Exam 1 ECG's Galore Flashcards
P wave
Atrial depolarization (phase 0) Normal = 0.06 -0.11 sec
Q wave
First negative deflection of QRS complex
Pathologic when in leads I, V1-3
R wave
First positive deflection of QRS complex
Increases in amplitude from right to left
S wave
First negative deflection following an R wave
Decreases in amplitude from right to left
T wave
Ventricular repolarization (phase 3) Should be in concordance with QRS complex
U wave
Usually not seen - may be related to electrolyte disturbances
QRS complex
Ventricular depolarization from start to finish
Normal = 0.07-0.11 sec
PR interval
Depolarization of atria and ventricles
Normal = 0.12-0.20 sec
QT interval
Ventricular depolarization and repolarization
Beginning of Q wave to end of T wave
Increases in length as heart rate decreases
ST segment
Ventricular plateau phase (phase 2)
Varies with heart rate
Generally isoelectric
Best indicator of ischemia
J point
Point where QRS joins ST segment
Degrees of Normal Axis
+30 to +100
Left atrial abnormality
P wave > 0.12 sec (3 small boxes)
Notched P wave in lead II
Wide, deep terminal P wave forces in V1
Left atrium depolarizes late
Right atrial abnormality
P wave > 0.12 sec (3 small boxes)
P waves tall and peaked in lead II and V1
Right atrium depolarizes late
Right ventricular hypertrophy (RVH)
Right axis deviation
Commonly have right atrial abnormality
Tall R waves in right leads
Deep S waves in left leads
ST depression with upward convexity and inverted T waves in right leads
Left ventricular hypertrophy (LVH)
Left axis deviation
Commonly have left atrial abnormality
Tall R waves in left leads
Right bundle branch block (RBBB)
Wide QRS ( >0.12 sec)
rsR’ pattern in V1
Deep, broad S wave in V6
Left bundle branch block (LBBB)
Wide QRS ( >0.12 sec)
Broad, slurred R wave in V6 with late peak
QS in V1
Left anterior fascicular block (LAFB)
Left axis deviation
Small Q in I and AVL
Small R in II, III, AVF
Normal QRS duration
Left posterior fascicular block (LPFB)
—rare—
Right axis deviation
Small Q in II, III, AVF
Small R in I and AVL
Normal QRS duration
NO EVIDENCE OF RVH
First degree AV block
PR interval > 0.20 sec (1 big box)
Generally benign
Second degree AV block description
Grouped QRS complexes - one or more (not all) atrial impulses fail to reach the ventricles, WITH NO PREMATURITY
Second degree AV block type I (Wenckebach)
PR interval progressively lengths until AV conduction is lost
Grouped QRS complexes, leads to periodicity, sometimes one is dropped
Second degree AV block type II
uncommon but bad
PR interval DOES NOT LENGTHEN
May drop QRS complexes but cannot predict where (no periodicity)
Almost always preceded by BBB
Third degree AV block
Wide QRS complexes
P rate »_space;» QRS complex rate
Atrial rates (P rates) are faster than ventricular rates QRS rates)
NO ATRIAL IMPULSES REACH THE VENTRICLES
AV dissociation
Rates of the atria and ventricles are SIMILAR (even though the rhythms are independent)
Narrow QRS complexes = using normal conduction pathway
p waves may enter QRS complex
Subendocardial ischemia
ST segment depression
may have inverted T waves
Transmural ischemia
ST segment elevation
May have tall peaked (hyperacute) T waves
May have elevated J point
Myocardial Infarction - general rules of thumb for ECG (acute vs. old)
QRS changes most helpful
ACUTE = ST elevation = STEMI = current of injury
OLD = pathologic Q waves = NECROSIS
EVOLVING = gradually losing ST elevation and developing Q waves
Anterior MI
Q waves in V1-3
Left anterior descending of LCA
Lateral MI
Q waves in I, AVL
Left anterior descending of LCA
Inferolateral or posterolateral MI
Q waves in V4-6
Left anterior descending of LCA
Inferior MI
Q waves in II, III, AVF
Right coronary artery (90% of the time)
May be characterized by AV block
Posterior MI
R waves progressively get bigger in V1-3
Mirror image of anterior MI
Left circumflex of LCA
Ventricular pre-excitation
MUST HAVE SHORT PR INTERVAL (<0.12 sec) AND DELTA WAVES
QRS usually > 0.10 sec
Conduction via Kent bundle
Atrial prematures
Occur early in cycle
Abnormally shaped P waves
P wave may superimpose on T wave
MOST COMMON CAUSE OF A PAUSE ON AN ECG IS A NON-CONDUCTED ATRIAL PREMATURE
May have…
Normal QRS or aberrant
Compensatory pause or not
Junctional prematures (supraventricular prematures)
Arise in AV junction = VERY SHORT PR
P waves may be absent, follow, or precede QRS
QRS usually narrowing (if no BBB present)
Ventricular prematures
Wide, bizarre QRS complexes
No P wave
ST segment slopes away from QRS
