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S2B6: MEDI > Tachyarrhythmias > Flashcards

Tachyarrhythmias Flashcards

1
Q

What is a normal heart rate range?

What qualifies as tachycardia?

What qualifies as bradycardia?

A

Normal: 60-100 bpm

Tachycardia: greater than 100 bpm

Bradycardia: less than 60 bpm

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2
Q

What are the inherent pacing rates of automaticiy for the following foci?

SA node

Atria

AV node/junction

Ventricle

A
  • SA node rate
    • 60-100 bpm
  • Atria automaticity rate
    • 60-80 bpm
  • AV node/junction rate
    • 40-60 bpm
  • Ventricular rate
    • 20-40 bpm
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3
Q

What are the steps to evaluating a normal EKG?

A
  1. Rate
    • find QRS that aligns with dark line on ECG, then cound “300, 150, 100, 70…”
  2. Look to see if there are P waves in front of QRS
    • are they upright?
    • How far are they from the QRS
  3. Are there T waves?
    • how far are they from the Q?
    • are they upright?
  4. Look to see if rhythm looks regular
  5. Check out the axises
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4
Q

What are the characteristics that define tachyarrhythmias?

A
  • Identified by location where foci originate
  • sinus node (SA) vs atrial ventricular (AV) node
  • supraentricular vs ventricular
  • most are propagated through reentry pathways
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5
Q

What is the difference between anatomical and functional reentry circuits?

A
  • Anatomic
    • by-pass tracts (accessory pathways)
    • pathways you have been born with and are not necessarily present in everyone
      • they can bypass the normal conduction pathway & create a circle pathway on their own
  • Functional
    • microcircuits in areas of the heart
    • w/ Afib, there is a lot of small foci throughout the atria & the form their own circular pathway
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6
Q

What is the dominant mechanism for supraentricular tachycardis & ventricular tachycardia?

What does it require?

A

Reentry

Requires bifurcating pathways of different velocities adn refractory periods

OR

accessory pathway

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7
Q

Describe what is happening in this image

A
  • A
    • Normal conduction pathway
    • A: long, fast pathway
      • refractory to come up to normal is slower
    • B: short, shlow pathway
      • going back to normal is faster
    • the impulses that split at the top will meet down at the distal common pathway to continue its course
      • sometimes it can go back up retrograde
      • when the retrograde pathway meets the slow pathway, they usually cancel each other out & you don’t have any problems
  • B
    • if there is a block in the fast pathway that interrupted the course
    • the slow pathway made it to the bottom first and was able to go up through the faster pathway & get back up before it was fully refractory, starting the reentry circuit
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8
Q

Supraventricular tachycardia is what type of tachycardia?

How common is it?

How are they classified?

What is the most common site of origin?

A
  • narrow complex tachycardia
  • most common of in all age groups
  • classification depends on
    • site of origin, nature of arrhythmia or mechanism
      • Origin (most commonly above bundle of His):
        • SA node, atrium, AV node and proimal bundle of His
      • automaticity, triggered or reentrant mechanism
      • some wide complex tachycardias can be supraventricular
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9
Q

What are the type of supraventricular tachycardia?

A
  • sinus tachycardia
  • AV node reentrant tachycardia (AVNRT)
  • AV reentrant tachycardia (AVRT)
  • SA nodal reentrant tachycardia (SANRT)
  • junctional tachycardia
  • atrial fibrillation
  • atrial flutter
  • multifocal atrial tachycardia (MAT)
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10
Q

What are the risk factors for supraventricular tachycardia?

A
  • Sympathomimetic use
    • caffein overdos, alcohol us, tocabo use
    • beta adrenergic medications used in asthma or COPD
    • Illicit drugs such as methamphetamines and cocaine
    • ADHD medications
    • other medications or supplements that can increase heart rate
      • OTC cold medications containing phenylephrine or pesudophedrine
      • Fat burners or pre-work out supplements
      • phentermine for weight loss
      • digoxin toxicity
  • Underlying medical conditions
    • hyperthyroidism, catecholamine producing tumors, previous MI
  • Stress, emotional upheaval or tiredness less commonly
  • congenital or acquired reentrant pathway, icreased automaticity
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11
Q

What is the clinical presentation of supraventricular tachycardia?

