Transcript Phase 1

Cardiac Arrhythmias
Andrea Székely
Objectives
• Identify common arrhythmias encountered
by the family physician
• Discuss arrhythmia etiologies
• Discuss initial primary care work-up and
treatment
• Practice questions
Physiology of cardiac rate and
rhythm
• Cardiac myocytes are electrically excitable
• Resting intracellular voltage of myocardial
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cells is negative -90mV (SA node is -40mV)
Resting state - K+ inside and Na+ outside cell
(Na+/K+ pump)
Action potential occurs when Na+ enters
the cell and sets up a depolarising current
Stimulation of a single muscle fibre causes
electrical activity to spread across the
myocardium
Phases of action potential of
cardiac cells
• Phase 0 rapid depolarisation
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(inflow of Na+)
Phase 1
Phase 1 partial repolarisation
(inward Na+ current deactivated,
outflow of K+)
0 mV
Phase 2 plateau (slow inward
calcium current)
Phase 0
I
Phase 3 repolarisation (calcium
current inactivates, K+ outflow)
Phase 4 pacemaker potential
-80mV
Phase 4
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(Slow Na inflow, slowing of K
II
outflow) ‘autorhythmicity’
Refractory period (phases 1-3)
IV
Phase 2
III
Phase 3
Mechanisms of arrhythmia
production
• Re-entry (refractory tissue reactivated due to
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conduction block, causes abnormal continuous
circuit. eg accessory pathways linking atria and
ventricles in Wolff-Parkinson-White syndrome)
Abnormal pacemaker activity in nonconducting/conducting tissue (eg ischaemia)
Delayed after-depolarisation (automatic
depolarisation of cardiac cell triggers ectopic
beats, can be caused by drugs eg digoxin)
Normal Sinus Rhythm
www.uptodate.com
Implies normal sequence of conduction, originating in the sinus node and
proceeding to the ventricles via the AV node and His-Purkinje system.
EKG Characteristics:
Regular narrow-complex rhythm
Rate 60-100 bpm
Each QRS complex is proceeded by a P wave
P wave is upright in lead II & downgoing in lead aVR
Sinus Bradycardia
• HR< 60 bpm; every QRS narrow, preceded by p wave
• Can be normal in well-conditioned athletes
• HR can be<30 bpm in children, young adults during
sleep, with up to 2 sec pauses
Sinus bradycardia--etiologies
• Normal aging
• 15-25% Acute MI, esp. affecting inferior wall
• Hypothyroidism, infiltrative diseases
(sarcoid, amyloid)
• Hypothermia, hypokalemia
• SLE, collagen vasc diseases
• Situational: micturation, coughing
• Drugs: beta-blockers, digitalis, calcium channel
blockers, amiodarone, cimetidine, lithium
Sinus bradycardia--treatment
• No treatment if asymptomatic
• Sxs include chest pain (from coronary
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hypoperfusion), syncope, dizziness
Office: Evaluate medicine regimen—stop all
drugs that may cause
Bradycardia associated with MI will often resolve
as MI is resolving; will not be the sole sxs of MI
ER: Atropine if hemodynamic compromise,
syncope, chest pain
Pacing
Sinus tachycardia
• HR > 100 bpm, regular
• Often difficult to distinguish p and t waves
Sinus tachycardia--etiologies
• Fever
• Hyperthyroidism
• Effective volume
• Hypotension and shock
• Pulmonary embolism
• Acute coronary ischemia
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depletion
Anxiety
Pheochromocytoma
Sepsis
Anemia
Exposure to stimulants
(nicotine, caffeine) or
illicit drugs
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and myocardial infarction
Heart failure
Chronic pulmonary
disease
Hypoxia
Sinus Tachycardia--treatment
• Office: evaluate/treat potential etiology
:check TSH, CBC, optimize CHF or COPD
regimen, evaluate recent OTC drugs
• Verify it is sinus rhythm
• If no etiology is found and is bothersome
to patients, can treat with beta-blocker
Sinus Arrhythmia
• Variations in the cycle lengths between p waves/ QRS
complexes
• Will often sound irregular on exam
• Normal p waves, PR interval, normal, narrow QRS
Sinus arrhythmia
• Usually respiratory--Increase in heart rate during
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inspiration
Exaggerated in children, young adults and
athletes—decreases with age
Usually asymptomatic, no treatment or referral
Can be non-respiratory, often in normal or
diseased heart, seen in digitalis toxicity
Referral may be necessary if not clearly
respiratory, history of heart disease
Sick Sinus Syndrome
•All result in bradycardia
•Sinus bradycardia (rate of ~43 bpm) with a sinus pause
•Often result of tachy-brady syndrome: where a burst of
atrial tachycardia (such as afib) is then followed by a
long, symptomatic sinus pause/arrest, with no
breakthrough junctional rhythm.
