Conduction Disorders (Cardio 1) Flashcards
What characteristics must a rhythm have to be considered a SINUS rhythm?
- regular, upright P waves
- normal PR interval (.12-.20)
- regular QRS with normal width (.08-.12)
- P:QRS relationship is 1:1
Normal Sinus Rhythm Characteristics
- rate is 60-100
- regular, upright P waves
- normal PR interval
- regular QRS with normal width
- P:QRS is 1:1
Sinus Bradycardia Characteristics
- rate < 60
- normal sinus P’s
- normal PR interval
- 1:1 AV conduction
Causes of Sinus Bradycardia
- physiologic: well-conditioned athlete, sleep, vagal stimulation
- pharmacologic: digoxin, beta blockers, calcium channel blockers
- pathologic: inferior MI, increased intracranial pressure, hypothyroidism
Clinical Significance of Sinus Bradycardia
-depends on cause
Sinus Tachycardia Characteristics
- acceleration of sinus rate (100-160)
- normal sinus P’s
- normal PR interval
- 1:1 AV conduction
Causes of Sinus Tachycardia
- physiologic: infants/kids, exertion, anxiety
- pharm: atropine, epinephrine, nicotine, caffeine, cocaine
- pathologic: fever, hypoxia, anemia, pulmonary embolus
Tx of Sinus Tachycardia
- usually none, but need to investigate underlying cause
- in setting of acute MI, consider beta blockers
Sinus Arrhythmia Characteristics
- variation in sinus node discharge rate (irregular)
- normal P waves
- normal PR interval
- 1:1 AV conduction
Sinus Arrhythmia Causes
- most common in kids, young adults
- usually results from change in vagal tone during respiration (rate does not speed up w/ inspiration, it SLOWS with expiration)
Clinical Significance of Sinus Arrhythmias
- benign
- usually asymptomatic
Tx of Sinus Arrhythmias
none
For irregular rates, how are these estimated and reported?
- take an average of the rate for the shortest QRS interval and longest interval
- for irregular rates, must put about 80 or 80I
How do you determine regular vs. irregular on a rhythm strip?
-look at the QRS spacing
Atrial Flutter Characteristics
- regular atrial rate 250-350 bpm (300 most common; get this by looking @ the P waves)
- sawtooth flutter waves
- AV block, usually P: QRS of 2:1 (ventricular rate 150)
Where in the heart is the problem spot in atrial flutter?
above the AV node b/c things are normal on the rhythm strip once it hits AV (QRS is normal)
Causes of Atrial Flutter
- 60% due to underlying heart dz (ischemic heart dz, acute MI, HTN)
- 30% no cause
- also seen with pulmonary embolus, digoxin toxicity
- may be transitional arrhythmia between sinus rhythm and atrial fibrillation
Symptoms of Atrial Flutter
- palpitations (heart jumping or feeling funny)
- fatigue
- dyspnea
Tx of Atrial Flutter
- carotid sinus massage may transiently slow conduction rate to make atrial flutter and make sawtooth more evident
- low energy electrical cardioversion >90% success
- may control ventricular rate with digoxin, calcium channel blockers, beta blockers
- chemical conversion using type Ia, Ic, III
What is actually happening in the heart during atrial flutter?
