1. Cardiac Arrhythmias
Andrea Székely

2. Objectives
Identify common arrhythmias encountered by the family physician
Discuss arrhythmia etiologies
Discuss initial primary care work-up and treatment
Practice questions

3. Physiology of cardiac rate and rhythm
Cardiac myocytes are electrically excitable
Resting intracellular voltage of myocardial 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
Resting intracellular voltage of myocardial cell is –90mV (high intracellular K maintained by Na/K pump)

4. Phases of action potential of cardiac cells
Phase 0 rapid depolarisation (inflow of Na+)
Phase 1 partial repolarisation (inward Na+ current deactivated, outflow of K+)
Phase 2 plateau (slow inward calcium current)
Phase 3 repolarisation (calcium current inactivates, K+ outflow)
Phase 4 pacemaker potential (Slow Na+ inflow, slowing of K+ outflow) ‘autorhythmicity’
Refractory period (phases 1-3)
Phase 4
Phase 0
Phase 1
Phase 2
Phase 3
0 mV
-80mV II I
III IV

5. Mechanisms of arrhythmia production
Re-entry (refractory tissue reactivated due to conduction block, causes abnormal continuous circuit. eg accessory pathways linking atria and ventricles in Wolff-Parkinson-White syndrome)
Abnormal pacemaker activity in non-conducting/conducting tissue (eg ischaemia)
Delayed after-depolarisation (automatic depolarisation of cardiac cell triggers ectopic beats, can be caused by drugs eg digoxin)
Re-entry is when tisue that is usually refractory is reactivated. Occurs if there is a ring of tissue that does not conduct normally. Usually the two paths of action potentials meet and die out, but if they do not meet then a circuit is set up.
Abnormal pacemaker activity can occur if myocardial cells are damaged eg ischaemic heart disease also via catecholamine overactivity
Delayed after-depolarisation occurs when in cardiac tissue that usually has to wait for the initiation of an action potential from pacemaker tissue, the cardiac cell automatically depolarises. This leads to a repetitive discharge (triggers ectopic beats -‘R on T phenomenon’) (related to extent of inward Ca current) caused by cardiac glycosides eg digoxin
Re-entry (partial conduction block eg accessory pathways linking atria and ventricles eg Wolff-Parkinson-White syndrome) halted by drugs that prolong the refractory period

6. Normal Sinus Rhythm
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 bpm
Each QRS complex is proceeded by a P wave
P wave is upright in lead II & downgoing in lead aVR

7. 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

8. 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
Situational—vagus nerve

9. Sinus bradycardia--treatment
No treatment if asymptomatic
Sxs include chest pain (from coronary 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

10. Sinus tachycardia HR > 100 bpm, regular
Often difficult to distinguish p and t waves

11. Sinus tachycardia--etiologies
Fever
Hyperthyroidism
Effective volume depletion
Anxiety
Pheochromocytoma
Sepsis
Anemia
Exposure to stimulants (nicotine, caffeine) or illicit drugs
Hypotension and shock
Pulmonary embolism
Acute coronary ischemia and myocardial infarction
Heart failure
Chronic pulmonary disease
Hypoxia
Effective Vol Depletion---CHF, cirrhosis, dehydration

12. 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

13. 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

14. Sinus arrhythmia
Usually respiratory--Increase in heart rate during 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

15. 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.

16. Sick Sinus Syndrome--etiology
Often due to sinus node fibrosis, SNode arterial 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

17. Sick sinus syndrome--treatment
Address and treat cardiac conditions
Review med list, TSH
Pacemaker for most is required

18. Paroxysmal Supraventricular Tachycardia
Refers to supraventricular tachycardia other than afib, aflutter and MAT
Occurs in 35 per 100,000 person-years
Usually due to reentry—AVNRT or AVRT

19. PSVT 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

20. 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)

21. 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

22. 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

23. Atrial Fibrillation Irregular rhythm Absence of definite p waves
Narrow QRS
Can be accompanied by rapid ventricular response

24. Atrial Fibrillation—causes and associations
Hypertension
Hyperthyroidism and subclinical hyperthyroidism
CHF (10-30%), CAD
Uncommon presentation of ACS
Mitral and tricuspid valve disease
Hypertrophic cardiomyopathy
COPD
OSA
ETOH
Caffeine
Digitalis
Familial
Congenital (ASD)

25. Atrial fibrillation--assessment
H & P—assess heart rate, sxs of SOB, chest 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 hours? Sudden onset? Or no sxs?

