LE3 Flashcards
Channels through which extracellular Ca2+ enters the cell during the plateau of the action potential
a) Na+/ Ca2+ Exchangers (nacax)
b) Receptor-operated Ca2+ channels
c) L-type Ca2+ channels
d) Ca2+ Channel Blockers
c) L-type Ca2+ channels
- Branch from the aorta supplying the myocardium with blood
- Exit from behind aortic valve cusps in very part of aorta and lead to a branching network blood vessels
a) Elastic Arteries
b) Airway Resistance
c) Varicose Veins
d) Coronary Arteries
d) Coronary Arteries
Receptors where Ca2+ binds, triggering the release of a larger quantity of Ca2+
a) Sarcoplasmic Reticula
b) Calmodulin
c) Ryanodine Receptors
d) Terminal Cisternae
c) Ryanodine Receptors
- Where most cardiac veins drain, emptying into the right atrium
- Empties into the right atrium
a) Coronary Sinus
b) Venous Pressure
c) Medullary
d) Coronary Arteries
a) Coronary Sinus
Cells found in the SA node, AV node, AV bundle, and Purkinjie fibers, causing uncoordinated atrial and ventricular contractions
a) Pacemaker Cells
b) Node Cells
c) Atrial Fibrillation
d) Oligodendrocytes
b) Node Cells
[SA Node/AV Node]
- Normal rate: 60-100 impulse/min
- Depolarization travels through internodal pathway
SA node
[SA Node/AV Node]
- Signal has 0.1s delay to allow atria to contract and completely fill ventricles before they contract
- Depolarization travels through AV bundle of His
AV Node
Go to the apex of the ventricular septum, then turn upwards
a) Bundle Branches
b) Purkinjie Fibers
c) Cardiac Output
d) Ventricular Fibrillation
b) Purkinjie Fibers
- Extracellular Ca2+ enters the cell through the L-type Ca2+ Channels during the plateau of AP
- Ca2+ binds to ryanodine receptors and triggers release of larger quantity of Ca2+
a) Cardiac Action Potential
b) Ca2+ channel blockers
c) Varicose veins
d) Flow-Pressure Relationship
a) Cardiac Action Potential
Uncoordinated atrial and ventricular contractions caused by a defect in the conduction system
a) Pleurisy
b) Hypertension
c) Arrhythmias
d) Heart Murmurs
c) Arrhythmias
Rapid and irregular contraction where the SA node no longer controls the heart rate
a) Hyperventillation
b) Hypertension
c) Fibrillation
d) Ventilation
c) Fibrillation
Controls electrical impulses causing contraction, potentially leading to clotting and inefficient ventricle filling
a) Pleural Fluid
b) Hypertension
c) Ventricular Fibrillation
d) Atrial Fibrillation
d) Atrial Fibrillation
More life-threatening than atrial fibrillation, causing ventricles to pump without filling
a) Atrial Flutter
b) Ventricular Fibrillation
c) Atrial Fibrillation
d) Hypertension
b) Ventricular Fibrillation
What happens after rhythm is not re-established in ventricular fibrillation?
Circulation stops; Brain death
Application of electrical stimulus to shock the heart back into normal SA rhythm
a) Transmural
b) Ventricular Fibrillation
c) Defibrillation
d) Hypertension
c) Defibrillation
Graphic record of the heart’s electrical activity, shows the composite of electrical events
a) Electroencephalogram
b) Trachea
c) Electrocardiogram
d) Fibrillation
c) Electrocardiogram
- Result of depolarization from SA to AV node
- Atria contracts 0.1s after this wave starts
a) P wave
b) Medullary
c) Type II alveolar
d) T wave
a) P wave
Result of ventricular depolarization and precedes ventricular contraction
a) T wave
b) Diastole
c) Systole
d) QRS complex
d) QRS complex
Result of ventricular repolarization
a) Diastole
b) Systole
c) T wave
d) QRS complex
c) T wave
What is the order of the sequence of excitation?
- Atrial excitation
- Ventricular excitation
- Ventricular relaxation
Contraction phase of cardiac muscle
a) Stroke Volume
b) Systole
c) T Wave
d) Diastole
b) Systole
Relaxation phase of cardiac cycle
a) Arteries
b) Systole
c) Diastole
d) Stroke Volume
Diastole
Abnormal heart sounds
a) Heart murmurs
b) Fibrillation
c) Hypertension
d) Arrhythmias
a) Heart murmurs
[TRUE/FALSE]
Blood flow should be silent
TRUE