Week 1 Flashcards
Define automaticity
Intrinsic ability to spontaneously depolarize to threshold and stimulate an action potential
Describe how abnormalities in automaticity lead to atrial fibrillation
altered automaticity, abnormal automaticity, or triggered activity
suggested causes in AF
- Heterogeneity of cardiac myocytes–>depolarization and repolarization at different times–>asynchronous contraction, opens the door for retrograde/feedback loops
- Cardiac cell injury–>leaking of ions, change in properties can lead to other cells developing the ability to fire an impulse–if depolarize faster than the SA node–>take over the role of primary pacemaker or cause ectopic beats; cells do not conduct the same impulse as SA node
- Pulmonary vein current can lead to increased impulse firing/tachycardia–> can outpace the SA node or overstimulate cells that are normally NOT pacemaker cells–>ectopic atrial impulses
expected rate of depolarization of the SA node and the conduction time to the AV node
- SA node rate of 60-100
- AV node rate 50-60
- Conduction time=PR interval, 0.12-0.2s
Explain the interpretive value of the shape and duration of the P wave and PR interval
- P
- PR interval
- P wave: atrial contraction; usually left and right happen almost concurrently so are superimposed into one P wave; normal size= <2.5 mm (2.5 small boxes) tall
- PR interval (from beginning of P wave to beginning of QRS): represents the pause between SA and AV node firing that allows ventricular filling; normal size= 0.12-0.2s (3-5 small boxes)
EKG differences in A-fib
- some sources say there aren’t any P waves, others say the P waves are polymorphic (varying sizes and shapes) and random firing of atria lead to fibrillation
Locate the site of a cardiac anatomical abnormality based on the conduction abnormalities identified in an ECG tracing
- p wave
- QRS
- T wave
- P wave abnormalities indicate atrial dysfunction
- QRS=ventricular, His-Purkinje system
- T wave= ventricular origin
Explain how multiple wandering re-entrance circuits can result in atrial fibrillation
- Re-entrance circuits–>continued re-stimulation–>self-propagating circuits that stimulate action potentials and may not respond to SA node (on different rate so could be in refractory when SA node try to stimulate)–>ectopic stimulation of cardiomyocytes
- If there are multiple–>multiple ectopic beats–>too many stimuli firing at different times–>lead to heterogeneity of cells (some depolarizing, some repolarizing, some getting excited)–>asynchronous, “vibrate”= AF
Relate changes in thyroid function to cardiac dysrhythmias
Hyperthyroidism=^ TH–>^ cardiac output–>^ heart rate; consistently high heart rate can stress or damage the cells–>lead to development of heterogenous properties, ^ risk of developing abnormal rhythm
components of the CHA2DS2-VASc Score
a. C: CHF
b. H: Hypertension
c. A: Age
d. D: Diabetes
e. S: Stroke/ TIA/ thromboembolism history
f. VA: VAscular disease history
g. S: Sex
types of atrial fibrillation
- Paroxysmal= lasts <1 week, convert spontaneously; episodes can recur
- Persistent= lasts >1week (weeks to months), can convert spontaneously but usually require intervention
- Permanent= choose not to convert
Describe the role of INR monitoring in anticoagulation therapy
Tell you if Warfarin (Coumadin) is appropriately “thinning” the blood to prevent clot formation; goal is 2-3 (2.5-3.5 if high risk of clot)
Summarize the difference between rate and rhythm control in the management of atrial fibrillation
- Rate control–usually through medications, but can also utilize ablation (stop impulse from conducting) or pacemaker placement
- Rhythm control–through electrical or pharmacologic conversion;
- rate control can only affect the PACE of beats, rhythm control corrects the PATTERN of beats
MOA of diltiazem
- nodal cell vs myocyte
L-type Ca2+ channel blocker–>slow depolarization (Phase 0 of slow-response/nodal action potentials) and slow Ca2+ sensitive-K+ channel from opening and allowing repolarization (delay Phase 3, prolong Phase 2)–> slow the rate; relaxation of smooth muscle and vasodilation
integrative approaches to atrial fibrillation
- Avoid large meals–can cause gastric distention–>^ vagal stimulus–>decrease heart rate (issue if already on rate control medication)
- Less Na+ in diet bc it stimulates catecholamine release
- Avoid alcohol and caffeine
- Exercise: can induce episode of atrial fibrillation, but is also important for heart health and training can decrease sympathetic activation/tone–>consider lower intensity exercise like walking, yoga
- Meditation and relaxation techniques to also decrease sympathetic control
- Coenzyme Q–helpful for control of hypertension–>decrease stress on the heart; decrease episodes of AF (unknown how)
- Magnesium–related to Ca2+ and K+ metabolism (poorly understood how); decrease arrhythmias by decreasing triggered activity and slowing conduction through AV node
- Fish oil–healthy fat acids, help protect cell membranes and decrease inflammation that can irritate the heart
