Cardio/Renal Lab 1 Flashcards
Depolarization
- Na, Ca, K move into the cell
Repolarization
K moves out of the cell
Resting potential (Phase 0)
-90 mV
Atrial and ventricular cardomyocyte depolarization
- Systole (contraction)
Resting membrane potentional corresponds to?
Diastole (relaxation)
Phase 0
- Na channels open
- influx of Na
- cell rapidly depolarizes and trigger muscle contraction
Phase 1
- Na channel closes
- K channels open to removed K+ out of the cells
- Partially repolarized
Phase 2
- calcium channels open and Ca+ flows into the cell
- cells remains depolarized for 0.3 seconds
- Plateau segment of action potential
Phase 3
- cell repolarizes
- Potassium channel opens and K+ flows out
- cell returns to resting potential
Absolute refractory period
- cariomyocytes are unable to generate, propogate or respons to the arriving action potential
Relative refractory period
- the cell is only able to respons when there is a strong enough stimulus from action potential
Electrocardiogram
- recording of the electrical activity of the heart
- currents generated can reach to the surface of the chest
- recorded by electrodes
P wave
- first wave of the ECG
- represents the depolarization of the atrium
- before atrial contraction
- short period after (straight line) allows for ventricular filling
QRS complex
- depolarization of the ventricles
- Q = depolarization from V septum (left to right)
- R = largest wave, depolarization of the V
- S = final stage of V depolarization
T wave
- ventricular repolarization
- before the end of ventricular contraction
ST segment
- zero potential between depolarization and repolarization
PQ interval
- time between the beginning of the P wave and the beggining of the QRS complex
QT interval
- ventricular contraction
- begins at Q wave until the end of T wave
Atrial fibrillation
- no P waves
- irregular narrow QRD complex at random irregular intervals
Atrial flutter
- sawtooth P wave form
Bradycardia
- sinus node dysfunction caused by coronary artery disease
- hypothyroidism
Tachycardia
- abnormal impulse formation / conduction
Sinus
tachycardia
- caused by drug toxicity or disease
Triggered activity
- when depolarization occurs before the cell is fully repolarized
- not related to SA node firing
Re-entry arrhythmias
- abnormal conduction
- retrograde conduction is blocked as the cells originating the stimuli are still in refractory period
- antrograde conduction is blocked in one of the paths and impulse travels through the paths which are not blocked
Class 1
- block inward Na (slow conduction velocity)
- block outward K channels (prolong APD)
Class 1B
- shorten APD (shorten rate of depolarization)
Class 1C
- slows conduction
- sympatholytic drugs
Class 2
- B-blockers
- slow heart rate, reduced the influx of calcium ions
Class 3
- potassium channel blockers
- slow down electrical impulses
Class 4
- calcium channel blockers
- decrease HR and contraction
Inverted T-wave
- due to mild ischemia in the apex of the ventricle
causes of cardiac arrhythmias
- damage to heart muscle leads to alterations to conduction and heart rhythm
Sinoatrial Block
- sudden stop of P waves, atrium is at standstill
- ventricles pick up rhythm
Atrioventricular block
- Prolonged PR or PQ interval
- P wave is present but conduction is slowed
- ventricle beats drop but still generate impulses
Ventricular Fibrillation
- Coarse contraction of ventricles disappear
- irregular spasmodic waves
Class 1A drugs – Sodium Channel Blocker
- quinidine
- procainamide
- dispyramide
Class 1B drugs
- lidocaine
- mexiletine
- tocainide
Class 1C drugs
- flecainide
- encainide
- propafenone
Class 2 – BB
- propranolol
- esmolol
- metoprolol
- atenolol
- timolol
Class 3 - K channel blocker
- Sotalol
- ibutilide
- bretylium
- dofetilide
- amiodarone
Class 4 – CCB
- diltiazem
- verapamil