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Mechanical Activity of Heart and the Cardiac Cycle

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Nancy Rich

on 12 February 2017

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Transcript of Mechanical Activity of Heart and the Cardiac Cycle

Mechanical Activity of Heart and the Cardiac Cycle
Cardiac Cycle
Electrical and Mechanical events that repeat with every beat of the cycle
Timing
Ventricular Diastole and Atrial Systole
Relaxation and Filling of Ventricles with Blood
1.) Early Diastole
Pressure changes in the ventricles
Isovolemic relaxation
All heart valves now closed- pressure less than arteries but more than atria
2.) Late Diastole
Pressure drops below atria- AV valves open
Rapid Ventricular filling
"Passive Filling"
Blood pours into ventricles
70-90%
3.) Atrial Systole
Ventricles topped off with blood from atrial contraction
10-30%
Some back flow occurs in the veins
EDV

End Diastolic Volume
Approximately 120 mL of blood left in the ventricles
Ventricular Systole

1st Phase
Occurs just as atrial systole ends
Ventricles begin to contract
Isovolemic contraction
Ventricle pressure increases
All heart valves are closed
Pressure rises steeply until ventricular pressure exceeds aortic pressure
2nd Phase
Ventriclaur pressure exceeds atrial pressure
Semilunar valves open
Rapid ejection
Ventricular pressure continues to rise
Big decrease in ventricular volume
Reduced Ejection
Less rapid decrease in ventricular volume
Ventricular and aortic pressures begin to fall
Notes:
Approximately 70 mL of blood ejected
STROKE VOLUME
Approximately 50 mL remaining in heart
END SYSTOLIC VOLUME
Remember:
EDV is about 120 mL
Heart Sounds
S1: Lubb
Closure of AV valves
S2: Dubb
Closure of semilunar valves
S3: Rapid passive filling
Normally not heard in adults
May be present in children and endurance athletes
S4: Atrial systole
Normally not heard in adults
Murmur:
Gurgling sound as blood moves through the damaged veins
Bruit:
Abnormal sound as blood runs past an obstruction through arteries
Overlapping Electrical and Mechanical Activity
Ventricular Systole
QRS
Ventricular depolarization
Contraction
Onset
AV valve closes when ventricular pressure exceeds atrial pressure
First heart sound
Isovolemic contraction causes steep increase in pressure
Ventricular ejection
Ventricular Diastole
T wave
Ventricular repolarization
Relaxation
Onset of diastole when T wave completed
Drop in ventricular pressure
Falls below aortic pressure
Aortic valves close
Second heart sound
Falls below atrial pressure
AV valve opens
P wave
Atrial depolarization
Atrial contraction
Small rise in ventricular pressure
Wigger's Diagram
1.) Atrial systole
During ventricular diastole
P wave
Atrial contraction
Slight increase in ventricular pressure
AV valves open
Slight increase in ventricular volume
Atrial kick
Topping off
2.) Ventricular systole
QRS
Ventricular contraction
Immediate rise in ventricular pressure above atrial
AV valve closes
First heart sound
Note: throughout this period blood is returning to the atrium
A: Isovolemic contraction
Against two closed valves
Sharp increase in pressure
No change in volume
B: rapid ejection
Ventricular pressure exceeds aortic pressure and aortic valve opens
Rapid decrease in ventricular volume
C: reduced ejection
T wave
repolarization spreading over ventricles
aortic and ventricular pressure begin to decrease
Ventricles begin to relax
Blood continues to leave ventricles
Continued decrease in ventricular volume
3.) Ventricular Diastole
Onset of diastole marked by completion of depolarization
End of T wave
A: Isovolemic relaxation
Ventricular pressure drops below aortic pressure
Aortic valve closes
Second heart sound
Both valves closed
Big drop in pressure
No change in volume
B: Rapid Filling
Pressure in ventricles drops below atria
AV valve opens
Blood passively pours into ventricle
Big increase in volume
Aortic pressure decreasing
Blood flows off to periphery
Depicting
Purpose
Simultaneous depiction of several parameters related to
blood flow
volume
ECG
Echocardiogram
Through the cycle of the cardiac systole and diastole
Cardiac Output
Cardiac output= Heart rate X Stroke Volume= (EDV-ESV)
Stroke volume
Affected by
Preload
Contractility
Afterload
Altering Heart Rate
Autonomic Nervous System
Sympathetic Innervation
Norepinephrine/epinephrine
Receptors
Adrenergic
Beta 1
Positive chronotropic effect
Parasympathetic Innervation
Acetylcholine
Receptor
Muscarininc Ach
M2
Negative chronotropic effect
Altering Stroke Volume
Intrinsic Regulation of Stroke Volume
Frank-Starling law of the Heart
Increased stretch of myocytes increases strength of contraction
Autonomic Regulation
Contractility
Increase in strnth of contraction due to an increased amount of ctosolic calcium
Primarily sympathetic
Ventricular cardiomyocytes not well innervated by parasympathetic
NE increases Ca++
Frank-Starling Law of the Heart
Strength of ventricular contraction will increase with an increase in vnous return
Length tension relation of the heart
Preload: stretch of ventricle just prior to contraction
Contractility

Increased strength of contraction of ventricle
Due to an increase in cytolsolic calcium
For any given preload
Contractility
Inotrope
Positive
epi
norepi
Negative
Mostly drugs
Release of CA from SR
1.) Size of inward calcium current during plateau of myocyte action potential
Trigger calcium
SNS enhances Ca channels
2.) Amount of calcium stored in SR
SNS increases reuptake of Ca into SR
Full transcript