Summary N254 cardiac exam study guide

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
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,  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

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, 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

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