Support

1
Drug Therapy
Haemodynamic
in
Support
Kitty Chan School of Nursing,The Hong Kong
Polytechnic University Email hskittyc_at_inet.polyu.
edu.hk Date 2004
2
Objectives

• Upon completion of the module, the students
  should have
• developed a basic understanding of anatomy and a
  basic understanding of the clinical application
  of drugs for haemodynamic support as well as for
  advanced cardiac life support (ACLS)

3
Indicative Readings
Darovic G O 2002 Haemodynamic Monitoring
Invasive and Noninvasive Clinical Application.
3rd ed. Philadelphia W B Saunders Company.
Chapter 14 Pharmacologic Influences on
Haemodynamic Parameters
4
Introduction
The correction of underlying causes or the
control of precipitating factors in heart failure
is always the first line of treatment.
Pharmacological therapy may modify or reverse
adverse consequences to improve the symptoms and
promote a beneficial outcome of the
clients. Multiple drug therapies are used to
manage the haemodynamic status of the clients in
critical care settings. Understanding the
mechanism of the action of the drugs and primary
effect in relation to the patients condition and
haemodynamic parameters may enhance evaluations
of the efficacy of drugs and determine their
therapeutic end point.
5
Introduction
In this module, cardiovascular medications that
are commonly used in critical care areas and the
principles of administering drugs are
highlighted. Rapid and ever-changing advances in
drug therapies occur in the field of
pharmacology. Recommended regimes of medication
may be revised from time to time. Healthcare
givers are advised to regularly verify the latest
changes. It is our responsibility to update and
broaden our knowledge and take appropriate
precautions when administering drugs.
6
Basic Concept of Cardiac Output
7
Desired Pharmacological Cardiovascular Effect

• Circulatory dysfunction a decrease in cardiac
  output are common urgencies in critical care
  settings.
• Drugs with a rapid effect are required for
  haemodynamic support to maintain stability
  accommodate physiologic changes.
• Goal Optimization of Cardiac Output
• Enhancing Stroke Volume
• Antiarrhythmia

8
Drugs Therapy Optimization of CO 1

• 1. Inotropes (? Contractility)
• Beta-adrenergic
• Alpha-adrenergic
• Digitalis
• e.g., Adrenaline, Nor-adrenaline, Dopamine
  Dobutamine
• Disadvantages These agents are arhythmogenic,
  and cause the heart rate increase, thereby
  affecting the cardiac workload and oxygen
  consumption
• 2. Diuretics (? Preload)
• Angiotensin-Converting Enzyme (ACE) Inhibitors
  e.g. Lisinopril, enalapril
• Loop diuretics e.g., Lasix
• Potassium-sparing diuretics e.g. spironolactone
  or amiloride
• Thiazide e.g., hydrochlorthiazide
• These agents relieve symptoms caused by
  peripheral pulmonary oedema

9
Drugs Therapy Optimization of CO 2

• 3. Vasodilators (? Afterload)
• Nitrates e.g., Nitroglycerin, nitroprusside
• ?-Antagonists Minipress, Cardura, Hytrin
• Beta-Blocking Agents (?-blockers) e.g. Betaloc,
  Carvedilol
• Angiotensin-Converting Enzyme (ACE) Inhibitors
  e.g., Captopril
• Calcium Channel Blockers (Ca Antagonists) e.g.,
  Verapamil, Nifedipine, Diltiazem
• Hydrallazine
• 4. Vasopressors (? SVR)
• ?-Agonists e.g., Phenylephrine, Nor-adrenaline
• 5. Volume Expanders (? Preload)
• Blood Transfusion
• Colloids Crystalloids

