N254 Cardiac Exam Study Guide
5 EKG interpretation questions:
Electrocardiogram
o Graphic record of hearts activity
o Electrodes detect the magnitude and direction of electrical currents produced in the heart.
o Need good skin contact, remove hair if needed, dry sweat if needed; change as needed, jelly dries up
in 2-3 days
o P wave
Represents atrial depolarization and contraction; 0.10 seconds in length
Impulse is from sinus node
Precedes QRS complex, is normally smooth, round, and upright
May be absent when SA node is not acting as a pacemaker
Atrial repolarization occurs during ventricular depolarization and usually is not seen on the
ECG
o PR interval
Represents time required for sinus impulse to travel to the AV node and into the Purkinje
fibers
Measured from beginning of P wave to beginning of QRS complex. (If no Q wave present,
measure to R wave)
0.12-0.20 seconds (up to 0.24 OK in pts >65)
Any greater indicates delay in conduction from SA node to ventricles
o QRS complex
Represents ventricular depolarization and contraction
0.06-0.10 seconds or <3 small squares
Any greater indicates delays in transmitting the impulse through the ventricular
conduction system
Impulse from Bundle of His throughout ventricular muscles
o ST segment
Signifies beginning of ventricular repolarization
End of QRS- beginning of T wave
Should be isoelectric
o T wave
Ventricular repolarization, no associated activity from ventricular muscle (resting phase)
Smooth, rounded shape less than 10mm tall
Abnormalities may indicate myocardial ischemia or electrolyte imbalances (peaked T wave
indicates earliest sign of hyperkalemia)
o QT interval
Beginning of QRS to end of T
Total time of ventricular depolarization and repolarization
Usually 0.32-0.44 seconds
Prolonged= greater risk for dysrhythmias due to prolonged refractory period
Shortened QT can be from meds or electrolyte imbalances
o U wave
Rare, can be seen in hypokalemia
INTERPRETING AN EKG (BOX 29-2, p. 848)
Step 1: Determine RATE
o Assess HR, use P waves to determine atrial rate and R waves for ventricular rate
Count # of complexes in 6 second strip and multiply by 10
1
, Step 2: Determine REGULARITY
o Consistency of which P waves or QRS complexes occur
o Use a caliper or paper method to measure
Start at peak of P wave (atrial rhythm) or R wave (ventricular rhythm)
P-P or R-R
Wave peaks that vary by more than 1-3 small boxes are considered irregular
Can be irregularly irregular or regularly irregular
Step 3: Assess P WAVE
o Presence or absence helps determine rhythm
o Should be alike in share and size (morphology)
o If they are different or not seen, rhythm may not originate in sinus node
Step 4: Determine interval durations
o Measure PR interval, QRS duration, and QT interval
o Evaluates impulse transmission through the cardiac conduction system
PHYSICAL ASSESSMENT
Apical impulse
Retraction- pulling of tissue in precordium
o Normal and may be seen in thin patients
Pulsations- other than normal apical pulsations (can be called heaves/lifts) are abnormal
o Occur as the result of an enlarged ventricle
5 Ps of peripheral vascular disease (PVD)
o Pulselessness, pallor, pain, paresthesias, paralysis
Diminished S1 sounds are associated with first-degree heart block, mitral regurgitation, CHF, CAD, or
pulm/systemic HTN
o Splitting of S1 may be associated with right BBB and PVCs
Diminished S2 occurs with aortic stenosis, shock, and increased chest diameter
o Wide splitting of S2 is associated with delayed emptying of right ventricle, resulting in delayed
pulmonary valve closure (mitral regurg, pulm stenosis, right BBB)
S3- also called a ventricular gallop; immediately follows S2
o Results from myocardial failure and ventricular volume overload (CHF, mitral or tricuspid regurg)
o No variation with respirations
o Lower pitched
S4- also called an atrial gallop; precedes S1
o Results from increased resistance to ventricular filling after atrial contraction (HTN, CAD, aortic
stenosis, cardiomyopathy)
o Can be normal without pathological evidence in 40-50yr olds after exercise
Pericardial friction rub results from inflammation of the pericardial sac, as with pericarditis
o Inflammation of the precordium
THE PATIENT WITH A CARDIAC DYSRHYTHMIA
Physiology review
o Automaticity- ability of pacemaker cells to spontaneously initiate an electrical impulse (action
potential)
SA node= dominant pacemaker @ 60-100bpm
o Excitability- ability of myocardial cells to respond to stimuli generated by pacemaker cells
o Conductivity- ability to transmit an impulse from cell to cell
When one cell is stimulated, the impulse rapidly spreads throughout the heart muscle
o Refractoriness- the inability of cardiac cells to respond to additional stimuli immediately following
depolarization
o Contractility- ability of myocardial fibers to shorten in response to a stimulus
Heart muscles respond in an all-or-nothing manner
2
, o SA node generates at a regular rate of 60-100bpm. Impulse spreads through the atria and is briefly
delayed at the AV node, and then spreads through conduction.