What is the first thing you need to differentiate?

A
  • Need to differentiate stable from unstable
  • may be asymptomatic & incidental finding on ECG or exam
    • most commonly atrial fibrillation
  • Sudden onset of palpitations is most common complaint
  • shortness of breath (mild to severe)
  • chest pain
  • dizziness
  • syncope
  • diaphoresis
  • acute heart failure
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12
Q

What is the initial workup for a patient presenting with supraventricular tachycardia?

A

ECG

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13
Q

Identify the differential diagnosis for each of the provided scenarios

A
  • Narrow
    • Regular
      • Sinus tachycardia
        • physiologic sinus tachycardia
        • inappropriate sinus tachycardia
      • AVNRT
      • AVRT
      • Focal AT
      • Atrial flutter
      • Junctional tachycardia
      • SANRT
      • rarely ventricular tachycardia
    • Irregular
      • AF
      • Multifocal AT (or sinus tachycardia with frequent atrial ectopy(
      • Focal AT with variable AV block
      • Atrial flutter with variable AV block
  • Wide
    • Regular
      • Monomorphic VT
      • Any SVT with aberrant conduction, ventricular pacing, preexcitation, certain antiarrhythmic medications, or significant electrolyte abnormalities
      • antidromic ARVT with antegrade AV conduction via accessory pathway (WPW syndrome)
    • Irregular
      • AF, atrial flutter, or focal AT with aberrant conduction
      • AF, atrial flutter or focal AT with antegrade conduction via accessory pathway (WPW syndrome)
      • Polymorphic VT (including torsade de pointes)
      • Ventricular fibrillation
      • Antidromic AVRT due to nodoventricular/nodofascicular accessory pathway with variable VA conduction
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14
Q

What is the next work up step following the EKG?

If there are no abnormalities?

If there are?

What labs are you ordering?

A
  • If no abnormalities / symptoms are intermittent can proceed to further work-up outpatient
  • If abnormality found on EKG
    • abnormal rhythm shoudl be treated & further work-up postponed until patient is stable
  • Labs
    • electrolytes
    • thyroid functin
    • anemia if suspect substance abuse (CBC)
    • urine drug screen
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15
Q

Describe the appropriate cardiac monitors to precribe for out-patient work up

A
  • Cardiac Monitors
    • Holter monitor
      • continuous ECG monitors
      • Not patient activated
        • but patients should write down when they have symptoms
      • Short duration of use (24-48hrs up to 2 weeks)
      • for use of daily or every other day symptoms
    • Event monitors
      • patient activation recording
        • if symptom happens at night, you may miss a recording
      • longer duration of monitoring sometimes up to 1 month
    • Mobile Cardiac Telemetry
      • Both patient activation and set parameter auto-trigger (HR, length of a pause, etc.)
      • Can be used for longer monitoring (30+ days)
    • Loop Recorder
      • implanted under the skin (usually over the heart)
      • can be work 2-3 years
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16
Q

Describe the possible out-patient work up procedures that can be used in addition to cardiac monitoring

A
  • Echocardiogram
    • rule out any structureal abnormalities and assess myocardial wall function/ejection fraction
  • Exercise Testing to induce exertional arrhythmias or underlying CAD
  • Electrophysical Study (EPS)
    • invasive, multipolar electrode catheter based study of area suspected to contain the reentry pathway to evaluate for or induce arrhythmia at time of study
      • complications: myocardial perforation with cardiac tamponade, pseudoaneurysms at arterial access site adn provocation of nonclinical arrhythmias
  • Direct cardiac mapping
    • potentials recorded directly from the heart are spatially depicted as functin of time in an integrated manner
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17
Q

What is the treatment for active, current supraventricular tachycardia?

A
  • In stable patients, you can do a vagal maneuver, carotid massage or cold water/ice on face
    • in older people must ensure no carotid artery disease prior to carotid massage
  • Adenosine can also be used if initial maneuvers are unsuccessful (into large vein)
    • 6mg x1 and may repeat at 12 mg x2
    • If adenosine does not work can use IV beta-blockers or non-dihydropyridine CCB (verapamil, diltiazem)
    • Class III or Clas IC drugs can be used as alternatives
    • Caution in WPW as can precipitate VF (choose procainamide or amiodarone)
  • If continued arrhythmia or patient become unstable, immediate direct current cardioversion with sedation required
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18
Q

What is the treatment for chronic intermittent supreventricular tachycardias?