10
Pharmacologic Effect on Haemodynamic Parameters
Many of the cardiovascular drugs have multiple
actions and can be classified in various
categories. Vasoactive medications should be
infused parenterally via the central line to
assure their bioavailability and employed as
precautionary measures of extravasation in the
peripheral line. Since the coexisting
ventricular dysfunction affects the effect of the
medication, a haemodynamic status that is of
normal value may not acheive optimal cardiac
output. The drugs efficacy are usually titrated
according to the haemodynamic parameters to the
clinical manifestations of the clients.
11
Pharmacologic Effect on Haemodynamic Parameters
Agents Agents HR MAP SV CO CVP PAP PCWP SVR
Inotropes Adrenaline ? ? ?? ? ? ? ? ?
Inotropes Noradreanline 0/? ? ?? ?? ? ? ? ?
Inotropes ?Dopamine 0/? 0/? ?? ? 0/? 0/? 0/? 0/?
Inotropes Dobutamine 0/? 0/? ? ? 0/? 0 0/? ?
Inotropes Digoxin ? 0 ? ? 0/? 0/? 0/? ?
Vasopressor Phenyephrine 0/? ? ? ?? ? ? ? ?
Vasodilator Nitroglycerin 0/? ? ? ? 0/? ? ? ?
Vasodilator Nitroprusside ? ? ? ? 0/? 0/? 0/? ?
Vasodilator Hydrallazine ? ? ? ? 0/? ? 0/? ?
Antiarrhythmic Lignocaine 0 0/? 0 0/? 0 0/? 0 0/?
Antiarrhythmic Propanolol ? ? 0/? ? 0/? 0/? 0/? 0/?
Antiarrhythmic Metoprolol ? ? ? ? 0/? 0/? 0/? 0
Antiarrhythmic Labetalol ? ? ? ? ? ? ? ?
Antiarrhythmic Diltiazem 0/? 0/? ?? ?? 0/? 0/? 0/? ?
Antiarrhythmic VerapamiL ? 0/? 0 ?? 0/? 0/? 0/? ?
?Points to Note The Effect of Dopamine is
Dose-dependent
12
Functional Classification of Adrenergic Receptor
Sites
13
Vasoactive Drugs
14
Vasoactive Drugs Inotropes Vasopressors
DOPAMINE ?1 (?2) ? DA
Adrenergic Receptor Stimulation Receptor-specif
ic Effects of Physiologic Pharmacologic
Catecholamines
Opie L H Gersh B J 2001 Drugs for the Heart
5th ed Philadelphia W B Saunders.
15
Vasodilators
Vasodilator (IV) Dosage Onset Duration Remarks
Nitroglycerin 5-10 mcg/min By 10mcg/min at 5min intervals 1-5 min 30min Venodilation ? ? preload Slight arterial dilation Preserve coronary blood flow Epicardial Collateral Coronary Arteries dilation Direct cerebral vasodilation ? headache Bradycardia Hypotension
Nitroprusside 0.3-2 mcg/Kg/min Max 10mcg/Kg/min for a few mins ONLY 30-60 sec POTENT Arterial AND Veno-dilator in systemic, coronary, pulmonary renal circulation BP ? to pre-therapy in 1-10min Labile BP may due to hypovolemia Contraindicated with coarctation of aorta or arteriovenous shunt induced hypertension In Dissecting Aortic Aneurysm, TREAT with aß1-Blocker Monitoring the Thiocyanate cyanide toxicity monitoring e.g., lactic acidosis, seizures psychosis PHOTOSENSITVE degrades rapidly in light POTENT Arterial AND Veno-dilator in systemic, coronary, pulmonary renal circulation BP ? to pre-therapy in 1-10min Labile BP may due to hypovolemia Contraindicated with coarctation of aorta or arteriovenous shunt induced hypertension In Dissecting Aortic Aneurysm, TREAT with aß1-Blocker Monitoring the Thiocyanate cyanide toxicity monitoring e.g., lactic acidosis, seizures psychosis PHOTOSENSITVE degrades rapidly in light
Hydrallazine 5-10mg to a max of 20mg at 5-20min intervals 5-20 min 2-6hrs Arterial dilation Minor venodilator effects Indicated for moderate to severe Hypertension Severe CHF Use with caution in coronary artery disease, rheumatoid mitral valve disease, dissecting aortic aneurysm CVA
16
Vasodilators Anti-Anginals
REDUCED AFTERLOAD
SYSTEMIC CIRCULATION
Ca2 Blockers ß- Blockers Nitrates
Beta-Blockers
-ve Chronotropic
Inotropic
SA
PERIPHERAL ARTERIOLES
Nitrates
Vasodilation
VENOUS CAPACITANCE
REDUCED PRELOAD
REDUCED VENOUS RETURN
Opie L H Gersh B J 2001 Drugs for the Heart
5th ed Philadelphia W B Saunders.
17
Vasodilator NitratesEffect on Circulation
18
ß-Blocking Agents (ß-adrenergic Antagonists)

