Final Exam Flashcards
(36 cards)
Determinants of stroke volume
Preload
Afterload
Contractility
Preload
The volume of blood in ventricles at end of diastole, before next contraction.
Determines the amount of stretch placed on myocardial fibres.
Afterload
Peripheral resistance against which left ventricle must pump.
Affected by size of ventricle, wall tension, and arterial blood pressure.
Contractility
Can be increased by norepinephrine, released by the sympathetic nervous system, as well as epinephrine.
Increasing contractility raises stroke volume by increasing ventricular emptying.
Starling’s Law
The more the fibres are stretched (i.e., the greater the preload), greater is their contractility.
Two main types of cells in the heart
Conducting cells
Contractile cells
Conducting cells
Generate and propagate electrical impulses
Contractile cells
Contract following receipt of electrical impulses.
They can propagate and on occasion generate electrical impulses.
Sinoatrial Node
A group of cells found high up in the right atrium, close to its junction with the superior vena cava.
Functions as the heart’s intrinsic pacemaker, regulating heart rate.
Spontaneously generates electrical impulses, which are transmitted to the right and left atrium.
These electrical impulses stimulate the atrial myocardium to contract.
Atrioventricular Node
A group of specialized cells situated in the atrioventricular septum just above the coronary sinus ostium.
Receives electrical impulses from the atria and then transmits the electrical impulse from the atria to the ventricles.
The Bundle of His
A collection of heart muscle cells specialized for electrical conduction. They receive input from the AVN.
Branches into the left and right bundle branches which travel down the intraventricular septum.
Propagate impulses to the left and right branches respectively.
Each branch terminates as several Purkinje fibres.
Purkinje fibres
They are situated in the subendocardium.
They transmit the wave of electricity to the ventricular myocardium.
This wave of electricity results in ventricular contraction.
Electrocardiograph Monitoring (ECG)
A graphic tracing of the electrical impulses produced in the heart. The waveforms on the ECG are produced by the movement of charged ions across the membranes of myocardial cells, representing depolarization and repolarization.
Cardiac Monitor (Telemetry)
the observation of a patient’s HR and rhythm to rapidly diagnose dysrhythmias, ischemia, or infarction.
What we look for on an ECG
1:1 conduction
Right rate (bpm)
Right time interval of P-wave and QRS complex
Regularity (same distance from P wave to next or QRS to next)
*Any variations from this suggest we do not have Sinus Rhythm
P-wave
Atrial depolarization
Lasts 0.12 - 0.20 seconds
PR interval
Beginning of atrial contraction to beginning of ventricular contraction (time for impulse to reach ventricles from sinus node)
PR Segment
End of P-wave to beginning of WRS complex.
Signifies AV nodal delay.
QRS complex
Ventricular depolarization
Lasts 0.04 - 0.12 seconds
T wave
Ventricular repolarization
QT interval
Time from start of Q wave to end of T wave.
Represents the time taken for ventricular depolarization and repolarization
U wave
Sometimes seen after T wave, represents Purkinje fibre repolarization. Usually not a good thing if you see this!
Atrial Fibrillation
Characterized by total disorganization of atrial electrical activity caused by multiple ectopic foci, resulting in loss of effective atrial contraction.
Most common dysrhythmia encountered in the ED.
Focus of treatment is rapid assessment of potential hemodynamic instability and identification and treatment of the underlying cause.
Atrial Fibrillation: Clinical Associations
Underlying heart disease, such as CAD, rheumatic heart disease, cardiomyopathy, hypertensive heart disease, HF, and pericarditis.
Often acutely caused by thyrotoxicosis, alcohol intoxication, caffeine use, electrolyte disturbances, stress, and cardiac surgery.
