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Transcript of The Heart. Chambers of the Heart Cardiac Cycle Ventricular systole - isovolumic contraction -...
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The Heart
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Chambers of the Heart
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Cardiac Cycle
Ventricular systole- isovolumic contraction- ejection
Ventricular diastole- isovolumic relaxation- rapid filling- atrial contraction
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4) Ventricular Filling 5) Atrial Contraction
1) Isovolumic Ventricular Contraction 2) Ventricular Ejection
3) Isovolumic Ventricular Relaxation
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Can the heart beat by itself ?
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AutorhythmThe heart can beat on its own without the need
for exogenous commands.
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Skeletal muscle
Motor nerve
Conclusion ?
The heart generates electricity.
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TERMINOLOGY
Excitation
- definition: generation of action potentials - different from contraction
Contraction- definition: shortening of muscle cells- triggered by excitation
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Excitation-Contraction coupling
Excitation Contraction[ Ca++ ]i
(Action Potentials) (shortening)
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Sinus-Atrial node (SA node)
Atria
Atrial-ventricular node (AV node)
Ventricles
Sequence of excitation
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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.
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Conduction of Electrical Impulses in the Heart
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Conduction of Action Potentials from Cell to Cell
through gap junctions in intercalated discs (electrical synapses)
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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.
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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
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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.
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From AV node to Ventricles
His bundle
- left branch (anterior/posterior division)
- right branch
His bundle
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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
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Rapid conduction in the ventricles
simultaneous excitation of the ventricles
functional syncytium
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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
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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.
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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.
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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
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Role of Long refractory period - 2
Prevent retrograde excitation
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ELECTROCARDIOGRAPHY
(ECG)
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QRS: potential changes during depolarization of ventricles
EELECTROCARDIOGRAPHY ((ECG)
the recording of electrical activities of the heart via electrodes placed on body surface.
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Applications of ECG
1) measure automaticityHR, rhythmicity, pacemaker
2) measure conductivity pathway, reentry, block
3) reveal hypertrophy
4) reveal ischemic damageslocation, size, and progress
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Waves and Intervals of ECG
P wave: atrial depolarizationQRS complex: ventricular depolarizationT wave: ventricular repolarization
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PR Interval
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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.
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Bradycardia slow heart rate ( < 60 beats/min)
Tachycardia
fast heart rate ( > 100 beats/min)
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- contract uncoordinatedly and extremely rapidly.
- Ventricular fibrillation is lethal.
Atrial or Ventricular Flutter and Fibrillation
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is when the heart beat is triggered by ectopic pacemakers (cells other than SA node).
Premature contraction
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Conduction Block
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Artificial Pacemaker
Application: sinus abnormality,
complete AV or ventricular block
Function:- generate electric pulses- sensing- antitachyarrhythmia
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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.
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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.
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- 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
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Heart Murmur
- abnormal heart sound - occur in valvular diseases and septal defects
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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.
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MECHANICAL PROPERTIES OF THE HEART
CONTENT
Heart RateStroke volumeCardiac Output (CO)Ejection FractionPreloadAfterloadContractility Frank-Starling MechanismFactors on Cardiac Output
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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
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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
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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
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End of diastole
133 ml
120 ml
End of systole
SV =
Ejection Fraction
120 ml 133 ml = 90%
increases during exercise
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Preload the force that stretches the muscle before contraction.
Afterload the force that stretches muscle during contraction.
preloadafterload
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Preload to ventricles = ventricular end diastolic pressure
- the degree of stretch of the ventricular muscle cells just before they contract.
- determined by ventricular filling.
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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
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Contractility
- the intrinsic strength of cardiac muscles.
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Factors on Cardiac Output
1) Preload: 2) Afterload:
3) Contractility: 4) Heart Rate:
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Factors on Cardiac Output
1) Preload:
Preload cardiac output
(Starling-Frank Mechanism)
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More in
More out
Factors on Cardiac Output
1) Preload:
Preload cardiac output
(Starling-Frank Mechanism)
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Factors on Cardiac Output
1) Preload: 2) Afterload:
afterload CO
R
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Factors on Cardiac Output
1) Preload: 2) Afterload:
3) Contractility:
contractility CO
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Factors on Cardiac Output
1) Preload: 2) Afterload:
3) Contractility: 4) Heart Rate:
dual effects
CO = Heart Rate x Stroke Volume
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less in
less out
Factors on Cardiac Output
1) Preload: 2) Afterload:
3) Contractility: 4) Heart Rate:
dual effects Heart Rate
Stoke Volume
CO = Heart Rate x Stroke Volume 300% 400%
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REGULATION OF THE HEART FUNCTION
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Regulation of the Cardiac Function
1) Nervous control
• Sympathetic control
• Parasympathetic control
• Higher centers
• Reflexes
2) Hormonal Control
3) Autoregulation
4) Other factors
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Regulation of the Cardiac Function
1) Nervous control
• Sympathetic control
• Parasympathetic
control
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Sympathetic Nervous System
- controls all components of the heart.
- release Norepinephrine (NE).
- increases heart rate (positive chronotropic) and
contractility (positive inotropic).
Cell
1
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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.
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Higher Centers of Autonomic Nervous System
- Medulla Oblongata
- Hypothalamus, Thalamus, Cerebral cortex
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Centers in Medulla OblongataSympathetic center:
distinct accelerator and augmentor
Parasympathetic center: Nucleus vagus and nucleus ambiguus
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Hypothalamus, Thalamus, Cerebral cortex
Involved in the cardiac response to environmental temperature changes, exercise, or during excitement, anxiety, and other emotional states
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Neural Control via Reflexes
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Baroreceptors
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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
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2) Chemoreceptor Reflex
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Chemoreceptors
Chemoreceptors
Chemoreceptors
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2) Chemoreceptor Reflex
- stimulated by oxygen, pH, or CO2
- overall effect: positive choronotropic and inotropic.
- less important in regulating cardiac function
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3) Proprioceptor Reflex
- Stimulated by muscle and joint movement
- Effects: increase heart rate during exercise
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Regulation by Hormones
Epinephrine - released from adrenal gland.- increases heart rate and contractility.
Thyroxin- released from thyroid gland.- increases heart rate.
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Autoregulation of the Heart
Stroke volume is autoregulated by ventricular filling (Frank-Starling law).
SVMore in
More out
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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
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Blood Supply to Cardiac Muscles
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Can cardiac muscles get nutrients from the blood in heart chambers?
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The cardiac muscles get nutrients from coronary circulation.
Anterior view Posterior view
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RV
LVepicardium
endocardium
Coronary arterial anastomosis
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Coronary venous blood is emptied into the right atrium through cardiac veins and coronary sinus.
coronary sinus
Posterior view
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Blockade of coronary artery causes myocardial infarction, or heart attack.
RV
LVepicardium
endocardium
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Coronary Atherosclerosis
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dull white and slightly elevated fibrous plaque (atheroma) on coronary arterial lumen.
Typical lesion of Coronary Atherosclerosis
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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
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occur often at arterial branching points
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Surgical Therapies
1)
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2) Coronary angioplasty
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3) Stenting