• Indications
• Hypertensive crisis
• SVT
• Ventricular Arrhythmias (especially those
  associated with digitalis toxicity or
  catecholamine excess)
• Absolute Cardiac Contraindications
• Severe bradycardia
• Preexisting High Degree Heart Block
• LV failure
• Pulmonary Contraindiations
• Asthma
• Severe Bronchospasm

19
ß-Blocking Agents (ß-adrenergic Antagonists)
Beta-blockers (IV) Onset Duration Remarks
Propanolol 1-5min 10-20min Non-selectiveß-Blocker NOT A FIRST LINE DRUG Predispose to status asthmaticus Synergistic effects with verapamil causing asystole
Atenolol 1min Peak5min 12hrs ß1-Blocker (cardioselective) Contraindicated in heart block, bradycardia or pulmonary oedema
Metoprolol 10min 5-8hrs ß1-Blocker (cardioselective) Contraindicated in heart block, bradycardia or pulmonary oedema
Esmolol 5min 20-30 min Short-acting ß1-Blocker (cardioselective)
Labetalol 2-5min Peak10 mins 2-6hrs Non-selectiveß-Blocker a1 adrenergic blocking NOT A TITRATABLE DRUG (to give a noticeable effect takes 10min with ? drip rate OR several hours after the dose has been reduced/ discontinued)
20
Calcium Channel Blocking Agents

• Actions
• Inhibits the influx of transmembrane Ca ions,
  arterial smooth muscles and myocardium
• ? Refractoriness Slows the conduction of AV
  Node
• Vasodilator (? SVR/Afterload) Coronary
  Vasodilatation
• Negative inotrope negative chronotrope
• Indications
• Antihypertensive
• Terminates reentrant tachyarrhythmias
• Controls HR in AF A flutters
• Chronic stable angina

21
Calcium Channel Blocking Agents
CCB (IV) Onset Duration Duration Remarks
Diltiazem 5-7 min 10-20 min Diltiazem LESS LIKELY TO PRECIPITATE HEART FAILURE OR HYPOTENSION than Verapamil NEVER administer to slow HR in SINUS TACHYCARDIA (e.g., fever hypovolemia where ? HR is a physiological response to compensate for CO) Contraindications SSS Wide complex VT Bradycardic or hypotensive clients Caution when combined with ß-Blocker digoxin use in Second Third Degree Heart Block Diltiazem LESS LIKELY TO PRECIPITATE HEART FAILURE OR HYPOTENSION than Verapamil NEVER administer to slow HR in SINUS TACHYCARDIA (e.g., fever hypovolemia where ? HR is a physiological response to compensate for CO) Contraindications SSS Wide complex VT Bradycardic or hypotensive clients Caution when combined with ß-Blocker digoxin use in Second Third Degree Heart Block
Verapamil Peak 5min 10-20 mins Diltiazem LESS LIKELY TO PRECIPITATE HEART FAILURE OR HYPOTENSION than Verapamil NEVER administer to slow HR in SINUS TACHYCARDIA (e.g., fever hypovolemia where ? HR is a physiological response to compensate for CO) Contraindications SSS Wide complex VT Bradycardic or hypotensive clients Caution when combined with ß-Blocker digoxin use in Second Third Degree Heart Block Diltiazem LESS LIKELY TO PRECIPITATE HEART FAILURE OR HYPOTENSION than Verapamil NEVER administer to slow HR in SINUS TACHYCARDIA (e.g., fever hypovolemia where ? HR is a physiological response to compensate for CO) Contraindications SSS Wide complex VT Bradycardic or hypotensive clients Caution when combined with ß-Blocker digoxin use in Second Third Degree Heart Block
22
ß-Blockers Calcium Channel Blockers
Haemodynamics
ß-Blockers
-ve Chronotropic ? CO HR x SV
? PVR ? ? BP
Initially ?PVR then? or ?
ß-Blockers
Opie L H Gersh B J 2001 Drugs for the Heart
5th ed Philadelphia W B Saunders
23
Diuretics Preload ReductionDiuretic Sites of
Action
Opie L H Gersh B J 2001 Drugs for the Heart
5th ed Philadelphia W B Saunders
24
Shock

• Classification
• Hypovolemic Shock - inadequate vascular volume
• Cardiogenic Shock - ? CO due to impaired
  ventricular function
• Distributive Shock - massive vasodilation caused
  by the abnormal distribution of intravascular
  volume
• Septic - severe systemic infection
• Neurogenic - loss of sympathetic tone
• Anaphylactic - severe hypersensitive reactions

25
Acute Pulmonary Oedema, Hypotension Shock

• Differentiate determine the source of the
  problem
• Volume
• Pump
• Rate
• Pulmonary Oedema

• Hypotension Acute Pulmonary Oedema are
  indicators of Cardiogenic Shock

26

• Acute Pulmonary Edema, Hypotension Shock
• Clinical Signs Shock, Hypoperfusion, CHF, APO?

