Cardiology #4 Conduction Disorders Flashcards
In an EKG, what are the following parts related to?
-P wave
-PR segment
-QRS complex
-T wave
P wave: atrium contraction
PR segment: AV node
QRS complex: Ventricular contraction
T wave: Ventricular repolarization
How do you calculate the rate of an EKG strip?
Count the large boxes in an R - R segment
300 / 1, 2, 3, 4, 5
=300, 150, 100, 75, 60
Explain the process of conduction and relate it to the parts of an EKG
-Sinus node sends impulse through RA to AV node (atrial contraction). PR segment (nothing happens) when it goes through AV node. Then, rapid condition through Bundle of His –> contraction of ventricle (QRS complex)
Normal sinus rhythm has a rate of ________
60-100 bpm
Sinus bradycardia, which is decreased HR with a rate of __________, has causes such as what?
HR < 60 bpm from sinus node
Causes: young athletes, BB, CCB, SA node ischemia, hypothyroid
Treatment for sinus bradycardia
-Symptomatic: Atropine (1st line)
–Epinephrine or Transcutaneous pacing
-Asymptomatic
–No treatment needed
Sinus tachycardia is HR > 100 bpm from the sinus node. What are some causes? What is the treatment?
-Exercise, stress, kids/infants, fever, pain, hypoxia, shock, cocaine
Treat underlying cause (1st line), BB if needed
What is sinus arrhythmia?
No treatment is needed in most cases.
Norma variation of sinus rhythm. Beat to beat variation with respiration. Increase in rhythm with inspiration, decrease in rhythm with expiration.
Sick sinus syndrome is dysfunction of the sinus node leading to what rhythm?
Combination of sinus arrest with alternating periods of tachycardia and bradycardia.
What is the MCC of sick sinus syndrome?
Sinus node fibrosis
Others: old age
Treatment for sick sinus syndrome
-Atropine (first line)
-Long term: Permanent pacemaker (definitive), AICD if alternating
What happens in a junctional rhythm?
What is seen on an EKG with this type of rhythm?
AV node becomes the dominant pacemaker
Inverted P waves or not seen at all. Narrow QRS
What segment of an EKG strip is the most useful in determining an AV Block?
PRI interval
What does the ECG with a First Degree AV block look like?
Treatment?
Prolonged PR interval, but all P waves are followed by a QRS complex
-Asymptomatic: observation
-Atropine (1st line)
-Pacemaker (definitive)
What is the pathophysiology of a 2nd degree AV block? What is the first type of second degree AV Block, what is seen on an ECG, and what is the treatment?
Not all atrial impulses are conducted to the ventricles, leading to P waves without QRS complexes
-Mobitz 1: Wenkebach
-ECG: P waves are constant, Progressive PRI lengthening –> dropped QRS
Atropine, Epi, Pacemaker
What is the other type of 2nd degree AV block, what is seen on an ECG, and what is the treatment?
Mobitz II
P waves constant, constant/prolonged PRI –> dropped QRS
Atropine or temporary pacing, pacemaker definitive
Both 2nd degree AV blocks occur where in the heart?
Bundle of His
Mobitz I causes
Mobitz II causes
1 (Wenkebach): inferior wall MI, BB/CCB/Digoxin, Myocarditis
2: Rarely in patients without structured heart disease (myocarditis, endocarditis, myocardial fibrosis)
A third degree AV block is due to AV dissociation. No atrial impulses are reaching the ventricles. Causes of this are similar to 2nd degree AV block because it can progress to a 3rd degree. Name them.
Inferior Wall MI
AV nodal blocking agents (BB, CCB, Digoxin)
Lyme, Endocarditis, Myocarditis
Hypothyroidism, Hyperkalemia
What does the ECG for a 3rd degree AV block look like?
Regular R-R and P-P intervals, but not related to each other
-P’s and Q’s don’t agree, then you have a third degree
Treatment for a 3rd degree AV block
-Transcutaneous pacing followed by permanent pacemaker (definitive)
What does an ECG look like in Paroxysmal Supraventricular Tachycardia (PSVT?)
Regular, narrow QRS complex
Tachycardia (no discernible P waves)
HR > 100 bpm
If you can’t tell if it’s a P or a T, it must be SVT
The treatment for PSVT differs based on the width of the QRS complex. What are the treatments for the following:
Stable (narrow complex)
Stable (wide complex)
Unstable
Definitive
Narrow: vagal maneuvers (Valsalva, carotid massage, Adenosine)
Wide: Amiodarone
Unstable: Synchronized (DC) Cardioversion
Definitive: Radiofrequency catheter ablation
Wolff-Parkinson White (WPW) is a form of PSVT. Explain the pathophysiology of this condition.
What are the three components of this on an ECG?
-Accessory pathway (Bundle of Kent) outside the AV node pre-excites the ventricles, bypassing the AV node, leading to a delta wave.
Wave = Delta Wave
P = PR Interval is short
W = Wide QRS Complexes
Management for WPW
-Stable: Procainamide (1st line), Amiodarone
-Unstable: DC Cardioversion
-Definitive: Radiofrequency catheter ablation (Destroys the normal pathway)
Treatment is the Same as PSVT
What medications should be avoided in PSVT and WPW?
AV node blockers (ABCD)
-Adenosine, BB, CCB, Digoxin
With atrial flutter, what are you at increased risk for?