- atria depolarize/contract and dump blood to ventricles, depolarize and dump, depolarize and dump
- ventricles now have more blood in them than they should
- blood not getting to lungs = SOB
- then ventricles contract
Atrial Fibrillation Characteristics
- no organized P waves, only shimmering baseline
- irregular ventricular rhythm (usually rapid 160-180)
- normal QRS width
Causes of Atrial Fibrillation
- most common: rheumatic heart dz, HTN, ischemic heart dz, thyrotoxicosis
- other: COPD, pulmonary embolus, pericarditis, ETOH
Clinical Significance of Atrial Fibrillation
- multiple areas of atria continuously depolarizing
- no uniform atrial depolarization (bag of worms, quivering)
- atrial depolarization rate >400, but refractory period of AV node means a slower ventricular response
- loss of atrial contraction can lead to heart failure in patients with underlying left ventricular dysfunction
- rapid ventricular response may lead to myocardial ischemia, hypotension, shock
- increased risk of stroke
Tx of Unstable A Fib Patient
-immediate electrical cardioversion (if hypotension, shock, pulmonary edema)
Tx of Stable A Fib Patient
- control ventricular rate with IV or oral calcium channel blockers or beta blocker
- chemical cardioversion Ia, Ic, III
- can consider electric cardioversion of stable pt prior to 7 days but do not cardiovert if a fib. present >48 hours (higher risk of systemic emboli; must anticoagulate coumadin at least 3 weeks prior to cardioversion)
Chemical Cardioversion Agents
- Ia: procainamide, qunidine
- Ic: flecanide, propafenone
- III: ibutilide, amiodarone
Supraventricular (Atrial) Tachycardia Characteristics
- regular, rapid atrial rhythm (160-200)
- P waves often difficult to see (might be buried in T waves)
- QRS complexes usually normal width
Causes of Supraventricular Tachycardia
- fairly common (2/1000)
- can occur in otherwise normal heart
- no age or sex predisposition
- sometimes seen in association with MI, rheumatic heart dz, pericarditis, mitral valve prolapse
- due to “reentry” of depolarization
Clinical Significance Supraventricular Tachycardia
- abrupt onset of tachycardia caused by reentry of electrical impulse in atria via closed loop of conducting tissue
- usually well-tolerated in young healthy patients; may cause palpitations, lightheadedness, dizziness, SOB
- in elderly patients or those with heart dz: syncope, pulmonary edema, myocardial ischemia
Tx of Supraventricular Tachycardia
very general categories… will ask for detail on other cards
- vagal maneuvers in stable, young patient
- adenosine
- verapamil
- electrical cardioversion if unstable and refractory to above methods
- can usually cure with radiofrequency ablation
Vagal Maneuvers for Supraventricular Tachycardia
- increase vagal tone
- slow conduction and prolong the refractory period in the AV node
- examples: carotid sinus massage, diving reflex, Valsalva maneuver (bearing down like pooping)
Adenosine for Supraventricular Tachycardia
- ultra-short acting AV nodal blocker
- most commonly used SVT med
- will stop the heart at first (5-7 secs)
Verapamil for Supraventricular Tachycardia
- a calcium channel blocker
- longer acting than adenosine
- blocks AVnode
Ventricular Tachycardia Characteristics
- three of more ectopic (aberrant) beats in a row
- wide QRS
- rate > 100 (usually 150-200)
- usually a regular rhythm
- may occur in short episodes or sustained
- in v tach, you usually cannot identify P waves
Causes of Ventricular Tachycardia
- rarely seen in pts w/o underlying heart dz
- usually seen w/ ischemic heart dz or acute MI
- other causes: drugs, metabolic abnormalities, cardiomyopathies
Clinical Significance of Ventricular Tachycardia
PATIENT MAY BE:
- relatively stable (alert, good BP, asymptomatic) but few are like this
- symptomatic (hypotension, chest pain, SOB, syncope)
- pulseless in cardiac arrest
Tx of Ventricular Tachycardia
- if unstable/pulseless: immediate electric biphasic shock (100-200 J)
- if stable, use IV antiarrhythmics: amiodarone, lidocaine, bretylium, procainamide; can try synchronized cardioversion (50-200 J) if needed
What is synchronized cardioversion?
-delivers shock at the peak of the QRS complex
What is really happening in the heart during Ventricular Tachycardia?
- ventricles in charge of rhythm
- atria sort of just depolarizing w/o inducing ventricular depolarization
Ventricular Fibrillation Characteristics
- irregular zigzag pattern with no P waves or QRS
- may be coarse (early) or fine (late) pattern
- looks like squiggles
Ventricular Fibrillation Causes
- usual etiology: severe ischemic heart dz with or w/o acute MI
- other: digoxin toxicity, hypothermia, blunt chest trauma, severe electrolyte imbalance (eg hyperkalemia)
Ventricular Fibrillation Clinical Significance
- totally disorganized, chaotic depolarization of small areas of the ventricle
- no effective ventricular pumping
- pt is pulseless and in cardiac arrest
Ventricular Fibrillation Tx
- immediate electrical defibrillation
- CPR!