26. Atrial fibrillation--management
Rhythm vs Rate control—if onset is within last 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 hours: need 4-6 weeks of anticoagulation prior to cardioversion, and warfarin for 4-12 weeks after

27. 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

28. Atrial fibrillation--management
Rate control with chronic anticoagulation is 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

29. Atrial fibrillation--management
Goal INR of 2.5 ( )
Rhythm control---second line approach, if unable to control rate or pt with persistent sxs
Can also consider radiofrequency ablation at pulm veins

30. PAC P wave from another atrial focus Occurs earlier in cycle
Different morphology of p wave

31. 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

32. 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

33. 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

34. Wenckebach, Mobitz type I
Usually asymptomatic, but with accompanying 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

35. 2nd degree block Type II (Mobitz 2)
Normal PR intervals with sudden failure of a p wave to 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

36. 3rd Degree AV Block
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

37. PVC
Extremely common throughout the population, both with and without heart disease
Usually asymptomatic, except rarely dizziness or fatigue in patients that have frequent PVCs and significant LV dysfunction

38. PVC No treatment is necessary, risk outweighs benefit Reassurance
Optimize cardiac and pulmonary disease management

39. 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

40. Non-sustained ventricular tachycardia
Need to exclude heart disease with Echo and 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

41. Ventricular fibrillation
Defibrillation

42. Pulseless Electrical Activity
Use the rhythms presented in the next slides to discuss PEA. Any pulseless rhythm that looks as if it could produce a pulse is considered PEA.
Therefore, any pulseless rhythm that is not VF, VT, or asystole should be considered PEA. This rhythm—sinus tachycardia with unifocal PVCs and no pulse—is one form of PEA that could be EMD or pseudo-EMD.
Question: Would anyone in the group give atropine to this patient?

43. Sinus Tachycardia With No Pulse
This rhythm—sinus rhythm without a pulse—is another form of PEA that could be EMD or pseudo-EMD. This patient also has first-degree AV block.
Question: Would anyone in the group give atropine to this patient?

44. PEA? Asystole?
Bradyasystolic rhythms without a pulse are another form of PEA. Mention that asystole is a flat line that will be discussed further in a later case.
Comment on the 2 drugs used for non-specific PEA.
Epinephrine is administered every 3 to 5 minutes during cardiac arrest.
Atropine is used to treat relative bradycardia (remind the group of their answers to the earlier rhythms in regards to giving atropine).
Informal surveys suggest that many ACLS providers consider atropine
one of the standard agents for treating PEA, without reference to the rate
of the electrical activity. Until specific evidence accumulates otherwise,
follow the ACLS recommendation of limiting atropine to absolute or
relative bradycardia. The shorter dosing interval (every 3 minutes) is
possibly helpful (Class IIb) in cardiac arrest.

45. Pulseless Electrical Activity?
Idioventricular rhythms without a pulse are another form of PEA.

46. Pulseless Electrical Activity?
Agonal rhythms without a pulse are another form of PEA.
Discuss that PEA may be due to true EMD, the end stage of many severe cardiac conditions. Review the findings in true EMD. Stress that because of its very poor prognosis, a rapid search for treatable causes is the key strategy. Stress that only a few reversible causes exist, and they must be found and treated quickly.

