Heart Anatomy and Muscle Function

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Questions and Answers

What is the primary effect of increasing preload on stroke volume?

It has no effect on stroke volume.

It results in a decrease in stroke volume.

It decreases the force of contraction.

It stretches the muscle, increasing stroke volume. (correct)

Which of the following agents is known to decrease contractility?

Thyroxine

Calcium channel blockers (correct)

Epinephrine

Sympathetic stimuli

How do hormones like epinephrine and norepinephrine affect myocardial contractility?

They increase calcium availability to sarcomeres. (correct)

They have no effect on contractility.

They reduce intracellular calcium availability.

They have a negative inotropic effect.

What is the impact of increased peripheral resistance on cardiac output?

It decreases cardiac output. Signup and view all the answers

What effect do beta-blockers have on the heart?

They block beta-receptors, reducing contractility. Signup and view all the answers

What are the two primary types of valves in the heart?

Atrioventricular valves and semilunar valves Signup and view all the answers

What is preload in the context of heart function?

The tension on the muscle when it begins to contract Signup and view all the answers

Which chamber of the heart is associated with the tricuspid valve?

Right atrium Signup and view all the answers

What is the role of pacemakers in the heart?

To generate and spread action potentials Signup and view all the answers

What is afterload in heart mechanics?

The load against which the muscle exerts contractile force Signup and view all the answers

Which phase of the cardiac cycle corresponds to the interval between heartbeats?

Diastole Signup and view all the answers

Which layer of the heart contains the specialized cells responsible for electrical conduction?

Myocardium Signup and view all the answers

What duration does a single contraction of the heart typically last?

280 ms Signup and view all the answers

What is the role of the sino-atrial (SA) node in cardiac function?

It regulates atrial systole and influences heart rate. Signup and view all the answers

What occurs during the isovolumic contraction phase of the cardiac cycle?

Intraventricular pressure rises without a change in volume. Signup and view all the answers

What condition must be met for the mitral valve to open?

Atrial pressure must exceed ventricular pressure. Signup and view all the answers

What happens during the ventricular systole phase of the cardiac cycle?

The blood is pumped from the ventricles into the arteries. Signup and view all the answers

During what part of the cardiac cycle is the majority of ventricular filling completed?

During early diastole. Signup and view all the answers

What defines afterload in the context of ventricular contraction?

The resistance the ventricle must overcome to eject blood. Signup and view all the answers

Which of the following statements about the spread of excitation in the heart is TRUE?

The atrio-ventricular node delays excitation for about 120 ms. Signup and view all the answers

What phase of the cardiac cycle follows ventricular systole?

Ventricular diastole. Signup and view all the answers

What percentage of blood is ejected during the rapid ejection period?

70% Signup and view all the answers

During isovolumic relaxation, what happens to the intraventricular pressure?

It falls rapidly. Signup and view all the answers

What is the normal stroke volume in milliliters at rest?

70 ml Signup and view all the answers

How is cardiac output calculated?

Stroke volume x heart rate Signup and view all the answers

What volume remains in each ventricle at end-systole?

40-50 ml Signup and view all the answers

What primarily affects end-diastolic volume (EDV)?

Venous return Signup and view all the answers

What is the consequence of increased preload on muscle contraction?

Increase in contraction force Signup and view all the answers

What effect does stretching of the SA node have?

Increases heart rate Signup and view all the answers

Study Notes

Heart Anatomy

The heart consists of two pumps, each with an atrium and a ventricle.
Flow between chambers is controlled by valves:
- Atrioventricular valves: tricuspid (right) and mitral (left)
- Semilunar valves: pulmonary (right) and aortic (left)

Heart Muscle

It is a specialized form of muscle with discrete, electrically connected cells.
Contraction occurs due to action potentials that increase intracellular calcium.
Action potentials have a long duration, leading to a single contraction lasting 280 ms (systole).
Excitation spreads from cell to cell, triggering action potentials.

Pacemakers

A small group of cells generate action potentials that spread throughout the heart, causing a coordinated contraction.
Pacemakers generate action potentials at regular intervals.

Phases of the Cardiac Cycle

Each action potential produces a single beat (systole).
The interval between beats is called diastole.

Electric Pathway of the Heart

The sino-atrial (SA) node in the right atrium is the primary pacemaker.
Excitation spreads from the SA node across the atria, leading to atrial systole.
It then reaches the atrio-ventricular (AV) node, where it is delayed for about 120 ms.

Spread of Excitation (Cont.)

From the AV node, excitation travels down the septum between the ventricles.
It spreads through the ventricular myocardium from the inner (endocardial) to the outer (epicardial) surface.
Ventricle contraction starts at the apex and moves upwards, pushing blood towards the outflow valves.

The Cardiac Cycle

The SA node generates an action potential about once a second at rest.
This produces a short atrial systole followed by a longer ventricular systole.
Ventricular systole lasts approximately 280 ms.
Relaxation follows and lasts about 700 ms before the next systole.

