Cardiology Part 2

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Abnormal heart rhythm:

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Arrhythmia

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slow heart beat:

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bradycardia

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203 Terms

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Abnormal heart rhythm:

Arrhythmia

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slow heart beat:

bradycardia

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too fast heart beat:

tachycardia

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Signs and symptoms of arrhythmias:

fluttering in chest

skipping a beat

dizziness

shortness of breath

fatigue

lightheadedness

chest pain

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What can be used to diagnose arrhythmias?

ECG

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Holter monitor:

an ambulatory ECG device that records the electrical activity of the heart continuously for 24-48 hours

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What type of arrhythmias can a Holter monitor or continuous ECG?

intermittent

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Describe the steps in the cardiac conduction pathway:

  1. electrical impulse begins in the SA node

  2. impulse travels from the SA node to the right and left atria, which causes atria contraction

  3. signals reaches the AV node, electrical conduction slows down

  4. impulse continues through the bundle of His and into the ventricles

  5. the bundle of His divides into the right bundle branch for the right ventricle

  6. left bundle branch for the left ventricle

  7. signal continues to spread through the ventricles via Purkinje fibers, which causes the ventricles to contract.

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The heart’s pacemaker:

SA node

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Normal HR:

60-100 BPM

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Describe the step of electrical signaling ( Cardiac action potential):

Phase 0: heartbeat is initiated when rapid ventricular depolarization occurs in response to an influx of sodium, which causes ventricular contraction ( QRS complex on ECG)

Phase 1: early rapid repolarization( Na channel close)

Phase 2: a plateau in response to an influx of calcium and efflux of potassium

Phase 3: rapid ventricular repolarization occurs in response to an efflux of K; which causes ventricular relaxation ( T wave on ECG)

Phase 4: resting membrane potential is established; atrial depolarization occurs ( P wave on ECG)

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What is the most common cause of arrhythmias?

myocardial ischemia infarction

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What are some non cardiac conditions that can trigger or predispose a patient arrhythmia?

electrolyte imbalances ( potassium, magnesium, sodium. and calcium)

elevated sympathetic state

drugs ( drugs that prolong QT and illicit drugs)

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What is the most common type of arrhythmia?

atrial fibrillation

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PVCs

premature ventricular contractions ( also known as skipped heartbeats)

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A series of PVCs that result in a HR > 100 BPM:

ventricular tachycardia

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If a patient has a pulseless VT:

it is a medical emergency and advanced cardiac life support should be started.

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What can happen if you leave and ventricular tachycardia untreated?

it can degenerate into ventricular fibrillation

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At what rate is a QTC interval considered to be prolonged?

> 440-460 milliseconds, but it is markedly prolonged > 500 msec.

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When a patient has a prolongation of their QT interval it put them at risk for?

torsade de pointes

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What medications can increase or prolong QT interval?

antiarrhythmics: class Ia, Ic, and III

anti-infectives: antimalarials, azole antifungals, macrolides, quinolones, lefamulin

antidepressants: SSRIs ( high risk with citalopram and escitalopram)

antiemetics: 5-HT3 receptor antagonists, droperidol, metoclopramide, promethazine

antipsychotics: 1st generation and second generation

onclongy medications: androgen deprivatio therapy, tyrosine kinase inhibitors, arsenic trioxide

cilostazol, donepizil, fingolimod, hydroxyzine, loperamide, methadone, ranolazine, solifenacin

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What should be done before starting any drug for a non life threatening arrhythmia?

electrolytes and toxicology screen should be checked to identify any potentially reversible causes

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Class I: sodium channel blockers:

Ia: disopyramide, quinidine, procainamide

Ib: lidocaine, mexiletine

Ic: flecainide, propafenone

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Vaughan Williams classification Class II:

beta blockers

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Vaughan williams classifications class III: potassium channel blockers

dronedarone

dofetilide

sotalol

ibutilide

amiodarone

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Vaughan Williams classification class IV: non-DHP CCBs

verapamil

diltiazem

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MOA of amiodarone:

class III antiarrythmic that blocks potassium channels and also blocks sodium, calcium, alpha, and beta adrenergic receptors.

