the heart

The Heart

Chambers of the Heart

Cardiac Cycle

Ventricular systole- isovolumic contraction- ejection

Ventricular diastole- isovolumic relaxation- rapid filling- atrial contraction

4) Ventricular Filling 5) Atrial Contraction

1) Isovolumic Ventricular Contraction 2) Ventricular Ejection

3) Isovolumic Ventricular Relaxation

Can the heart beat by itself ?

AutorhythmThe heart can beat on its own without the need

for exogenous commands.

Skeletal muscle

Motor nerve

Conclusion ?

The heart generates electricity.

TERMINOLOGY

Excitation

- definition: generation of action potentials - different from contraction

Contraction- definition: shortening of muscle cells- triggered by excitation

Excitation-Contraction coupling

Excitation Contraction[ Ca++ ]i

(Action Potentials) (shortening)

Sinus-Atrial node (SA node)

Atria

Atrial-ventricular node (AV node)

Ventricles

Sequence of excitation

SA node- located in the right atrial wall, just inferior to the entrance of the superior vena cava.

Original Impulses from S-A Node

The electrical impulses are normally generated by a group of specialized pacemaker cells at sinoatrial (SA) node.

Conduction of Electrical Impulses in the Heart

Conduction of Action Potentials from Cell to Cell

through gap junctions in intercalated discs (electrical synapses)

Conduction in AtriaThe electrical impulses from SA node spread through the entire right and left atrial muscle mass, triggering contraction of the right and left atrium.

Delay at A-V Node

- The impulses from S-A node travel to atrioventricular (A-V) node.

- A-V node is located in lower end of the interatrial septum near the tricuspid valve.

A-V node

Delay at A-V Node

- A-V node is the only normal route that impulses from SA node are transmitted into ventricles.

- Conduction speed in A-V node is slow (delay).

- This delay allows time for the atria to finish contraction and empty their contents into the ventricles before ventricles start to contract.

From AV node to Ventricles

His bundle

- left branch (anterior/posterior division)

- right branch

His bundle

1) Purkinje fibers

- located in the subendocardial layer

- fastest conduction (4 m/s)

2) Ordinary ventricular myocardial cells

able to conduct AP at a slower speed

After the delay at A-V node, the impulses rapidly spread to the ventricles via specialized fibers, Purkinje fibers.

Rapid Conduction in Ventricles

Rapid conduction in the ventricles

simultaneous excitation of the ventricles

functional syncytium

NNote:

- Each electrical impulse can trigger cardiac muscle contraction normally only once.

- A normal heart generates 60 to 100 impulses in 1 minute at resting state.

1

1

Excitation Contraction[ Ca++ ]i

(Action Potentials) (shortening)

Properties of Cardiac Muscle

Excitation of the heart is triggered by electrical impulse rather than neural transmitters.

Contraction of the heart is triggered by elevation of intracellular calcium influx.

Properties of Cardiac Muscle

- Myocytes depend heavily on oxygen and blood supply. - Not fatigue

- Excitability Cycle

The myocytes have Long refractory

period during which they do not respond

to any electrical impulses.

RRole of a Long Refractory Period – 1

prevent ventricles from contracting at too high rates so that enough time is allowed for refill of the ventricles

Role of Long refractory period - 2

Prevent retrograde excitation

ELECTROCARDIOGRAPHY

(ECG)

QRS: potential changes during depolarization of ventricles

EELECTROCARDIOGRAPHY ((ECG)

the recording of electrical activities of the heart via electrodes placed on body surface.

Applications of ECG

1) measure automaticityHR, rhythmicity, pacemaker

2) measure conductivity pathway, reentry, block

3) reveal hypertrophy

4) reveal ischemic damageslocation, size, and progress

Waves and Intervals of ECG

P wave: atrial depolarizationQRS complex: ventricular depolarizationT wave: ventricular repolarization

PR Interval

Disorders of the Cardiac Conduction System ---- Arrhythmias

- refers to abnormal initiation or conduction of electrical impulses in the heart.

- caused by ischemia, fibrosis, inflammation, or drugs.

Bradycardia slow heart rate ( < 60 beats/min)

Tachycardia

fast heart rate ( > 100 beats/min)

- contract uncoordinatedly and extremely rapidly.

- Ventricular fibrillation is lethal.

Atrial or Ventricular Flutter and Fibrillation

is when the heart beat is triggered by ectopic pacemakers (cells other than SA node).

Premature contraction

Conduction Block

Artificial Pacemaker

Application: sinus abnormality,

complete AV or ventricular block

Function:- generate electric pulses- sensing- antitachyarrhythmia

Heart Sounds

Four heart sounds can be recorded via phonocardiography, but normally only two, the first and the second heart sounds, are audible through a stethoscope.

First heart sound:

- occurs when the atrioventricular (AV) valves close at the beginning of ventricular contraction.

- generated by the vibration of the blood and the ventricular wall

- is louder, longer, more resonant than the second heart sound.

- occurs when aortic and pulmonary semilunar valves close at the beginning of ventricular dilation

- generated by the vibration of the blood and the aorta

- Aortic valve closes slightly before pulmonary valve.

Second heart sound

Heart Murmur

- abnormal heart sound - occur in valvular diseases and septal defects

Two Basic Types of Valvular Diseases

1) valvular stenosis, a narrowing of the valve

2) valvular insufficiency (incompetence). A valve is unable to close fully; so there is some backflow (regurgitation) of blood.