Acute Pulmonary Oedema
Volume Problem
Pump Problem
Rate Problem
Bradycardia or Tachycardia Algorithms

• 1st line - APO
• Frusemide IV 0.5-1.0MG/Kg
• Morphine IV 2-4mg
• Nitroglycerin S.L.
• Oxygen/Intubation as needed

• Administer
• Fluids
• Blood Transfusions
• Cause-specific interventions
• ?Consider vasopressors

BLOOD PRESSURE ?
Systolic BP BP defines 2nd line of action
Systolic BP lt 70mmHg S/S of Shock
Systolic BP 70- 100 mmHg S/S of Shock
Systolic BP 70- 100 mmHg NO S/S of Shock
Systolic BP gt 100mmHg
Nitroglycerin 10-20 ?g/min IV
Dopamine 5-15 ?g/Kg/min IV
Dobutamine 2-20 ?g/Kg/min IV
Norepinephrine 0.5-30 ?g/min IV

• 2nd line - APO
• Nigroglycerin/Nitroprusside if BP gt 100mmHg
• Dopamine if BP 70-100mmHg S/S of shock
• Dobutamine if BP gt100mmHg NO S/S of shock

• Further diagnostic/therapeutic considerations
• Pulmonary artery catheter
• Intra-aortic Balloon Pump
• Angiography for AMI/Ischaemia
• Additional diagnostic studies

27
Haemodynamic Changes Interventions
PULMONARY OEDEMA
OPTIMAL FILLING PRESSURE
Marino, P. L. (1998) The ICU Book. (2nd ed)
Philadelphia Lippincott Williams Wilkins. P248
fig.16.5
28
Haemodynamic Changes Interventions
Circulatory Support Aim Assessment
Fluid Therapy Fluid Challenge 250ml over lt20min Optimize preload sustained ? CVP, PCWP, but little/no ? CO gtgt Risk of Pulmonary oedema with further fluid admininstration Transient ? CO BP gtgt more fluid replacement indicated
Inotropes and Vasoactive Drugs Optimize HR Haemodynamic Support Titrate to MAP 65-70mmHg Transient ? CO BP gtgt more fluid replacement indicated
Cardiac pacemakers ventilatory support ? cardiopulmonary work Improve coronary systemic perfusion ? cardiopulmonary work Improve coronary systemic perfusion
IABP ? cardiopulmonary work Improve coronary systemic perfusion ? cardiopulmonary work Improve coronary systemic perfusion
Left Ventricular Assistive Devices ? cardiopulmonary work Improve coronary systemic perfusion ? cardiopulmonary work Improve coronary systemic perfusion
Leach, R. (2004). Crticial Care Medicine at a
Glance. UK Blackwell Publishing.
29
Haemodynamic Changes Interventions
From Cardiovascular compensatory mechanisms and
the detrimental positive feedback effects they
exert in heart failure. The location of action of
key drugs, by Leach, R. (2004). Critical Care
Medicine at a Glance. p. 48. UK Blackwell
Publishing.
30
Dysrhythmias Resuscitation Algorithms

• 1. Ventricular Tachycardia (VT)/Ventricular
  Fibrillation (VF)
• 2. Asystole
• 3. Pulseless Electrical Activity (PEA)
• Electromechanical Dissociation (EMD)
• Pseudo-EMD
• Idoventricular Rhythms
• Ventricular Escape Rhythms
• Bradyasystolic Rhythms
• Post-defibrillation Idoventricular rhythms

VT VF are the most common rhythms in cardiac
arrest aim to reestablish cardiac rhythm
early defibrillation improves the outcome
31
Dysrhythmias Resuscitation Algorithms

• 4. Tachydysrhythmias
• Atrial Fibrillation/Atrial Flutter
• Narrow-complex tachycardias
• Stable Wide-complex tachycardias
• monomorphic
• polymorphic
• 5. Bradycardia

