Topic 3 Flashcards
CARDIAC PHYSIOLOGY REVIEW
- Pacemaker cells and?
- Electrical signals generated by?
- Cells can generate stimulus without?
- Cardiac cycle Composed of?
- Pacemaker cells and automaticity
- Electrical signals generated by pacemaker cells
- Cells can generate stimulus without outside stimulation
- Automaticity
- Cardiac cycle Composed of two activities
1) Electrical (caused by automaticity)
2) Mechanical (muscular), known as a contraction
CARDIAC ELECTROPHYSIOLOGY
- Cardiac muscle cells generate an electrical current = cardiac action potential
- Sinoatrial node (SA node)
- Exchange of electrolytes
CARDIAC CYCLE
- Two phases of electrical activity
1) Depolarization = active
2) Repolarization = resting - Two mechanical responses
1) Systole
2) Diastole
- Depolarization =
- Repolarization =
- Electrical activity precedes?
- Electrical + mechanical =
- Depolarization = systole = contraction
- Repolarization = diastole = resting or filling phase
- Electrical activity precedes mechanical activity
- Electrical + mechanical = cardiac contraction
CARDIAC ACTION POTENTIAL
- Depolarization
- Na outside cell; K inside the cell
- Change cell permeability
- Na enters cells; K leaves cells
- Ca slowly enters cells
- ATP needed to move electrolytes back to resting state
- Repolarization begins
ECG is evidence of?
electrical activity, not contraction
MUSCULAR CONTRACTION
- Depolarization leads to contraction
- Repolarization leads to resting and filling of ventricles from atria
- ECG is evidence of electrical activity, not contraction
SA node rate
(inherent rate of 60 – 100 beats per minute)
- SA node
- SA node (inherent rate of 60 – 100 beats per minute)
- Depolarization begins
- Atrial contraction or atrial kick
- Intraatrial and internodal pathways to AV node
AV node rate
(inherent rate of 40-60 beats per minute)
Bundle of His rate
(inherent rate of 20-40 beats per minute)
CARDIAC CONDUCTION PATHWAY
- AV node
- AV node (inherent rate of 40-60 beats per minute)
- Delays impulse to ventricles; allows for filling
- Backup pacemaker
- Bundle of His (inherent rate of 20-40 beats per minute) - Left and right bundle branches; fascicles
- Purkinje fibers
Cardiac physiology review from beginning to end
1) Atrial diastole
- atrial fills
- all valves are closed
2) Early atrial systole
- increased atrial pressure opens AV valves
- ventricles fill
3) Atrial systole, atrial kick
- atria contract and empty
- ventricles are full
4) Early ventricular systole
- ventricles begin contraction
- pressure closes AV Valves
- atria relax
5) Ventricular systole
- ventricles contract
- increased pressure in ventricles
- aortic and pulmonary valves open
- blood ejected into aorta and pulmonary artery
6) Early atrial diastole
- ventricles empty
- ventricles relax
- aortic and pulmonary valves close
Autonomic nervous system
2 pathways
1) sympathetic nervous system> epinephrine and norepinephrine> increased HR, increased contractility, vasoconstriction
2) parasympathetic nervous system>acetylcholine> decreased HR, decreased contractility, vasodilation
INHERENT RATES
- SA node =
- AV node =
- Ventricles (Purkinje fibers) =
- SA node = 60 to 100 beats/min
- AV node = 40 to 60 beats/min
- Ventricles (Purkinje fibers) = 20 to 40 beats/min
12-LEAD ECG
- Lead I
- Lead II
- Lead III
- Lead I
- Records flow from right arm to left arm
- Lead II
- Records flow from right arm to left leg
- Lead III
- Records flow from left arm to left leg
Augmented limb leads; unipolar center of heart to lead
- aVR =
- aVL =
- aVF =
- aVR = from heart to right arm
- aVL = from heart to left arm
- aVF = from heart to left foot
P Wave
Atrial depolarization
- Normally indicates firing of the sinoatrial node
- Not to exceed three boxes high
QRS Complex
Ventricular depolarization
- Q wave first negative deflection after P wave
- R wave first positive deflection after P wave
- S wave negative waveform after R wave
- Not everyone has a traditional QRS
Pathological Q waves
