Cardiac action potentials Flashcards
How is AP generation in a pacemaker cell distinct from AP generation in contractile cardiac muscle
cells?
In pacemaker cells, depolarization is triggered when the pacemaker potential reaches about -40mV,
causing Ca2+ channels to open and Ca2+ diffuses into the cell.
In contractile cardiac muscle cells, depolarization is triggered when neighboring cells depolarize,
opening voltage-gated Na+ channels on the next cell and allowing Na+ diffuses into the cell.
The right coronary artery branches into:
Right marginal artery
Posterior descending artery
Coronary arteries
Supply the heart
The two major coronary arteries that branch off from the aorta
Left main coronary artery
Right coronary artery
Circumflex artery is a branch of
Left main coronary artery
The left main coronary artery branches into:
Circumflex artery
Left Anterior Descending artery (LAD)
circumflex artery supplies?
supplies blood to the left atrium, side and back of the left ventricle
LAD supplies?
supplies the front and bottom of the left ventricle and the front of the septum
The right coronary artery branches into:
Right marginal artery
Posterior descending artery
The right coronary artery supplies:
Right atrium
Right ventricle
Bottom portion of both ventricles and back of the septum
What’s happening with pressure when mitral valve closes?
LV pressure is higher than LA pressure.
After mitral valve closes?
Isovolumetric contraction.
Main function: ventricular contraction
Occurs in early systole, directly after the atrioventricular valves (AV valves) close and before the semilunar valves open
All valves are closed
Ventricle contracts (i.e., pressure increases) with no corresponding ventricular volume change
LV pressure: 8 mm Hg → ∼ 80 mm Hg (when aortic and pulmonary valves open passively)
LV volume: remains ∼ 150 mL
The period of highest O2 consumption
After isovolumetric contraction?
Aortic valve opens
Systolic ejection: Blood is pumped from the ventricles into the circulation and lungs.
Occurs during systole, between the opening and closing of the aortic valve
Ventricles contract (i.e., pressure increases) to eject blood, thereby decreasing the ventricular volume
Pressure: first increases from ∼ 80 mm Hg to 120 mm Hg and then decreases until aortic and pulmonary valves close
Volume: ejection of ∼ 90 mL SV (150 mL → 60 mL)
When LV pressure is higher than aortic pressure?
Aortic valve opens
Aortic valve closes?
When LV pressure is lower than aortic pressure
S2 heart sound, diastole begins
What occurs between aortic valve closing and mitral valve opening
Isovolumetric relaxation
slight increase of aortic pressure in the early diastole that corresponds to closure of the aortic valve
Dicrotic notch
Rapid vs reduced filling
Both occur in diastole.
Rapid: early diastole, right as mitral valve opens
Reduced: Late diastole, right before mitral valve closes
Define cardiac output
Formula?
Cardiac output (CO) is the total volume of blood ejected by the ventricles per minute
Cardiac output = Heart rate × Stroke volume
Cardiac reserve?
The difference between CO at rest and during maximum exercise
Parasympathetic vs sympathetic stimulation on heart rate?
Parasympathetic (rest and digest) decreases it. Sympathetic (fight or flight) increases it
How does sympathetic stimulation increase heart rate?
Norepinephrine released from the sympathetic nerve endings activates the β1 receptors in the SA node.
Activation of the β1 receptors in the SA node leads to an increase of inward Na+ and Ca2+ movement via enhanced “funny” Na+- and T-type voltage-gated Ca2+ channels.
This speeds the depolarization phase of the SA node’s action potential by reaching the threshold faster, that in turn increases the heart rate.
Furthermore, sympathetic stimulation reduces the AV nodal delay and increases the conduction of the action potentials throughout the conductive system.
Negative Chronotropic Effects (Parasympathetic Stimulation) Decreases the Heart Rate. How?
