Critical Care Medicine
Abnormal heart rhythm
1. Description of the problem
- Overview of causes and general treatments
- Etiology of arrhythmias in ICU
- Clinical features of arrhythmias
- Initial investigations of an arrhythmia
- Overview of arrhythmia treatment
- Classification of arrhythmias
- Supraventricular tachycardias
- Atrial fibrillation
- Atrial flutter
- Unifocal atrial tachycardia (UAT)
- Multifocal atrial tachycardia (MAT)
- AV node re-entrant tachycardia (AVNRT)
- AV re-entrant tachycardia (AVRT) (e.g. Wolff-Parkinson-White syndrome [WPW])
- Ventricular tachycardia (VT)
- Monomorphic VT
- Polymorphic VT
- Ventricular fibrillation
- Atrioventricular block (AV block) + bundle branch block (BBB)
- AV block
- Bundle branch block (BBB)
- Sick sinus syndrome (Tachy-brady syndrome)
2. Emergency Management
- 4. Specific Treatment
5. Disease monitoring, follow-up and disposition
Special considerations for nursing and allied health professionals
What's the evidence?
Cardiac Arrhythmias in ICU
1. Description of the problem
Overview of causes and general treatments
Arrhythmias are rarely the cause of admission to critical care, but as many as 50% of patients develop an arrhythmia, usually early in the course of their illness. Atrial fibrillation is the most common arrhythmia encountered.
Etiology of arrhythmias in ICU
These occur as a result of cardiac pathology and/or systemic factors. In critical care, systemic factors play a more significant role than in the general population.
· Cardiac pathology: Common conditions include ischemic heart disease, myocardial infarction, hypertension, and valvular heart disease (particularly mitral). Rarer causes are cardiomyopathies, infiltrative conditions such as sarcoid, and pericardial inflammation.
· Systemic factors: Systemic inflammatory response, electrolyte abnormalities, drugs, hyperthyroidism and alcohol.
Clinical features of arrhythmias
· Patients may be asymptomatic or experience palpitations.
· Clinical features of the cause of the arrhythmia (e.g. chest pain).
· Clinical features of the complications of the arrhythmia (e.g. respiratory failure due to ↓left ventricular function)
Initial investigations of an arrhythmia
ECG: For detection of diagnosis, ventricular rate and ischemia.
ABG: PO2, PCO2, pH, lactate, bedside Hb and electrolytes.
Blood Tests: Urea and Electrolytes (K+, Mg++, Ca++), Cardiac Enzymes (Troponin, CK, BNP) and @12 hours, CRP/Procalcitonin, Full Blood Count, Drug levels (digoxin/phenytoin),Thyroid Function tests if not already done (TFT's in ICU are difficult to interpret)
Radiology: CXR (consolidation or pulmonary edema)
Cardiac Imaging: Echocardiography looking at atrial size (and thrombus), ventricular size/function/regional wall motion abnormalities, valvular pathology. Coronary angiogram (if AMI is thought to be cause).
Overview of arrhythmia treatment
The principles are:
1. Diagnosing the arrhythmia
2. Providing appropriate anti-arrhythmic treatment
3. Treating the underlying cause. For example, early revascularization of a coronary infarct decreases early arrhythmias and VF, although reperfusion arrhythmias do occur. Unless the cause of the arrhythmia is managed, recurrence is likely.
Anti-arrhythmic treatment involves a combination of general and directed measures. General measures include:
· Treatment of hypoxia or hypercapnia
· Optimize hemodynamics and fluid balance. Monitoring intravascular fluid balance can be difficult with an arrhythmia, but there may be clues prior to development of the arrhythmia (such as large removal of fluid with hemofiltration). A fluid bolus is often warranted.
· Electrolytes should be normalized.
§ K+ >4.0mmoI/L and probably >4.5mmoI/Lin high-risk patients.
§ Mg++ >1.0mmoI/L.
§ Metabolic pH<7.1 may benefit from HC03-.
· Cease any pro-arrhythmic medication if possible
· Sympathetic surges often induce arrhythmias. Ensure appropriate sedation (ventilator dyssynchrony or respiratory rate may be apparent).
Directed measures include: DC cardioversion, pacing or anti-arrhythmic drugs.
· Urgent DC cardioversion for cardiovascular collapse, respiratory distress, or ↑rate-related cardiac ischemia.
· Urgent pacing for symptomatic bradycardia (or a broad complex QRS rate <30bpm). This can be transcutaneous until a transvenous system can be placed.