This delay causes atria to contract, delivering an extra bolus of blood to the ventricles before
they contract (atrial kick)
o AV node also controls the number of impulses that reach the ventricles, preventing extremely rapid
HRs
Pathophysiology
o Dysthymias arise through disruption of the very properties that stimulate and control the heart beat
(listed above)
o Bradydysrhythmias and tachydysrhythmias result from change in automaticity of cardiac cells
o Ectopic beats- interrupt normal conduction sequence and may not initiate a normal muscle
contraction
o Conduction abnormalities cause varying degrees of heart block (block in normal conduction
pathways)
Supraventricular Rhythms
o Sinus rhythm
Normal sinus rhythm
Originates is the SA node and travel through all normal conduction pathways without delay
Rate 60-100
o Sinus node dysrhythmias
Sinus arrhythmias
Rate varies with respirations, causing irregular rhythm
Rate increases during inspiration and decreased with expiration
Common in very young and very old
Caused by: increase in vagal tone, dig toxicity, morphine
Sinus tachycardia
Rate >100; QRS <0.12 seconds
From enhanced automaticity in response to changed in internal environment
Normal response to any event that increases the body’s need to oxygen and
nutrients (hypoxia, hypovolemia, anemia, hyperthyroidism (Graves), MI, HF,
cardiogenic shock, PE, caffeine, epinephrine, atropine)
Increases cardiac work and O2 use
Increased pulse rate, dizziness, SOB
Sinus bradycardia
Rate <60, may be from increased vagal (parasymp) activity or depressed
automaticity die to injury of ischemia to sinus node
Normal in pts with athletic heart syndrome
May be from IICP, hypothermia, acidosis, acute MI
o Supraventricular dysthymias
When an action potential originates in atrial tissue outside the sinus node
Ectopic pacemaker overrides the SA node
May be paroxysmal (abrupt onset and termination)
Premature atrial contractions (PACs)
Ectopic atrial beat that occurs earlier then next expected sinus beat
Usually asymptomatic and benign
Usually require no tx, reduce alc and caffeine; may tx with beta-blocker
Irregular rhythm, with normal rhythm interrupted by early beats arising in the atria
May cause palpitations or fluttering sensation in chest
Paroxysmal supraventricular tachycardia (PSVT)
Tachycardia of sudden onset and termination ; initiated by reentry loop in or around
AV node
3
5 EKG interpretation questions:
Electrocardiogram
o Graphic record of hearts activity
o Electrodes detect the magnitude and direction of electrical currents produced in the heart.
o Need good skin contact, remove hair if needed, dry sweat if needed; change as needed, jelly dries up
in 2-3 days
o P wave
Represents atrial depolarization and contraction; 0.10 seconds in length
Impulse is from sinus node
Precedes QRS complex, is normally smooth, round, and upright
May be absent when SA node is not acting as a pacemaker
Atrial repolarization occurs during ventricular depolarization and usually is not seen on the
ECG
o PR interval
Represents time required for sinus impulse to travel to the AV node and into the Purkinje
fibers
Measured from beginning of P wave to beginning of QRS complex. (If no Q wave present,
measure to R wave)
0.12-0.20 seconds (up to 0.24 OK in pts >65)
Any greater indicates delay in conduction from SA node to ventricles
o QRS complex
Represents ventricular depolarization and contraction
0.06-0.10 seconds or <3 small squares
Any greater indicates delays in transmitting the impulse through the ventricular
conduction system
Impulse from Bundle of His throughout ventricular muscles
o ST segment
Signifies beginning of ventricular repolarization
End of QRS- beginning of T wave
Should be isoelectric
o T wave
Ventricular repolarization, no associated activity from ventricular muscle (resting phase)
Smooth, rounded shape less than 10mm tall
Abnormalities may indicate myocardial ischemia or electrolyte imbalances (peaked T wave
indicates earliest sign of hyperkalemia)
o QT interval
Beginning of QRS to end of T
Total time of ventricular depolarization and repolarization
Usually 0.32-0.44 seconds
Prolonged= greater risk for dysrhythmias due to prolonged refractory period
Shortened QT can be from meds or electrolyte imbalances
o U wave
Rare, can be seen in hypokalemia
INTERPRETING AN EKG (BOX 29-2, p. 848)
Step 1: Determine RATE
o Assess HR, use P waves to determine atrial rate and R waves for ventricular rate
Count # of complexes in 6 second strip and multiply by 10
1
, Step 2: Determine REGULARITY
o Consistency of which P waves or QRS complexes occur
o Use a caliper or paper method to measure
Start at peak of P wave (atrial rhythm) or R wave (ventricular rhythm)
P-P or R-R
Wave peaks that vary by more than 1-3 small boxes are considered irregular
Can be irregularly irregular or regularly irregular
Step 3: Assess P WAVE
o Presence or absence helps determine rhythm