- 0.04 seconds in width
- More than one fourth of the R-wave amplitude
- Indication of a myocardial infarction
PR INTERVAL
- Atrial depolarization/delay in AV node
- Beginning of P wave to beginning of QRS complex
- 0.12 to 0.20 seconds
- Shorter interval = impulse from AV junction
- Longer interval = first-degree AV block
QRS INTERVAL
- Ventricular depolarization
- 0.06 to 0.10 seconds
- Various configurations
- Wide: slowed conduction
- Bundle branch block (BBB)
- Ventricular rhythm
ST SEGMENT
- Look for depression or elevation
- ST elevation: myocardial injury
- ST depression: reciprocal changes, digoxin, and ischemia
T wave
- Ventricular repolarization
- Follows a QRS complex
- Bigger than a P wave
- No greater than five small boxes high
- Inversion indicates ischemia to myocardium
QT INTERVAL
- Beginning of QRS complex to end of T wave
- 0.32 to 0.50 seconds
- Varies with heart rate
U WAVE
- Sometimes seen after T wave
- Unknown origin
- May be normal
- May indicate hypokalemia
RHYTHMICITY
- Regularity or pattern of heartbeats
- PP intervals (atrial)
- RR intervals (ventricles)
- PP intervals (atrial)
- Is regular when distance between PP intervals is equal 3. RR intervals (ventricles)
- Is regular when distance between RR intervals is equal
BASIC DYSRHYTHMIAS
Grouped by anatomical areas
- SA node
- Atria
- AV node-Junctional
- Ventricles
- AV blocks
1-NORMAL SINUS RHYTHM
- Regular rhythm
- Rate 60 to 100 beats/min
- Normal P wave in lead II
- P wave before each QRS
- Normal PR, QRS, and QT intervals
SINUS TACHYCARDIA
- Sinus rhythm with a rate of 100 to 150 beats/min
- Causes: Hyperthyroidism, hypovolemia, heart failure, anemia, exercise, use of stimulants, fever, and sympathetic response to fear or pain and anxiety may cause sinus tachycardia.
- Assess for symptoms of low cardiac output
SINUS BRADYCARDIA
- Sinus rhythm with rate less than 60 beats/min
- Causes: vagal, drugs, ischemia, disease of the nodes, ICP, hypoxemia, and athletes (normal)
- Produces various hemodynamic responses
SINUS ARRHYTHMIA
- Sinus rhythm
- Rate varies with respirations
- Inspire = increase
- Expire = decrease
- Rarely affects hemodynamic status
SINUS ARREST OR EXIT BLOCK
- Sinoatrial node fails to initiate impulse
- Causes: vagal, heart disease, and drugs that slow heart rate
- Heart rate can be normal or slow
- Irregular rhythm
- Can decrease cardiac output
ATRIAL DYSRHYTHMIAS
- Increased automaticity in the atrium
- Generally have P-wave changes
ATRIAL DYSRHYTHMIAS Causes
- Stress
- Electrolyte imbalances
- Hypoxia
- Atrial injury
- Digitalis toxicity
- Hypothermia
- Hyperthyroidism
- Alcohol
- Pericarditis
PREMATURE ATRIAL CONTRACTIONS
- Early beats initiated by atrium
- P waves and PR interval may vary
- Noncompensatory pause
- P wave may be found in T wave
WANDERING ATRIAL PACEMAKER
- Varying configurations of P waves
- At least three different P-wave shapes must be seen
- Heart rate not greater than 100
- PR interval varies
- Irregular rhythm
ATRIAL TACHYCARDIA
- Rapid rhythm
- Ectopic focus in atria
- 1:1 conduction (ventricle responds to every atrial impulse)
- 2:1 conduction (ventricle responds to every two atrial impulses)
MULTIFOCAL ATRIAL TACHYCARDIA
- Almost identical to wandering atrial pacemaker
- Heart rate exceeds 100 beats/min
- Common in COPD patients
Common in COPD patients
MULTIFOCAL ATRIAL TACHYCARDIA
PAROXYSMAL ATRIAL TACHYCARDIA
- Heart rate 150 to 250 beats/min
- Regular rhythm
- P waves (if present) may merge in T waves
- QRS complex width is normal
- Hemodynamic effects vary
ATRIAL FLUTTER
- Ectopic foci in atria, heart disease
- Classic “sawtooth” pattern in leads II, III, and aVF
- Atrial rate fast and regular (250 to 350 beats/min) with AV block
- Description of atrial flutter might be constant at 2:1, 3:1, 4:1, 5:1, and so forth, or it may be variable
- Causes: Lung disease, ischemic heart disease, hyperthyroidism, hypoxemia, heart failure, and alcoholism can cause atrial flutter.