· Anti-arrhythmic drugs that cardiovert or provide rate control.
· Cardioversion can also be performed on a semi-elective basis to hasten the return to sinus rhythm. Loading with anti-arrhythmic drugs improves cardioversion success rates and decreases arrhythmia recurrence.
Classification of arrhythmias
Classification of Arrhythmias
|Supraventricular Tachycardia (SVT): originates from atrial tissue (outside the sino-atrial node) or from the AV node.||SVT (AV node independent)||Atrial fibrillationAtrial flutterUnifocal atrial tachycardiaMultifocaI atriaI tachycardia|
|SVT (AV node dependent)||AV nodal re-entrant tachycardia (AVNRT)AV re-entrant tachycardia (AVRT)|
|Ventricular Tachycardia (VT): originates from ventriculartissue.||Ventricular Tachycardia||Monomorphic VTPolymorphic VT|
|Heart Blocks (HB) and Bundle Branch Blocks (BBB): abnormalities of heart conduction pathways||Heart Blocks||1st degree2nd degree: Mobitz Type 1Mobitz Type 23rd degree|
|Bundle Branch Blocks||Left Bundle BranchRight Bundle branchHemiblocks|
|Sino-atrial node abnormality ±AV node involvement||Tachy-Brady or Sick Sinus Syndrome|
AF is the chaotic contraction of many different segments of the atria at rates between 300 and 600 bpm. Only a fraction of these are conducted through the AV node in an irregularly irregular pattern. AF is most common in older patients with ischemic heart disease.
In the critically ill, AF can result from systemic upset (the systemic inflammatory response, pH and electrolyte abnormalities, high inotrope requirements and acute withdrawal of β-blockers). Any cardiac pathology enlarging the atria or inducing abnormal electrophysiology in the atria/pulmonary veins can also be a trigger. Over time thrombus can form in the akinetic atria. This can be a particular problem in low cardiac output and prothrombotic states (e.g. post AMI).
ECG: absence of P waves, irregular narrow QRS complexes (unless there is associated pathology widening the QRS). ECG is usually diagnostic, although multifocal atrial tachycardia (MAT) can be misdiagnosed as AF.
Management of new-onset AF
Cardiovascular collapse, respiratory distress, or ↑rate-related cardiac ischemia needs synchronized DC cardioversion.
· Rate or rhythm control.
· Treat the underlying cause.
· AF is associated with thromboembolism (population figures: 4% risk of stroke per year), but critical illness affects "thrombotic state" and these statistics probably do not apply. If possible, anticoagulation should be commenced within 48 hours.
Anti-arrhythmic drugs: Amiodarone may revert to sinus rhythm or ↓rate (see Anti-arrhythmic Drugs section).
Rate Control: β-adrenergic blockers, diltiazem, or digoxin (see Anti-arrhythmic Drugs section).
Anticoagulation: (see Anti-arrhythmic Drugs section).
Chronic/paroxysmal AF management
· Valvular AF has a 17× higher incidence of thrombotic complications, and should be warfarinized.
· Non-valvular AF may benefit from either aspirin or warfarin. The CHADS 2score guides therapy.
Elective cardioversion: If cardioversion is being considered, then 3 weeks of anticoagulation is needed beforehand. Alternatively, transoesophageal echocardiography demonstrating no thrombus can be sufficient. There is a significant risk of AF recurrence, and the atria (particularly the appendages) suffer from stunning and so less coordinated contractions. Therefore, anticoagulation should be continued for 4 weeks.
Ablation therapy: Surgical and left atrial catheter ablations are demonstrating success rates of 80% with complications rates of less than 1%. A key feature is isolation of the pulmonary veins using radiofrequency ablation. Complications from these advanced ablative techniques include pulmonary vein stenosis, perforation and producing a re-entrant tachycardia.
Atrial flutter is another common arrhythmia in ICU. The atrial rate is increased to near 300 bpm due to a re-entrant loop in the right atrium. Conduction ratio through the AV node is 1:2, 1:3 or higher.
ECG has sawtooth flutter waves best seen in lead V1 and in the inferior leads. The flutter waves have a rate of approximately 300, while the QRS complex rate will depend on the conduction ratio (1:2→150bpm, 1:3→100bpm).
Similar to AF. Low-energy (25-50J) synchronized cardioversion is the most reliable method of reverting atrial flutter. Concerns about thrombus development are similar to AF, and the same precautions apply.
