Conduction system disorders Flashcards
symptoms of conduction system disorders
-Palpitations
-“Extra beat”
-“Fluttering”
-“Heart beating out of chest”
-Shortness of breath
-Chest pain
-Diaphoresis
-Dizziness(room spinning- rule out vertigo)/lightheadedness(sit to stand)
-Syncope
-Cough
-Fatigue
-Weakness
dx of conduction system
-12 lead Electrocardiogram (EKG)
-Holter monitor- 24hrs – 30 days
-Implantable Loop Recorder (ILR)- Useful for cryptogenic CVA
-ILR- left of sternum -> records for 3 years
implanted loop recorder
-3 year monitor
-Triggered symptom events recorded
-Spontaneous recording of:
-Tachycardia
-Bradycardia
-Pauses
-Irregular rhythms
-Blue tooth home monitor transmissions
-MRI Compatible
-also records when pt hits the activator
-if cryptogenic stroke (recently) pts will get loop recorder to check for afib -> left atrium clot
paroxysmal supraventricular tachycardia
-rate 150-250 bpm/min
-MC paroxysmal tachycardia
-Includes:
-Irritate focus above or at the AV junction
-Most commonly AV node re-entry***-P-wave hidden in T-wave
-Narrow QRS complex
-Others:
-Atrial Tachycardia
-Multifocal Atrial Tachycardia
-Junctional Tachycardia- rapid firing from AV
causes of PSVT
-Excessive caffeine
-Alcohol consumption
-Ischemic heart disease
-Post myocardial infarction (MI)
-Structural heart disease
-Myocarditis/pericarditis
-Pulmonary embolism- right heart typically affected
-Chronic lung disease
-Medications -Amphetamines
-Idiopathic
SVT tx and prevention
-Acute phase
-Hemodynamically unstable vs. stable
-Vagal maneuvers:
-Bearing down, cough, holding breath
-*Carotid massage not recommended
-Narrow complex: Adenosine -6mg IV then 12 mg IV push (makes it go in quicker) -> makes AV node arrest
-if you did adenosine with afib it wouldnt do anything -> not coming from AV node
-Wide complex: Amiodarone (prof doesnt recommend)
-Unstable: synchronized cardioversion- reset heart
-Prevention
-Beta-blockers: atenolol, metoprolol, carvedilol
-Calcium cannel blockers: diltiazem, verapamil
-Definitive treatment: radiofrequency ablation
SVT medications: adenosine
-causes vasodilation
-Transient heart block at the AV node
-Half life is less than 10 seconds
-Most common:
-Chest pain
-SOB
-Facial flushing
-Lightheadedness
-Metallic taste*
-“Impending doom”*
-Contraindications:
-Asthma
-Long QT syndrome
-2nd/3rd degree heart blocks
SVT medications: amiodarone- class 3 antiarryhthmic
-“<65 yo, ablation not this, this is a very toxic drug”
-Half life is 58 hours
-Common side effects:
-Nausea
-Fatigue
-Tremors
-Adverse effects:
-Hepatotoxicity- every 6 months bw
-Pulmonary fibrosis!!- worst- PFTs 1x year
-Optic neuritis*
-Thyroid dysfunction- MC - every 6 months bw
-Skin Discoloration- blue skin in sun
-Contraindications:
-2nd/3rd degree heart block
-Prolonged QT
-Pregnancy
-Sinus node dysfunction
atrial fibrillation
-rate 350 – 450 bpm
-Multiple foci in the atria rapidly firing - Irregularly irregular rhythm
-NO P-wave present
-Irregular QRS intervals
-Length:
-1) Paroxysmal- Less than 7 days
-2) Persistent- Longer than 7 days
-3) Chronic- Arrhythmias presents for at least 1 year without resolution
-Commonly caused by excessive alcohol or withdrawal
-“Holiday heart” syndrome - excessive alcohol or withdrawal
3 questions when looking at afib
-hows the rate
-hows the rhythm
-protect from stroke
rate of afib
-Rate:
-Based on ventricular rate
