Final Exam Flashcards
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.
Atrial Fibrillation: Clinical Significance
Can result in a decrease in CO due to ineffective atrial contractions and rapid ventricular response.
Thrombi may form in atria as a result of blood stasis.
Embolus may develop and travel to brain, causing a stroke.
Management of A-Fib Priorities
Control heart rhythm and heart rate
Prevent stroke
Optimize quality of life
Heart rate controlling medications
Beta-blockers
Calcium channel blockers
Digoxin
Heart rhythm controlling medications
Sodium channel blockers
Potassium channel blockers
Synchronized Cardioversion
The therapy of choice for patients with hemodynamically unstable ventricular or supraventricular tachydysrhythmias.
A synchronized circuit in the defibrillator is used to deliver a countershock that is programmed to occur on the R wave of the QRS complex
Sinus Bradycardia
Conduction pathway is the same as in sinus rhythm, but SA node fires at rate of less than 60bpm.
Treatment of sinus bradycardia
Atropine (Anticholinergic drug that increases HR and improves atrioventricular conduction by blocking parasympathetic influences on heart.
A pacemaker may be required.
Ventricular Tachycardia
Too fast/sometimes collapses
Can be stable (patient has pulse) or unstable (patient is pulseless).
Ventricular Fibrillation
Collapse rhythm. HR is not measurable. Rhythm is irregular and chaotic. P wave is not detectable. PR and QRS intervals are not measurable.
Ventricular Fibrillation: Clinical significance
Unresponsive, pulseless, and apneic state
If not treated rapidly, death will result
Ventricular Fibrillation: Treatment
Immediate initiation of CPR and ACLS measures with the use of defibrillation and drug therapy.
Implantable Cardioverter-Defibrillator (ICD)
Appropriate for patients who:
Have survived SCD
Have spontaneous sustained VT
Have syncope with inducible ventricular tachycardia/fibrillation during EPS
Are at high risk for future life-threatening dysrhythmias.
