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 Isovolumic Ventricular Contraction 2) Ventricular Ejection 3) Isovolumic Ventricular Relaxation

Isovolumic

Ventricular Contraction

Can the heart beat by itself ?

Autorhythm The 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

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)

through gap junctions in intercalated discs

(electrical synapses)

Conduction in Atria The 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

From AV node to Ventricles

His bundle

left branch (anterior/posterior division)

- right branch

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

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

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)

EELECTROCARDIOGRAPHY ((ECG) the recording of electrical activities of the heart via electrodes placed on body surface.

Applications of ECG 1) measure automaticity HR, rhythmicity, pacemaker 2) measure conductivity pathway, reentry, block 3) reveal hypertrophy 4) reveal ischemic damages location, size, and progress

Applications of ECG

1) measure automaticity

HR, rhythmicity, pacemaker

2) measure conductivity

pathway, reentry, block

3) reveal hypertrophy

4) reveal ischemic damages

location, size, and progress

Waves and Intervals of ECG P wave : atrial depolarization QRS complex : ventricular depolarization T 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)

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.

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 Rate Stroke volume Cardiac Output (CO) Ejection Fraction Preload Afterload Contractility Frank-Starling Mechanism Factors on Cardiac Output

CONTENT

Heart Rate

Stroke volume

Cardiac Output (CO)

Ejection Fraction

Preload

Afterload

Contractility

Frank-Starling Mechanism

Factors on Cardiac Output

Heart Rate the number of heart beats in 1 minute. Normal value: 60-100/min Stroke volume the 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 ml x 75 beat/min = 5,250 ml/min 70 75 beat/min ml

Ejection Fraction = stroke volume  end-diastolic ventricular volume 70 ml  130 ml = 54% 60 ml End of diastole 130 ml 70 ml End of systole SV =

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. preload afterload

Preload

the force that stretches the muscle before contraction.

Afterload

the force that stretches muscle during contraction.

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 Preload : 2) Afterload : 3) Contractility : 4) Heart Rate :

Factors on Cardiac Output

Preload :

2) Afterload :

3) Contractility :

4) Heart Rate :

Factors on Cardiac Output Preload :  Preload   cardiac output (Starling-Frank Mechanism)

Factors on Cardiac Output

Preload :

More in More out Factors on Cardiac Output Preload :  Preload   cardiac output (Starling-Frank Mechanism)

Factors on Cardiac Output

Preload :

Factors on Cardiac Output Preload : 2) Afterload :  afterload   CO R

Factors on Cardiac Output

Preload :

2) Afterload :

Factors on Cardiac Output Preload : 2) Afterload : 3) Contractility :  contractility   CO

Factors on Cardiac Output

Preload :

2) Afterload :

3) Contractility :

Factors on Cardiac Output Preload : 2) Afterload : 3) Contractility : 4) Heart Rate : dual effects  CO =  Heart Rate x Stroke Volume

Factors on Cardiac Output

Preload :

2) Afterload :

3) Contractility :

4) Heart Rate :

less in less out Factors on Cardiac Output Preload : 2) Afterload : 3) Contractility : 4) Heart Rate : dual effects Heart Rate Stoke Volume  CO =  Heart Rate x  Stroke Volume 300% 400%

Factors on Cardiac Output

Preload :

2) Afterload :

3) Contractility :

4) Heart Rate :

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

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

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

Sympathetic Nervous System

- controls all components of the heart.

- release Norepinephrine (NE).

- increases heart rate (positive chronotropic) and contractility (positive inotropic) .

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.

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

Higher Centers of Autonomic Nervous System

- Medulla Oblongata

- Hypothalamus, Thalamus, Cerebral cortex

Centers in Medulla Oblongata Sympathetic 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  CO 2 - 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.

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 ). SV More in More out

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

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

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

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 .

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