Cardiac Flash Cards

ATRIAL DEPOLARIZATION

• Usually upright in leads I and II and has a rounded configuration.
• Amplitude of P wavce is measured at the center of the waveform normally does not exceed 3 boxes.

A change in the form of the P wave = impulse did not come from the SA node but from an alternate pacemaking site such as the atria or the AV node.

The PR interval measures the time it takes for the impulse to depolarize the atria, travel to the AV node, and then dwell there briefly before entering the bundle of His.

Normal PR interval is 0.12 to 0.20 second, which is three to five small boxes wide.

Shorter interval = abmormally slow conduction speed.

A set of three distinct waveforms that are indicative of VENTRICULAR DEPOLARIZATION.

Q wave is sometimes not present. If present, it is assessed for abnormalities.

ABNORMAL Q WAVE: 0.04 seconds in width and measures more than one fourth of the R wave amplitude. (Pathological wave/ significant Q wave-- usually found on ECGs of patients who had MIs)

U waves, if present, immediately follows the T wave and is of the same deflection.

ELECTROLYTE IMBALANCE = HYPOKALEMIA

Can also be seen in myocardial infarciton. Sometimes a normal finding, indicative of late depolarization of the Purkinje fibers.

VENTRICULAR REPOLARIZATION

• Normally follows the QRS complex. Usually greater in size and amplitude than the P wave.
• Usually asymmetrical.
• Amplitude should be no greater than 5 small boxes or 5 mm.

HYPERKALEMIA - Tall peaked T waves.

measured from the beginning to the end of the QRS complex.

When greater than 0.10 seconds = suspected bundle branch block (BBB), or an intraventricular conduction delay -- most commonly seen in coronary artery disease.

Right BBB - QRS interval with TWO DISTINCT R WAVES

Left BBB - wide, negative QRS complex in V₁ (widening occurs because of a delay in the impulse's entry into the left ventricle.

Segment that connect the QRS complex to the T wave. Usually ISOELECTRIC or flat.

REPORT and DOCUMENT an ST segment that is above or below the isoelectric line. Use the PR segment as a reference for baseline.

A displacement in the ST segment = MI or myocardial injury

ECG monitors should be set to alarm to detect ST-segment changes.

measured from the beginning of the QRS complex to the end of the T wave.

MEASURES: time taken for ventricular depolarization and repolarization.

PROLONGED QTI = may cause monomorphic ventricular tachycardia, polymorphic ventricular tachycardia (torsades de pointes) and sudden cardiac death.

Normal QTIs are based on HEART RATE:

• slower HR = longer QTI
• faster HR = shorter normal QTI

Regularity or pattern of hearbeats. P waves are used to establish atrial rhythmicity and R waves for ventricular rhythmicity. Regular: P to P / R to R are equal distances.

IF the point lands one small box or less away the next P or R wave, the rhythm is essentially regular.

IF the point lands more than one small box AWAY = IRREGULAR rhythm.

• Regularly irregular rhythms - have a pattern
• Irregularly irregular - no pattern and no predictability; example: atrial fibrillation.

Equal how fast the heart is DEPOLARIZING.

Under normal conditions: atria and ventricles depolarize at same rate.

Two ways to determine rate:

• 1.) Rule of 1500 = EXACT rate of a REGULAR rhythm: locate two consecutive P or R waves. Count the small boxes in between the peaks. Divide into 1500.
• 2.) Rule of 10 = approximate rate. Count number of P or R waves in a 6-second strip. Multiply by 10.

• Rhythm is regular or essentially regular.
• Both the atrial rate and ventricular rate are the same, and that rate is between 60 and 100 beats per minute.
• Upright, small, rounded P waves are present in lead II.
• P waves preced each QRS complex.
• The PR interval is 0.12 to 0.20 seconds in duration.
• The QRS interval is 0.06 to 0.10 seconds in duration.