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What is the ½ life of amiodarone?

40-60 days

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Amiodarone is the most commonly prescribed and is a preferred:

antiartrhythmic in patients with HF

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Amiodarone

nexterone

pacerone

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Boxed warnings for amiodarone:

pulmonary toxicity

hepatotoxicity

life threatening arrhythmias only

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What are some contraindications to taking amiodarone?

iodine hypersensitivity

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What things should you look out for in patients taking amiodarone?

hyper and hypothyroidism

optic neuropathy

corneal microdeposits

photosensitivity: blue-gray skin discoloration

peripheral neuropathy

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SE of amiodarone:

hypotension

bradycardia ( may decrease infusion rate)

photosensitivity

DILE

SJS/TEN

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What do you monitor in patients taking amiodarone?

ECG

HR

BP

Electrolytes

LFTs ( every 6 months)

thyroid function

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How do you administer amiodarone IV infusions?

iv infusions > 2 hours require a non-PVC container: polyolefin or glass

preixed IV bags: nextreone comes in non-PVC , non-DHEP galaxy plastic container

use 0.22 micron filter; central line preferred

incompatible with heparin

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What is recommended to prevent drug interactions when taking amiodarone with digoxin?

decrease digoxin by 50%

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What do you do to prevent drug interactions between amiodarone and warfarin in patients on both medications?

decrease dose of warfarin by 30-50%

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If a patient needs to take both amiodarone and simvastatin, what is the maximum dose per day of simvastatin?

20mg/day

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If a patient has to take lovastatin and amiodarone together what is the maximum dose of lovastatin?

40 mg/day

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What can enhance the bradycardia effects of amiodarone if used with amiodarone?

sofosbuvir when used together with amiodarone

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How do you take quinidine?

take with food or milk to help decrease GI upset

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What are some warning for disopyramide?

proarrhythmic

anticholinergic effects

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What are some warnings for quinidine?

pro arrhythmic

hemolysis risk: avoid in G6PD deficiency

can cause positive coombs test

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SE of quinidine:

DILE

diarrhea

stomach cramping

rash

lightheadedness

cinchonism ( toxicity): tinnitus, hearing loss, blurred vision, headache, delirium

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SE of disopyramide:

anticholinergic effects: dry mouth, constipation, urinary rentention

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Dosage form of procainamide

injection

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How is the active metabolite , N-acetyl procainamide is cleared?

renally cleared

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What is the therapeutic level of procainamide?

4-10 mcg/mL

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Boxed warning for procainamide:

agranulocytosis

long termuse leads to positive antinuclear antibody in 50% of patients which can result in DILE

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How does metabolism of procainamide to NAPA occur?

by acetylation: slow acetylators are at risk for drug accumulation and toxicity

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Class Ib antiatrhymics are used in the treatment of what type of arrhythmias?

ventricular arrhythmias only

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MOA of Class Ib drugs:

block sodium channels

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Dosage form of lidocaine for arrhythmias:

injection

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IV lidocaine is useful for:

refractory VT/cardiac arrest

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MOA of flecanide:

block sodium channels

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Boxed warnings for flecanide:

proarrhythmic

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Contraindications to using flecanide and propafenone:

heart failure

MI

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Side effects of propafenone:

taste disturbance: metallic taste in mouth

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Contraindications to dronedarone:

patients with decompensated HF or permanent AF due to increased risk of death, stroke, and HF

CYP3A4 inhibitors and QT prolonging drugs

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What are some warnings of dronedarone?

hepatic failure

pulmonary toxicity

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SE of dronedarone:

proarrhythmic

diarrhea

bradycardia

asthenia

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Tue/False: dronedarone does not contain iodine and has little effect on thyroid function

True

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How do you initiate dofetilide?

it has to be started in a setting with continuous ECG monitoring.

assess CrCl for a minimum of 3 days

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True/False: Dofetilide is not a preferred antiarrhythmic in HF

False; it is preferred in HF

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How do you dose sotalol if a patients CrCl <60 mL/min?

decrease frequency

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Side effects of sotaol:

bradycardia

palpitations

chest pain

dizziness

fatiue

dypsnea

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Dosage form of ibutilide

Injection

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When is adenosine used?

to treat supraventriular re-entrant tachycardias

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Dosage form of adenosine:

injection

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What is the ½ life of adenosine?

