Electrocardiography + PE Flashcards
(36 cards)
Explain why this is an example of A fib
- no clear P waves before the QRS
- some of the QRS are close together, some are far apart
- irregularly irregular pattern
Describe normal conduction in the heart and then conduction with A fib
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
Differences between Paroxysmal, Persistent, and Permanent Atrial Fibrillation
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)
Major symptoms of A fib, and consequences if left untreated
- many asymptomatic
- palpitations, fatigue, dyspnea
- if rapid (HR<150) and untreated:
- tachycardia-induced cardiomyopathy
- decreased LVEF
- Systolic heart failure
Who is at at higher risk for A fib?
- elderly patients and with heart disease
- anything that dilates atria
- CHF
- Valvular disease
- Coronary Disease, Diabetes, Hypertension
A fib triggers
- “holiday heart” (binge drinking)
- increased catecholamines (drive up SNS)
- infection
- surgery
- pain
- often no trigged identified
What determines the heart rate in in Afib?
List the atrial and ventricular rate in afib
**AV node refrctory period **
Atrial rate is double the ventricular rate:
Afib atrial rate: 300-500 bpm
Ventricular rate: 70-180 bpm
Valvular Afib vs. non-valvular
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
Two very high risk factors for stroke
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
Path of an Afib embolism
Embolus can travel to any sight that comes off the aorta:
- brain (stroke)
- gut (mesenteric ischemia)
- spleen
Tool used to assess stroke risk in Afib patients
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
Anticoagulation in Afib patients (3) and important alarm re thrapy
- Warfarin (INR monitoring, goal: 2-3)
- Factor 10 inhibitors
- Rivaroxiban
- Apixiban
- Direct thrombin inhibitor
- Dabigatran
Alarm: whether AFib persists or sinus rhythm restored, you MUST address anticoagulation, and pt must remain on an AC
Atrial Kick in A fib patients
- 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
What conditions require emergent cardioversion
Unstable patient in A fib _WITH hypotension _
Caution: look for other causes critical illness
Summary of approach to Afib patients
- Are they sick?
- sick = catecholamines, which drive Afib
- infection, trauma, recent surgery
- treat underlying condition
- sick = catecholamines, which drive Afib
- 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
- Anticoagulation?
- use CHAD score regulations
- 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”
For symptomatic A fib patients, how do you know whether to treat with cardioversion immediately or use anticoagulation first?
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
Long Term Therapy options for A fib patients
- Rate control: remain in A fib
- beta blocker, Ca-blocker, digoxin
- anti-coagulation
- 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 _
How do you treat recurrent a fib?
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
Formation of pulmonary embolism
- blot clot in leg (usually femoral artery)
- travels to lung via IVC –> R atrium –> R ventricle
Virchow’s triad: 3 conditions necessary for thombus formation
- endothelial damage
- stasis of blood
- hypercoaguable state
What are the risks for pulmonary embolism?
- Post op state
- hypercoaguable (surgery)
- stasis, not moving much
- endothelial damage (surgery)
- Fall/hip fracture
- stasis
- endothelial damage (trauma)
- long plane flight
- Malignancy (hypercoaguable state which leads to blood clots)
- Oral contraceptive pills
- increase platelet adhesions and clotting factors
Factor V Leiden Mutation
mutant factor V that cant be degraded by Protein C
Prothrombin gene mutation
Increased prothrombin production
Antithrombin deficiency
Blunted increase PTT after heparin (heparin resistance)