32
Antiarrhythmic Drug Therapy Class Action
Hudak C M, Gallo B M Morton P G (ed) 2002
33
Combination of Antiarrhythmic Drug

• A combination of drugs is favoured
• When a single medication fails
• Reduce the dose to diminish side effects
• DO NOT combine agents of the same class or
  subclasses
• Has potentially additive side-effects
• ? risk of dysrhythmias

34
Use of Adenosine

• Adenosine Triphosphate (ATP)
• Actions
• Depresses sinus automaticity
• Changes atrial tissue repolarizaton
• Slow AV node conduction
• Indications
• DRUG OF CHOICE FOR SYMPTOMATIC PSVT (RE-ENTRY
  PATHWAYS)
• NOT for chaotic Atrial Flutter or Atrial
  Fibrillation
• DIAGNOSTIC for Tachycardia with wide QRS
  complexes

35
Diagnostic Use of Adenosine
? Onset of Atriaoventricular Block
? Atrial Flutter Revealed
? PSVT with Wide QRS Complexes
The onset of ATP action takes only a few seconds.
The underlying dysrhythmia is due to atrial
flutter/fibrillation or a ventricular origin is
revealed. Caution must be taken against the
serious tachycardia due to the risk of atrial
flutter with a 11 AV block.
Opie L H Gersh B J 2001 Drugs for the Heart
5th ed Philadelphia W B Saunders
36
Diagnostic Use of Adenosine
Preparation for Adenosine Challenge Preparation for Adenosine Challenge
1. Patient History NO Asthma Adenosine will lead to bronchospasm
2. Warning Reassurance Chest tightness, flushing , headache may arise during Adenosine administration but last for 20 seconds Symptoms usually develop when an effective dose is reached
3. ECG Recording Lead II (good P waves)
4. Resuscitation Trolley Standby
5. IV Access Available 0.9 NS for flushing (10ml)
6. Dosage 3mg IV Bolus, Note the Occurrence of AV Block on ECG. If there is NO Effect within 30 seconds ? ? 6mg ? ? 9mg ? ? 12mg
7. Evaluation Adenosine will Either Terminate the Tachycardia (AVNRT) in 90-100 clients OR Cause a Transient AV Block (revealing an underlying Atrial Rhythm)
37
Amiodarone

• Amiodarone
• Powerful antiarrhythmic agents
• arrhythmias in congestive heart failure
• prophylaxis treatment for recurrent atrial
  fibrillation or VT
• cardiac arrest in non-clinical settings
• Risk of hypotension (IV)
• multisystem side-effects
• serious pulmonary infiltration fibrosis
• Toxicity screening required for long-term use

38
Sotalol

• Sotalol
• Effective in sinus tachycardia, PSVT, WPW, AF, VT
  VF
• Contraindicated in bradycardia, heart blocks
  SSS
• greater risk of torsades de pointes

Opie L H Gersh B J 2001 Drugs for the Heart
5th ed Philadelphia W B Saunders.
39
Effect of Amiodarone Sotalol
Generally, Amiodarone is more powerful than
Sotalol
Agt S
S gt A
Atrial Ectopies
WPW
Negative Effect
Negative Effect
PSVT
Sustained VT
Post-Infarction Prophylaxis
Arrhythmia of CHF
Agtgt S
ONLY Amiodarone
Opie L H Gersh B J 2001 Drugs for the Heart
5th ed Philadelphia W B Saunders
40
Lidocaine

• Lidocaine
• Suppression of serious ventricular arrhythmias in
  AMI or post-cardiac surgery ( ?correct hypoK)
• NOT for chronic recurrent ventricular arrhythmias
  
• Free of haemodynamic effects

41
Quinidine

• Quinidines
• Conversion of atrial flutter atrial
  fibrillation
• Monitor widened QRS ? serious conduction delay
  Toxicity ? idiosyncrasy
• Contraindicated in VT predisposed to Torsades
  de pointes

42
Emergency Treatment of Hyperkalemia

• 3 Principles
• Antaganize Calcium Chloride
• Shift into Cells
• Sodium Bicarbonate
• Dextrose Insulin Infusion
• Albuterol Nebulizer
• Remove from Body
• Diuresis with Lasix
• Cation-exchange Resin (Kayexalate)
• Peritoneal Dialysis
• Hemodialysis

