period of isovolumic contraction is briefer for the RV
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What is the difference between Right and Left atrial contraction?
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it begins and ends earlier in the R atrium
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On which side of the heart does ejection last longer?
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the right side from RV
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Why does the aortic valve close before the pulmonary valve?
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b/c of higher downstream pressure in the aorta than the pulmonary trunk (pulmonary valve with lower downstream pressure opens first and closes last)
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Which valve opens first: mitral or tricuspid?
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tricuspid b/c RV fills before the LV
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What is the definition of stroke volume?
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the volume of blood ejected on one ventricular contraction (IVC-IVR volume)
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What is the equation for determining stroke volume?
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EDV-ESV (ml/beat)
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What is the definition of ejection fraction?
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the effectiveness of the ventricles in ejecting blood, fraction of the EDV that is ejected in one SV, it is an indicator of contractility
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What is the equation for determining ejection fraction?
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SV/EDV X 100
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What is the definition of cardiac output?
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total volume of blood ejected per unit time
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What is the equation for determining cardiac output?
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CO=HR X SV
-it is the product of SV and HR |
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How is the cardiac index calculated?
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CO / SA (body surface area)
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What percent of ejection fraction is indicative of heart failure?
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<45%
this greatly reduces survivability |
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What pathologies can widen the S2 split?
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-pulmonic stenosis (narrowed pulmonary valve)
-right ventricular failure (associated w/increased preload) -right bundle branch block (delayed depolarization of right ventricle |
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What pathology can cause the S2 split to narrow or disappear?
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left bundle branch block (delayed depolarization of LV)
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What causes a paradoxical split of the S2 sound?
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severe aortic stenosis (P2 heard before A2)
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What are heart murmurs?
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they are abnormal heart sounds that originate from abnormal flow of blood across valves or between heart chambers
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What is an insufficient valve?
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a valve that cannot close completely so blood flows backward and collides with incoming blood creating turbulence which can be heard as a murmur
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What is the definition of a systolic murmur?
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one that is heard during systole or after S1 heart sound
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What can cause a systolic murmur?
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aortic valve stenosis, pulmonary valve stenosis (blood flow occurs through a narrowed opening during systole of ventricles)
-mitral valve regurgitation or tricuspid valve regurgitation (closure of the valve not complete and blood is forced back into atrium under pressure) |
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What is the definition of a diastolic murmur?
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heard during diastole after S2 heart sound
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What can cause a diastolic murmur?
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aortic or pulmonary valve regurgitation (backflow of blood into ventricles during diastole of ventricles)
-mitral or tricuspid valve stenosis |
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What 2 things determine conduction velocity in the heart?
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1)the rate of change in membrane potential as a function of time (upstroke phase of AP)
2) resistance |
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What 2 kinds of membrane junctions are present within intercalated discs?
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gap junctions-electrical connections
desmosomes-mechanical junctions |
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Describe the length of cardiac action potentials in comparison to skeletal mm.
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they have a long duration compared to sk. mm.
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What are the 2 types of action potentials in cardiac cell and what types of cell are responsible for them?
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1)fast action potentials: contractile cells
2)slow action potential-pacemaker cells |
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What is Phase 0 of the fast action potential?
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upstroke, rapid depolarization
-similar to that in sk. mm. -due to fast inward Na+ current |
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What is Phase 1 of the fast action potential?
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early repolarization
-due to activation of some transient K+ channels (outward) -inactivation gates on Na channels close -electrochemical gradient favors K movement out of the cell |
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What is Phase 2 of the fast action potential?
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the plateau phase
-major diff. btwn. cardiac mm. and sk. mm. or nerve -responsible for very long AP -due to balance btwn. Ca (L-type) channel inward current and K outward current |
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What can inhibit the plateau phase in cardiac mm?
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Ca channel blockers
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What are L-type channels in cardiac mm?
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they are "long lasting" channels that have slower kinetics than Fast Na channels
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What is phase 3 of the fast action potential?
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repolarization
-caused by turn off of Ca channels and further increase of K currents -K current reduced near end of this phase b/c membrane potential closer to K equilibrium |
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What is Phase 4 of the fast action potential?
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resting potential
-caused by large background K outward current (different channels than in phase 3) -balanced by inward Na and Ca current |
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Why are summation and tetanus unlikely in cardiac mm?
