Cardiovascular Anatomy, Physiology, Pathology, and Pharmacology Flashcards
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
endocardium
MAP=
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 CO= SV x HR
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
