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Atrial Fibrillation (dysrhythmias) Flashcards

1
Q

what is a dysrhythmia

A

it is an abnormal heart rate or rhythm that alters the cardiac cycle (filling and emptying)

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2
Q

what are the two main problems that arise from arrythmias

A
  • dec CO. (up to 30% dec)

- when the blood isnt being pushed through the atria it pools and can put pt at risk of clots

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3
Q

Etiology of arrythmias

(her suggestions) 12

A 
her notes:
-cardiomyopaty
-alcohol
-age
-hyperthyroid
•	CAD
•	HTN
•	MI
•	CHF
•	Digoxin toxicity
•	Valvular damage
•	Electrolyte imbalance. Paricularly potassium.
•	COPD
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4
Q

what is an atrial fibrillation (from patho)

A

irreg, chaotic contractions of atria (400-600)

-irreg, rapid Ventricle rate (~80-180BPM)

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5
Q

what is an ectopic beat or rhythm

A

Ectopic beat (or cardiac ectopy) is a disturbance of the cardiac rhythm frequently related to the electrical conduction system of the heart, in which beats arise from fibers or group of fibers outside the region in the heart muscle ordinarily responsible for impulse formation (i.e., the sinoatrial node)

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6
Q

signs and symptoms of atrial fibrillation

in class

A 
from ppt
Dizzy
Weakness
SOB
Fainting
Palpitations  (skipped beats)
Irregular pulse
(in class)
dt dec CO
•	Sob
•	Dizziness
•	Weak
•	Fatigue
•	Some pts feel palpitations, chest pain (esp w comorbidities)
Clot formation can cause
•	Stroke/CVA
•	PE
•	MI
•	DVT
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7
Q

S/S of arrythmias patho

A

o May be asymptomatic
o May experience significant hemodynamic collapse (hypotension, chest pain, pulmonary edema, altered level of consciousness) esp if they have HTN, mitral stenosis, hypertrophic cardiomyopathy or other restrictive heart failure
o Usually theres a pulse deficit
o Inc likelihood of thrombi and dec myocardial perfusion

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8
Q

what is the number one problem that a. fib can lead to

A

strokes or CVAs

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9
Q

interventions for atrial fibrillation

A

drugs
cardioversion (shock them)
give oxygen

ablation

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10
Q

how do you diagnose a. fib

A

ECG

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11
Q

contraindications for antidysrhythmics

A
  • Allergy
  • All antidysrhymic drugs are potentially dysrhythmogenic (they can worsen dysrhythmias especially in those with structural heart damage) therefore use of them with the following may be contraindicated and careful judgment must be used when prescribing
  • 2nd or 3rd degree AV block
  • Sick Sinus syndrome
  • Any other major ECG changes
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12
Q

Adverse effects of antidysrhythmics in general

A 
Adverse effects of antidysrhythmics
•	Hypersensitivity rxn
•	Nausea
•	Vomiting
•	Diarrhea
•	Dizziness
•	Headache
•	Blurred vision
•	New dysrhythmias (prodysrhythmic effect)
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13
Q

what is a common interaction that one should be aware of with most antidysrhythmics
-how should this be addressed

A

they potentiate warfarin (Coumadin)
-monitor PTT and INR and maybe dec warfarin dose
also grapefruit juice and quinidine increases the risks of the drug

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14
Q

how do beta blockers affect dysrhythmias

A

o Beta adrenergic blockers. Reduce or block SNS stimulation to the heart and therefore block/reduce the impulses in the hearts conduction system.
• Results in dec heart rate, delayed AV node conduction, dec myocardial contractility, dec myocardial automatacity

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15
Q

how is an echocardiogram be useful in a pt w arrythmias

A

it shows the ejection fraction

also An echocardiogram (ECHO) uses sound waves (ultrasound) to create a picture of your heart. The recorded waves show the shape, texture and movement of your heart valves, as well as the size of your heart chambers and how well they are working.