Usually have compensatory pause (R-R lengthens)
R on T ventricular premature description
Grade 5 = REALLY BAD
Repolarization is occurring then a depolarization event occurs and triggers a reentrant ventricular tachycardia
Multiform ventricular premature description
Grade 3
Varying QRS complexes (some negative, some positive, some different shapes)
Left ventricular prematures
Usually monophasic R or qR in V1
qS or monophasic QS in V6
Left peak in V1 with greater amplitude
Atrial flutter
Generally regular with periodicity
Flutter waves make the baseline look like sawtooth
Atrial rate ~300 (QRS rate usually 150ish)
Most common presentation = 2:1 AV conduction
Atrial fibrillation
Variable baseline = coarse to fine with f waves
IRREGULARLY IRREGULAR
QRS complexes do what they want
Controlled (HR 60-100) vs. uncontrolled (tachycardia)
No p waves
Orthodromic AV bypass tachycardia
Normalization of QRS and no delta waves
P waves after QRS
Go to ventricles via normal conduction pathway and reenter atria via Kent bundle
Antidromic AV bypass tachycardia
–rare–
QRS wide
P waves after each QRS
Delta waves present
Slow upslope of QRS
Go to ventricles via Kent bundle and reenter atria via normal conduction pathway
AV (reentrant) junctional tachycardia (SVT)
P waves USUALLY ABSENT (but can be before or after QRS)
NARROW QRS (conduction through normal pathway)
HR about 200
GETS BACK TO SINUS RHYTHM WITH CAROTID MASSAGE
Reentrant ventricular tachyarrhythmia
WIDE QRS complexes
Tall R wave in V1
Deep S wave in V6
Torsades de pointes
QRS complex twists around the baseline
R on T reentrant ventricular tachyarrhythmia
Premature hits on the end of the T wave»_space; can lead to A fib.
Class IA anti-arrhythmic drugs
Moderate Na channel blockers
Quinidine, Procainamide, Disopyramide
Class IB anti-arrhythmic drugs
Mild Na channel blockers
Lidocaine, Mexiletine
Class IC anti-arrhythmic drugs
Marked Na channel blockers
Flecinide, propafenone
Class II anti-arrhythmic drugs
Beta Blockers
Metoprolol, atenolol
Class III anti-arrhythmic drugs
Marked K channel blockers
sotolol, amiodarone, ibutilide
Class VI anti-arrhythmic drugs
Calcium channel blockers
verapamil, diltiazem
AE quinidine
cinchonism
AE procainamide
QT prolongation
AE disopyramide
significant anticholinergic effects
Lidocaine use
works only on ventricular arrhythmia’s (no atrial effects)
Important fact about class I anti-arrhythmic drugs
increase mortality in CHF patients
Important fact about beta blockers as anti-arrhythmic drugs
ONLY class to reduce mortality in these patients
AE of sotolol
QT prolongation
AE’s of amiodarone
pulmonary toxicity
corneal deposits
blue-green skin discoloration
2 conditions that cause widened splitting of S2
RBBB, pulmonic stenosis
2 conditions that cause paradoxical splitting of S2
LBBB, aortic stenosis
What causes an opening snap to be heard?
Stenosis in mitral or tricuspid valve
Aortic Stenosis
Between S1, S2
Harsh, diamond shape
2nd right ICS
Aortic Regurgitation
Diastolic decrescendo
3rd/4th ICS
High pitch, blowing
Mitral Stenosis
Mild = presystolic accentuation
Severe = OS sooner in diastole
Low, rumbling, opening click, Down + up
Apex
Mitral Regurgitation
Pansystolic
Apex»_space; axilla
Heart failure patients
High pitched, blowing
3 determinants of stroke volume
ventricular contractility **
EDV/preload
afterload
3 factors affecting afterload
ventricular outflow tract
aortic valve function
peripheral arterial resistance
ANREP Effect
relates afterload to contractility
increase in aortic pressure abruptly will have a positive inotropic effect for 1-2 min = true inotropic effect (independent of muscle length)
Metabolic changes: increase sodium + calcium in cytosol cause an increase myocardial contraction
Force Frequency Relationship
Increased HR progressively enhances the force of ventricular contraction
When stimulation becomes too rapid, force decreases (Decreased heart rate has negative staircase effect)
Opposing factor = ventricular filling time (if it increases then there is more in the ventricle, so contraction is stronger)
Decrease duration of filling a high HR
Relates HR to contractility
Most common cause of increased afterload
hypertension
2 modes of passive regulation of pulmonary circulation
distension and recruitment (opening capillaries)
2 modes of active regulation of pulmonary circulation
hypoxic vasoconstriction and ventilation-perfusion matching
Difference in QRS between supraventricular and ventricular arrhythmia’s
Supraventricular = narrow QRS (supra skinny) Ventricular = wide QRS
