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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
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
Indicative Readings
4
IntroductionThe 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 patient’s 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.
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Basic Concept of Cardiac Output Cardiac Cardiac OutputOutput
Heart Rate
Stroke Volume
Contractility
Preload
Ventricular
Compliance
Venous
Return
Afterload
Blood Volume
Peripheral Vascular
Resistance(PVR)
Aortic Impedance
7
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 OutputGoal: Optimization of Cardiac Output
1.1. Enhancing Stroke VolumeEnhancing Stroke Volume
2.2. AntiarrhythmiaAntiarrhythmia
Desired Pharmacological Cardiovascular Effect
8
Drugs Therapy: Optimization of CO [1]1. Inotropes ( Contractility)
Beta-adrenergicAlpha-adrenergic Digitalise.g., Adrenaline, Nor-adrenaline, Dopamine & DobutamineDisadvantages: 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, enalaprilLoop diuretics: e.g., LasixPotassium-sparing diuretics: e.g. spironolactone or amilorideThiazide: e.g., hydrochlorthiazideThese 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, CarvedilolAngiotensin-Converting Enzyme (ACE) Inhibitors: e.g., CaptoprilCalcium Channel Blockers (Ca Antagonists): e.g., Verapamil, Nifedipine, DiltiazemHydrallazine
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 ParametersAgents HR MAP SV CO CVP PAP PCWP SVR
InotropesInotropes Adrenaline ↑ ↑ ↑↓ ↑ ↑ ↑ ↑ ↑Noradreanline 0/↑ ↑ ↑↓ ↑↓ ↑ ↑ ↑ ↑
Dopamine 0/↑ 0/↑ ↑↓ ↑ 0/↑ 0/↑ 0/↑ 0/↑
Dobutamine 0/↑ 0/↑ ↑ ↑ 0/↑ 0 0/↓ ↓
Digoxin ↓ 0 ↑ ↑ 0/↓ 0/↓ 0/↓ ↑
VasopressorVasopressor Phenyephrine 0/↑ ↑ ↓ ↑↓ ↑ ↑ ↑ ↑
VasodilatorVasodilator Nitroglycerin 0/↑ ↓ ↑ ↑ 0/↓ ↓ ↓ ↓
Nitroprusside ↑ ↓ ↑ ↑ 0/↓ 0/↓ 0/↓ ↓Hydrallazine ↑ ↓ ↑ ↑ 0/↓ ↓ 0/↓ ↓
AntiarrhythmicAntiarrhythmic Lignocaine 0 0/↓ 0 0/↑ 0 0/↓ 0 0/↓
Propanolol ↓ ↓ 0/↑ ↓ 0/↓ 0/↓ 0/↑ 0/↑
Metoprolol ↓ ↓ ↑ ↓ 0/↓ 0/↓ 0/↑ 0Labetalol ↓ ↓ ↑ ↓ ↓ ↓ ↓ ↓
Diltiazem 0/↓ 0/↓ ↑↓ ↑↓ 0/↓ 0/↓ 0/↑ ↓
VerapamiL ↓ 0/↓ 0 ↑↓ 0/↓ 0/↓ 0/↓ ↓
Points to Note: The Effect of Dopamine is Dose-dependent
12
Functional Classification of Adrenergic Receptor Sites
Receptor Location Responses to Stimulation
Alpha (1) Vessels of: Skin Kidneys Intestines
Vasoconstriction of peripheral arterioles
Alpha (2) Presynaptic Nerve Terminals
Inhibition of the release of catecholamine Peripheral Vasodilation
Beta1 (1) Cardiac tissue: SA node AV node Myocardium
Heart rate (chronotropic) conduction (dromotropic) contractility (inotropic)
Beta2 (2) Smooth muscles of: Vascular Bronchial
Vasodilation of peripheral arterioles Bronchodilation
Dompaminergic Vascular smooth muscles:
Renal Coronary Mesenteric
Vasodilation
13
Vasoactive DrugsADRENERGIC EFFECT VASOPRESSORS IV INFUSION
Dose 1 2
DOPAMINERGIC ARRHYTHMOGENIC POTENTIAL
EPINEPHRINE 2-10 µg/min ++++ ++++ ++ - +++ NOREPINEPHRINE 2-8 µg/min ++++ +++ - - ++
1-5 µg/Kg/min - - ++ +++ + 5-10 µg/Kg/min + ++ ++ - ++
DOPAMINE
10-20 µg/Kg/min
+++ +++ - - +++
DOBUTAMINE 2-20 µg/Kg/min + ++++ ++ - ++ ISOPROTERENAL 2-10 µg/min + ++++ ++ - +++
14
Vasoactive Drugs: Inotropes & Vasopressors
Opie L H & Gersh B J 2001 Drugs for the Heart 5th ed Philadelphia: W B Saunders.