Rate Control: β-adrenergic blockers, diltiazem, and digoxin.
Antiarrhythmic drugs: Amiodarone
Anticoagulate within 48 hours.
Anticoagulation: The guidelines for anticoagulation in atrial flutter are the same as atrial fibrillation, although there are fewer data supporting this practice.
Prevention of recurrence: Amiodarone, sotalol and flecainide are used. Radiofrequency ablation (between tricuspid valve and entrance of the inferior vena cava) may provide a longer-term cure outside the critical care setting.
Unifocal atrial tachycardia (UAT)
The generation of an ectopic atrial contraction at a rate faster than the SA node. Digoxin toxicity is the most common cause (and is often associated with a degree of AV block).
ECG: altered P wave morphology with high rate.
Treatment of the underlying cause is necessary. Cardioversion can be achieved with a DC shock or amiodarone while rate control can be achieved with β-adrenergic blockers or diltiazem. In digoxin toxicity, cardioversion and amiodarone should be avoided (see Anti-arrhythmic Drugs section).
Multifocal atrial tachycardia (MAT)
MAT occurs in patients with chronic lung disease and cor pulmonale. Atrial contraction is generated at a high rate from a number of different locations. The ECG has irregular P waves with at least 3 distinct P-wave morphologies. The ventricular rate is also irregular due to the irregular P waves.
Treatment: Cardioversion is usually unsuccessful until underlying right heart strain is managed. Diltiazem and β-blockers are effective. β-blockers will often be contraindicated due to chronic lung disease. Amiodarone may be useful in patients with a poor LV function. Digoxin is ineffective.
AV node re-entrant tachycardia (AVNRT)
A re-entrant loop develops within the AV node generating a narrow complex tachycardia.
ECG: Regular narrow complex tachycardia. Retrograde P waves are usually buried in the QRS complex.
The AV loop can be terminated by temporarily blocking conduction through the AV node.
· Physiological: Carotid sinus massage or Valsalva maneuver
· Pharmacological: Adenosine, β-blockers, diltiazem, amiodarone
· DC shock: Especially if there are critical consequences
Longer-Term Management: Radiofrequency ablation of the AV re-entrant circuit
AV re-entrant tachycardia (AVRT) (e.g. Wolff-Parkinson-White syndrome [WPW])
An accessory pathway connects the atria to ventricle. The accessory pathway is sometimes visible on the resting ECG as a pre-excitation component. Some accessory pathways only conduct retrograde and so have normal resting ECGs.
Two problems can arise from accessory pathways.
The generation of a circular re-entrant rhythm around the AV node and accessory pathway. The majority of tachycardias conduct antegrade through the AV node and retrograde through the accessory pathway, resulting in a narrow complex tachycardia. Rarely conduction can be the other way, resulting in a broader complex tachycardia.
Abnormal ventricular conduction in atrial fibrillation resulting in an irregular broad complex tachycardia (and often hemodynamic compromise)
ECG: Usually a narrow complex regular tachycardia. An inverted P wave can be within or behind the QRS complex. The resting ECG may demonstrate a pre-excitation complex. This is typified in WPW by a short PR interval and delta wave (slurred upstroke on QRS). In AF, the ventricular rate can be very high and the QRS complexes of variable width.
Hemodynamic compromise → synchronized DC cardioversion
AVRT narrow complex tachycardias are terminated by slowing AV node conduction: Valsalva, adenosine, β-blockers, or amiodarone. Nodal slowing drugs MUST be avoided in AVRT with a broad QRS.
AVRT broad complex tachycardia (from retrograde conduction through the AV node) and broad complex AF should be treated as a ventricular tachycardia.
Long-term management: Radiofrequency ablation of the accessory pathway.
Ventricular tachycardia (VT)
Definition: Three or more consecutive ventricular beats at a rate of greater than 120bpm. VT lasting more than 30 seconds is sustained VT.
VT is a malignant rhythm that can induce hemodynamic collapse, or degenerate into ventricular fibrillation. VT is often the result of an ischemic region or scar tissue within the ventricle.
ECG: Regular broad complex (QRS>120msecs) tachycardia (HR>120).
Management: Cardioversion with DC shock ± amiodarone. Lignocaine may not be as effective as previously thought. Amiodarone also reduces recurrence rate, but treating underlying pathology is most important.
Long-term management: An implantable defibrillator can recognize and terminate VT. Pharmacological prevention with sotalol, amiodarone or other β-blockers may help.