- IV amiodarone, lidocaine and/or bretylium with repeated shocks after each dose
AV Block First Degree Characteristics
- delay in AV conduction
- each atrial impulse is conducted to ventricles, but slower than normal
- PR interval > .20 seconds
AV Block First Degree Cause
- sometimes found in normal hearts
- increased vagal tone
- digoxin toxicity
- inferior MI
- myocarditis
AV Block First Degree Clinical Significance
- delay usually at level of AV node
- generally benign
AV Block First Degree Tx
none
Second Degree Block Type 1 Characteristics
- progressively longer PR interval until a dropped beat (blocked, non-conducted P wave)
- cycle usually repeats itself
- conduction ratio describes atrio-ventricular depolarizations
Second Degree Block Type 1 Causes
- acute inferior MI
- digoxin toxicity
- myocarditis
- cardiac surgery
- rheumatic heart dz
- seen in high level athletes (increased parasympathetic tone)
Second Degree Block Type 1 Clinical Significance
- occurs at level of AV node
- thought to be due to progressive prolongation of refractory period of AV node w/ each depolarization until AV node completely blocked; then AV node resets itself
- generally does not progress to complete heart block
Second Degree Block Type 1 Tx
- if pt stable, no tx necessary
- if slow ventricular rate causes hypoperfusion, consider atropine and/or cardiac pacing
Second Degree Block Type 2 Characteristics
- constant PR interval (either normal or long), then a non-conducted P wave (missing QRS)
- QRS may be narrow or wide, depending on whether or not bundle branch block also present
Second Degree Block Type 2 Causes
- acute anteroseptal MI
- cardiomyopathy
Second Degree Block Type 2 Clinical Significance
- block usually occurs in infranodal conducting system
- prognosis worse than 2nd degree type 1
- usually permanent
- in setting of acute MI, may progress to complete heart block
Second Degree Block Type 2 Tx
- if slow perfusion rate produces hypoperfusion, atropine or pacing
- most pts ultimately require pacemaker
Third Degree Block Characteristics
- atrial and ventricular depolarizations are independent of each other
- P waves and QRS complexes have no consistent relationship
- PR interval varies
- QRS may be either narrow or wide
Third Degree Block Causes
- usually acute MI
- drug effect (digoxin, beta blocker)
- may be transient or permanent
Third Degree Block Clinical Signficance
–no atrioventricular conduction
–escape pacemaker kicks in
+if nodal block: pacemaker above His bundle, produces narrow QRS escape rhythm (40-60)
+if infranodal block: pacemaker at or below His bundle, produces wide QRS escape rhythm (<40 bpm, unstable)
Third Degree Block Tx
- atropine and/or pacing
- nodal blocks (narrow complex) more likely to respond to atropine
- infranodal probably won’t respond to atropine and will require pacing
Premature Atrial Contractions (PAC) Characteristics
- ectopic P wave occurs sooner than expected
- ectopic P wave has different shape than other Ps (originates from site other than sinus node)
- ectopic P may or may not be conducted through AV node
Premature Atrial Contractions (PAC) Causes
- common in all ages, often in absence of heart dz
- possible precipitants: stress, alcohol, caffeine, fatigue, tobacco
- frequent PACs may be seen in chronic lung dz, heart dz, digoxin toxicity
Premature Atrial Contractions (PAC) Clinical Significance
- usually benign
- occasionally PACs may trigger other atrial arrhythmias (like atrial flutter/fib)
Premature Atrial Contractions (PAC) Tx
- stop any precipitating drugs
- tx underlying disorder
- PACs that trigger flutter/fib can be suppressed with quinidine, beta blockers
Premature Ventricular Contractions (PVC) Characteristics
- impulses arising prematurely from single or multiple areas in the ventricles
- occurs before next expected sinus beat
- no preceding P wave
- wide and bizarre appearing QRS ( >.12 sec)
- PVCs may be unifocal (same morphology) or multifocal (different morphs)
Premature Ventricular Contractions (PVC) Causes
- very common even in absence of heart dz
- stress, alcohol, caffeine contribute
- frequently occur in ischemic heart dz, acute MI, CHF
- hypokalemia
- hypoxia most common cause
- sympathomimetic drugs
Premature Ventricular Contractions (PVC) Clinical Sig.
- common in AMI due to myocardium being electrically unstable
- may lead to v fib
- in absence of heart dz, PVCs have no prognostic significance
- in pts w/ heart dz and decreased ejection fraction, frequent PVCs are risk for v fib and sudden death (need implantable defibrillator)
Premature Ventricular Contractions (PVC) Tx
- if otherwise healthy: give O2, avoid caffeine/alcohol/etc
- for PVCs with acute MI: treat underlying cause rather than the PVCs
- chronic PVCs: no evidence that anti-arrhythmics enhance survival; consider implantable defibrillator
Asystole Characteristics
- no atrial or ventricular activity
- check lead placement
- check circ, airway, breathing
- CPR!!!