-Rate ≥ 100 - Rapid ventricular response
-Rate 60-100- Moderate -> ventricular response
-Rate < 60- Slow ventricular response
causes of atrial fibrillation
-Ischemic heart disease
-Structural heart disease -Most commonly mitral stenosis
-Cardiomyopathy- Dilated and hypertrophic
-Pulmonary embolism
-Hyperthyroidism
-Sepsis
-Anemia
-Pheochromocytoma
-Post-operative stress
-Alcohol consumption
-Electrolyte disturbance
afib treatment
-Acute phase- Less than 48 hours from onset -> Synchronized cardioversion
-Greater than 48 hours:
-Anticoagulation + rate control 3 weeks then cardioversion -> Increased risk of thromboembolic events*
-clot breaks down in 3 weeks
-Rate control:
-Beta-blockers
-Calcium channel blockers
-Digoxin
-Rhythm control- Antiarrhythmic medications
-TEE – visualize left atrial appendage*- look for clots
-this is for pts you have high concern of clots or if you dont want to wait 3 weeks
-Anticoagulation and rate/rhythm control
-Who do we anticoagulant? -> CHADS2 score vs. CHADSVASC score
-Ablation therapy
CHA2DS2VASc score
-CHF - 1 point
-hypertension- 1 point
-age- 65-74 - 1 point, >75 2 points
-diabetes- 1 point
-CVA or TIA- 2 points
-vascular disease (h/o MI, PAD, or aortic atherosclerosis- 1 point
-sex- female- 1 point (only if they have a diff point elsewhere)
-0 points- none or ASA
-1 point- ASA or full anticoagulation
-2 or greater- full anticoagulation
atrial fibrillation: anticoagulation- warfarin
-Warfarin- (Coumadin)
-Blocks vitamin K production in the liver-> Factors II, VII, IX, and X, Protein C and Protein S
-Metabolized by Cytochrome P450
-Monitor INR- Standard goal 2-3 and Mechanical valves 2.5 – 3.5 -> if even goes .1 under -> start over therapy
-Can be reversed with Vitamin K or fresh frozen plasma**
-Affecting factors
-Decreasing INR:
-Leafy green vegetables: spinach, broccoli, brussels sprouts
-Phenytoin, phenobarbitol
-St. Jonhs wart- OTC
-Increasing INR:
-Alcohol
-Antibiotics: quinolones, amoxicillin, metronidazole
-Steroids
-Amiodarone
-if INR Is too high -> risk bleeding event
antiarrhythmics- class 1
-sodium channel blockers
-depolarization
antiarrhythmics- class 2
beta blockers
antiarrhythmics- class 3
-K channel blockers
-amiodarone
-sotalol
-repolarization
-messes with QT interval
-high risk
antiarrhythmics- class 4
-Ca channel blocker
-plateu phase
afib- anticoagulation- direct oral anticoagulants (DOAC)
-for pts with non-valvular afib -> what is valvular afib -> mitral stenosis and mechanical heart valves
-types:
-Dabigatran (Pradaxa)- Direct thrombin inhibitor
-Rivaroxaban (Xarelto)- Factor Xa inhibitor
-Apixaban (Eliquis)- Factor Xa inhibitor
-No monitoring of INR
-Reversal agents (dont need to know):
-Pradaxa = idarucizumab (Praxbind)
-Xarelto/Eliquis = andexanet alpha (Andexxa)
-All metabolized through the kidneys- Warning in renal impairment patients
HASBLED score- bleed risk
-Hypertension (uncontrolled)- 1 point
-Abnormal liver or renal function (Cr > 2.26) (bili x2 or AST/ALT/AkP x3)- 1 or 2 points
-Stroke- 1 point
-Bleeding (major bleeding event)(labile INR)- 1 point
-Elderly (>65)- 1 point
-Drugs or alcohol (drugs causing bleeding) (>8 drinks a wk)- 1 or 2 points
atrial flutter
-rate 250 – 350 bpm (rate of atrium not HR)
-Rapid firing of atrial focus
-Reentry circuit in the atrium
-*Produces a “saw-tooth” pattern
-Classified as atrial to ventricular conduction ratio