High risk for pulmonary or systemic emboli
ATRIAL FIBRILLATION
ATRIAL FIBRILLATION
- Erratic impulse formation in atria
- No discernible P wave
- Irregular ventricular rate
- Aberrant (abnormal) ventricular conduction can occur
- Results in loss of atrial kick
- High risk for pulmonary or systemic emboli
A patient comes to the emergency department complaining of headache, numbness of his left arm and hand, and slurred speech. His pulse is 120 and irregular. His blood pressure is 136/88 mm Hg. What is a probable cause for his symptoms?
These symptoms may indicate an acute stroke. The irregular heart beat may be caused by atrial fibrillation. A common complication of atrial fibrillation is thromboembolism. The blood that collects in the atria is agitated by fibrillation, and normal clotting is accelerated. Small thrombi, called mural thrombi, begin to form along the walls of the atria. These clots may dislodge, resulting in pulmonary embolism or stroke.
What is meant by symptomatic bradycardia? What signs and symptoms would you see?
Many patients continue to maintain adequate cardiac output, despite a lowered heart rate. Symptomatic bradycardia results in deceased cardiac output. Symptoms include decreased level of consciousness, hypotension, chest pain, shortness of breath, pulmonary congestion, and syncope.
What drugs cause bradycardia?
Drugs with negative chronotropic actions decrease the heart rate. These include digoxin, beta blockers, and calcium channel blockers.
Why might prolonged tachycardia result in heart failure?
The faster the heart rate, the less time there is for ventricular filling, resulting in a decreased cardiac output.
Why are multifocal PVCs considered more dangerous than unifocal PVCs?
Multifocal PVCs are a sign of multiple areas of irritability and present a greater chance for lethal dysrhythmia than unifocal PVCs.
The nurse is talking with the patient. Suddenly, the nurse looks up at the monitor and sees a ventricular fibrillation pattern. What should he or she do?
If the nurse is talking with the patient, the rhythm on the monitor is not likely ventricular fibrillation. The nurse should immediately assess the patient and check the patient’s leads to see if one has fallen off. A disconnected lead can sometimes mimic fibrillation.
Why is the demand mode of pacing preferred?
Pacemakers can be operated in a demand mode or asynchronous mode. The demand mode paces the heart based on need. The asynchronous mode may compete with the patient’s own rhythm and deliver an impulse on the T wave (R on T), with the potential for producing ventricular tachycardia or ¬fibrillation. The demand mode is safer and is the mode of choice.
What is the benefit of a dual-chamber pacemaker?
Dual-chamber pacing allows for stimulation of both atria and ventricle as needed to produce a near-normal cardiac contraction.
AV-JUNCTIONAL RHYTHMS
- Dysrhythmias from the AV junction
- Junctional escape rhythm
- Premature junctional contractions
- Accelerated junctional rhythms
- Junctional tachycardia
- Paroxysmal supraventricular tachycardia
- P-wave changes
- Shorter PR intervals
- No P wave
- Retrograde P waves
JUNCTIONAL ESCAPE RHYTHM
- Regular rhythm
- PR interval low end of normal
- P-wave changes
- Rate usually 40 to 60 beats/min
- Possible decreased cardiac output
ACCELERATED JUNCTIONAL RHYTHM
AND
JUNCTIONAL TACHYCARDIA
- Rhythm initiated from the AV junction
- Rate is 60 to 100 beats/min for accelerated junctional tachycardia
- Rate is greater than 100 beats/min for junctional tachycardia
PREMATURE JUNCTIONAL CONTRACTIONS
- Early beats initiated by AV junction
- P-wave changes
- PR interval is shorter than normal
- Usually a noncompensatory pause
VENTRICULAR DYSRHYTHMIAS
- Impulses initiated from lower portion of the heart
- Depolarization occurs, leading to abnormally wide QRS complex
- Ectopic and escape beats
- Common causes
- Myocardial ischemia, injury, and infarction
- Low potassium or magnesium
- Hypoxia
- Acid-base imbalances
Common causes VENTRICULAR DYSRHYTHMIAS
- Myocardial ischemia, injury, and infarction
- Low potassium or magnesium
- Hypoxia
- Acid-base imbalances
When two PVCs occur in a row, this is termed: A. Bigeminy B. Couplet C. Multifocal D. Ventricular tachycardia
B. Couplet
when a PVC follows every atrial beat, it is called?
bigeminy
when a PVC occurs every 3rd beat, it is called?
trigeminy
PREMATURE VENTRICULAR CONTRACTIONS
- Wide and bizarre beats
- Compensatory pause
- Patterns
- Bigeminy and trigeminy
- Couplets and triplets
- Unifocal vs. multifocal
- QRS complex greater than 0.10 seconds
- Irregular rhythm
- Compensatory pause
- Absent P waves
PREMATURE VENTRICULAR CONTRACTIONS
- Assess and treat cause
- Hypoxia
- Ischemia
- Electrolyte imbalance
- May need antidysrhythmic agents
WHEN ARE PVCS DANGEROUS?