Sick Sinus Syndrome--etiology
• Often due to sinus node fibrosis, SNode arterial
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atherosclerosis, inflammation (Rheumatic fever,
amyloid, sarcoid)
Occurs in congenital and acquired heart disease
and after surgery
Hypothyroidism, hypothermia
Drugs: digitalis, lithium, cimetidine, methyldopa,
reserpine, clonidine, amiodarone
Most patients are elderly, may or may not have
symptoms
Sick sinus syndrome--treatment
• Address and treat cardiac conditions
• Review med list, TSH
• Pacemaker for most is required
Paroxysmal Supraventricular
Tachycardia
• Refers to supraventricular tachycardia other than
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afib, aflutter and MAT
Occurs in 35 per 100,000 person-years
Usually due to reentry—AVNRT or AVRT
PSVT
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Initial eval: Is the patient stable?
Determine quickly if sinus rhythm
If not sinus and unstable, cardioversion
Unstable sinus tachycardia---IV beta-blocker, and
treat cause
• Sxs of instability would include: chest pain,
decreased consciousness, short of breath, shock,
hypotension—unstable sxs require shock
PSVT
• If stable, determine whether regular
rhythm (sinus or PSVT) vs irregular
(afib/flutter, MAT)? p waves (MAT vs. AF)?
• If regular, determine whether p waves are
present, if can’t see---administer
adenosine (6mg, can give 2 doses) or CSM
or other vagal maneuvers)
PSVT
• CSM or adenosine commonly terminate
the arrhythmia, esp, AVRT or AVNRT
• Can also use CCB or beta blockers to
terminate, if available
• Counsel to avoid triggers, caffeine, Etoh,
pseudoephedrine, stress
PSVT
• No p waves —junctional tachycardia, AVRT
or AVNRT, Afib
• AVRT and AVNRT: can have retrograde p
waves and short RP interval
• Abnormal p waves morphology: MAT
Atrial Fibrillation
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Irregular rhythm
Absence of definite p waves
Narrow QRS
Can be accompanied by rapid ventricular response
Atrial Fibrillation—causes and
associations
• Hypertension
• Hyperthyroidism and
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subclinical
hyperthyroidism
CHF (10-30%), CAD
Uncommon presentation
of ACS
Mitral and tricuspid valve
disease
• Hypertrophic
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cardiomyopathy
COPD
OSA
ETOH
Caffeine
Digitalis
Familial
Congenital (ASD)
Atrial fibrillation--assessment
• H & P—assess heart rate, sxs of SOB, chest
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pain, edema (signs of failure)
If unstable, need to cardiovert
Echocardiogram to evaluate valvular and overall
function
Check TSH
Assess for RVR
Assess onset of sxs—in the last 24-48 hours?
Sudden onset? Or no sxs?