-can be lifetime -> recircuit
-around the valves
-Causes:
-COPD*
-Cardiomyopathy
-Structural heart disease -Atrial septal defect
-Myocarditis
-Hyperthyroidism
-Idiopathic
-these things just exacerbate the deformity thats already there
-Treatment:
-Anticoagulation
-Treatment for atrial fibrillation
-More successful with ablation therapy
-ablation is tx for life
ventricular tachycardia
-Rapid ventricular focus
-3 of more premature ventricular contractions in a row
-Unifocal (monomorphic)
-Multifocal (polymorphic)
-Nonsustained vs. sustained
-NSVT: < 30 seconds
-Sustained VT: > 30 seconds -> Even if spontaneous resolution
-sustained- deliberator
ventricular tachycardia causes
-Coronary artery disease- MC in patient after MI
-Cardiomyopathy
-Congenital defects
-Prolonged QT syndrome- can be candidate for defibrillator- sudden death
-Illicit drug use
-Medications
watchman procedure
(nonvalvular) NVAF with atrial fibrillation
-reduce stroke risk that originate in LAA
-seals the pocket in the LA
-high CHAD and bleeding risk -> consider this
ventricular tachycardia tx
-pulseless tx- ACLS
-stable sustained- synchronized cardioversion + antiarrhythmic
-unstable sustained- synchronized cardioversion
-nonsustained-beta blocker therapy
-treating underlying cause:
-myocardial ischemia- catheter
-cardiomyopathy- echo
-electrolytes
-medication
ventricular tachycardia treating the underlying cause
-Myocardial ischemia- Cardiac catheterization
-Cardiomyopathy:
-Echocardiogram to assess ejection fraction and walls
-Medical management of cardiomyopathy
-Electrolyte abnormalities (find the cause: diuretics, dialysis):
Potassium
Magnesium
Calcium
-Medications: Sotalol, Amiodarone, Mexiletine
torsades de pointes
-form of polymorphic ventricular tachycardia
-“Twisting of the points”
-QRS complex twists around axis
-Warning sign of ventricular fibrillation - prolonged QT
-Treatment:
-First line: magnesium 1g IV push*
-Defibrillation
-can sometimes pop out on its own but not typical and you should be ready
ventricular fibrillation
-ventricular rate of 300 - 400bpm
-Rapid firing of multiple foci leading to no uniform ventricular contraction
-No cardiac output
-No blood pressure
-Irregular and shapeless QRS pattern on EKG
-Most commonly caused by ischemic heart disease*
ventricular fibrillation causes
-Ischemic heart disease*
-Antiarrhythmics-Prolongation of the QT interval
-Atrial fibrillation with rapid ventricular response
-Drug toxicity
-Sepsis
-Hemorrhagic shock
-Electrolyte abnormalities
ventricular fibrillation treatment
-Definitive treatment: defibrillation
-CPR
-Follow ACLS protocol- Defibrillation -> Epinephrine -> Defibrillation -> Epinephrine*
-Amiodarone IV - 24 to 48 hours following conversion
-Treat the underlying cause- Requires an ischemic evaluation
-Prevention- AICD placement
cardiac arrest
-sudden cessation of blood flow due to failure of the heart
-Inability of contractility
-Death within minutes
-MC cause is coronary artery disease
-MC rhythm is ventricular fibrillation
causes of cardiac arrest
-Coronary artery disease**- ischemic
-Heart failure
-Genetics: pro-longed QT syndrome, -Brugada syndrome, Hypertrophic cardiomyopathy (thick septum obstructs- congenital)
-Low magnesium, potassium
-Anemia, hemorrhage
-Trauma
brugada syndrome
-Genetic inheritance- Autosomal dominant disorder
-Mutation of the sodium ion channels in the cardiac muscle- >60 mutations