Determining SVT + BBB vs VT
A broad complex tachycardia should be treated as VT unless there is proof it is an SVT with bundle branch block. See
Characteristics separating VT from SVT+BBB
|Characteristic||Example of characteristic|
|Presence of AV dissociation→ Highly suggestive of VT||Independent P wave activityCapture beats: Normally conducted QRS in among the broad ventricular beatsFusion beats: Normally conducted QRS fusing with a ventricular beat|
|Morphology of the QRS (less definite and open to interpretation)||RS complexes <100ms (not a QRS, QR, QS, R and rSR) in precordial leads suggests SVTTypical bundle branch pattern may suggest SVT|
A broad complex tachycardia with a twisting QRS morphology about the baseline. It most commonly occurs in the setting of a long QT (>0.44msec).
The prolonged QT represents a long and heterogeneous ventricular repolarization. Arrhythmia can be due to either:
· Depolarization on the extended plateau phase of the cardiac action potential
· Re-entrant loops created by the heterogeneity of the action potential
Causes of Long QT
|Idiopathic||Familial in 90%. Majority autosomal dominant.Sporadic 10%|
|Acquired||Cardiac pathology: Myocardial ischemia/infarctionPharmacological: Class 1A, 1C, III anti-arrhythmics. Amiodarone and sotalol commonMacrolide antibioticsPhenothiazides and Tricyclic AntidepressantsElectrolytes: ↓K+, Mg++|
Synchronized DC cardioversion with magnesium loading is recommended for the polymorphic VT.
Recurrence is prevented by decreasing QT:
Remove factors that ↑QT (drugs/electrolytes)
Temporary ↑HR with isoprenaline or ventricular pacing
Persistent ↑QT will need assessment for an implantable defibrillator.
VF is one of the 3 "rhythms of cardiac arrest".
ECG: Irregular broad complex waves of varying morphology and amplitude associated with a loss of cardiac output. The complexes can be larger and appear more synchronized (termed coarse VF) or can be low-voltage rapid fibrillation waves (fine VF).
VF is often associated with coronary artery disease. Other causes include cardiomyopathies, valvular heart disease or systemic factors such as electrolyte imbalance and pro-arrhythmic drugs.
Treatment is urgent unsynchronized DC shock ± amiodarone with CPR, following the ALS guidelines. Amiodarone is currently the favored anti-arrhythmic. The cause of the VF arrest should be investigated and treated with an urgent angiogram ± stenting (hemodynamic stability permitting).
Cardiac, respiratory and neurological problems commonly arise following a cardiac arrest. The cardiac problems include recurrence of arrhythmias, myocardial depression (globally and regionally), valvular impairment and even pericardial inflammation. Early reperfusion therapy reduces the incidences of these complications.
Long-term management: Suitable patients need assessment for implantable defibrillators as long-term survival is significantly improved.
Atrioventricular block (AV block) + bundle branch block (BBB)
AV block is the delay or failure of some or all of the electrical conduction from the atria to the ventricles. See
Heart Block by ECG and Pathology
|Type of heart block||ECG description||Pathology||Treatment options|
|1st degree heart block (1st HB)||Prolongation of PR interval (>200ms). All P waves are followed by a QRS (P waves may be hidden in the previous T wave).||Slowed conduction through the AV node||None needed.|
|2nd degree heart block (2nd HB)||Mobitz Type 1 (Wenckebach): Progressive lengthening of PR interval resulting in missed beats||Delayed conduction at the AV node||None needed. Atropine will ↑HR if needed.|
|Mobitz type 2: PR interval constant, but regularly dropped QRS. P:QRS ratio is constant at 2, 3 or 4.||Lesion at Bundle of His||Pacing is needed. Atropine or β1-agonists are not indicated and can worsen block.|
|3rd degree heart block (3rd HB)||P waves and QRS completely dissociated. QRS rate slower than P rate.||Lesion at AV node or bundle of His. Nature of escape rhythm will be determined by lesion level.||Pacing is needed. Atropine or β1-agonists are indicated only if the escape rhythm is narrow complex (and originating from AV node).|
1st HB can be a normal variant. Pathologically it can be associated with inferior myocardial ischemia/infarction or certain drugs (such as digoxin). 1st HB does not need treating, but in an acute developing situation monitoring for extension of the heart block is wise.