o Should be alike in share and size (morphology)
o If they are different or not seen, rhythm may not originate in sinus node
Step 4: Determine interval durations
o Measure PR interval, QRS duration, and QT interval
o Evaluates impulse transmission through the cardiac conduction system
PHYSICAL ASSESSMENT
Apical impulse
Retraction- pulling of tissue in precordium
o Normal and may be seen in thin patients
Pulsations- other than normal apical pulsations (can be called heaves/lifts) are abnormal
o Occur as the result of an enlarged ventricle
5 Ps of peripheral vascular disease (PVD)
o Pulselessness, pallor, pain, paresthesias, paralysis
Diminished S1 sounds are associated with first-degree heart block, mitral regurgitation, CHF, CAD, or
pulm/systemic HTN
o Splitting of S1 may be associated with right BBB and PVCs
Diminished S2 occurs with aortic stenosis, shock, and increased chest diameter
o Wide splitting of S2 is associated with delayed emptying of right ventricle, resulting in delayed
pulmonary valve closure (mitral regurg, pulm stenosis, right BBB)
S3- also called a ventricular gallop; immediately follows S2
o Results from myocardial failure and ventricular volume overload (CHF, mitral or tricuspid regurg)
o No variation with respirations
o Lower pitched
S4- also called an atrial gallop; precedes S1
o Results from increased resistance to ventricular filling after atrial contraction (HTN, CAD, aortic
stenosis, cardiomyopathy)
o Can be normal without pathological evidence in 40-50yr olds after exercise
Pericardial friction rub results from inflammation of the pericardial sac, as with pericarditis
o Inflammation of the precordium
THE PATIENT WITH A CARDIAC DYSRHYTHMIA
Physiology review
o Automaticity- ability of pacemaker cells to spontaneously initiate an electrical impulse (action
potential)
SA node= dominant pacemaker @ 60-100bpm
o Excitability- ability of myocardial cells to respond to stimuli generated by pacemaker cells
o Conductivity- ability to transmit an impulse from cell to cell
When one cell is stimulated, the impulse rapidly spreads throughout the heart muscle
o Refractoriness- the inability of cardiac cells to respond to additional stimuli immediately following
depolarization
o Contractility- ability of myocardial fibers to shorten in response to a stimulus
Heart muscles respond in an all-or-nothing manner
2
, o SA node generates at a regular rate of 60-100bpm. Impulse spreads through the atria and is briefly
delayed at the AV node, and then spreads through conduction.
This delay causes atria to contract, delivering an extra bolus of blood to the ventricles before
they contract (atrial kick)
o AV node also controls the number of impulses that reach the ventricles, preventing extremely rapid
HRs
Pathophysiology
o Dysthymias arise through disruption of the very properties that stimulate and control the heart beat
(listed above)
o Bradydysrhythmias and tachydysrhythmias result from change in automaticity of cardiac cells
o Ectopic beats- interrupt normal conduction sequence and may not initiate a normal muscle
contraction
o Conduction abnormalities cause varying degrees of heart block (block in normal conduction
pathways)
Supraventricular Rhythms
o Sinus rhythm
Normal sinus rhythm
Originates is the SA node and travel through all normal conduction pathways without delay
Rate 60-100
o Sinus node dysrhythmias
Sinus arrhythmias
Rate varies with respirations, causing irregular rhythm
Rate increases during inspiration and decreased with expiration
Common in very young and very old
Caused by: increase in vagal tone, dig toxicity, morphine
Sinus tachycardia
Rate >100; QRS <0.12 seconds
From enhanced automaticity in response to changed in internal environment
Normal response to any event that increases the body’s need to oxygen and
nutrients (hypoxia, hypovolemia, anemia, hyperthyroidism (Graves), MI, HF,
cardiogenic shock, PE, caffeine, epinephrine, atropine)
Increases cardiac work and O2 use
Increased pulse rate, dizziness, SOB
Sinus bradycardia
Rate <60, may be from increased vagal (parasymp) activity or depressed
automaticity die to injury of ischemia to sinus node
Normal in pts with athletic heart syndrome
May be from IICP, hypothermia, acidosis, acute MI
o Supraventricular dysthymias
When an action potential originates in atrial tissue outside the sinus node
Ectopic pacemaker overrides the SA node
May be paroxysmal (abrupt onset and termination)
Premature atrial contractions (PACs)
Ectopic atrial beat that occurs earlier then next expected sinus beat
Usually asymptomatic and benign
Usually require no tx, reduce alc and caffeine; may tx with beta-blocker
Irregular rhythm, with normal rhythm interrupted by early beats arising in the atria
May cause palpitations or fluttering sensation in chest
Paroxysmal supraventricular tachycardia (PSVT)
Tachycardia of sudden onset and termination ; initiated by reentry loop in or around
AV node
3