-Characterized by ST elevations with negative T wave in precordial leads V1-V3 appearance without structural cardiac abnormalities
-Increased risk for sudden death for ventricular fibrillation
-Onset occurs during adulthood
-Definitive treatment: ICD placement
defibrillator
-leads go into the subclavian vein
-snake into right ventricle
-dual chamber- RA lead
-if they have left? bundle branch block they can snake it through coronary sinus (biventricular device)
sick sinus syndrome
-chronic dysfunction of the sinoatrial (SA) node
-Encompasses alternating dysrhythmias including:
-Sinus bradycardia
-Sinus tachycardia
-Sinus pauses
-Sinus arrest
-MC in the elderly*
-MC asymptomatic*
causes of sick sinus syndrome
-Myocardial scarring
-Medications:
-Beta-blockers, CCB
-Antiarrhythmics
-Digitalis
-Lithium
-Methyldopa
-Genetic: Familial sick sinus syndrome
-Sarcoidosis, amloydosis
-lyme disease
sick sinus syndrome treatment
-Discontinuation of medication
-Definitive treatment: permanent pacemaker placement*
bundle branch blocks
-Blocked conduction of the right or left bundle branch leading to delay in activation of correlating ventricle
-Ventricular conduction is not in sync
-1) Right bundle branch block - Left conduction -> right conduction
-2) Left bundle branch block- Right conduction -> left conduction
-right-left contraction
-if pt also has left ventricle HF the left is weak and has to contract against the already contracted right ventricle
-Measured by QRS complex:
-> 0.12 seconds -> >3 small boxes
-“Rabbit ears”- Overlapping of QRS complex
right bundle branch block (RBBB)
-leads V1 and V2
-RsR complex
-T-wave inversions
-Causes:
-Idiopathic
-Increased right ventricular pressures:
-Cor pulmonale
-PE
-Myocardial ischemia
-Treatment- Rule out underlying cause
left bundle branch block (LBBB)
-Leads V5 and V6
-Broadened R wave
-T-wave inversions
-Widened QRS in V1 and V2
-Causes:
-Myocardial fibrosing:
-HTN
-Myocardial ischemia- LAD
-Cardiomyopathies
-Treatment- Rule out underlying disease
atrioventricular (AV) block
-Intermittent or complete failure of the conduction system between the atria and ventricles
-3 classifications of heart block
-First degree AV block
-Second degree AV block:
-1) Mobitz I (Wenckebach)
-2) Mobitz II
-Third degree AV block aka complete heart block
AV block causes
-Aging
-Coronary artery disease- MI
-Rheumatic heart disease
-Lyme disease
-Sarcoidosis
-Hematomachrosis
-Hyperthyroidism
-Congenital
-Hyperkalemia
AV block treatment
-First degree: no treatment required
-Second degree:
-Type I: No treatment required unless symptomatic
-Type II: more likely to progress to third degree -> Requires permanent pacemaker
-Third degree: Requires permanent pacemaker (PPM)
first degree heart block
-not a true block -> conduction delay
-delay in the AV node
-fix prolonged PR interval > .2 s and > 5 small boxes
second degree type 1
-Intermittent block within the AV node
-Progressive lengthening of PR interval with eventual non-conducting P wave*
-Caused by conduction arriving at time when AV node is absolutely refectory
second degree type 2
-Intermittent block within the His-Purkinje system
-Fixed PR interval with eventual non-conducting P-wave*
-Wide QRS complex
-Can progress to complete heart block
third degree heart block
-complete
-dissociation of electrical activity between the atria and ventricles