Ventricular Pumping

The alternating systole and diastole, combined with inflow and outflow valves, allows the heart to function as a reciprocating pump.
The ventricles fill with blood from veins during diastole.
The ventricles pump blood into arteries during systole.

The Left Ventricle

Inflow valve: The mitral valve permits blood flow from the atrium to the ventricle but not vice versa. It opens when atrial pressure exceeds intraventricular pressure and closes when ventricular pressure exceeds atrial pressure.
Outflow valve: The aortic valve allows blood flow from the ventricle to the aorta but not vice versa. It opens when intraventricular pressure exceeds aortic pressure and closes when aortic pressure exceeds ventricular pressure.

Ventricular Filling

During systole, blood accumulates in the atria.
At the end of systole, higher pressure forces open the AV valves, causing rapid ventricular filling. This lasts about 1/3 of the diastole, approximately 200-300 ms.
Minimal flow occurs during the middle 1/3 of diastole.
The atria contract during the last 1/3 of diastole, delivering up to 20% of the total ventricular volume.

Isovolumic Contraction

As systole starts, intraventricular pressure rises, closing the AV valves.
For approximately 20-30 ms, pressure continues to rise but is less than the pressure required to open the semilunar valves.
This is called isovolumic contraction because ventricular volume remains constant.

Ejection Period

The ejection phase starts once the semilunar valves open.
About 70% of the blood ejected occurs in the first 1/3 of systole, termed the rapid ejection period.
The last 30% empties in the next 2/3, known as the slow ejection period.

Isovolumic Relaxation

Ventricular relaxation begins suddenly at the end of systole, causing intraventricular pressure to fall rapidly.
The semilunar valves close when aortic pressure surpasses intraventricular pressure.
For 30-60 ms, the muscle continues relaxing, and pressure continues to fall, but no filling occurs because the AV valves are still closed. This is the period of isovolumic relaxation.

Normal Blood Volume in the Ventricles

After atrial contraction, each ventricle contains 110-120 ml (end-diastolic volume).
Contraction ejects roughly 70 ml (stroke volume output).
40-50 ml remain in each ventricle after ejection (end-systolic volume).

Cardiac Output and Venous Return

Cardiac output is the volume of blood pumped into the aorta per minute. Cardiac output = stroke volume x heart rate.
Venous return is the volume of blood flowing from veins to the right atrium.
Normal resting cardiac output:
- Stroke volume: 70 ml
- Heart rate: 72 beats/minute
- Cardiac output: ~5 litres/minute
During exercise, cardiac output can increase to over 20 liters/minute.

Cardiac Output (Cont.)

Stroke volume: The volume of blood pumped by either the right or left ventricle during ventricular contraction. SV = EDV – ESV (End Diastolic Volume - End Systolic Volume).
Cardiac output: CO = SV x HR (heart rate).

Factors Affecting Stroke Volume

EDV (End Diastolic Volume):
- Influenced by venous return and preload (EDV itself).
ESV (End Systolic Volume):
- Influenced by contractility and afterload.

Frank-Starling Mechanism

The force of cardiac muscle contraction increases as the muscle stretches, within limits. This is due to optimal overlap of actin and myosin filaments during stretch, similar to skeletal muscle.
Increased venous return and stretching lead to increased contraction force and stroke volume.
Stretching of the SA node increases the firing rate of the pacemaker, resulting in increased heart rate.
Frank-Starling Law of the Heart: Preload → stretch of muscle → force of contraction → stroke volume.

Extrinsic Factors Influencing Stroke Volume

Contractility:
- Increased by:
  - Increased sympathetic stimuli
  - Certain hormones
  - Ca2+ and some drugs
- Decreased by:
  - Acidosis
  - Increased extracellular K+
  - Calcium channel blockers

Extrinsic Control of Contractility

Contractility: Strength of contraction at any given fiber length.
Sympathoadrenal system: Norepinephrine (NE) and epinephrine (Epi) increase contractile strength (+ inotropic effect). This occurs through increased Ca2+ availability to sarcomeres.
Parasympathetic stimulation: Does not directly influence contraction strength.

Contractility and Norepinephrine

Sympathetic stimulation releases norepinephrine, initiating a cyclic AMP second messenger system.

Effects of Hormones on Contractility

Epinephrine, norepinephrine, and thyroxine all have positive inotropic effects, increasing contractility.
Digitalis elevates intracellular Ca++ concentrations, interfering with its removal from the sarcoplasm of cardiac cells.
Beta-blockers (e.g., propranolol) block beta-receptors, preventing sympathetic stimulation of the heart (negative chronotropic effect).

Cardiac Output and Peripheral Resistance

Increasing peripheral resistance decreases cardiac output.

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Description

Explore the intricacies of heart anatomy, including its two pumps and how valves control blood flow. Understand the electrical activity of heart muscle cells and the role of pacemakers in coordinating heartbeats. Dive into the phases of the cardiac cycle and the overall electric pathway of the heart.