Atrial fibrillation--management
• Rhythm vs Rate control—if onset is within last
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24-48 hours, may be able to arrange
cardioversion—use heparin around procedure
Need TEE if valvular disease (high risk of
thrombus)
If unable to definitely conclude onset in last 2448 hours: need 4-6 weeks of anticoagulation
prior to cardioversion, and warfarin for 4-12
weeks after
Atrial Fibrillation
• Cardioversion: synchronized (w/QRS)
delivery of current to heart; depolarizes
tissue in a reentrant circuit; afib involves
more cardiac tissue, but cardiovert
• Defibrillation: non-synchronized delivery of
current
Atrial fibrillation--management
• Rate control with chronic anticoagulation is
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recommended for first line approach for majority
of patients; overall Afib is a stable rhythm
Beta-blockers (atenolol and metoprolol) or
calcium channel blockers (verapamil or
diltiazem) recommended. Digoxin not
recommended for rate control
Anticoagulation: LMWH and then warfarin; can
use aspirin for anticoagulation if CI to warfarin,
not as effective
Atrial fibrillation--management
• Goal INR of 2.5 (2.0-3.0)
• Rhythm control---second line approach, if
unable to control rate or pt with persistent
sxs
• Can also consider radiofrequency ablation
at pulm veins
PAC
• P wave from another atrial focus
• Occurs earlier in cycle
• Different morphology of p wave
PAC
• Benign, common cause of perceived
irregular rhythm
• Can cause sxs: “skipping” beats,
palpitations
• No treatment, reassurance
• With sxs, may advise to stop smoking,
decrease caffeine and ETOH
• Can use beta-blockers to reduce frequency
1st Degree AV Block
• PR interval >200ms
• If accompanied by wide QRS, refer to cardiology, high
risk of progression to 2nd and 3rd deg block
• Otherwise, benign if asymptomatic
2nd Degree AV Block Mobitz type I
(Wenckebach)
• Progressive PR longation, with eventual non•
conduction of a p wave
May be in 2:1 or 3:1
Wenckebach, Mobitz type I
• Usually asymptomatic, but with accompanying
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bradycardia can cause angina, syncope esp in elderly—
will need pacing if sxs
Also can be caused by drugs that slow conduction (BB,
CCB, dig)
2-10% long distance runners
Correct if reversible cause, avoid meds that block
conduction
2nd degree block Type II (Mobitz 2)
• Normal PR intervals with sudden failure of a p wave to
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conduct
Usually below AV node and accompanied by BBB or
fascicular block
Often causes pre/syncope; exercise worsens sxs
Generally need pacing, possibly urgently if symptomatic
3rd Degree AV Block
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Complete AV disassociation, HR is a ventricular rate
Will often cause dizziness, syncope, angina, heart failure
Can degenerate to Vtach and Vfib
Will need pacing, urgent referral
PVC
• Extremely common throughout the population, both with
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and without heart disease
Usually asymptomatic, except rarely dizziness or fatigue
in patients that have frequent PVCs and significant LV
dysfunction
PVC
• No treatment is necessary, risk outweighs
benefit
• Reassurance
• Optimize cardiac and pulmonary disease
management
Non-sustained Ventricular
tachycardia
• Defined as 3 or more consecutive ventricular beats
• Rate of >120 bpm, lasting less than 30 seconds
• May be discovered on Holter, or other exercise testing
Non-sustained ventricular
tachycardia
• Need to exclude heart disease with Echo and
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stress testing
If normal, there is no increased risk of death
May need anti-arrhythmia treatment if sxs
In presence of heart disease, increased risk of
sudden death
Need referral for EPS and/or prolonged Holter
monitoring
Ventricular fibrillation
• Defibrillation
Pulseless Electrical Activity
Sinus Tachycardia
With No Pulse
PEA? Asystole?
Pulseless Electrical Activity?
Pulseless Electrical Activity?