DOPAMINE
1 (2) DA
DOPAMINE
1 (2) DA
* Adrenergic Receptor Stimulation:
Receptor-specific Effects of Physiologic & Pharmacologic Catecholamines
* Adrenergic Receptor Stimulation:
Receptor-specific Effects of Physiologic & Pharmacologic Catecholamines
Inotropic 1 (2)
Inotropic 1 (2)
11
DA1DA1
DOBUTAMINE
1 > 2 >
DOBUTAMINE
1 > 2 >
Inotropic
High Dose
Vasoconstriction
Peripheral Vasodilatio
n
Renal Blood Flow
DA1 DA2
1 (2)
InotropicNOREPINEPHRINE
1 > > 2
NOREPINEPHRINE
1 > > 2
EPINEPHRINE
1 = 2 >
EPINEPHRINE
1 = 2 >
15
VasodilatorsVasodilator (IV)
Dosage Onset Duration Remarks
Nitroglycerin
5-10 mcg/minBy 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/minMax 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 aβ1-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
Ischaemic Zone
Ischaemic Zone
Vasodilators: Anti-Anginals
Opie L H & Gersh B J 2001 Drugs for the Heart 5th ed Philadelphia: W B Saunders.
REDUCED PRELOADREDUCED PRELOADREDUCED VENOUS RETURN
REDUCED VENOUS RETURN
REDUCED AFTERLOAD
REDUCED AFTERLOAD
Vasodilation
PERIPHERALARTERIOLESPERIPHERALARTERIOLES
VENOUSCAPACITANCE
VENOUSCAPACITANCE
SYSTEMICCIRCULATION
SYSTEMICCIRCULATION
Ca2+ Blockersβ- BlockersNitrates
Ca2+ Blockersβ- BlockersNitratesInotropi
cSASA
-ve Chronotropic
17
Opie L H & Gersh B J 2001 Drugs for the Heart 5th ed Philadelphia: W B Saunders.
REDUCED
PRELOAD
REDUCED
PRELOAD
REDUCED
VENOUS RETURN
REDUCED
VENOUS RETURN
REDUCED
AFTERLOAD
REDUCED
AFTERLOAD
Vasodilation
PERIPHERAL
ARTERIOLES
PERIPHERAL
ARTERIOLES
VENOUS
CAPACITANCE
VENOUS
CAPACITANCE
SYSTEMIC
CIRCULATION
SYSTEMIC
CIRCULATION
ToleranceTolerance
ToleranceTolerance
Renin Angiotension II
Renin Angiotension II
Blood Volume ↑Blood Volume ↑
Ischaemic Ischaemic ZoneZone
Ischaemic Ischaemic ZoneZone
Vasodilator: NitratesEffect on Circulation
18
β-Blocking Agents (β-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
β-Blocking Agents (β-adrenergic Antagonists)
Beta-blockers (IV)
Onset Duration Remarks
Propanolol 1-5min 10-20min Non-selectiveβ-Blocker
NOT A FIRST LINE DRUGPredispose to status asthmaticusSynergistic effects with verapamil causing asystole
Atenolol 1minPeak~5min
12hrs β1-Blocker (cardioselective)
Contraindicated in heart block, bradycardia or pulmonary oedema
Metoprolol 10min 5-8hrs
Esmolol 5min 20-30 min Short-acting β1-Blocker (cardioselective)
Labetalol 2-5minPeak~10 mins
2-6hrs Non-selectiveβ-Blocker + α1 adrenergic blockingNOT 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)
On
set
Dura
tion
Remarks
Diltia
zem5-7 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 β-Blocker & digoxin use in Second & Third Degree Heart Block
Vera
pamilPeak:5min
10-20 mins
22
β-Blockers & Calcium Channel Blockers: Haemodynamics
Opie L H & Gersh B J 2001 Drugs for the Heart 5th ed Philadelphia: W B Saunders
AVAVSASA
-ve Chronotropic CO = HR x
SV
Contraindicated ∵ it causes
bronchospasms
Inhibits contraction of heart muscles
Decrease
Coronary Tone
PVR → BP
Initially PVR then
or
23Opie L H & Gersh B J 2001 Drugs for the Heart 5th ed Philadelphia: W B Saunders
Diuretics: Preload ReductionDiuretic Sites of ActionDiuretic Sites of Action
Impermeable to H2O
Impermeable to H2O
H2O with
ADH
H2O
NaNa++ Pump Pump
NaNa++ HH22OO NaNa++
KK++ 2Cl2Cl--
NaNa++ KK++
2Cl2Cl--
ClCl- - NaNa++
ClCl- - NaNa++
KK++KK++
NaNa++NaNa++
NaNa++NaNa++
HH++HH++
24
ShockClassification:
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
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
Differentiate & determine the source
of the problem:
Volume
Pump
Rate
Pulmonary Oedema
Hypotension & Acute Pulmonary Oedema are
indicators of Cardiogenic Shock
Hypotension & Acute Pulmonary Oedema are
indicators of Cardiogenic Shock
26
Systolic BPBP defines 2nd line of action
Systolic BPBP defines 2nd line of action
Acute Pulmonary Edema, Hypotension & ShockAcute Pulmonary Edema, Hypotension & ShockClinical Signs: Shock, Hypoperfusion, CHF, APO?
