Cardiac action potentials

Question 1

How is AP generation in a pacemaker cell distinct from AP generation in contractile cardiac muscle
cells?

Answer 1

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.

Question 2

The right coronary artery branches into:

Answer 2

Right marginal artery

Posterior descending artery

Question 3

Coronary arteries

Answer 3

Supply the heart

Question 4

The two major coronary arteries that branch off from the aorta

Answer 4

Left main coronary artery

Right coronary artery

Question 5

Circumflex artery is a branch of

Answer 5

Left main coronary artery

Question 6

The left main coronary artery branches into:

Answer 6

Circumflex artery

Left Anterior Descending artery (LAD)

Question 7

circumflex artery supplies?

Answer 7

supplies blood to the left atrium, side and back of the left ventricle

Question 8

LAD supplies?

Answer 8

supplies the front and bottom of the left ventricle and the front of the septum

Question 9

The right coronary artery branches into:

Answer 9

Right marginal artery

Posterior descending artery

Question 10

The right coronary artery supplies:

Answer 10

Right atrium
Right ventricle
Bottom portion of both ventricles and back of the septum

Question 11

What’s happening with pressure when mitral valve closes?

Answer 11

LV pressure is higher than LA pressure.

Question 12

After mitral valve closes?

Answer 12

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

Question 13

After isovolumetric contraction?

Answer 13

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)

Question 14

When LV pressure is higher than aortic pressure?

Answer 14

Aortic valve opens

Question 15

Aortic valve closes?

Answer 15

When LV pressure is lower than aortic pressure

S2 heart sound, diastole begins

Question 16

What occurs between aortic valve closing and mitral valve opening

Answer 16

Isovolumetric relaxation

Question 17

slight increase of aortic pressure in the early diastole that corresponds to closure of the aortic valve

Answer 17

Dicrotic notch

Question 18

Rapid vs reduced filling

Answer 18

Both occur in diastole.
Rapid: early diastole, right as mitral valve opens
Reduced: Late diastole, right before mitral valve closes

Question 19

Define cardiac output

Formula?

Answer 19

Cardiac output (CO) is the total volume of blood ejected by the ventricles per minute

Cardiac output = Heart rate × Stroke volume

Question 20

Cardiac reserve?

Answer 20

The difference between CO at rest and during maximum exercise

Question 21

Parasympathetic vs sympathetic stimulation on heart rate?

Answer 21

Parasympathetic (rest and digest) decreases it. Sympathetic (fight or flight) increases it

Question 22

How does sympathetic stimulation increase heart rate?

Answer 22

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.

Question 23

Negative Chronotropic Effects (Parasympathetic Stimulation) Decreases the Heart Rate. How?

Answer 23

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.

Question 24

Stroke volume, define

Answer 24

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).

Question 25

Classic clinical examples of increased afterload

Answer 25

hypertension and aortic stenosis, hypertrophic cardiomyopathy

Question 26

Preload

Answer 26

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.

Question 27

clinical example of a decreasing preload

Answer 27

severe hemorrhage or dehydration that can result in a reduction of stroke volume or cardiac output.

Question 28

Afterload, define

Answer 28

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.

Question 29

Contractility

Answer 29

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

Question 30

Ejection fraction formula

Answer 30

Ejection fraction = Stroke volume/End-diastolic volume

Question 31

Effect of exercise?

Answer 31

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.

Question 32

How to increase preload?

Answer 32

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)

Question 33

How to decrease preload

Answer 33

Remove volume (bleeding, dehydration)
Raise heart rate (less time to fill, less volume)
Pool blood in veins (like nitrates)

Question 34

To increase contractility?

Answer 34

Sympathetic nervous system activity. Triggered by stress, exercise, circulating catecholamines leads to increased calcium release from sarcoplasmic reticulum

Sympathomimetic drugs

Question 35

To decrease contractility?

Answer 35

Heart failure, MI, verapamil, diltiazem (CCBs) and beta blockers

Question 36

T/F Stroke volume rises with increased HR

Answer 36

True.
SNS always raises HR with contractility

Stroke volume and cardiac output can drop when HR becomes too high, eg in arrhythmia

Question 37

How does increase in HR and contractility affect EDV and ESV

Answer 37

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.

Question 38

When will ESV increase?

Answer 38

When contractility falls or with negative inotropic drugs like beta blockers

Question 39

LVEDV will increase with

Answer 39

Heart rate slows to allow more filling

Increase in preload (fluid infusion)

Question 40

LVEDV will decrease with

Answer 40

Fast heart rate (less filling time )

Question 41

How does vasodilation affect after load?

Answer 41

Vasodilation will Decrease afterload

Question 42

Determinants of cardiac output

Answer 42

HR, contractility, preload, after load

Question 43

What increases with a fall in after load?

Answer 43

Stroke volume and cardiac output increase.

Question 44

Decrease in after load decreases work of the heart?

Answer 44

True

Fewer forces resist the flow of blood out of LV

Question 45

How does skeletal muscle vasodilation affect peripheral resistance

Answer 45

Decrease

Question 46

How does exercise affect ESV, Pulse pressure, LVEF

Answer 46

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

Question 47

Systole and diastole on EKG?

Answer 47

Systole starts right before the QRS complex, diastole starts right after the T wave