MECHANICAL PROPERTIES OF THE HEART

CONTENT

Heart RateStroke volumeCardiac Output (CO)Ejection FractionPreloadAfterloadContractility Frank-Starling MechanismFactors on Cardiac Output

Heart Rate the number of heart beats in 1 minute. Normal value: 60-100/min

Stroke volumethe volume of blood pumped out by each ventricle per each contraction.

SV

Cardiac Output (CO)

the amount of blood pumped out by each ventricle in 1 minute.

Cardiac output = stroke volume x heart rate

Example:70

75 beat/min

ml

70 ml x 75 beat/min = 5,250 ml/min

Ejection Fraction

= stroke volume end-diastolic ventricular volume

70 ml 130 ml = 54%

End of diastole

130 ml

70 ml

End of systole

SV =

60 ml

End of diastole

133 ml

120 ml

End of systole

SV =

Ejection Fraction

120 ml 133 ml = 90%

increases during exercise

Preload the force that stretches the muscle before contraction.

Afterload the force that stretches muscle during contraction.

preloadafterload

Preload to ventricles = ventricular end diastolic pressure

- the degree of stretch of the ventricular muscle cells just before they contract.

- determined by ventricular filling.

Afterload to left ventricle: aortic arterial pressure

Afterload to right ventricle: pulmonary arterial pressure

Afterload to the left ventricle is greater than that to the right ventricle.

Aortic arterial pressure

Contractility

- the intrinsic strength of cardiac muscles.

Factors on Cardiac Output

1) Preload: 2) Afterload:

3) Contractility: 4) Heart Rate:


1) Preload:

Preload cardiac output

(Starling-Frank Mechanism)

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1) Preload:

Preload cardiac output

(Starling-Frank Mechanism)



afterload CO

R



3) Contractility:

contractility CO




dual effects

CO = Heart Rate x Stroke Volume

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less out




dual effects Heart Rate

Stoke Volume

CO = Heart Rate x Stroke Volume 300% 400%

REGULATION OF THE HEART FUNCTION

Regulation of the Cardiac Function

1) Nervous control

• Sympathetic control

• Parasympathetic control

• Higher centers

• Reflexes

2) Hormonal Control

3) Autoregulation

4) Other factors

Regulation of the Cardiac Function

1) Nervous control

• Sympathetic control

• Parasympathetic

control

Sympathetic Nervous System

- controls all components of the heart.

- release Norepinephrine (NE).

- increases heart rate (positive chronotropic) and

contractility (positive inotropic).

Cell

1

Cell

m

Parasympathetic Nervous System (PNS)

- controls SA node and AV node.

- releases Acetylcholine (Ach).

- decreases heart rate (negative chronotropic).

- prolongs delay at AV node.

- has little effect on contractility.

Higher Centers of Autonomic Nervous System

- Medulla Oblongata

- Hypothalamus, Thalamus, Cerebral cortex

Centers in Medulla OblongataSympathetic center:

distinct accelerator and augmentor

Parasympathetic center: Nucleus vagus and nucleus ambiguus

Hypothalamus, Thalamus, Cerebral cortex

Involved in the cardiac response to environmental temperature changes, exercise, or during excitement, anxiety, and other emotional states

Neural Control via Reflexes

Baroreceptors

1) Baroreceptor Reflex

- stimulated by increase in arterial pressure (stretch)

- Effect: negative chronotropic and inotropic

- regulate the heart when BP increases or drops

- involved in short term regulation of BP

2) Chemoreceptor Reflex

Chemoreceptors

Chemoreceptors

Chemoreceptors

2) Chemoreceptor Reflex

- stimulated by oxygen, pH, or CO2

- overall effect: positive choronotropic and inotropic.

- less important in regulating cardiac function

3) Proprioceptor Reflex

- Stimulated by muscle and joint movement

- Effects: increase heart rate during exercise

Regulation by Hormones

Epinephrine - released from adrenal gland.- increases heart rate and contractility.

Thyroxin- released from thyroid gland.- increases heart rate.

Autoregulation of the Heart

Stroke volume is autoregulated by ventricular filling (Frank-Starling law).

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4) Other Factors

- Blood level of ionic calcium, sodium, and

potassium

Hypercalcemia (high plasma Ca++):

positive inotropic

Hypernatremia (high plasma Na+):

negative

chronotropic

Hyperkalemia (high plasma K+):

negative

chronotropic

used in lethal

injection

- Age, gender, exercise, and body temperature

Blood Supply to Cardiac Muscles

Can cardiac muscles get nutrients from the blood in heart chambers?

The cardiac muscles get nutrients from coronary circulation.

Anterior view Posterior view

RV

LVepicardium

endocardium

Coronary arterial anastomosis

Coronary venous blood is emptied into the right atrium through cardiac veins and coronary sinus.

coronary sinus

Posterior view

Blockade of coronary artery causes myocardial infarction, or heart attack.

RV

LVepicardium

endocardium

Coronary Atherosclerosis

dull white and slightly elevated fibrous plaque (atheroma) on coronary arterial lumen.

Typical lesion of Coronary Atherosclerosis

composed of lipid, smooth muscle, macrophages, and connective tissues.

cause stenosis of coronary arteries

Histology of the plaque

occlude arterial lumen when combined with internal hemorrhage, thrombosis, and arterial spasm

occur often at arterial branching points

Surgical Therapies

1)

2) Coronary angioplasty

3) Stenting

the heart

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