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16
Q

what are the two most prevalent complications that arise from atrial fibrillation

A

CVA and DVT

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17
Q

name a hemodynamic complication of atrial fibrillation and assoc symptoms you would assess

A

dec CO

  • SOB
  • light headed
  • fatigue
  • dizzy
  • chest pain if it were serious
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18
Q

which class of drug might you use for DVT and for a fib

A

anticoagulant

19
Q

what is the effective refractory period and how do you want it to be if pt has atrial fibrillation

A

ERP (effective refractory period: the period after the firing of an impulse during which a cell may respond to a stimulus but the response will not be passed along or continued as another impulse)
-you want this to be prolonged to dec the tachycardia

20
Q

what types of drugs are used to treat dysrythmias (ppt)

A 
Sodium channel blockers
Beta-Blockers 
Potassium channel blockers
Calcium channel blockers
Miscellaneous antidysrhythmic drugs
Digoxin
Amiodarone
21
Q

what is cardioversion. consideration for its use in Tx of a fib pt

A

• Cardioversion-put paddles on pt and shock them. Problem is that you must catch the a fib within 48hrs, dt risk of clot. You can treat them w pharmacology for the clots
Cardioversion is a medical procedure by which an abnormally fast heart rate (tachycardia) or cardiac arrhythmia is converted to a normal rhythm using electricity or drugs. Synchronized electrical cardioversion uses a therapeutic dose of electric current to the heart at a specific moment in the cardiac cycle.

22
Q

what is a cardiac glycoside used to treat pt with a fib. what other heart condition is this drug used for

A

digoxin

heart failure

23
Q

digoxin MOA

A

by inhibiting sodium-potassium pumo which results in inc calcium concentration->inc in myocardial contractility (it is a positive inotrope)

aslo augments vagal tone>inc diastolic filling between heartbeats and reduces heart rate (negative chromotropic effect) which inc CO and cardiac eficiency

dec velocity of conduction ( this is a negative dromotopic) the dec conduction slows heart rate(negative chromotropic))

24
Q

i also wrote abut digoxin in heart failure cards

adverse effects of cardiac glycosides

what is the worst thing that could happen

A

Increase myocardial workload by increasing oxygen demands

  • other negative effects include:
  • dysrhythmias
  • anorexia, nausea, vomiting, abd pain
  • headache, faituge, malaise, confusion, convulsions
  • coloured vision, halos
25
Q

how can you tell if someone is dig toxic

A

anorexia, nausea, vomiting, fatigue, depression, malaise (all early signs)

  • changes in heart rythm or rate, irreg
  • ECG changes
26
Q

how do you treat digoxin toxicity

A

hold the med while monitoring the pts symptoms and serum levels

  • start continuous ECG monitoring, give any dysrhythmic drugs
  • check drug serum levls and elecrtrolyte levels
  • may need to give potassium supplement for hypokalemia
  • if toxicity is extreme then give digoxin immune fab (antidote) which binds to digoxin. when meas serum levels after this it will be inaccurate as it cant differentiate between bound and unbound digoxin
27
Q

what is the therapeutic window with digoxin

consideration for this

A

1-2.5nmol/L

this is a smll window. monitor pt response carfully as well as drug serum levels

28
Q

life threatening digoxin overdose

kids and adults

A

> 10mg in adults

>4mg in kids

29
Q

what to assess for giving antidysrhythmics

A

Basically assess everything. What seems important to me is heart rate etc, BPs (including posturals), electrolytes, clotting problems, edema, pulse deficits, JVD and ECG??

  • Do thorough physical exam, history
  • Another focus of assessment is to get a baseline ECG w interpretation of the results w attention to heart rate, rhythm, character
  • Note heart sounds
  • BP (including postural BPs)
  • Assess apical-radial pulse deficits
  • JVD
  • Edema
  • Prolonged cap refill (longer than 5 seconds)
  • Dec urinary output
  • Activity intolerance
  • Chest pain or pressure
  • Dyspnea
  • Syncope
  • Dizziness
  • Fatigue
  • Nausea
  • Changes in alertness\anxiety
  • Abnormal serum electrolyte levels
  • Kidney and liver fx tests are usually ordered to check if doses are correct
  • Look at blood counts for problems with clotting eg thrombocytopenia
  • Document baseline neuro fx and any neuromuscular deficits such as muscle weakness
  • If pt is on antidysrhythmic you must inspect the skin closely for bruising and bleeding as well as looking for bleeding elsewhere
  • Assess grapefruit juice (interacts with quinidine and inhibits metabolism of cytochrome P450 3A4 liver enzymes
  • Other drugs have specific assessments that aren’t on our list
30
Q

what are the therapeutic responses to antidysrhythmics

A

Summary
• The therapeutic responses to antidysrhythmics include a dec in edema, restoration of reg pulse rate without major irreg or an improvement from earlier in therapy