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because of the long refractory period along with the prolonged plateau phase
-this is important to ensure periods of contraction followed by relaxation which ensure blood pumping action |
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What are the 3 main differences btwn. fast action and slow action potentials?
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In slow action potentials:
1)automaticity 2)unstable RMP 3)no sustained plateau |
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What phases are absent from slow action potentials?
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phases 1 and 2
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Describe Phase 0 of slow AP.
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upstroke
-slow due to L type Ca current inward |
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Describe phase 3 of slow AP.
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repolarization
-caused by turn off of Ca current and further increase in K current |
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Describe phase 4 of the slow AP.
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the pacemaker potential
-spontaneous depolarization -longest portion of AP due to inward Na current and a transient Ca current (T-type) inward -Na current turned on by repol. from preceeding AP -max. diastolic potential=-65 mV |
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What sets the heart rate? (in terms of APs)
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the rate of phase 4 of the slow action potential
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What is the source of initiating Ca in the heart?
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extracellular
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What effect does stretching cardiac mm. fibers have on the force of contraction?
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it increases the strength of the contraction
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Equation for Stroke volume?
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EDV-ESV
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Ejection fraction equation.
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usually 50-70%
SV/EDV X 100 |
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Cardiac output equation.
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SV X HR
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Cardiac Index equation.
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CO/SA (where SA equals body surface area in m(squared))
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Left ventricular stroke work equation. (LVSW)
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SV X left ventricular pulse pressure
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What is the definition of preload?
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the tension in the ventricular wall at end of diastole (proportional to EDV)
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How do we measure preload ?
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since tension cannot be measured we usually measure EDV or DP (EDP)
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What effect does increasing the EDV have on the SV?
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it increases it (due to Frank Starling law) b/c the heart contracts with more force
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Name some factors that determine preload.
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ventricular filling time (dependent on heart rate), ventricular compliance, filling pressure (w/negative intrathoracic P increase venous return to right heart, contribution of atrial systole to filling (important when filling time is reduced), pericardial constraint
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In the absence of sympathetic stimulation, what effect will increasing the heart rate to approx. 150 BPM have on filling time and CO?
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filling time will be reduced (reduced filling phase), but CO will usually not be affected since decreased SV is compensated for by increased HR
-CO adversely affected by HR>150 to 180 BPM |
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With sympathetic stimulation, what would happen to CO?
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SV is preserved due to increased contractility, CO can increase dramatically tho b/c of increased HR
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What is ventricular compliance?
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the ability of ventricle to distend under pressure,
-a highly compliant chamber will undergo a large change in volume with a relatively small change in pressure -low compliance ventricles develop higher pressure during diastole which retard filling |
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What will increase RV stroke volume?
What effect will this have on the Left ventricle? |
decreasing intrathoracic pressure or increasing central venous pressure (very important!!)
-this will increase the preload on the left ventricle |
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When does atrial systole become very important in determining EDV (preload)?
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in cases where filling time is limited
-atrial contractility can actually increase in these scenarios |
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What is afterload?
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resistance against which the ventricles contract
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What are the major components affecting afterload for the left ventricle?
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arterial pressure, arterial wall compliance, Peripheral vascular resistance, mass of the column of blood in the aorta, viscosity of the blood,
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How is afterload estimated? (using what value?)
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mean arterial pressure
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Equation for mean arterial pressure?
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DP + 1/3 PP
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noi mettiamo
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we put
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Clinically, how is afterload increased?
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aortic stenosis, elevated arterial pressure, increased peripheral vascular resistance, increased blood viscosity, decreased arterial compliance
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How do we compensate for increased afterload in the heart?
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by the Frank-Starling mechanism, with an increased ESV, the ventricle still fills normally so EDV increases which restores the normal SV but the heart is doing more work
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What is contractility?
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ability of heart to do work at any given fiber length (distinct from changes in end diastolic fiber length =preload, and different from afterload)
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What are some factors that affect myocardial contractility?
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ANS, hormones, Ca influx and availabiltiy (more X-bridges activated=more force generated)
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What does SNS stimulation do to filling and contraction times?
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the total force of contraction increases as well as the rate of that force production, the rate of relaxation is also very rapid in order to allow sufficient time for filling (filling time are maintained)
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What effect will increasing contractility have on the parameters of cardiac performance?