Pulseless Electrical Activity
Review for most frequent causes
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Hypovolemia
Hypoxia
Hydrogen ion—acidosis
Hyper-/hypokalemia
Hypothermia
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“Tablets” (drug OD, accidents)
Tamponade, cardiac
Tension pneumothorax
Thrombosis, coronary (ACS)
Thrombosis, pulmonary (embolism)
Epinephrine 1 mg IV push,
repeat every 3 to 5 minutes
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Atropine 1 mg IV (if PEA rate is slow),
repeat every 3 to 5 minutes as needed, to a total
dose of 0.04 mg/kg
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Vaughan Williams classification of
antiarrhythmic drugs
• Class I: block sodium channels
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– Ia (quinidine, procainamide,
disopyramide) AP
– Ib (lignocaine) AP
– Ic (flecainide) AP
Class II: ß-adrenoceptor
antagonists (atenolol, sotalol)
Class III: prolong action
potential and prolong refractory
period (suppress re-entrant
rhythms) (amiodarone, sotalol)
Class IV: Calcium channel
antagonists. Impair impulse
propagation in nodal and
damaged areas (verapamil)
Phase 1
IV
Phase 2
0 mV
Phase 0
-80mV
I
Phase 4
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III
Phase 3
Management of arrhythmias
• Acute management (clinical assessment of
patient and diagnosis)
• Prophylaxis
• Non-pharmacological
• Pharmacological (some antiarrhythmics
are also proarrhythmic)
Non-pharmacological treatment
• Acute
– Vagal manoeuvres
– DC cardioversion
• Prophylaxis
– Radiofrequency ablation
– Implantable defibrillator
• Pacing (external, temporary, permanent)
Pharmacological treatmentLignocaine (Lidocaine)
• Class Ib (blocks Na+ channels, reduces AP
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duration)
Ventricular arrhythmias (acute Rx)
IV infusion only (2 hour half life, high first pass
metabolism)
Hepatic metabolism (inhibited by cimetidine,
propranolol)
SE mainly CNS - drowsiness, disorientation,
convulsions, hypotension
Flecainide
• Class Ic (block Na+ channels, no change to
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AP)
Slows conduction in all cardiac cells
Acute Rx /prophylaxis
Supraventricular tachycardias
Paroxysmal atrial fibrillation
Ventricular tachycardias
Oral/IV
Long acting (T1/2 14 hours)
Hepatic metabolism, urinary elimination
Flecainide
• CAST (Cardiac Arrhythmia Suppression
Trial) 1989 – increased mortality post MI
(VF arrest)
• SE- cardiac failure, ventricular
arrhythmias, blurred vision, abdominal
discomfort, nausea, paraesthesia,
dizzyness, tremor, metallic taste
Amiodarone
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Class III - increases refractory period and AP
Major effect acutely is depression of AV node
Acute Rx/prophylaxis
Atrial and ventricular arrhythmias
Oral or IV (central line)
Loading and maintenance doses
T1/2 54 days
Large volume of distribution
Accumulates
Hepatic metabolism- biliary and intestinal excretion
Amiodarone – adverse effects
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Photosensitive rashes
Grey/blue discolouration of skin
Thyroid abnormalities 2%
Pulmonary fibrosis
Corneal deposits
CNS/GI disturbance
Pro-arrhythmic effects (torsade de pointe)
Heart block
Nightmares 25%
Abnormal LFT 20%
Interacts with digoxin, warfarin (reduces clearance)
Adenosine
• Not in Vaughan Williams class
• Purine nucleotide (activates adenosine
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receptors)
Slows AV nodal conduction
Acute Rx
Termination of SVT/ diagnosis of VT
Given IV only (rapid bolus)
T1/2 < 2seconds
Adenosine- adverse effects
• Feeling of impending doom!