A
  • Chronic pharmacological suppression in mild, less frequent cases “pill in the pocket”
    • oral beta-blockers, non-dihydropyridine calcium channel blockers, class IC antiarrhythmic drug flecainide typically used
  • Cryoablation or radiofrequence catheter ablation in recurrent, severe cases is definitive treatment
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19
Q

Describe the characteristics of Sinus Tachycardia

Rate?

ECG findings?

Causes?

Clinical presentation?

Treatment?

A
  • Rate: 100-180 bpm
  • P-wave before every QRS with stable PR interval
  • Causes vary but include
    • excessive caffein use
    • Illicit drug use
    • Normal resonse to exercise
    • pulmonary emboli
    • hyperthyroidism
    • stress/andiety disorders
    • pheochromocytoma
    • sepsis
  • Presentation
    • gradual onset & termination
    • In patients with underlying coronary artery disease (CAD) can precipitate chest pain
  • Treatment
    • typically aimed at cessation of of offending agends or target underlying disease
    • beta-blockers or nondihydropyridine calcium channel blockers may be used to decrease heart rate
    • Ivabradine has been usefulin patients with inappropriate or refractory sinus tachycardia
20
Q

Describe the characteristics of Premature Atrial Complexes

Origination?

How common are they?

ECG?

Causes?

Clinical Presentation?

Treatment?

A
  • Origination
    • originate froma ny area of the atrium
  • Frequency
    • most common cause of irregular pulse & palpitations
    • common in normal hearts & increase with age
  • ECG
    • P-wave is typically different from teh p-wave of the dominating rhythm indicating different focus or origin
      • P-R interval can often exceed 120 ms
    • non-conducted PACs can often be buried in the T-wave if occurrign late int eh cardiac cycle
  • Cause - may situations
    • infection
    • inflammation
    • MI
    • anxiety
    • excessive caffeine
    • illicit drugs
  • Clinical features
    • can precipitate the occurrence of SVT
  • Treatment
    • do not generally require therapy except in symptomatic persons, then beta blocker or calcium channel blocker can be attempted
21
Q

Describe the characteristics of Atrial Flutter

Rate?

How common are they?

Origination?

ECG?

Causes?

A
  • Rate
    • 250-350 bpm
  • Frequency
    • less common than atrial fibrillation
  • Origination
    • Reentrant tachycardia in the right atrium
      • use 2 similar circuits clockwise (upright waves) or counterclockwise (inverted waves) around the tricuspid annulus
      • rates and flutter pattern consistent and predictable
  • ECG
    • Regulat “saw-tooth” flutter waves without isoelectric wave between flutter waves
      • seen best in II, III, aVF, or V1
    • Atrial conduction to ventricular conduction
  • Causes
    • reentry without significant heart disease
    • septal defects
    • pulmonary emboli
    • mitral or tricuspid stenosis and regurgitation
    • heart failure
    • scaring from previous ablations
    • aging
    • toxic & metabolic derangements
      • thyrotoxicosis, alcoholism, pericarditis
22
Q

What are things to be aware of during an physical exam on a patient with atrial flutter?

A
  • anxious patient
  • may be hypotensive
  • rapid flutter waves in the jugular venous pulse
  • palpable pulse is typically regular
  • EKG consistent with regularly regular sawtooth flutter waves
23
Q

Treatment/Management for Atrial Flutter?

A
  • Carotid massage or adenosine can slow rate but rarely terminates
  • Acute therapy: rate vs. rhythm
    • early restoration of sinus rhythm preferred
    • IV beta or calcium channel blockers, amiodarone, digoxin
    • if pharmacological agents not tolerated, direct cardioversion
    • If rhythm initiated by acute event (sepsis, surgery, etc) treatment for up to 1 month
  • Therapy for transient, chronic episodes
    • long term oral beta-blocker, calcium channel blocker, amiodarone, flecainide, sotalol
    • similar to treatment for trial fibrillation
    • requires anticoagulation
    • definitive treatment is catheter ablation
24
Q

Describe the characteristics of Atrial Fibrillation

Clinical Presentation?