• Sinus Tachycardia
• Sinus Bradycardia
• Sinus Dysrhythmia
• Sinus Pauses and Sinus Arrest

• Premature Atrial Contractions
• Blocked Premature Atrial Contractions
• Atrial Tachycardia (sometimes called supraventricular tachycardia)
• Wandering atrial pacemaker
• Mutifocal Atrial Tachycardia
• Atrial Flutter
• Atrial Fibrillation

• Junctional Rhythm
• Premature Junctional Contractions
• Acclerated Junctional
• Junctional Tachycardia

• Premature Ventricular Contractions
• Ventricular Tachycardia
• Ventricular Fibrillation
• Idioventricular Rhythm
• Accelerated Idioventricular Rhythm
• Ventricular Standstill (Asystole)

• First Degree Block
• Second Degree Block
• Second Degree Block Type II
• Third Degree Block (Complete Heart Block)

SA nodes generates > 100 beats per minute.

Normal finding in children younger than 6 years.

Could be caused by:

• Exercise
• Stimulants
• Increased Body Temp
• Alteration in Fluid Status

Leads to decrease in ventricular filling time = less blood volume in the ventricle for next systole = lower CO

Same as for NSR except for HR is > 100 bpm

Same as NSR except for HR < 60 bpm

It may be:

• A normal finding (atheletes and other who are physically fit)
• Increased Vagal Nerve Stimulation
• (When Vagal Nerve is stimulated, an impulse is sent to the heart and the HR is decreased)
• Drug effects (bradycardia = negative chronotropic effect)
• SA node ischemia (less able to generate impulses)
• Effects of hypoxemia
• Increased Intracranial Pressure (ICP) - Cushing's Reflex (a hemodynamic response to increased ICP = HR decreases and often becomes irregular)

• The Valsalva Maneuver
• Coughing
• Suctioning
• Gagging
• Vomiting
• Vagal Nerve Stimulation = Sinus Bradycardia

• Many pts can maintain adequate CO, despite lowered HR.
• Others experience decreased CO and related symptoms.

Drugs that affect speed or velocity of conduction.

Drugs that affect the HR.

Drugs that affect contractility.

• Decreased LOC
• Hypotension
• Chest Pain
• Shortness of Breath
• Pulmonary congestion, crackles
• Syncope

• A cardiac rhythm disturbance associated with respiration.
• (Inspiration) negative intrathoracic pressure = increased venous return = HR increases to compensate to increased volume.
• (Expiration) positive intrathoracic pressure = flow of blood returns to normal, as does HR.

• Same as NSR except for a CYCLICAL increasing and decreasing of HR
• Changes in HR is associated with respiration
• Rhythm is regularly irregular

Normally tolerated well unless assoc. with tachy/bradycardia.

SA node occasionally temporarily fails as the dominant pacemaker. Failure may be cause of by inability of the node to to generate the impulse or the impulse may be generated but blocked from exiting the node = no atrial or ventricular depolarization occurs for one heartbeat or more.

• Enhanced Vagal Tone
• Coronary Artery Disease (due to decreased perfusion of the SA node)
• Effects of drugs (cardiac drugs that slow HR can lead to episodes of sinus arrest and exit block)

• The heart rate can be normal (60 to 100) or slower than normal
• Pauses caused by missed beats are noted on the ECG
• The rhythm is irregular as the result of missed beats
• Pauses may be interrupted by an escape beat from the AV node or the Purkinje fibers.

• Depends on the number of beats that are arrested/blocked, and the length of the resulting pause. Changes in CO depend on how low HR falls.
• Multiple beats arrested/blocked = asystole = no CO.

• Caused by increased automaticity in the right/left atrium or both.
• Conditions that affect automaticity:
• Stress
• Electrolyte Imbalances, particularly hypokalemia
• Hypoxemia (atria become irritable when deprived of oxygen)
• Injury to the atria
• Digitalis Toxicity (stimulation of the myocardium, especially the atria. May convert atrial dysrhytmia to a sinus rhythm, or it may only slow the ventricular response to atrial tachycardias. Toxicity should be suspected in pts. receiving digoxin - WITHHOLD subsequent doses until toxicity is ruled out.
• Hypothermia
• Hyperthyroidism
• Alcohol Intoxication (cardiac stimulant, irritating effect on heart)
• Pericarditis

• Common; usually seen in the setting of NSR.
• Generated very near the SA node.
• The generation of PACs near the SA node frequently leads to depolarization of surround tissue and causes a pause in teh ECG.

