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Cardiology > Conduction system disorders > Flashcards

Conduction system disorders Flashcards

1
Q

symptoms of conduction system disorders

A

-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

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2
Q

dx of conduction system

A

-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

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3
Q

implanted loop recorder

A

-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

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4
Q

paroxysmal supraventricular tachycardia

A

-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

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5
Q

causes of PSVT

A

-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

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6
Q

SVT tx and prevention

A

-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

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7
Q

SVT medications: adenosine

A

-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

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8
Q

SVT medications: amiodarone- class 3 antiarryhthmic

A

-“<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

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9
Q

atrial fibrillation

A

-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

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10
Q

3 questions when looking at afib

A

-hows the rate
-hows the rhythm
-protect from stroke

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11
Q

rate of afib

A

-Rate:
-Based on ventricular rate
-Rate ≥ 100 - Rapid ventricular response
-Rate 60-100- Moderate -> ventricular response
-Rate < 60- Slow ventricular response

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12
Q

causes of atrial fibrillation

A

-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

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13
Q

afib treatment

A

-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

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14
Q

CHA2DS2VASc score

A

-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

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15
Q

atrial fibrillation: anticoagulation- warfarin

A

-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

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16
Q

antiarrhythmics- class 1

A

-sodium channel blockers
-depolarization

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17
Q

antiarrhythmics- class 2

A

beta blockers

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18
Q

antiarrhythmics- class 3

A

-K channel blockers
-amiodarone
-sotalol
-repolarization
-messes with QT interval
-high risk

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19
Q

antiarrhythmics- class 4

A

-Ca channel blocker
-plateu phase

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20
Q

afib- anticoagulation- direct oral anticoagulants (DOAC)

A

-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

21
Q

HASBLED score- bleed risk

A

-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

22
Q

atrial flutter

A

-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

23
Q

ventricular tachycardia

A

-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

24
Q

ventricular tachycardia causes

A

-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

25
Q

watchman procedure

A

(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

26
Q

ventricular tachycardia tx

A

-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

27
Q

ventricular tachycardia treating the underlying cause

A

-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

28
Q

torsades de pointes

A

-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

29
Q

ventricular fibrillation

A

-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*

30
Q

ventricular fibrillation causes

A

-Ischemic heart disease*
-Antiarrhythmics-Prolongation of the QT interval
-Atrial fibrillation with rapid ventricular response
-Drug toxicity
-Sepsis
-Hemorrhagic shock
-Electrolyte abnormalities

31
Q

ventricular fibrillation treatment

A

-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

32
Q

cardiac arrest

A

-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

33
Q

causes of cardiac arrest

A

-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

34
Q

brugada syndrome

A

-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

35
Q

defibrillator

A

-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)

36
Q

sick sinus syndrome

A

-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*

37
Q

causes of sick sinus syndrome

A

-Myocardial scarring

-Medications:
-Beta-blockers, CCB
-Antiarrhythmics
-Digitalis
-Lithium
-Methyldopa

-Genetic: Familial sick sinus syndrome

-Sarcoidosis, amloydosis
-lyme disease

38
Q

sick sinus syndrome treatment

A

-Discontinuation of medication
-Definitive treatment: permanent pacemaker placement*

39
Q

bundle branch blocks

A

-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

40
Q

right bundle branch block (RBBB)

A

-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

41
Q

left bundle branch block (LBBB)

A

-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

42
Q

atrioventricular (AV) block

A

-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

43
Q

AV block causes

A

-Aging
-Coronary artery disease- MI
-Rheumatic heart disease
-Lyme disease
-Sarcoidosis
-Hematomachrosis
-Hyperthyroidism
-Congenital
-Hyperkalemia

44
Q

AV block treatment

A

-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)

45
Q

first degree heart block

A

-not a true block -> conduction delay
-delay in the AV node
-fix prolonged PR interval > .2 s and > 5 small boxes

46
Q

second degree type 1

A

-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

47
Q

second degree type 2

A

-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

48
Q

third degree heart block

A

-complete
-dissociation of electrical activity between the atria and ventricles

Cardiology (11 decks)

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