Acetylcholine (ACh) release from the parasympathetic nerve endings bind to muscarinic receptors in the SA node to decrease the heart rate as a result of
(1) slowing down the rate of spontaneous depolarization as a result of a decreased Na+ inward current via Na+ “funny” channels—this occurs through coupling of the muscarinic receptors with the Gi proteins that consequently inhibits adenylyl cyclase;
(2) hyperpolarization of the resting potential because of the increase of the K+ permeability and the outward current via the K+-ACh channels; and
(3) a decreased Ca2+ inward current as a result of decreasing functional Ca2+ channels. Thus, more depolarization is needed to reach the threshold and fire an action potential.
Stroke volume, define
Stroke volume (SV) is the volume of blood ejected from each ventricle during the contraction in 1 heartbeat.
EDV - ESV
It is equivalent to the difference between the volume of blood in the ventricle just before the contraction (end-diastolic volume) and the volume of blood left in the ventricle after the contraction (end-systolic volume).
Classic clinical examples of increased afterload
hypertension and aortic stenosis, hypertrophic cardiomyopathy
Preload
Preload in the heart can be defined as the stretching of the myocardial muscle fibers just prior to a contraction or ventricular wall tension at the end of diastole.
clinical example of a decreasing preload
severe hemorrhage or dehydration that can result in a reduction of stroke volume or cardiac output.
Afterload, define
the resistance that the ventricle needs to overcome in order to eject its content. Clinically, it is the amount of aortic pressure that the heart ejects blood against in order to empty the left ventricle.
Contractility
Contractility or inotropy is the property that accounts for the changes in the strength of myocardium contraction independent of the preload and the afterload.
It is affected by the neurotransmitters or hormonal influences and is mainly mediated by the change of the intracellular calcium concentration in the cardiomyocytes.
Ejection fraction is the index for contractility
Ejection fraction formula
Ejection fraction = Stroke volume/End-diastolic volume
Effect of exercise?
The overall effect of exercise is an increased heart rate, increased stroke volume due to an increased preload and increased contractility, and decreased afterload. The total peripheral resistance is decreased and blood perfusion to the muscles is increased.
How to increase preload?
Add volume (blood, IV fluids)
Slow heart rate (more time to fill, more volume )
Constrict veins: Sympathetic stimulation of alpha 1 receptors in veins
(In the setting of blood loss, venous constriction helps maintain volume)
How to decrease preload
Remove volume (bleeding, dehydration)
Raise heart rate (less time to fill, less volume)
Pool blood in veins (like nitrates)
To increase contractility?
Sympathetic nervous system activity. Triggered by stress, exercise, circulating catecholamines leads to increased calcium release from sarcoplasmic reticulum
Sympathomimetic drugs
To decrease contractility?
Heart failure, MI, verapamil, diltiazem (CCBs) and beta blockers
T/F Stroke volume rises with increased HR
True.
SNS always raises HR with contractility
Stroke volume and cardiac output can drop when HR becomes too high, eg in arrhythmia
How does increase in HR and contractility affect EDV and ESV
ESV decreases
B-1 activation increases LV contractility and HR. The ventricles squeeze harder and push more blood into the vascular system. As such, less blood remains in the LV chamber at the end of systole.
When will ESV increase?
When contractility falls or with negative inotropic drugs like beta blockers
LVEDV will increase with
Heart rate slows to allow more filling
Increase in preload (fluid infusion)
LVEDV will decrease with
Fast heart rate (less filling time )
How does vasodilation affect after load?
Vasodilation will Decrease afterload
Determinants of cardiac output
HR, contractility, preload, after load
What increases with a fall in after load?
Stroke volume and cardiac output increase.
Decrease in after load decreases work of the heart?
True
Fewer forces resist the flow of blood out of LV
How does skeletal muscle vasodilation affect peripheral resistance
Decrease
How does exercise affect ESV, Pulse pressure, LVEF
Exercise increases SNS activity = increased contractility = increased ejection fraction as the heart squeezes harder = decreased ESV
With exercise, skeletal muscle vasodilation decreases peripheral resistance. As a result, the diastolic BP may fall or remain unchanged.
Systolic bp rises due to higher cardiac output
Systole and diastole on EKG?
Systole starts right before the QRS complex, diastole starts right after the T wave