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at a given EDV, EDP, and afterload, the SV will be increased, the ESV will decrease, Ejection fraction increased,
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What 2 main things is ESV dependent on?
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afterload, and contractility
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How is contractility actually measured in the body?
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by measuring the isovolumic indices, AKA getting the rate of ventricular Pressure changes during isovolumic contraction with catheterization (pressure change/time)
-can also measure ejection indices (ejection fraction comparing SV to EDV) |
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What is considered a normal ejection fraction?
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50-75%
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In what 2 ways does HR influence cardiac performance?
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1)Treppe-aka bowditch staircase effect where increasing HR causes Ca accumulation with increases contractility (small positive inotropic effect)
2)rlthp. btwn. HR and CO -increased HR will increase CO only if SV is maintained or increased by SNS sitmulation |
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How is SV maintained at high heart rates?
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b/c of Treppe, increased Ca accumulation allows some of the Ca to be stored in SR for use in subsequent beats, increased Ca increases contractility which maintains the SV
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How is LVSW calculated using MAP?
When would we want to use this method over using LVPP? |
SV X MAP
would want to use this in cases of aortic stenosis when the LVPP is going to be elevated |
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How is LVMW (left ventricular minute work) calculated?
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LVSW X HR or SV X MAP X HR
-contractile work per minute instead of per beat |
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Equation for left ventricular stroke index?
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LVSW/SA
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What is the Fick method of calculating cardiac output?
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it is the oldest method and it says:
Oxygen consumption/(arterial O2-venous O2) |
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Where are venous O2 levels measured in the Fick method?
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in the pulmonary artery (right atrium not OK, blood not mixed, but R ventricle OK)
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What is cardiac efficiency in basic terms?
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the ratio of work performed to the energy consumed (through O2 consumption)
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What is the usual efficiency of the myocardium?
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5-15%
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When does the efficiency of the heart improve?
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during exercise
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What type of work increases during exercise?
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volume work increases which is more efficient than increasing pressure work which is more costly
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How much more work does the LV do than the RV?
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6-7 times as much
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Which vessels contain more collagen fibers?
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veins
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Which vessels contain more elastic fibers and smooth mm?
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arteries
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Which vessels have the largest x-sectional area?
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capillaries
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Volume of blood is highest in which vessels?
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veins, but pressure is low so called "unstressed volume"
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Equation for velocity of blood flow.
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v=Q/A
v=velocity of blood flow (cm/sec) Q=flow (mL/sec) A=cross sectional area (cmsquared) (A=pi R^2) |
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Why is it important for capillaries to have a low v?
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because it allows sufficient time for cross-wall exchange
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Equation for flow.
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Q=pressure change/R
P=mmHg R=mmHg/mL/min Q=mL/sec |
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Equation for pulse pressure.
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systolic pressure-diastolic pressure
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What is vascular resistance?
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a measure of hindrance to blood flow caused by friction between moving blood and the vessel flow
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What is Poiseuilles's equation and what does it help to determine?
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R=8nl/pi(r)^4
expresses factors that determine resistance of a blood vessel n=viscosity l=length of vessel r=radius |
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What is the most important factor that determines vascular resistance?
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radius
smaller radius confers more resistance b/c blood rubs against a larger surface area |
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What happens to the resistance if another circuit is added to vessels arranged in parallel?
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it decreased the total resistance (as in growth of the placenta in women)
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What is laminar flow?
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the ideal blood flow in a vessel, elements of the fluid move in streamlines and demonstrate a paraboloid profile of velocity of blood flow in which the layer of fluid in contact with the wall is motionless and then the layer central to this externa lamina moves slowly and then the next more central layer moves still faster,etc..
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What is Reynold's number?
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it predicts whether turbulent or laminar flow will occur in a vessel
-it considers: diameter of vessel, mean velocity, fluid density and viscosity, <2000 is laminar >3000 is turbulent |
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What is the equation for Reynold's number?
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Nr=pdv/n
p=density of blood d=diameter of vessel v=velocity of flow n=viscosity of blood main factor is velocity! |
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What does a Reynold's number btwn. 2000 and 3000 signify?
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flow is transitional btwn. laminar and turbulent
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Equation for vessel compliance?
