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ECG and Dysrhythmias - perfusion
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ECG and Dysrhythmias - perfusion
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Perfusion
I. Cardiac Mechanical System
A. Cardiac Cycle
The contraction and relaxation of the heart constitute
one heartbeat
Ventricular filling is followed by ventricular
systole, during which the ventricles contract and
eject blood into the pulmonary and systemic
circuits.
Systole (ventricular contraction/pump of heart) is
followed by a relaxation phase known as diastole.
During diastole (ventricular relaxation), the atria
contract, the ventricles refill, and the myocardium is
perfused; volume in the ventricles increases to
approx. 120 mL (end-diastolic volume)
At the end of systole, approx. 50 mL of blood
remains in the ventricles (end-systolic volume)
The complete cardiac cycle occurs about 70-80
times per minute
B. Cardiac Output (HR x SV = CO)
Cardiac Output is the amount of blood pumped by each ventricle in one minute
The difference between end-diastolic volume & the end-diastolic volume is Stroke Volume
Stroke Volume: the amount of blood ejected from the ventricle with each heartbeat; ranges from 60 to 100 mL/beat and
averages approx. 70 mL/beat in an adult
Numerous factors can affect either the heart rate or stroke volume, therefore, affecting cardiac output
Heart Rate primarily affected by Autonomic Nervous System
C. Factors Affecting Stroke Volume
1. Preload (Venous Return)
amount of blood left in the ventricles at the end of diastole, before the next contraction
determines the amount of stretch placed on myocardial fibers; overstretching can result in ineffective contraction
Starlings Law: the more the myocardial fibers are stretched, the greater the force of the contraction
vasoconstriction increases venous return and thereby increases preload
too little circulating blood volume results in decreased venous return and therefore decreased preload.
Decreased preload reduces SV and leads to decreased CO (hemorrhage, third-spacing)
2. Contractility
inherent capability of the cardiac muscle fibers to shorten
can be increased by sympathetic nervous system.
increasing contractility raises SV by increasing ventricular emptying
3. Afterload (Arterial System)
the force the ventricles must overcome to eject their blood volume
peripheral resistance against which the left ventricle must pump (ventricle size, wall tension, BP)
afterload of the left ventricle is measured as systemic vascular resistance
as pulmonary or arterial BP increases (vasoconstriction), pulmonary and/or SVR increases, and the work of the
ventricles increases. As workload increases, consumption of myocardial oxygen increases. A compromised
heart cannot effectively meet this increase demand for oxygen.
low afterload decreases the forward flow of blood into the systemic circulation and the coronary arteries
D. Ejection Fraction (hallmark of systolic function)
the percentage of total ventricular filling volume that is ejected during each ventricular contraction
fraction or percent of the diastolic volume that is ejected from the heart during systole
SV divided by the end-diastolic volume
o An end-diastolic volume of 120 mL divided by a SV of 80 mL equals an ejection fraction of 66%
normal = greater than 55%
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II. Cardiac Conduction System (Electrical): a series of pathways
that conduct electrical impulses through the heart, stimulate
depolarization and resulting muscle contraction of chambers in
a specific sequence, and initiate the pumping action of the heart.
Conduction takes place because of special electrophysiological
properties of the heart.
A. Properties of Cardiac Cells
Automaticity: pacing function or ability of cardiac
pacemaker cells to initiate an electrical impulse. Normally
only
Excitability: characteristic shared by all cardiac cells that
refers to the ability to respond to an electrical impulse
generated by pacemaker cells or other external stimulus, such
as from a chemical, mechanical, or electrical source.
Conductivity: ability of the cardiac cells to transmit electrical
impulses to adjacent cardiac cells. This allows an electrical
impulse in any part of the myocardium to spread throughout
the heart as excitable cells depolarize in rapid succession.
B. Components of Cardiac Conduction System
Sinoatrial (SA) node: natural pacemaker; concentration of cells responsible for initiating conduction impulse in a health
heart; located in right atrium at juncture with superior vena cava; rate 60-100 beats per minute in an adult
Internodal pathways: carry impulse from SA node to AV node through both right and left atria; impulse initiates process
of depolarization in both atria; depolarization results in myocardial contraction of both atria
Atrioventricular (AV) node: located at base of atrial septum; slows impulse; allows atria to fully empty before initiating
depolarization of ventricles; when SA node is not functioning, can initiate an impulse at a rate of 40-60 beats per minute in an
adult
Bundle of His: short branch of conductive cells connecting AV node to bundle branches at intraventricular septum
Bundle branches: right (RBB) and left (LBB) split off on either side of intraventricular septum carry impulse to
Purkinje fibers
Purkinje fibers: diffuse network of conduction pathways; terminal branches of conduction system; conduct impulses rapidly
throughout ventricles; initiate rapid depolarization wave throughout myocardium and resulting ventricular contraction; when
SA and AV nodes fail, can initiate impulses at rate of 20-40 beats per minute in an adult
C. Cardiac Action Potential: refers to the change in the electrical charge inside
the cardiac cell when it is stimulated. Impulses from the SA and AV nodes
stimulates a series of changes in ion concentration across the membrane of
each cardiac muscle cell. This movement of sodium, potassium, and calcium
ions causes an electrical impulse that stimulates muscle contraction. The whole
process of depolarization and repolarization is called the action potential.
Polarization: electrical state that exists at the cardiac cell membrane
when the cell is at rest. Positive & negative ions align on either side of
the cell membrane, producing a relatively negative charge within the
cell and a positive extracellular charge. (Flat isoelectric line on ECG)
Depolarization: phase when the heart contracts. The opposite of
polarization & occurs when there is a reversal of the electrical charges at
the cell membrane. The inside of the cell becomes more positive due to
the rapid influx of sodium ions into the cell. (P-wave is atrial
depolarization & QRS complex is ventricular depolarization on ECG)
Repolarization: process that returns the cell to it's resting, polarized
state. Sodium channels close keeping sodium ions from diffusing into
the cell, potassium ions defuse out, and the cell begins to regain its
negative charge. (ST segment and T wave is ventricular
repolarization)
D. Refractory Periods: resistance of the cell membrane to respond to stimulus. Many dysrhythmias are triggered during
relative refractory and supernormal periods.
Absolute refractory period: cells will not respond to further stimulation.
Relative refractory: greater than normal stimulus required to generate action potential.
Supernormal period: mild stimulus will cause depolarization.
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