• Flushing, dyspnoea, chest pain, transient
arrhythmias
• Contraindicated in asthma, heart block
Verapamil
• Class IV (calcium channel blocker)
• Prolongs conduction and refractoriness in AV
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node, slows rate of conduction of SA node
Acute Rx /prophylaxis
Used IV/oral
SUPRAVENTRICULAR NOT VENTRICULAR
ARRHYTHMIAS (cardiovascular collapse)
Do not use IV verapamil with ß- blocker (heart
block)
T1/2 6-8 hours
Verapamil- adverse effects
• Heart failure
• Constipation
• Bradycardia
• Nausea
Digoxin
• Not in Vaughan Williams class
• Cardiac glycoside (digitalis, foxglove)
• Act on Na/K-ATPase of cell membrane (inhibits
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Na+/K+ pump, increases intracellular Na+ and
calcium)/ increases vagal activity
Increase cardiac contraction and slows AV
conduction by increasing AV node refractory
period
Digoxin
• Atrial fibrillation or flutter (controls ventricular
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rate)
Acute Rx/prophylaxis
Oral/IV
Loading and maintenance doses
T1/2 36 hours
Excreted by kidneys
Narrow therapeutic index
Therapeutic drug monitoring
Reduce dose in elderly/renal impairment
Digoxin – adverse effects
• Arrhythmias, heart block, anorexia,
nausea, diarrhoea, xanthopsia,
gynaecomastia, confusion, agitation
• AE potentiated by hypokalaemia and
hypomagnesaemia
• Overdose –Digibind (digoxin binding
antibody fragments), phenytoin for
ventricular arrhythmias, pacing, atropine
Clinical cases
36 year old woman with asthma
has ‘thumping in chest’
76 year old man with
breathlessness
54 year woman collapses 24
hours post MI
60 year old man with recurrent
blackouts
Summary
• Anti-arrhythmic drugs are classified by their
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effect on the cardiac action potential
Not all drugs fit this classification
In clinical practice treatment of arrhythmias is
determined by the type of arrhythmia (SVT,
VT) and clinical condition of the patient
Anti-arrhythmic drugs are efficacious but may
have serious adverse effects
Not all arrhythmias are treated with drug
therapy alone
Practice Questions—Case 1
• 37-year old male comes to office for
“skipping heart beats.” Going on over last
8 months, no other sxs: no sweating,
palpitations, wt loss, chest pain, anxiety or
pleuritic chest pain.
On PE, BP is 100/70, normal S1S2, no
murmurs/gallops. You hear about 5
premature beats.
Practice Questions
1. What is the most commonly encountered
“premature contraction?”
a. a ventricular premature beat
b. an atrial premature beat
c. atrial flutter
d. atrial fibrillation
e. none of the above
Practice questions
Answer B: atrial premature beats
• Most common premature beat in adults
• Almost always asxs
• Often patients c/of sxs during stress, or
while laying quietly
Practice Questions
2. Most atrial premature beats discovered on
clinical examination are:
a. associated with COPD
b. completely benign
c. associated with valvular heart disease
d. associated with an increase in
cardiovascular mortality
e. None of the above
Practice Questions
Answer B: completely benign
• require no treatment except reassurance
Practice Questions
3. Most ventricular premature beats
discovered on clinical exam are:
a. associated with COPD
b. completely benign
c. associated with valvular heart disease
d. associated with increased
cardiovascular mortality
e. none of the above
Practice Questions
Answer B: completely benign
• Patients need reassurance
• Usually asymptomatic
• Occasionally can be associated with severe
heart disease with multiple PVCs in a row--Vtach---which can cause syncope, chest
pain, dyspnea and cardiac arrest
Practice Questions—Case 2
A 51 year old male presents to the
emergency room with an acute episode of
chest pain. He has a history of afib. On
exam BP is 70/50, and ventricular rate is
160. He is in acute distress. His resp rate
is 32. ECG shows afib with rapid
ventricular response.