31
Q

what is digitalization

A

the restoration of acritically ill pt to near normal states within hours due to digoxin therapy

32
Q

effect of diltiazem on arrythmias/the heart

A

-prolongs AV nodal ERP
reduce AV nodal conduction
reduce rapid ventricular conduction caused by atrial futter

33
Q

how does amiodarone (not on case study) affect arrythmias/the heart

A

it prolongs the ERP

  • prolongs myocardial contraction
  • blocks both alpha and beta adrenergic heart stimulation
34
Q

what is the most significant concern with amiodarone

other concerns

A

pulmonary toxicity which is fatal in 10% of pts

skin can develop a blue tinge

  • it is lipophilic and can accumulate in adipose
  • can cause hyper or hypothyroidism
  • advrse rxns happen in 75% of pts on the drug
  • very common effect is corneal microdeposits->visual halos and dry eyes
35
Q

how long does amiodarone stay in the body

A

half life is several days therefore adverse effects can last up to 3 months

36
Q

with its multitude of side effects when is amiodarone used/not used

A

it is a last resort choice
given when pt has life threatening V tachycardia or V fibrillation thats resistant to other drug therapy
also used w atrial issues

37
Q

what are the two or three drugs or classes discussed in class to treat a fib

what else does the book suggest using

A

digoxin and amiodarone
beta blockers

sodium channel blockers
calcium channel blockers
dugs that inc action potential duration

38
Q

what do you assess before giving a cardiac glycoside

A

Most important from this Im guessIing=1. Blood pressure, pulse rate (apical and radial for 1 full minute)

  1. Heart sounds
  2. Peripheral pulse location and grading
  3. Capillary refill
  4. Presence of edema
  5. Breath sounds
  6. Weight
  7. Intake and output amounts
  8. Serum lab values such as potassium, sodium, magnesium, and calcium
  9. Electrocardiogram
  10. Kidney function lab tests (BUN and creatinine levels)
  11. Liver function tests
  12. Medication history
  13. Dietary habits, recall of all food in past 24 hours
  14. Intake of bran ( increases drug absorption)
  15. Smoking history
  16. Alcohol intake
39
Q

dont forget that we should be giving meds for the clots as well!

A

heparin
LMWH
warfarin
ASA

40
Q

heparin what do we need to know

A

Drug name: Heparin (used acutely)
MOA: Potentiates the inhibitory effect of antithrombin on factor Xa and thrombinprevents clots formation; used in sicker pt; 3 hr ½ life
Pre/post assessments: PTT (2.5x normal) prolongation in seconds of coagulation, bleeding
Worst side effect: bleeding

41
Q

LMWH what do we need to know

A

Drug name: LMWH (prophylaxis)
MOA: potentiates the inhibitory effect of antithrombin on factor Xa and thrombinprevents clots; used often for immobility in hospitals
Pre/post assessments: Labs (PTT, PT-INR and platelets- look to see for bleeding tendency; not done anymore), bleeding
Worst side effect: bleeding

42
Q

warfarin what do we need to know

A

Drug name: Warfarin (used long term, only PO)
MOA: interferes w hepatic synthesis of Vit KInhibit the formation of clotting factors therefore increasing clotting time (clotting time is in seconds) to prevent thrombi
Pre/Post assessments: PT-INR (therapetuc-2.5x normal so around 2.5), bleeding
Worst side effect: bleeding

43
Q

other than anticoagulants what else can be used to prevent clots

A

Drug name: Asprin, Plavix
MOA: inhibit platelet aggregation; prolong bleeding time, used to prevent MI or stroke.
Pre/Post assessments: evidence of addition or inc thrombosis; assess for symptoms of stroke, peripheral vascular disease, or MI. PT-INR should be prolonged.
Worst side effect: an allergic reaction, so take an antihistamine/epinephrine.

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