< 10 seconds

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Intermittent Afib that terminates within 7 days of onset:

paroxysmal Afib

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Continuous Afib sustained for > 7 days:

persistent Afib

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What is used to reduce the risk of clots/stroke in Afib patients?

anticoagulation

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What are the two ain strategies in the treatment of AFib?

rate and rhythm control

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What is the goal resting HR in patients with symptomatic AFib?

< 80 BPM

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What is the goal resting HR in patients who are asymptomatic and have preserved left ventricular function?

< 110 BPM

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What are the recommended medications for controlling ventriular rate in patients with AFib?

beta blockers and non-DHP CCBs

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If a patient has AFib and HFrEF they should not recieve:

non-DHP CCBs

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What is the goal of rhythm control in AFib patients?

restore and maintain normal sinus rhythm

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What antiarrythmics are used for rhythm control in AFib patients?

Class Ia, Ic, or III anti-arrhythmic drugs or electrical cardioversion

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What should be avoided in permanent AFib?

a rhythm control strategy with antiarryhtmic drugs

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Therapeutic range of digoxin for AFib:

0.8-2 ng/mL

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Dose of digoxin for AFib:

0.125-0.25 mg`

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A patient taking digoxin and have a CrCl <60 mL/min:

decreased dose or frequency and hold in acute renal failure

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How do you stwitch from oral to IV dose?

decrease dose by 20-25%

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What are signs and symptoms of digoxin toxicity?

Nausea and vomiting

loss appetite

blurred/double vision

greenish-yellow halos

bradycardia

life threathening arrhythmias

increase risk of toxicity with: hypokalemia, hypomagnesemia, hypercalcemia

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When is digoxin used in Afib patients?

used in combination with beta blocker or non-DHP CCBs for rate control

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What causes an acute ischemic stroke?

thrombus that forms during cerebral atherosclerotic infarction ( non-cardioembolic stroke)

embolus that forms in the heart and travels to the brain ( cardioembolic stroke)

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TIA:

a mini stroke caused by temporary clot in the brain

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Modifiable risk factors of stroke:

hypertension

atrial fibrilation

dyslipidemia

diabetes

physical inactivity

smoking

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Non-modifiable risk factors:

prior stroke or TIA

advanced age > 80 years old

race: higher risk in African American Patients

genetic diseases

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Signs and symptoms of stroke:

F: face dropping

A: arm weakness

S: speech difficulty

T: time to call 911

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What imaging is preformed within 20 minutes of arrival to the ER to quickly identify if a stroke symptoms are due to hemorrhage?

brain imaging using CT

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What is the goal of managing an ischemic stroke?

restore blood flow

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MOA of alteplase (tPA or rtPA):

tissue plasminogen activator that binds to fibrin in a thrombus and converts plasminogen to plasmin, which results in fribrinolysis

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True/False; alteplase is the only fibrinolytic FDA approved for ischemic strokes

True

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When is a patient a candidate for alteplase administration?

when their is no bleeding seen on the imaging

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Criteria that must be met to start alteplase:

no bleeding is seen on the brain imaging

stroke symptom onset is < 4.5 hours

alteplase can be administered within 60 minutes of hospital arrival

no contraindications to alteplase

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What are the contraindications to alteplase?

active internal bleed: ICH

risk of internal bleed due to;

  • severe hypertension: BP >185/110 mmHg ( lower BP to <185/110 mmHg with IV labetalol and nicardipine before alteplase administration)

  • head trauma

  • labs: elevated INR ( >1.7) , low platelet counts

  • drug interactions: anticoagulants usage ( treatment doe of LMWH within previous 24 hours, use of direct thrombin inhibitor or direct factor Xa inhibitor within previous 48 hours or taking warfarin)

history of recent stroke( within past 3 months)

blood glucose < 50 mg/dL