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C=delta V/delta P
C=compliance (ml/mmHg) V=volume (mL) P=pressure (mmHg) |
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Which vessels have the highest compliance?
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veins b/c they hold the largest volume of blood at the lowest pressures
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What are the 2 pools which serve as sources for fuel for the heart?
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1)exogenous pool (blood)=glucose, lactate, ketone bodies, fatty acids
2)endogenous pool (intracellular stores)=glycogen, triglycerides |
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What determines uptake of fuels by the heart?
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energy demand as workload (transition from rest to exercise), metabolic state (fasting to feeding-hormonal status, associated with changes in the arterial concentrations of fuels)
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What % of ATP is provided by carbohydrates under normal resting conditions of the heart?
By fatty acids? |
30-40%
60-70% by fatty acids |
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What are some sources of fatty acid uptake and metabolism?
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lipolysis of triglycerides and B-oxidation of the fatty acid, lipoprotein and chylomicron oxidation, ketone body oxidation
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What cycle allows the heart to switch to rely entirely on carb. oxidation for its energy needs?
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the Randle cycle
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As level of fatty acids increases in the heart, what happens to other metabolism?
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palmitate oxidation increases (B-oxidation), and glucose metabolism decreases
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What metabolic pathways are inhibited by fatty acids in the heart?
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glucose oxidation and glycolysis (inhibition greater on glucose oxidation)
-inhibiting glucose oxidation can lead to LV failure |
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What is the clinical significance of the Randle cycle?
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it can be manipulated in cases of angina, infarct, diabetes, and post cardiac surgery,
-all these conditions are associated with high levels of fatty acid oxidation |
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Why are high rates of fatty acid metabolism detrimental to the heart?
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induce cardiac arrhythmias, increase oxygen consumption, promotes oxygen wasting, reduces cardiac performance, leads to heart failure
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Why would metabolic intervention be necessary in people with diabetes?
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b/c both glucose uptake and oxidation are low in diabetics, their hearts rely solely of fatty acid oxidation which contributes to heart failure and potentiates post infarct injury
-restoring glucose use restores cardiac performance |
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Why would metabolic intervention be necessary in infarct and cardiac surgery?
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b/c both are associated with extremely high levels of plasma FFAs b/c of the release of epinephrine= ventricular dysfunction
-reducing fatty acid oxidation improves cardiac performance and reduces injury to the heart |
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What do Ranolazine and trimetazidine do?
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they inhibit ketoacyl CoA thiolase which is an enzyme of B-oxidation
= reduces Fatty acid oxidation |
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What do etomoxir and oxfenicine do?
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they inhibit carnitine palmitoyl transferase = inhibition of FA uptake into the mitochondria
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What does L-carnitine do?
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it's a cardiac metabolism modulator, it modulates mitochondrial acetyl CoA levels, it buffers acetyl CoA by producing acetylcarnitine which decreases mito. levels of Acetyl CoA which removes the inhibition on pyruvate dehydrogenase and allows glycolysis to resume
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What does dichloroacetate do?
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it stimulates pyruvate dehydrogenase (aka activates an enzyme of glucose metabolism)
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What factors have a positive inotropic effect on the heart?
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increased HR, SNS, catecholamines
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What factors have a negative inotropic effect on the heart?
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PNS, heart failure
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What are the 2 main ways that force production in the heart is regulated/changed?
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contractility (Ca)
length/tension rlthshp. |
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How does Digitalis work to increase contractility or tension development in the heart?
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it inhibits the Na/K ATPase and therefore reverses the Na/Ca exchanger so that now there is higher intracellular Ca=enhanced force of contraction
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What is NCX?
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it is the Na/Ca exchanger found in heart cells that pumps one Ca ion out for every 3 Na in, it is a secondary active transporter that relies on the Na/K ATPase to work
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What would cause increased peak tension in the heart myocytes?
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greater intracellular Ca
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What would increase the rate of tension development?
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phosphorylation of sarcolemmal Ca channels increase inward Ca current during plateau phase,
-increased Ca induced Ca release |
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What would cause faster relaxation in the heart?
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phosphorylation of phospolamban b/c it increases the activity of the SERCA pump
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Which leads view current in the frontal plane?
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bipolar limb leads or einthoven leads(1, 2, 3) and augmented unipolar limb leads (aVR, aVL, aVF)
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Which leads provide information in the transverse plane of the body?