Practice Questions
4. What should your first step in
management be?
a. digitalize the patient
b. give the patient IV verapamil
c. give the patient IV adenosine
d. start synchronized cardioversion
e. start rapid IV hydration
Practice Questions
Answer D: this patient has an acute onset
afib with RVR, with chest pain and
hypotension. Treatment of choice per
ACLS protocol is cardioversion.
Practice Questions—Case 3
A 44 year old male comes to your ER saying
he has palpitations. Denies chest pain or
SOB. No known history of CAD or risk
factors except mild obesity. Does admit to
drinking heavily the night before.
On PE, BP is 120/80 and heart rate is 160.
ECG confirms afib with rapid ventricular
response.
Practice Questions
5. What should you do at this time?
a. digitalize the patient
b. treat the patient with IV verapamil
c. treat the patient with IV procainamide
d. cardiovert the patient
e. have him perform a Valsalva maneuver
by rebreathing into a paper bag
Practice Questions
Answer B: this patient has the same
condition but is hemodynamically stable.
His afib is following Etoh ingestion, not
uncommon after holidays and weekends.
Initial management would be rate control
Practice Questions
6. What is the recommended treatment for
PSVT with hemodynamic compromise?
a. synchronized cardioversion
b. direct-current counter shock
c. IV adenosine
d. IV verapamil
e. IV digoxin
Practice Questions
Answer A: cardioversion. If a patient
presents with stable PSVT, start with vagal
maneuvers or adenosine. Vagal
maneuvers can help diagnosis, by slowing
rate, and treat arrhythmia. CSM, ice pack,
Valsalva are all possible maneuvers.
Pressing eyeballs---not recommended.
This patient however is unstable--shock
Practice Questions
Which of the following statements about treatment
of atrial premature beats is true?
a. the benefit outweighs the risk
b. the risk outweighs the benefit
c. the risk and benefit are equal
d. the risk and benefit depend on the patient
e. nobody really knows for sure
Practice Questions
Answer B: risk outweighs benefit
Practice questions
Which of the following statements about treatment
of ventricular premature beats is true?
a. the benefit outweighs the risk
b. the risk outweighs the benefit
c. the risk and benefit are equal
d. the risk and benefit depend on the patient
e. nobody really knows for sure
Practice Questions
Answer B: risk outweighs benefit.
For both PACs and PVCs, unless
circumstances are unusual and
documented by EPS studies, multiple trials
have shown that the risk outweighs the
benefit for both.
Practice questions
• A 50 year old male is brought to the
emergency department via EMS c/of
severe substernal chest pain, w/nausea,
diaphoresis. BP is 90mm Hg systolic, HR
120 bpm. Pulse disappears on arrival and
monitor shows Vtach. Venous access is
established and he has O2 via mask.
Practice Questions
True or false, the appropriate management
at this time includes:
1. Lidocaine 1 mg/kg IV push
2. Procainamide, 20mg/min IV infusion
3. Defibrillation
4. Transvenous pacemaker
Practice Questions
• 1. False, 2. False, 3. True, 4. False
The patient is having an MI. Unstable,
pulseless Vtach is treated with
defibrillation---unstable pts with Vtach
include those with sxs (chest pain, SOB),
hypotension, CHF, ischemia or infarction, if
still with pulse—cardioversion first, then
defibrillate if necessary.
Practice Questions
His rhythm stabilizes and you note evidence
of acute MI on EKG. Which of the
following should be taken into account
when considering thrombolytic therapy?
5. Degree of coronary occlusion
6. Whether the patient has a hx of stroke
7. Time interval from onset of sxs
Practice Questions
5. false, 6. true, 7. true
tPa is contraindicated in persons with recent
(<3 months) hx of internal bleeding; known
hemorrhagic diathesis; hx of stroke, intracranial
AV malformation, neoplasm, aneurysm; severe,
uncontrolled htn just prior to administration;
recent intracranial, intraocular, intraspinal
surgery; recent trauma or cpr; recent tPa.
Thrombolytics are considered appropriate up to
12 hours after sxs onset.