43
Electrolytes Disturbance

• Indications of Sodium Bicarbonate in
  resuscitation
• Class I known pre-existing ? K
• Class IIa pre-existing H2CO3- responsive
  acidosis
• Class IIb
• prolonged resuscitation with effective
  ventilation
• spontaneous circulation after a long arrest
  interval
• Class III hypercarbic acidosis

e.g., DKA, tricyclic antidepressant overdose such
as cocaine
e.g., CPR without intubation

• In cardiac arrest patients
• Misconception Bicarbonate is the buffering
  agent
• CPR Adequate Ventilation is the Key to
  eliminating acidosis

44
References

• Hazinski M F, Cummins R O Field J M (ed) 2000
  2000 Handbook of Emergency Cardiovascular Care
  for Healthcare Providers. American Heart
  Association.
• Jackson K (ed) 2002 Mastering ACLS. Springhouse
  Springhouse.
• Leach R 2004 Critical Care Medicine at a Glance.
  UK Blackwell Publishing.
• Opie L H Gersh B J 2005 Drugs for the Heart.
  5th ed Philadelphia W B Saunders.
• Swearingen P L Keen J H 2002 Manual of Critical
  Care Nursing Nursing interventions and
  Collaborative Management. 4th ed St Louis Mosby.
• Urden L D, Stacy K M Lough M E 2002 Thelans
  Critical Care Nursing Diagnosis and Management.
  4th ed St Louis Mosby.
• Wiegand L-M D J Carlson K K (ed) 2005 AACN
  Procedure Manual for Critical Care. 5th ed
  Philadelphia Saunders.

45
References

• Lo C B WONG T W 2003 AE Clinical Guidelines
  No.14 Guidelines on Rapid Sequence Intubation
  (RSI). Hospital Authority in Hong Kong,
  Electronic Knowledge Gateway.
• Lau C C, Tong H K, Liu H W, Hung C T, Tsang D,
  Yam L Yung R 2003 AE Clinical Guidelines
  No.16 Guideline for in-hospital resuscitation of
  patients at risk of SARS . Hospital Authority in
  Hong Kong, Electronic Knowledge Gateway.

46
Journals

• American Heart Association. Guidelines 2000 for
  Cardiopulmonary Resuscitation and Emergency
  Cardiovascular Care International Consensus on
  Science 2000 Part 3 Adult Basic Life Support
  Section 1 - 8. Circulation, Vol 102 (8)
  Supplement August ppI-22-59.
• American Heart Association. Guidelines 2000 for
  Cardiopulmonary Resuscitation and Emergency
  Cardiovascular Care International Consensus on
  Science 2000 Part 6 Advanced Cardiovascular Life
  Support Section 1 - 8. Circulation, Vol 102 (8)
  Supplement August ppI-86-171.
• Burns S M 2001 Safely caring for patients with a
  laryngeal mask airway. Critical Care Nurse, Vol
  21 (4) pp72-76.

47
Journals

• Cummins R Hazinski M F 2000 Guidelines Based on
  the Principle First, Do No Harm New Guidelines
  on Tracheal Tube Confirmation and Prevention of
  Dislodgment. Circulation, Vol 102 (8) Supplement
  I-380-I384.
• Carroll P 1999 Respiratory Monitoring
  EVOLUTIONS CAPNOGRAPHY. RN Vol 62 (5) 68-71.
• Soliz J M, Sinha A C Thakar D R 2002 Airway
  Management A Review Update. The Internet
  Journal of Anesthesiology, Vol 6 (1).
  http//216.39.195.244/ostia/index.php?xmlFilePath
  journals/ija/vol6n1/airway.xml Accessed on 20
  February 2003.

48
e-Book

• Lippincott Clinical Choice
• Harwood-Nuss, A., Wolfson, A. B., Linden, C. H.,
  Shepherd, S. M. Stenklyft, P. H. (ed) (2001)
  The Clinical Practice of Emergency Medicine.
  Philadelphia Lippincott Williams Wilkins.
• Chapter 129 Cardiac arrest and
  resuscitation

Video

• Sudbury M 2001 Professional Rescuer CPR Academy
  or American Orthopaedic Surgeons, National Safety
  Council Jones Barlett Publishers (Call no.-
  RC87.9.P76)