Arterial thrombus formation that leads to stroke (like A-fib)
Symptoms of atrial flutter
-Palpitations, fatigue, dyspnea, refractory chest pain, hypotension, AMS
What does an ECG show for atrial flutter?
Flutter (sawtooth) atrial waves usually around 300 bpm but no clear P waves
Treatment for atrial flutter
-Stable: Vagal maneuvers, BB or CCB (Diltiazem, Verapamil)
-Unstable: DC Cardioversion
Radiofrequency catheter ablation is definitive
Etiologies of Atrial fibrillation
-Infection, cardiomyopathies, age, thyroid disorders genetics, drugs, alcohol (use and withdrawal), men, whites
What is seen on an ECG for A-fib?
-Irregularly irregular rhythm with fibrillatory waves
What is Ashman’s Phenomenon in regards to A-fib?
Wide QRS after short R-R cycles
Treatment for stable A-fib
-BB or CCB (Diltiazem or Verapamil)
-Digoxin if heart failure
If unstable, what is the treatment for A-fib
DC Cardioversion
Long term treatment for A-fib
-rate control (BB or CCB)
-DC Cardioversion
-RF catheter ablation
-Anticoagulation
Describe the timing rule for cardioversion and anticoagulation
How long should anticoagulation be continued afterwards?
-AF > 48 hours: anticoagulation for 3 weeks before cardioversion
-AF < 48 hours: anticoagulation prior
Continue anticoagulation for 4 weeks after cardioversion
Explain the scoring with the CHA2DS2-VASc Score
What score gives you chronic oral anticoagulation (Warfarin or Novel anticoagulation)?
Congenital Heart Failure = 1
Hypertension = 1
Age > 75 = 2
Diabetes = 1
Stroke, TIA = 2
Vascular Disease (PAD, MI) = 1
Age 65-74 = 1
Sex (female) = 1
2 or more is the cutoff
Explain non-vitamin K antagonistic oral anticoagulants (NOAC)
-Lower risks of ….
-Don’t need to…
-There are two kinds. Name them and explain what they do
-Lower risk of bleeding and stroke
-Don’t need to check INR, less drug interactions
-Dabigatran: binds and inhibits thrombin
-Rivaroxaban, Apixaban, Edoxaban: factor Xa inhibitors
Regarding Warfarin, when is it preferred and what is the INR goal with this medication?
Preferred if HIV+, CKD or anti-epileptic medications (Phenytoin, Carbamezapine)
Bridge with Heparin until therapeutic
INR goal of 2-3
Also monitor PT
Is Dual-antiplatelet therapy (Aspirin + Clopidogrel) less or more effective than anticoagulant mono therapy?
Less effective
Explain what a PVC is, what is seen on ECG, and what the treatment is?
Premature Ventricular Complexes (PVC)
Premature beat originating from ventricle
Wide, bizarre QRS complexes occurring earlier. T wave in opposite direction of QRS
No treatment needed
What is ventricular tachycardia?
What are some etiologies?
3 or more PVC’s at > 100 bpm
Ischemic heart disease (MC) - Post MI
Prolonged QT
Digoxin Toxicity
Hypomagnesemia, Hypokalemia
Treatment for V-tach
Stable/Sustained (>30 seconds): Amiodarone
Unstable with Pulse: DC Cardioversion
No Pulse = Defibrillation + CPR
Explain what Torsades de Pointes looks like on an ECG and name some etiologies
-Alterations of QRS amplitude around the isoelectric line (twisting)
Prolonged QT (antipsychotic use!!), hypomagnesemia, hypokalemia, macrolides, Digoxin, Procainamide
Treatment for Torsades de Pointes
-IV Mag Sulfate
What does a patient look like with ventricular fibrillation?
Unresponsive, pulselessness, syncope
Treatment for ventricular fibrillation?
What is the MCC?
Defibrillation + CPR
Ischemic heart disease (Post MI)
What are the components of a RBBB on an ECG?
-QRS > 120ms
-RsR1 (bunny ears) in V1-V3
-Slurred S waves in I, avL, V5, V6
What are the components of a LBBB on an ECG?
-QRS > 120ms (wider)
-Broad, notched M-shaped R in V6
-Dominant S wave in V1
Adenosine
MOA:
Use:
Adverse Effects:
-Slows AV node conduction time and blocks AV nodal reentry pathways
-Used in PSVT and pharmacological stress testing
–vasodilation of coronary arteries mimics increased demand
-Adverse Effects: CP, dyspnea, flushing, bronchospasm, hypertension, MI
Atropine
MOA:
Use:
Adverse Effects:
-Parasympathetic acetylcholine inhibition –> increased cardiac output
-Used in bradycardia
-Adverse Effects: Xerostomia, blurry vision, flushing
Amiodarone
MOA:
Use:
Adverse Effects:
-Class III antiarryhthmics (K+ channel blocker) that prolongs the action potential
-Used for stable, wide complex tachycardia
-Adverse Effects: Hypotension, LFT’s increased, thyroid disorders, corneal deposition > 6 months
What is Brugada syndrome?
What is seen on the EKG for this condition?
Abnormal myocardial depolarization that predisposes young, otherwise healthy people to V-fib and sudden cardiac death.
ST segment elevated and T wave inversion in V1-V3
