Cardiovascular Anatomy, Physiology, Pathology, and Pharmacology Flashcards Preview

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Flashcards in Cardiovascular Anatomy, Physiology, Pathology, and Pharmacology Deck (32)
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Where is the apex of the heart

located at the bottom


orientation of the heart

the right ventricle is more front facing


innermost layer of the heart




DBP + 1/3(SBP-DBP)


What are the events responsible for the generation of the action potential in the
sinoatrial node?

the depolarizing current is carried into the cell primarily by relatively slow Ca++ currents instead of by fast Na+ currents. There are, in fact, no fast Na+ channels and currents operating in SA nodal cells. This results in slower action potentials
At the end of repolarization, when the membrane potential is very negative (about -60 mV), ion channels open that conduct slow, inward (depolarizing) Na+ currents. These currents are called "funny" currents and abbreviated as "If". These depolarizing currents cause the membrane potential to begin to spontaneously depolarize, thereby initiating Phase 4. As the membrane potential reaches about -50 mV, another type of channel opens. This channel is called transient or T-type Ca++ channel. As Ca++ enters the cell through these channels down its electrochemical gradient, the inward directed Ca++ currents further depolarize the cell. When the membrane depolarizes to about -40 mV, a second type of Ca++ channel opens. These are the so-called long-lasting, or L-type Ca++ channels. Opening of these channels causes more Ca++ to enter the cell and to further depolarize the cell until an action potential threshold is reached (usually between -40 and -30 mV). It should be noted that a hyperpolarized state is necessary for pacemaker channels to become activated. Without the membrane voltage becoming very negative at the end of phase 3, pacemaker channels remain inactivated, which suppresses pacemaker currents and decreases the slope of phase 4. This is one reason why cellular hypoxia, which depolarizes the cell and alters phase 3 hyperpolarization, leads to a reduction in pacemaker rate (i.e., produces bradycardia). During Phase 4 there is also a slow decline in the outward movement of K+ as the K+ channels responsible for Phase 3 continue to close. This fall in K+ conductance (gK+) contributes to the depolarizing pacemaker potential.
Phase 0 depolarization is primarily caused by increased Ca++ conductance (gCa++) through the L-type Ca++ channels that began to open toward the end of Phase 4. The "funny" currents, and Ca++ currents through the T-type Ca++ channels, decline during this phase as their respective channels close. Because the movement of Ca++ through these channels into the cell is not rapid, the rate of depolarization (slope of Phase 0) is much slower than found in other cardiac cells (e.g., Purkinje cells).
Repolarization occurs (Phase 3) as K+ channels open (increased gK+) thereby increasing the outward directed, hyperpolarizing K+ currents. At the same time, the L-type Ca++ channels become inactivated and close, which decreases gCa++ and the inward depolarizing Ca++ currents.


What information does an electrocardiogram provide about cardiac function

P wave= atria depolarization
PR interval= delay in AV node
QRS= depolarization of ventricles
S wave= depolarization of ventricles
T wave= repolarization of ventricles


What is the impact of the absolute and relative refractory periods on cardiac function

During the absolute refractory period, a new action potential cannot be elicited. During the relative refractory period, a new action potential can be elicited


How do stroke volume and heart rate affect cardiac output

CO= amount of blood pumped per minute for each ventricle

SV= amount of blood pumped out


How is stroke volume regulated

preload- an increase in venous return to the heart increases the filled volume (EDV) of the ventricle, which stretches the muscle fibers thereby increasing their preload. This leads to an increase in the force of ventricular contraction and enables the heart to eject the additional blood that was returned to it. Therefore, an increase in EDV results in an increase in SV. Conversely, a decrease in venous return and EDV leads to a decrease in SV by this mechanism.

afterload- pressure that the ventricle must generate in order to eject blood into the aorta. Changes in afterload affect the ability of the ventricle to eject blood and thereby alter ESV and SV. For example, an increase in afterload (e.g., increased aortic pressure) decreases SV, and causes ESV to increase. Conversely, a decrease in afterload augments SV and decreases ESV. It is important to note, however, that the SV in a normal, non-diseased ventricle is not strongly influenced by afterload because of compensatory changes in preload. In contrast, the SV of hearts that are failing are very sensitive to changes in afterload.

inotrophy -(contractility) alter the rate of ventricular pressure development, thereby affecting ESV and SV. For example, an increase in inotropy (e.g., produced by sympathetic activation of the heart) increases SV and decreases ESV. Conversely, a decrease in inotropy (e.g., heart failure) reduces SV and increases ESV.


limb lead sites

lead I: right arm–left arm
lead II: right arm–left leg (inferior view)
lead III: left leg–left arm
(inferior view)

look at the heart in the vertical plane


augmented leads and their respective limb electrodes

aVR lead: right arm
aVL lead: left arm
aVF lead: left leg
(inferior view)


What is the origin of cardiac arrhythmias

the SA node fails to function normally (e.g., sinus bradycardia or tachycardia)

impulses are not conducted from the atria to the ventricles through the AV node (termed AV block)

abnormal conduction pathways are followed (e.g., accessory pathways between atria and ventricles)

other pacemaker sites within the atria or ventricles (e.g., ectopic pacemakers) trigger depolarization


How does each class of antiarrhythmics (I-IV) function to control arrhythmia and
what are the common and important adverse effects

I- Na+ channel blockers
decrease the rate of depolarization to decrease conduction velocity therefore suppressing tachycardia

II- Beta blockers
block the binding of NE and Epi therefore inhibiting sympathetic activity resulting in decreased HR and contractility

III- prolong AP ( potassium channel blockers)
bind and block K+ therefore delaying repolarization leading to an increased AP which suppresses tachy

IV- Ca2+ channel blockers
cause vascular smooth muscle relaxation (vasodilation), decreased myocardial force generation (negative inotropy), decreased heart rate (negative chronotropy), and decreased conduction velocity within the heart (negative dromotropy)


When the electrical activity of the heart travels towards a lead you get a

positive deflection


When the electrical activity travels away from a lead you get a

negative deflection


lead II shows the most positive deflection because...

it is the most closely aligned to the overall direction of electrical spread


lead II shows the most positive deflection because...

it is the most closely aligned to the overall direction of electrical spread


ejection fraction =



ventricular systole summary

isovolumic contraction
rapid ejection
slower ejection
closure of aortic valve`


ventricular diastole summary

isovolumic relaxation
mitral valve opening
rapid ventricular filling
slower ventricular filling
sinus node depolarization and atrial


how to calculate BP

= TPR x HR x SV


at rest how much of the blood volume is in the veins



how long does systole last in the cardiac cycle

1/3 of the time


the mitral valve is ____ during systole



the aortic valve is ____ during systole



coronary artery disease

major blood vessels that supply your heart with blood, oxygen and nutrients (coronary arteries) become damaged or diseased. Cholesterol-containing deposits (plaque) in your arteries and inflammation are usually to blame for


risk factors for CAD

blood lipids
elevated cholesterol
elevated LDL
low HDL
elevated TG
high fat, calorie diet
excess alcohol consumption
family history
prior history of cardiac event


cause of acute coronary syndrome

plaque instability and rupture


right sided heart failure characteristics

dependent edeam
distention of jugular veins
liver engorgement
elevation of peripheral venous pressure


left sided heart failure characteristics

exertional dyspnea
blood tinged sputum
elevation in pulmonary capillary wedge pressure