Acute Pulmonary Edema, Hypotension & ShockAcute Pulmonary Edema, Hypotension & ShockClinical Signs: Shock, Hypoperfusion, CHF, APO?
1st line - APO◈ Frusemide IV 0.5-1.0MG/Kg◈ Morphine IV 2-4mg◈ Nitroglycerin S.L.◈ Oxygen/Intubation as needed
1st line - APO◈ Frusemide IV 0.5-1.0MG/Kg◈ Morphine IV 2-4mg◈ Nitroglycerin S.L.◈ Oxygen/Intubation as needed
Bradycardia or
Tachycardia Algorithms
Bradycardia or
Tachycardia Algorithms
Acute Pulmonary OedemaAcute Pulmonary Oedema
Norepinephrine
0.5-30 g/min IV
Norepinephrine
0.5-30 g/min IV
Further diagnostic/therapeutic considerations:◈ Pulmonary artery catheter◈ Intra-aortic Balloon Pump◈ Angiography for AMI/Ischaemia◈ Additional diagnostic studies
Further diagnostic/therapeutic considerations:◈ Pulmonary artery catheter◈ Intra-aortic Balloon Pump◈ Angiography for AMI/Ischaemia◈ Additional diagnostic studies
Volume ProblemVolume Problem
Pump ProblemPump Problem
Rate ProblemRate Problem
Systolic BP < 70mmHg
S/S of Shock
Systolic BP < 70mmHg
S/S of Shock
Systolic BP 70- 100 mmHg
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 70- 100 mmHg
NO S/S of Shock
Systolic BP > 100mmHg
Systolic BP > 100mmHg
Administer◈ Fluids◈ Blood Transfusions◈ Cause-specific interventions◈ ✼Consider vasopressors
Administer◈ Fluids◈ Blood Transfusions◈ Cause-specific interventions◈ ✼Consider vasopressors
BLOOD BLOOD
PRESSURE ?PRESSURE ?
BLOOD BLOOD
PRESSURE ?PRESSURE ?
2nd line - APO
◈ Nigroglycerin/Nitroprusside if BP > 100mmHg
◈ Dopamine if BP = 70-100mmHg; S/S of shock
◈ Dobutamine if BP >100mmHg; NO S/S of shock
2nd line - APO
◈ Nigroglycerin/Nitroprusside if BP > 100mmHg
◈ Dopamine if BP = 70-100mmHg; S/S of shock
◈ Dobutamine if BP >100mmHg; NO S/S of shock
Dopamine
5-15 g/Kg/min IV
Dopamine
5-15 g/Kg/min IVDobutamine
2-20 g/Kg/min IV
Dobutamine
2-20 g/Kg/min IVNitroglycerin
10-20 g/min IV
Nitroglycerin
10-20 g/min IV
27
HEARTFAILURE
Haemodynamic Changes & Interventions
Pulmonary Capillary Wedge Pressure (mmHg)
10 20 30
1
2
3
Card
iac
Ind
ex (
L/m
in/m
2)
NORMAL
OPTIMALFILLING
PRESSURE
PULMONARYOEDEMA
Volume
Diuresis
Inotropesor
Vasodilators
Marino, P. L. (1998) The ICU Book. (2nd ed) Philadelphia: Lippincott Williams & Wilkins. P248 fig.16.5
28
Haemodynamic Changes & Interventions
Leach, R. (2004). Crticial Care Medicine at a Glance. UK: Blackwell Publishing.