• The ectopic beats are premature
• The PR interval is usually normal but often differs from the PR interval seen during NSR
• The P wave of the premature beat may be found in the T wave just before the premature beat.

• A pause is noted on the ECG tracing.
• A premature P wave which differs from the normal P wave, is found in the T wave of the last normal beat before the pause.

• PACs usually do not alter CO
• Many patients report palpitations.
• Increasing numbers of PACs ma herald development of A fib/A flutter

• A rapid rhythm that rises from the atrial muscle.
• Can be LIFE THREATENING. Usually seen in pts. with cardiac disease, but can also be seen in healthy patients.
• Increased number of PACs can sometimes precede onset of Atrial Tachycardia.
• Sometimes referred to as a SUPRAVENTRICULAR TACHYCARDIA or SVT

Atrial flutter and Atrial Fibrillation

Wolff-Parkinson-White Syndrome (WPW) - related to the presence of a bypass tract that connects the atria and the ventricles, "bypassing" the AV node.

• The rhythm is absolutely REGULAR
• Heart rate is usually 150-250 bpm
• Occurs suddenly, usually without warning
• P waves, if present, usually merge with preceding T wave, altering its appearance.
• AV block that may be fixed or varying degree is present.
• Width of the QRS is usually normal.

• Vary from none to shock.
• Faster HR = lower CO

• QRS complex may be widened, giving the apperance of a BBB
• PR is shortened (but not always <0.12 seconds) because of ventricular preexcitation.
• The QRS upstroke may be slurred or notched - DELTA WAVE (may be more visible in some leads more than others)
• If the patient has atrial fibrillation with WPQ, the rhythm will me irregular.

• 1. Short PR
• 2. Wide QRS
• 3. Delta Wave

• Varied pacemaking activity throughout the atria. At least 3 SITES of atrial pacemaking must be documented. (P waves would look different in shape, slope, or orientation).
• PR intervals will vary because the impulses originate from different locations within the atria, taking various times to reacht the AV node.

• Rhythm - irregular
• HR is less than 100 bpm
• At least 3 different-looking P-waves are seen.
• PR intervals may vary.

• May result in less effective atrial depolarization
• Ventricular filling may be altered = decreased CO

Essentially the same as wandering pacemaker, except the HR > 100 bpm

• Same as wandering pacemaker.
• Faster HR = less time for ventricular filling = decreased CO

• Arises from a single irritable focus in the atria
• Most commonly seen in pts with heart disease, particularly valvular disease
• Flutter waves best seen in leads II, III and aVF
• They are BIPHASIC: the first part of the waveform is negative, and it is followed by an upright or positive waveform.
• Appearance of TEETH or a SAWBLADE.
• Usually generated at a rate of 250 to 350 bpm with perfect regularity.
• Irritable focus in the atria never stops firing.

• Atrial rate is usually 250 to 350 bpm.
• The ventricular rate varies with the degree of AV block.
• The onset is usually rapid.

• Dependent on ventricular rate/ventricular response
• Pts. who sustain an atrial flutter with a fast ventricular response often have low CO symptoms.

• The most common clinically important rhythm.
• Characterized by erratic impulse formation throughout the atria, classicaly described as "irregularly irregular."
• Widespread irritability and increased automaticity lead to a chaotic state of impulse formation.
• Wavy baseline without any discernable P wave.
• Depolarization of the ventricles takes longer = widened QRS complex.

• In A-fib: aberrantly conducted beats.
• More likely to occur when an atrial impulse arrives at the AV node just after a previously conducted impulse.
• Often seenw hen rate changes from slower to faster, which is referred to as long-short cycle.
• Not clinically significant.

• Thromboembolism.
• The blood that collects in the atria is agitated by fibrillation and normal clotting is accelerated.
• SO: if pt has been in A-Fib for less than 48 hours, and if BP is stable, pt should receive anticoagulation therapy before any attempt is made to convert the A-Fib to NSR. (Usually IV heparin or SQ low-molecular weight heparin is administered).
• IF A-Fib persists or is recurrent, long-term warfarin (Coumadin) therapy is usually prescribed to diminish the risk of thromboembolism.