47. Pulseless Electrical Activity
Review for most frequent causes 1
Hypovolemia
Hypoxia
Hydrogen ion—acidosis
Hyper-/hypokalemia
Hypothermia
“Tablets” (drug OD, accidents)
Tamponade, cardiac
Tension pneumothorax
Thrombosis, coronary (ACS)
Thrombosis, pulmonary (embolism) 2
Epinephrine 1 mg IV push,
repeat every 3 to 5 minutes
Use this algorithm to present an overview of the diverse conditions that can present as PEA. Return to this slide often to reorient the group to the overall list of causes of PEA and their management.
Explain that the algorithm is merely a summary of the conditions that can cause PEA and their management. Reemphasize that the management of almost all of the conditions includes a fluid challenge and assessment and improvement of ventilation. Note also that several of the causes of EMD result in inadequate venous return to the heart, a condition that can be treated.
Because hypovolemia or blood loss is often the easiest cause of PEA to treat and has the best prognosis, it is the most important to seek and treat. Patients with hypovolemia or blood loss may have a history of vomiting, diarrhea, other causes of fluid loss, GI bleeding, major trauma, or other acute bleeding. Several scenarios illustrate cases that might respond to a fluid challenge.
Agonal rhythms without a pulse are another form of PEA.
Discuss that PEA may be due to true EMD, the end stage of many severe cardiac conditions. Review the findings in true EMD. Stress that because of its very poor prognosis, a rapid search for treatable causes is the key strategy. Stress that only a few reversible causes exist, and they must be found and treated quickly.
Discuss that PEA may be a very severe form of hypotension and that a rapid search for treatable causes is the key strategy. Stress that only a few reversible causes exist, and they must be found and treated quickly. Note that almost all patients will benefit from a fluid challenge, which may be the only treatment needed. Also, hypoxia may cause or worsen PEA, so ventilation with supplemental oxygen is essential for all cases.
Use this algorithm to present an overview of the diverse conditions that can present as PEA.
Return to this slide often to reorient the group to the overall list of causes of PEA and their management. Explain that the algorithm is merely a summary of the conditions that can cause PEA and their management. Reemphasize that the management of almost all of the conditions includes a fluid challenge and assessment and improvement of ventilation. Note also that several of the causes of EMD result in inadequate venous return to the heart, which can be treated.
Because hypovolemia or blood loss is often the easiest cause of PEA to treat and has the best prognosis, it is the most important to seek and treat. These patients may have a history of vomiting, diarrhea, other causes of fluid loss, GI bleeding, major trauma, or other acute bleeding. Several scenarios illustrate cases that might respond to a fluid challenge.
Although rare, tamponade may cause PEA. Tamponade is reversible in many cases. The history may include trauma, chest pain, recent CPR, AMI, prior cardiac surgery, metastatic cancer, recent fever, or viral infection. Describe pericardiocentesis, complications, equipment, and choices of approach; demonstrate technique. For more detail, discuss some or all of slides 6 through 17.
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 3

48. Vaughan Williams classification of antiarrhythmic drugs
Class I: block sodium channels
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
III
Phase 0 I
Phase 3
-80mV
Phase 4 II

49. Management of arrhythmias
Acute management (clinical assessment of patient and diagnosis)
Prophylaxis
Non-pharmacological
Pharmacological (some antiarrhythmics are also proarrhythmic)

50. Non-pharmacological treatment
Acute
Vagal manoeuvres
DC cardioversion
Prophylaxis
Radiofrequency ablation
Implantable defibrillator
Pacing (external, temporary, permanent)

51. Pharmacological treatment-Lignocaine (Lidocaine)
Class Ib (blocks Na+ channels, reduces AP 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

52. Flecainide Class Ic (block Na+ channels, no change to 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

53. 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

54. Amiodarone 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

55. Amiodarone – adverse effects
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)

56. Adenosine Not in Vaughan Williams class
Purine nucleotide (activates adenosine receptors)
Slows AV nodal conduction
Acute Rx
Termination of SVT/ diagnosis of VT
Given IV only (rapid bolus)
T1/2 < 2seconds

57. Adenosine- adverse effects
Feeling of impending doom!
Flushing, dyspnoea, chest pain, transient arrhythmias
Contraindicated in asthma, heart block

58. Verapamil Class IV (calcium channel blocker)
Prolongs conduction and refractoriness in AV 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

59. Verapamil- adverse effects
Heart failure
Constipation
Bradycardia
Nausea

60. Digoxin Not in Vaughan Williams class
Cardiac glycoside (digitalis, foxglove)
Act on Na/K-ATPase of cell membrane (inhibits Na+/K+ pump, increases intracellular Na+ and calcium)/ increases vagal activity
Increase cardiac contraction and slows AV conduction by increasing AV node refractory period

61. Digoxin Atrial fibrillation or flutter (controls ventricular 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

62. 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
Digoxin-specific binding (Fab) fragment, antibody to digoxin, neutralises digoxin in the plasma

63. Clinical cases

64. 36 year old woman with asthma has ‘thumping in chest’

65. 76 year old man with breathlessness

66. 54 year woman collapses 24 hours post MI

67. 60 year old man with recurrent blackouts

68. Summary
Anti-arrhythmic drugs are classified by their 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

69. 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.

70. Practice Questions
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

71. 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

72. 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

73. Practice Questions Answer B: completely benign
require no treatment except reassurance

74. 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

75. 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

76. 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 He is in acute distress. His resp rate is 32. ECG shows afib with rapid ventricular response.

77. 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

78. 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.

79. 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.

80. 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

81. 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

82. 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

83. 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

84. 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

85. Practice Questions
Answer B: risk outweighs benefit

86. 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

87. 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.

88. 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.

89. Practice Questions
True or false, the appropriate management at this time includes:
Lidocaine 1 mg/kg IV push
Procainamide, 20mg/min IV infusion
Defibrillation
Transvenous pacemaker

90. 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.

91. 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

92. 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.