ECG?

Causes?

Treatment?

A
  • Clinical Presentation
    • chaotic atrial rhythm relted to continuous, variable activation of the atria
    • recurrent, paroxysmal, perisistent or permanent
  • ECG
    • irregularly irregular QRS comlplexes on ECT with no distinct P-waves
    • rates are variable & can fluctuate widely
  • Cause
    • higher risk with age & other chronic conditions
    • can be heriditary
  • Treatment
    • similar to atrial flutter
    • anticoagulation based on risk for stroke
      • CHADS2
      • CHA2DS2-VASc
25
Q

Describe the ECG characteristics of Focal Atrial Tachycardias (FAT)

A
  • ECG
    • irregularly irregular rath WITH visible P-waves
    • Atrial rates of 150-200 bpm
    • P-wave contour typically differrent from that of sinus P-wave
      • those AT with foci near SA node may resenble sinus P-wave
      • there are isoelectric intervals between P-waves (unlike A-flutter)
      • positive or biphasic P-wave in V1=left atrial focus
      • negative P-wave in V1 = right atrial focus
    • can occur in short, recurrent bursts with spontaneous termination
26
Q

Describe the clinical presentation fo FAT.

What is the managment?

A
  • Clinical Presentation/Exam
    • Often occur in patients with CAD, HF, corpulmonale, digitalis toxicity
    • Symptoms correlate to underying cause
      • chest pain
      • shortness of breath
      • palpitations
      • presyncope
    • stimulants can provoke episodes
    • Physical exam findings:
      • variable rhythm on auscultation
      • cariable intensity of S1 on auscultation
      • variable systolic blood pressure
      • Patient may anxious only or exhibit signs of heart failure
  • Management
    • carotid masage and adenosine typically do not terminate arrhythmia but can slow AV conduction and ventricular rate
    • If digoxin toxicity, replace K if low and reverse digoxin with DIGIfab
    • Beta-blockers or calcium channel blockers to slow ventricular rate initially
    • Class IA, IC, or III drugs as add ons
    • Catheter ablation generally effective
27
Q

Describe the characteristics of Multifocal Atrial Tachycardia (MAT)

ECG?

Clinical presentation?

Treatment?

A
  • ECG
    • Marked variation in P-wave morphology
    • Very irregular P-P intervals and variable P-R intervals
    • Atrial rates between 100-130 bpm
    • Most P-waves are conducted o the ventricles
  • Clinical presentation
    • occurs in teh elderly with COPD & CHF
    • May transition to AF
    • seen more frequently when theophyline was used for severe COPD
  • Treatment
    • directed at underlying disease
    • antiarrhythmic drugs often ineffective at slowing the rate
    • beta blockers should be avoided in patients with bronchospasm pulmonary disease but can be effective if tolerated
    • calcium channel blockers (verapimil) and amiodarone are useful
    • ablation may be effective in some cases
28
Q

Describe the characteristics of Atrioventricular Nodal Reentry Tachycardia (AVNRT)

ECG?

Origincation

Clinical presentation including symptoms?

Treatment?

A
  • ECG
    • HR between 150-280 bpm
    • P-waves buried in QRS complex but when visible are positive & narrow appearing
  • Origination
    • reetry circuit located within the right atrium or AV node
  • Clinical presentation
    • most common form of reentry SVT
    • often triggered by PAC and PVC less commonly (1/3)
    • paroxysmal, more common in women (~75%)
    • categorized as slow-fast (90%- top ECG) or fast-slow (~10%- bottom ECG) depending on which reentry pathway is activated
    • Symptoms
      • sudden onset, rapid regular palpitations
      • may have sudden fall in BP with presyncope or syncope
      • may have chest pain and shortness of breath
  • Treatment
    • vagal maneuvers, carotid massage
    • adenosine, beta-blockers, calcium channel blockers if nonresponsive to adenosine
    • class III (amiodarone) or class IC agents can be used
    • catheter ablation definitive treatment
29
Q

Describe the characteristics of Atrioventricular Reentry Tachycardia (AVRT)

Origination?

ECG?

Clnical presentation?

Treatment?