Circulatory Support
Aim Assessment
Fluid TherapyFluid Challenge ~250ml over <20min
Optimize preload sustained ↑ CVP, PCWP, but little/no ↑ CO >> Risk of Pulmonary oedema with further fluid admininstrationTransient ↑ CO & BP >> more fluid replacement indicated
Inotropes and Vasoactive Drugs
Optimize HR& Haemodynamic Support
Titrate to MAP 65-70mmHgTransient ↑ CO & BP >> more fluid replacement indicated
Cardiac pacemakers & ventilatory support
↓ cardiopulmonary workImprove coronary & systemic perfusion
IABP
Left Ventricular Assistive Devices
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
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
4. Tachydysrhythmias
Atrial Fibrillation/Atrial Flutter
Narrow-complex tachycardias
Stable Wide-complex tachycardias:
monomorphic
polymorphic
5. Bradycardia
32
Class Common Antiarrhythmic Drug
Channel Effect Repolarization Time
Class I Membrane Stabilizing: automaticity of ectopic pacemaker foci & slow conduction abolish re-entry circuit
Class IA
Quinidine Disopyramide Procainamide
Markedly inhibitory effect on sodium movement Reduces the maximal velocity of phase 0 depolarization
Prolongs
Class IB Lidocaine Phenytoin
Block sodium movement Slows phase 0 depolarization at a fast HR action potential duration
Shortens
Class IC
Flecainide Propafenone
Blocks sodium movement reduces phase 0 depolarization at normal rates
Unchanged
Class II -blockers *sotalol has class III effect
Block sympathetic stimulation of the conduction system Limits spontaneous depolarization Calcium channel, phase IV current
Unchanged
Class II I
Amiodarone Sotalol Bretylium
Prolongs action potential duration Repolarizes a K+ currents
Markedly prolongs
Class IV
Adenosine (ATP) Calcium channel blockers; e.g., verapamil, diltiazem
AV nodal Ca2+ antagonists conduction velocity
Unchanged
Antiarrhythmic Drug Therapy: Class & Action
Hudak C M, Gallo B M & Morton P G (ed) 2002
33
Combination of Antiarrhythmic DrugA 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
Opie L H & Gersh B J 2001 Drugs for the Heart 5th ed Philadelphia: W B Saunders
AdenosineAdenosine Onset of Atriaoventricular
Block
Onset of Atriaoventricular
Block Atrial Flutter
Revealed
Atrial Flutter
Revealed
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 1:1 AV block.
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 1:1 AV block.
PSVT with Wide QRS Complexes
PSVT with Wide QRS Complexes
36
Diagnostic Use of Adenosine 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
AmiodaroneAmiodarone:
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
Opie L H & Gersh B J 2001 Drugs for the Heart 5th ed Philadelphia: W B Saunders.
Sotalol:
Effective in sinus tachycardia, PSVT, WPW,
AF, VT & VF
Contraindicated in bradycardia, heart
blocks & SSS
greater risk of torsades de pointes
39
Effect of Amiodarone & Sotalol
Opie L H & Gersh B J 2001 Drugs for the Heart 5th ed Philadelphia: W B Saunders
Generally, Amiodarone is more powerful than Sotalol:Generally, Amiodarone is more powerful than Sotalol:
S > A A> S
ONLY Amiodarone
PSVTPSVT
WPWWPW
A>> S
Sustained
VT
Sustained
VT
Atrial Ectopi
esAtrial Ectopi
es
Arrhythmia of
CHFArrhythmia
of CHF
Post-Infarction Prophylaxi
s
Post-Infarction Prophylaxi
s
Negativ
e Effect
Negativ
e Effect
Negativ
e Effect
Negativ
e Effect
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
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 DisturbanceIndications 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
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., DKA, tricyclic antidepressant overdose such as cocaine
In cardiac arrest patients: Misconception: Bicarbonate is the buffering agent
CPR & Adequate Ventilation is the Key to eliminating acidosis
In cardiac arrest patients: Misconception: Bicarbonate is the buffering agent
CPR & Adequate Ventilation is the Key to eliminating acidosis
e.g., CPR without
intubation
e.g., CPR without
intubation
44
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 Thelan’s 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.
References
45
Lo C B & WONG T W 2003 A&E 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 A&E Clinical Guidelines No.16 Guideline for in-hospital resuscitation of patients at risk of SARS . Hospital Authority in Hong Kong, Electronic Knowledge Gateway.
References
46
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Chapter 129: Cardiac arrest and resuscitation
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