• An irregularly irregular ventricular rhythm exists
• A wavy baseline exists with not discernable P waves
• The width of the QRS comples may vary between normal and slightly widened.
• Ashman's beats may be present.

• The atria are never fully depolarized and therefore do not contract = loss of atrial kick.
• Ventricular response determines effect on CO.
• Pts with markedly high or low rates are more likely to have decreased CO.

• Dysrhythmiass of the AV node. Also called nodal rhythms.
• Two primary causes of Junctional Rhythm:
• 1.)When a singular beat or ongoing rhythm is originated in an area other than the sinus node, it is considered ectopic. Ectopic means out of the normal place.
• Caffeine/nicotine/stress = Increased automaticity = Ectopic Rhythms
• Digitalis toxicity can produce all forms of junctional rhythms.
• At toxic levels, digitalis can suppress the HR or can act as a myocardial stimulant.
• 2.) Escape rhythms can be generated from the AV node should the sinus node fail. The AV node is capable of generating 40 to 60 bpm as a back up pacemaker.

• The rhythm is usually regular
• The heart rate is 40 to 60 per minute
• P waves may be absent, inverted, or follow the QRS complex.
• The PR interval is at the low end of normal or shorter than normal.
• The QRS complex is of normal width.

Atrial kick is usually less effective or absent, resulting in decreased ventricular filling. Diminished CO may occur.

Same as junctional rhythm EXCEPT for rate is between 60 and 100 bpm

Same as junctional rhythm EXCEPT for rate is between 100 to 150 bpm

Same as junctional rhythm. However, ventricular filing may be further compromised by the faster HR. Conversely, the faster HR may actually improve CO if SV is decreased.

• Irritable areas in the AV node and junctional tissue can generate beats that are earlier than the next expected beat.
• The premature beats most often occur in NSR and temporarily upset rhythmicity.
• A compensatory or noncompensatory pause may occur after a PJC.

• The ectopic beats are premature.
• P waves may be absent or inverted or may occur after the QRS complex.
• If a P wave is present before the QRS complex, the PR interval is usually shorter than normal.
• PJCs are usually followed by a noncompensatory pause.

• Do not usually alter CO.
• However, many pts. report palpitations.

• Common.
• The beats can be generated anywhere in the ventricles. Could be unifocal or multifocal.
• Compensatory pause follows a PVC because the SA node is usually able to compensate.

When only one focus of irritability exists=all the ectopic beats appear the same.

When ventricular ectopic beats come from multiple areas = each QRS complex looks different.

• Bigeminy: occur every other beat
• Trigeminy: every third beat
• Quadrigeminy: every fourth beat

• Couplet = two PVCs in a row, and the morphology of each is different
• Pair = two PVCs in a row, and the morphology is similar
• Triplet/Salvo = Three PVCs in a row

• From the peak of the T wave through the downslope of the T wave.
• If a PVC is generated durin this time = V Tach may occur.

• Rarely treated.
• Considered signs of underlying disease that requires attention (eg. hypoxemia, ischemia, or electrolyte imbalance).
• PVCs in a pt with MI are treated when associated with such symptoms as angina/hypotension.
• NURSE: assist in identifying causative factors and be alert for the development of worsening dysrhythmias.

• The rhythm is irregular as a result of premature beats. However, the premature beats can occur in a regular pattern.
• The ectopic beat occurs prematurely, before the next anticipated sinus beat.
• P waves are usually absent before the ectopic beat.
• The premature beat is usually followed by a compensatory pause.
• The QRS complex of the prematur beat is wider than 0.12 seconds
• The T wave of the PVC is in the opposite direction of the QRS of the PVC. (If QRS is upright/positive, the T wave is points downward/negative)

• Varied.
• Some patients may be asymptomatic.
• Others report lightheadedness or palpitations.
• Symptoms usually worsen with an increase in number of PVCs.

• Chaotic rhythm characterized by a quivering of the ventricles that results in total loss of cardiac output.
• State of clinical death = the heart has stoppped contracting = no blood flow to the vital organs.

V-Fib that occurs without the presence of cardiac disease or other explainable cause.