A
  • Origination
    • Accessory pathway that connects the atrium or AV node to the ventricle outside the normal AV nodal His-Purkinje conduction system
    • Accessory pathway can conduct anterograde (antidromic) and retrograde pathway (orthodromic)
      • retrograde or orthodromic pathway is the most common
  • ECG
    • RP- interval is often short, rate is 200-300 bpm and regular
    • antidromic will have wide QRS due to abnormal ventricle depolarization from accessory pathway
  • Clinical Presentation
    • symptoms when activated are palpitations, dizziness, presyncope/syncope, chest pain
    • physical exam
      • unvarying, regular ventricular rhythm, with constant intensity of the first heart sound and blood pressure
      • jugular vein may show larger A wave
  • Treatment
    • similar to AVNRT except with antidromic reentry pathway, consider class IC and III antiarrhythmics
    • DC cardiovert is unstable or refractory to medications
    • ablation definitive therapy
30
Q

What is Wolfe-Parkinson White Syndrome?

Origination?

How common is it?

Clinical features?

Treatment?

A
  • Origination
    • Congenital accessory pathway: bundle of Kent
      • as the pathwy goes through the ventricle & bypasses the AV node it excites the ventricle first (delta wave)
  • Common
    • Prevalence 1:1000
  • Clinical features
    • sudden onset & termination
    • symptoms similar to AVNRT
  • Treatment
    • acute episode caution using adenosine, beta-blockers or Ca-channel blockers
      • can cause decompensation
    • chronic suppression with class IA, IC or III agents
      • medication side effects
    • ablation curative 95%
31
Q

What ECG features would you see on an asymptomatic atient with WPW?

What are the other general characteristics of WPW on ECG?

A
  • Asymptomatic
    • delta waves on ECG
    • WPW Pattern (type A- top image; and B- bottom image)
      • A: large R wave in V1
      • B: deep S wave in V1
    • have good prognosis & rarely need treatment
  • Characteristics of WPW on ECG
    • PR interval less than 120 miliseconds durign sinus rhythm
    • QRS complex duration exceeding 120 miliseconds with a slurred, slowly rising onset of the QRS in some leads (delta wave) and usually a normal terminal QRS portion
    • ST-T wave discordant changes
  • Ventricular rates of 150-250 bpm with regular rhythm
32
Q

What is the major risk associated with WPW?

Treament?

Prevention?

A
  • Risk
    • High risk or progression to ventricular fibrillation
      • must avoid adenosine, beta-blockers, digoxin or non-dihydropyridien calcium-channel blockers
  • Treatment
    • Unstable requires immediate cardioversion
    • Can use procainamide IV to terminate arrhythmias
  • Prevention
    • Waiting for ablation can use oral class IC or III antiarrhythmic drugs
      • IC: flecainide, propafenone
      • Class III: amiodarone
  • ablative therapy is curative
33
Q

What are ventricular arrhythmias?

Origination?

Types?

A
  • Wide complex tachycardias
  • Origination
    • do not depend on SA node, AV node or atrium
    • similar physiologic mechanism as SVT
      • reentrant most common
  • Types
    • monomorphic ventricular tachyardia (including ventricular flutter)
    • polymorphic ventricular tachycardia (Torsade de Pointes)
    • Ventricular fibrillation
34
Q

What constitututes a Pre-ventricular contraction (PVC)?

Clinical Presentation?

ECG features?

A
  • less than 4 consecutive extrasystole contractions originating from the ventricle
  • Clinical presentation
    • frequently found in excessive sympathomimetic (caffeine/tobacco) agent use
    • may feel like heart sipped a beat
    • do not require work up
    • frequent PVVs seen on monitory or ECG in persons with structural heart disease can be concerning
  • ECG
    • wide QRS complex
  • Treatment
    • cessation of offendign agents
35
Q

What constitutues ventricular tachycardis (VT)?

Clinical features/origination?

Types?

A
  • 4 or more consecutive beats that origiinate from the ventricle
  • Clincal features
    • rate must be at least 100 beats per minute
    • trigger by similar mechanism as other tachyarrythmias
      • reentry, enhanced automaticity or triggered activity
      • reentry typically around area of prior MI scar
  • Types
    • nonsustained VT (NSVT)
      • lasts less than 30 seconds
      • does not require intervention due to hemodynamic instability
      • otherwise is called sustained VT
    • monomorphic VT
      • sometimes includes ventricular flutter
    • polymorphic VT
      • torsades de pointes
36
Q

What are the risk factors for ventricular tachycardia?

