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MOD 2 > Electrocardiography + PE > Flashcards

Electrocardiography + PE Flashcards

1
Q

Explain why this is an example of A fib

A
  • no clear P waves before the QRS
  • some of the QRS are close together, some are far apart
  • irregularly irregular pattern
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2
Q

Describe normal conduction in the heart and then conduction with A fib

A

Normal:

SA node= dominante pacemaker, starts electrical activity –> R and L atria –>AV conduction system –> L and R Bundle branch–> R and L ventricles –> purkinje fibers

In A fib:

  • atria depolarizes itself without the AV nodes
  • irregular depolarization, flickering in atria
  • some conducted down to ventricles
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3
Q

Differences between Paroxysmal, Persistent, and Permanent Atrial Fibrillation

A

Paroxysmal: A fib with HR >120, sudden episodes last 12-24 hours, then spontaneously resolve

Persistent: A fib persists for longer period of time (2 weeks), requires help/electrical cardioversion to get back to sinus rhythm

Permanent: developed A fib in past, remains in rhythm, asymptomatic (i.e. walks daily without limitations, no palpitations or fatigue)

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4
Q

Major symptoms of A fib, and consequences if left untreated

A
  • many asymptomatic
  • palpitations, fatigue, dyspnea
  • if rapid (HR<150) and untreated:
    • tachycardia-induced cardiomyopathy
    • decreased LVEF
    • Systolic heart failure
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5
Q

Who is at at higher risk for A fib?

A
  • elderly patients and with heart disease
  • anything that dilates atria
    • CHF
    • Valvular disease
  • Coronary Disease, Diabetes, Hypertension
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6
Q

A fib triggers

A
  • “holiday heart” (binge drinking)
  • increased catecholamines (drive up SNS)
    • infection
    • surgery
    • pain
  • often no trigged identified
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7
Q

What determines the heart rate in in Afib?

List the atrial and ventricular rate in afib

A

**AV node refrctory period **

Atrial rate is double the ventricular rate:

Afib atrial rate: 300-500 bpm

Ventricular rate: 70-180 bpm

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8
Q

Valvular Afib vs. non-valvular

A

Valvular:

  • associated with rheumatic heart disease
  • usually mitral stenosis

(endocarditis affects the mitral valve–think of pyogenes chef with M cap)

Non-valvular:

  • not associated with rheumatic disease
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9
Q

Two very high risk factors for stroke

A

Mitral stenosis + A fib

  • mitral valve stenosis: sluggish blood flow because mitral valve is thick
  • Note: arrythmia itself is NOT life threatening, but thrombus formation is dangerous- can break off and form embolism
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10
Q

Path of an Afib embolism

A

Embolus can travel to any sight that comes off the aorta:

  • brain (stroke)
  • gut (mesenteric ischemia)
  • spleen
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11
Q

Tool used to assess stroke risk in Afib patients

A

CHADs Score

higher value = higher risk of stroke = more intense blood thinner drug

CHADs VASC score also factors in being female, adds age group 67-75, and valvular disease

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12
Q

Anticoagulation in Afib patients (3) and important alarm re thrapy

A
  1. Warfarin (INR monitoring, goal: 2-3)
  2. Factor 10 inhibitors
    1. Rivaroxiban
    2. Apixiban
  3. Direct thrombin inhibitor
    1. Dabigatran

Alarm: whether AFib persists or sinus rhythm restored, you MUST address anticoagulation, and pt must remain on an AC

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13
Q

Atrial Kick in A fib patients

A
  • normal: atrial kick / atrial contraction prefills the L ventricle
  • Afib: atria contract irregularly, you lose LV prefilling, preload drops
  • develop heart failure, hypotension (lose prefilling, not enough blood gets through valves), aortic stenosis, severe LVH (stiff ventricle)
  • tolerated in young patients
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14
Q

What conditions require emergent cardioversion

A

Unstable patient in A fib _WITH hypotension _

Caution: look for other causes critical illness

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15
Q

Summary of approach to Afib patients

A
  1. Are they sick?
    • sick = catecholamines, which drive Afib
      • infection, trauma, recent surgery
    • treat underlying condition
  2. Is HR fast?
    • fast = >100
    • control heart rate
      • beta blockers (B1 seletive agents- metoprolol)
      • Ca2+ channel blockers (slows conduction in AV node-verapimil, dilitiazem)
      • Digoxin (oral inoptrope, slows AV node conduction
  3. Anticoagulation?
    • use CHAD score regulations
  4. Rate or rhythm control?
    • Asymptomatic: leave in A fib, “rate control” strategy, just keeping HR under control
    • Symptomatic, some asymptomatic: electrical cardioversion, “rhythm control strategy”
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16
Q

For symptomatic A fib patients, how do you know whether to treat with cardioversion immediately or use anticoagulation first?