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chest leads (V1-V6)
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What do leads measure?
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the potential difference btwn. 2 points
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What does aVR look at in the heart?
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it sees the cavities of the ventricles, atrial and ventricular depol. and ventric. repol. move away from electrode= all waves are negative or downwards
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What do aVL and aVF look at in the heart?
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the ventricles, deflections are predominately positive or upwards unline aVR
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What are the "lateral" leads?
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the leads in which the positive electrode is placed on the LA(laterally)
-leads I and AVL |
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What are the "inferior" leads?
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the leads in which the positive electrode is placed on the LF (II, III, and AVF)
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What charge is the electrode for all the chest leads?
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positive
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Which chest leads are over the right side of the heart?
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V1, V2 and QRS mainly negative
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Which chest leads are over the IV septum?
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V3 and V4
V3 nearer RV V4 nearer LV |
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WHich chest leads are over the L. side of heart?
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V5 and V6
QRS mainly positive |
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WHy do we want to determine vectors from an EKG trace?
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to calculate mean axis of deviation or mean axis of depolarization
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What could cause Left axis deviation in the heart?
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pregnancy, obesity, LV hypertrophy
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What could cause R axis deviation in the heart?
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RV hypertrophy, tall and slender, chronic lung disease (emphysema)
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Which part of the conduction system is the fastest?
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purkinje fibers
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What causes depolarization of the AV node?
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Ca, the rest of the conduction tissue uses Na
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Conduction velocity of the SA node?
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0.05 m/sec
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What are internodal tracts?
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there are 3 specialized internodal tracts in the RA that go between the SA and AV nodes (ant, middle, and post.)
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What happens to the rate of SA node discharge with inspiration?
Expiration? |
inspiration=increases
decreases with expiration |
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Which regions of the AV node have automaticity foci?
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not proximal, just middle and distal
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Rate of pacing for Atrial foci?
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60-80 beat/min
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Rate of pacing for ventricular foci?
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20-40 BPM
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Rate of pacing for junctional foci?
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40-60 BPM
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What is the PR interval?
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extends from beginning of P wave to beginning or QRS complex
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What is the QT interval?
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extends from the beginning of the QRS complex to the end of the T wave
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HOw long is a normal P wave?
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0.1 seconds
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Normal PR interval range?
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0.12-.20 seconds (anything greater than 0.2 s considered lengthened)
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Normal length of QRS?
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0.08-.10s
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What is the J-point (junction point) on an EKG tracing?
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where ST segment joins QRS complex
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What would cause depression of the ST wave?
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digitalis
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What does a depressed/elevated ST segment indicate?
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serious pathology, inflammation of the membrane surrounding the heart
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How long is a normal T wave?
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0.16 sec
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What does the QT interval represent?
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duration of ventricular systole, it is a good indicator of repolarization since it comprises most of the QT interval
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QT interval is considered normal if...
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it is half the R-R interval
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What does QT vary with?
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heart rate b/c repol and depol occur with greater efficiency at rapid HRs
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What does the U wave represent when present?
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repolarization of papillary mm.
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Equation relating HR and cycle length.
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HR=1/cycle length
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How much time between 2 dark lines on an EKG?
2 light lines? |
0.2 s
0.04 s |
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What does the amplitude (voltage) tell us about the heart in an EKG??
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gives an idea of the mass(number) of active cells
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Ratio of P:QRS in Type I mobitz Wenkebach?
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4:3 , 5:4, etc
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Normal serum K levels.
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3.5-4.5 mmol/L
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Characteristics of Hyperkalemia on EKG.
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high K=prolonged PR interval, P waves smaller/flatter may even disappear
initially peaking of T waves Really high K=intraventricular conduction delay, depol takes longer and QRS widens really really high K=QRS even wider, becomes undulating sine wave pattern |
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EKG of hypokalemia.
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ST depressions, prominent U waves, prolonged repolarization, T waves can become flatter of inverted
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Hypercalcemia on EKG.
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ventric depol and repol shortened, shortening of QT interval
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What is normal serum Ca levels?
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2.25-2.75 mmol/L
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What 2 things are diagnostic for hypercalcemia?
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decrease in QT interval and altered mental status
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Hypocalcemia on EKG.
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ventric repol. is lengthened, prolonged QT interval by stretching out ST segment,
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