A
  • Acue MI
  • chronic ischemic heart disease
  • structural cardiad disease
    • dilated cariomyopathy, reduced ejection fraction HF, hypertrophic cardiomyopathy (HCOM), inherited arrhythmogenic cardiomyopathy, chagas heart disease
  • inherited channelopathhies
    • long QT syndrome (LQTS)- defibrilator at young age
    • brugada syndrome
  • electrolyte abnormalities
    • magnesium, calcium, potassium
  • Infiltrative disease
    • sarcoidosis, amyloidosis
  • congenital heart disease
    • HOCM
  • drugs that prolong the QT interval
    • certain antibiotics, antiarrhythmics, antipsychotics and antidepressants
37
Q

The following ECG is an example of what type of syndrome?

A

Long QT syndrome

can be inherited or acquired from long-term use of drugs known to cause Long QT-syndrome

38
Q

The following ECGs are an example of what type of syndrome?

A

Brugada Syndrome

inherited disease

Type 1 is most common- sometimes mistaken for a heart attack

39
Q

What are the symptoms of ventricular arrhythmisa & what should you be looking for onteh physical exam?

A
  • Symptoms
    • shortness of breath
    • chest pain
    • palpitations
    • syncope or presyncope
    • malaise
    • exertional symptoms
    • sudden cardiac arrest
  • Physical exam
    • often non specific findings
    • tachycardia typically greater than 100 bpm
    • marked fluctuations in blood pressure
    • difficulty differentiating heart sounds due to rate of tachycardia but may vary in intensity
    • cannon “A” waves
40
Q

The provided ECG show what cardaic condition?

A

regular appearing rhythm, wide complex

41
Q

Describe the characteristics of monomorphic ventriculat tachycardia (MMVT)

Origination?

ECG?

Clnical presentation?

A
  • Origination
    • usually originate from the saem area of the ventricle
  • Clinical features
    • beats appear to be identical
    • ventricular flutter may be included
      • rates a greater than 300 beats per minute
  • ECG
    • SVT may appear as wide complex tachycardia in some cases
      • with aberrancy in bundle branch blocks
      • accessory pathway such as WPW syndrome
      • can use Brugada slgorithm to determine origin of wide complex tachycardias
42
Q

What is the treatment for monomorphic VT?

A
  • Acute MMVT treatment per ACLS protocol
  • After acute treatment
    • treat underlying cause
      • electrolyte replacement, cardiac cath if MI
    • echocardiogram to assess underlying structural disease
    • may consider cardiac MRI if suspect infiltrative cause
    • holter monitor
    • stress test if suspect is underlying CAD but without acute MI
    • electrophysiological studies with possible ablation
    • suppression with oral antiarrhythmics
      • beta-blocker, amiodarine, sotalol
    • consider ICD in those high risk patients
43
Q

Describe the characterisitcs of Polymorphic VT (Torsadees de Pointe)

A
  • ECG
    • undulatign baseline with varying QRS complexes
    • like a ribbon being twisted
    • unstable rhythm, often progresses to Vfib
  • Clinical Presentation
    • associated with electrolyte imbalance, specifically hypomagnesium
    • patient may be responsive or unresponsive
    • Symptoms
      • extreme palpatations
      • chest pain
      • shortness of breath
      • dizziness
      • syncope
      • confusion
      • hypotension
44
Q

What is treatment for polymorphic VT?

A
  • Magnesium
  • Unstable PVT WITH a pulse, follow ACLS protocol
  • If no pulse, go straight to pulseless ACLS resuscitation protocol
45
Q

The provided ECG is an example of what cardiac condition?

A

polymorphic VT into ventricular fibrillation

46
Q

The provided ECG is an example of what cardiac condition?

A

Ventricular Fibrillation

47
Q

What is ventricular fibrillation & what is the treatment?

A
  • Erratic irregular rhythm with no meaninful cardiac output
  • Requires immediate CPR & initiaion of ACLS resuscitation protocol
    • Start CPR
    • shock
    • epinephrine
  • Causes vary but often fatal

S2B6: MEDI (15 decks)

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