A

Symptoms >48 hours: not enough time for blood clot to have formed, can safetly perform cardioversion

Symptoms > 48 hours or unsure: anti-coagulation for 3 weeks, THEN cardioversion

17
Q

Long Term Therapy options for A fib patients

A
  1. Rate control: remain in A fib
    • beta blocker, Ca-blocker, digoxin
    • anti-coagulation
  2. Rhythm control: convert to Sinus
    • usually stay on beta blocker, Ca-blocker, digoxin
    • anti-coagulation

_so essentially the same for either: HR control drug and anticoagulation drug _

18
Q

How do you treat recurrent a fib?

A

Antiarrhthmic drugs:

  • Class I Na blockers (for patients with structurally normal hearts:
    • flecanide
    • propafenone
  • Amiodaron, Sotalol, Dofetilide
  • Pulmonary vein isolation (PVI) - burn tissue around each vein so no longer conduct electricity
19
Q

Formation of pulmonary embolism

A
  • blot clot in leg (usually femoral artery)
  • travels to lung via IVC –> R atrium –> R ventricle
20
Q

Virchow’s triad: 3 conditions necessary for thombus formation

A
  1. endothelial damage
  2. stasis of blood
  3. hypercoaguable state
21
Q

What are the risks for pulmonary embolism?

A
  1. Post op state
    • hypercoaguable (surgery)
    • stasis, not moving much
    • endothelial damage (surgery)
  2. Fall/hip fracture
    • stasis
    • endothelial damage (trauma)
  3. long plane flight
  4. Malignancy (hypercoaguable state which leads to blood clots)
  5. Oral contraceptive pills
    • increase platelet adhesions and clotting factors
22
Q

Factor V Leiden Mutation

A

mutant factor V that cant be degraded by Protein C

23
Q

Prothrombin gene mutation

A

Increased prothrombin production

24
Q

Antithrombin deficiency

A

Blunted increase PTT after heparin (heparin resistance)

25
Q

Protein C/S defiency

A

Cannot inactivate Factors 5 and 7

*also see skin necrosis after warfarin administration in Protein C deficiency *

26
Q

Scenario where you see an increased PT/PTT, decreased platelet, but also arterial and venous clots

A

Antiphospholipid Syndrome

  • primary or secondary to lupus
  • antibodies directed against plasma proteins, so takes longer to clot (increased PT/PTT)
  • but you also get a lot of clotting
27
Q

What usually precedes pulmonary embolism?

A

Deep vein thrombosis

  • calf pain
  • palpable cord (thrombosed vein)
  • unilateral edema
  • warmth, tenderness, erythema
  • Homan’s sign (calf pain with dorsiflexion of foot)
28
Q

What’s characteristic sign of a pulmonary embolism?

A

-pleuritic chest pain: worsens with deep breath

(other classical signs like dyspnea, hypoxia, tachypnea)

29
Q

The classic ECG finding in the setting of a pulmonary embolism

A

-sinus tachycardia, however the “S1Q3T3” pattern of is classic

  • lead I: QRS has deep S wave
  • lead III: Q wave and inverted T wave
  • V1: Pseudo RBBB
30
Q

Well score

A

determines likelihood of DVT or PE

31
Q

In DVT/PE, what happens to D-dimer levels?

A
  • elevated (elevated in many other conditions, which is why this is a sensitive test but not specific)
  • D-dimer is degraded FIBRIN product: tells us how much clotting is going on
  • recall: thombin cleaves fibrinogen to fibrin = clot

plasmin snips off pieces of fibrin, and left with different fragments. D-dimer is a specific fragment of fibrin

32
Q

How do you diagnose PE?

A
  1. CT angiogram
  2. VQ scan: inhale gaseous radionucleotide, shows where air goes in the lungs, then administered an IV nucleotide to show where blood flow goes in the lungs
    - looking for deficit (good perfusion by air but bad perfusion of blood)
33
Q

What is treatment for DVT/PE?

A
  • Heparin or LMWH
  • Warfarin
  • If massive PE: tPA
34
Q

Why might a blood clot travel from venous side to arterial system?

A
  • Patent Foramen Ovale
  • failure of FO to close after birth
  • in embryo, FO allows blood to pass from RA to LA
  • PFO can allow clot to reach brain
35
Q

Type of emoblism that usually occurs after a long bone fracture

A

fat embolism

  • fat may cross lungs –> small artery infarctions
  • on ARTERIAL side of body, so can get brain infarcts
  • petechia-microemboli into the skin
36
Q

Type of emboli that usually occurs during labor or shortly after

A

Amniotic fluid embolism

  • fluid causes massive inflammatory reaction
  • shock, respiratory failure, DIC, seizures

MOD 2 (13 decks)

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