- Frequent
- Multifocal
- Two or more in a row
- R on T
- PVC falls into the vulnerable period of the T wave
- Ventricular tachycardia or fibrillation can result
VENTRICULAR TACHYCARDIA
- Rapid, life-threatening dysrhythmia
- Three or more PVCs in a row
- Fast rate (>100 beats/min)
- Initiated by ventricles
VENTRICULAR TACHYCARDIA
- Wide QRS complex; greater than 0.10 seconds
- Usually regular
- May or may not have pulse
- Treat pulseless same as ventricular fibrillation
- Significant loss of cardiac output
- Hypotension
VENTRICULAR FIBRILLATION
- Chaotic pattern
- No discernible P, Q, R, S, or T waves
- Coarse versus fine
- No cardiac output; life-threatening
- Emergent defibrillation
Do not give lidocaine! for which EKG?
IDIOVENTRICULAR RHYTHM
IDIOVENTRICULAR RHYTHM
- Escape ventricular rhythm from Purkinje fibers
- Rate 15 to 40 beats/min
- Regular rhythm
- Wide QRS interval
- No P waves
- Do not give lidocaine!
ACCELERATED IDIOVENTRICULAR RHYTHM
- Same as idioventricular rhythm
- Rate more than 40 beats/min
- Hemodynamic effects correspond to heart rate
ASYSTOLE
- NoP,Q,R,S, or T waveforms
- Assess in two leads
- Why?
- No cardiac output
- Death
PULSELESS ELECTRICAL ACTIVITY
- How can it be assessed?
- What are its causes?
- Must treat the cause
- How can it be assessed?
- What are its causes?
Hypovolemia and Hypoxia - Must treat the cause
PULSELESS ELECTRICAL ACTIVITY (PEA) Causes
- Hypoxia
- Hypovolemia
- Hypothermia
- H+ ions (acidosis)
- Hypokalemia or hyperkalemia
- Tablets (overdose)
- Tamponade (cardiac)
- Tension pneumothorax
- Thrombosis (coronary)
- Thrombosis (pulmonary)
ATRIOVENTRICULAR BLOCKS
- Block of conduction from atria to ventricles
- Coronary artery disease
- Myocardial infarction (e.g., inferior wall)
- Infections
- Enhanced vagal tone
- Drug effects (e.g., digoxin toxicity)
ATRIOVENTRICULAR BLOCKS
Always assess for decreased cardiac output and treat cause
Four types
1) First-degree block
2) Second-degree block, Mobitz type I Wenckebach
3) Second-degree block, Mobitz type II
4) Third-degree block (complete)
FIRST-DEGREE BLOCK
- Delayed conduction from SA node to AV node
- Prolonged PR interval
- Greater than 0.20 seconds
- Same PR interval for each beat
SECOND-DEGREE BLOCK: MOBITZ TYPE I
- Steadily lengthening PR interval
- Nonconducted P waves
- PP interval regular
- RR interval irregular
- QRS normal
- Self-limiting; rarely progresses
- May decrease cardiac output
SECOND-DEGREE BLOCK: MOBITZ TYPE II
- More severe AV block
- Often associated with bundle branch block
- PR interval is fixed
- PP interval is regular
- Occasional P wave not followed by QRS
- What is the danger of this block?
THIRD-DEGREE BLOCK (COMPLETE)
- Atria and ventricles beat independently of each other
- P waves not associated with QRS complex
- PP intervals regular
- RR intervals regular
THIRD-DEGREE BLOCK
- Complete heart block
- Junctional or ventricular escape rhythms
- May need pacemaker
- Hemodynamic status based on ventricular rate
ELECTRICAL PACEMAKERS (CONT.)
- Method of pacing
- Can pace:
- Method of pacing
- Transcutaneous: emergency
- Transvenous
- Epicardial
- Can pace:
- Atrium
- Ventricle
- Both chambers
ELECTRICAL PACEMAKERS Complications
- Failure to pace
- Failure to capture
- Failure to sense