Mobitz Type 1 is a benign condition and should be managed similarly to 1st HB. Mobitz Type 2 is always pathological, and usually related to ischemic or structural heart disease. Progression to 3rd HB over time or in the presence of other drugs (notably anesthetic and analgesic drugs) occurs. Temporary ventricular pacing may be required until a permanent pacing system can be fitted.
3rd HB (complete) is usually associated with an escape ventricular rhythm. The cause should be investigated. It often results from gradual fibrosis of the conduction system, or acute inferior or anterior ischemia. Cardiac pacing is usually required.
Bundle branch block (BBB)
3 bundles conduct the action potential from the AV node to the ventricles:
· Right bundle
· Left anterosuperior fascicle
· Left inferoposterior fascicle
Right bundle branch block (RBBB)
When the right bundle is unable to conduct there is normal activation of the left ventricle but delayed activation of the free wall of the right ventricle.
ECG: A broad QRS (>120ms) with an rSR pattern in V1 (and V2), and Rs (R>S) in V6 (and lead 1). Partial RBBB applies to a similar morphology, but with the QRS 110-120ms.
RBBB may be a normal variant, but it is also associated with RV strain (e.g. acute pulmonary emboli or chronic lung disease) or with myocardial ischemic events.
Left bundle branch block (RBBB)
A block high in the conduction pathway can affect both left fascicles. There is abnormal depolarization of the septum and delayed depolarization of the left ventricle.
ECG: A broad QRS (>120ms). V1 has an rS or a QS morphology, while V6 has an RR' pattern (M or plateau-shaped). Q waves are not seen in V4-V6. Partial LBBB has similar morphology but QRS duration 110-120ms.
LBBB is often caused by coronary artery disease, cardiomyopathy or left ventricular hypertrophy. If it is new onset then an acute myocardial infarction can be assumed.
The left anterosuperior fascicle is the most susceptible, as it is thinner and runs close to the aortic valve. Blockage results in left axis deviation. The inferoposterior fascicle is thicker and has a dual blood supply. Blockage of this fascicle results in right axis deviation. Hemiblocks in the presence of RBBB indicate extensive bundle branch pathology with a high likelihood of deteriorating to complete heart block. Pacing may be required.
Sick sinus syndrome (Tachy-brady syndrome)
Alternating patterns of tachycardia (or even atrial flutter or fibrillation) with sinus bradycardia. The pathology lies in the SA node. There may be associated AV node abnormality, causing heart block.
Clinical features: Most common presentation is with syncope or near syncope.
Treatment: A combination of pacing for the bradycardias, and antiarrhythmics for the tachycardias. Anticoagulation may be needed if atrial fibrillation occurs.
2. Emergency Management
4. Specific Treatment
DC cardioversion has a role in:
SVT: AF/atrial flutter/AVNRT/AVRT (urgently if compromised)
VT (urgently if compromised)
The dose of energy (Joules) will depend on:
Thoracic impedance, which is influenced by paddle position, patient size, gel use, number of previous shocks
The waveform (monophasic damped sinusoidal wave vs. biphasic truncated exponential) alters the efficiency of cardioversion for a given energy.
It is important to use synchronized energy to prevent an R-on-T phenomenon inducing VT or VF. Examples of biphasic truncated exponential energies used:
AF, Atrial Flutter, AVNRT, AVRT: Synchronized 50J, then 100J and maximum 150/200J. Paddle position can be changed to right parasternal to left infrascapular as this may have a more direct vector for atrial involvement.
VT: Synchronized 100J, then maximum 150/200J. Polymorphic VT may be hard to synchronize and time should not wasted trying too hard to achieve this, as this is very close to VF.
VF/pulseless VT: Unsynchronized maximum 150/200J immediately.
Digoxin toxicity: High digoxin levels and DC cardioversion can induce ventricular arrhythmias (see "Digoxin").
These are most effective in arrhythmias associated with increased adrenergic stimulation, such as postoperative states or sepsis. They principally act through slowing of the SA node and conduction through the AV node. There is little effect on the remainder of conduction system, but there is acute reduction in myocardial contractility. Useful in:
Rate control in AF and atrial flutter
Cardioversion of a re-entrant circuit involving the AV node (AVNRT, AVRT)
Early use of IV β-blockers following thrombolysis for AMI improves mortality, through decreased work of the heart, and possibly additional prophylactic anti-arrhythmic effects.
Caution should be taken using β-blockers in those with poor LV function, potential bronchospasm or severe peripheral vascular disease. Co-prescription of multiple node-slowing drugs (β-blockers, Ca++ channel blockers and digoxin) is not recommended.
Esmolol: An ultrashort-acting cardioselective β-blocker. Metabolism is via the esterases in red blood cells. Re-distribution t1/2 is 2 minutes, and elimination t1/2 is 9 minutes. A trial bolus (0.2-0.5mg/kg) of esmolol can be used when tolerance of β-blockers is uncertain for cardiac or respiratory reasons. A continuous infusion can also be used.
Metoprolol: A short-acting (t1/2=3-4 hours) cardioselective β-blocker metabolized in the liver. Adult IV bolus dosage is 2mg up to a maximum of 20mg. Oral usage requires ≈10× higher doses.
Ca++ channel blocker that has a significant slowing effect on the AV node with moderate reduction in contractility, and moderate vasodilatation. Effective at:
Rate-controlling AF and AFl
Cardioversion of narrow complex AVNRT, AVRT (see section on WPW)
Cautions: Avoided in VT. It will induce even broader complexes, ventricular dyssynchrony, and contractility.
Diltiazem has a t1/2 of 3 hours and is metabolized by the liver. IV dose up to 0.25mg/kg in divided doses. Oral doses are higher due to reduced bioavailability.
Mg++ is a co-factor for the Na/K ATPase pump. It stabilizes the resting membrane potential, speeds up action potential propagation, lengthens the absolute refractory period, and reduces the relative refractory period. These properties result in reduced automaticity, reduced re-entrant vulnerability and ↑ synchronized contraction. Mg++ also vasodilates (especially if given quickly) and high levels (>5mmol/L) result in skeletal (and respiratory) muscle weakness.
Treatment of SVTs and rate-controlling AF
VT (especially polymorphic VT or digoxin-associated VT)
Prophylaxis following cardiac surgery
Mg++ plasma levels are 0.7-1.0mmol/L. The anti-arrhythmic effects of Mg++ are probably at 1-2.5 mmol/L. Dose: 20mmol over 20 minutes to 0.1mmol/kg/hr. Daily levels needed in renal failure.
Amiodarone affects the Na+/K+/Ca+ channels and the α+β receptors, resulting in:
↓ conduction through the AV node
↑ refractory period (and ↑QTc) in the remainder of the cardiac tissue
Due to its potency, broad spectrum of effects and relative hemodynamic stability its short-term use in the ICU is very common.
Revert AF and AFl + prevent recurrence
Terminate AVRT and AVNRT + prevent recurrence
Revert VT + prevent recurrence
ALS guidelines for shock-resistant VF
An initial IV dose will have an anti-arrhythmic effect within 5 minutes. Amiodarone undergoes extensive redistribution to other compartments, and may require repeat boluses (1-2mg/kg) in the first 24-48 hours. The elimination t1/2 is >40 days.
Rapid IV loading can be associated with transient myocardial depression and vasodilatation. The QTc also increases shortly after administration. Co-prescription with other node blocking drugs or in bradycardias can result in 3rd HB. The long-term side effects are extensive but these are kept to a minimum by short-term usage in the ICU:
Abnormal liver function tests. Stop amiodarone if LFT's ↑ 2-3 times. Cirrhosis.
Hyper- or hypothyroidism
Corneal microdeposits (of no clinical significance) and photosensitivity are also seen.
An ultra-short-acting drug generating a high-grade AV block. Used to:
Cardiovert AVRT or AVNRT
Assess atrial activity in a narrow complex tachycardia (e.g. to detect flutter waves)
Adenosine (6mg then 12mg) should be administered through a large peripheral or central vein followed by a 20ml flush.
Broad complex tachycardia, as can significantly worsen VT.
Reactive airways diseases due to bronchospasm.
Dipyridamole enhances adenosine effect.
Theophylline antagonizes adenosine effects.
Direct muscarinic activity
Inhibition of Na+/K+ATPase pump. ↑intracellular Na+ leads to ↑activity of the Na+/Ca++ exchanger and so ↑intracellular Ca++.
Net effects: ↑systolic function, ↓AV node conduction, ↓diastolic function (by impairing relaxation) and pro-arrhythmic (particularly in hypertrophied, ischemic ventricles). It has limited use in critical care patients as:
↓ potency in high adrenergic states
Delayed (a few hours) rate control
Avoid in patients suffering from ischemia or significant diastolic failure, or on alternative AV node-blocking drugs
It has a narrow therapeutic index. Potential for toxicity is high, especially in renal failure.
Electrolyte (K+, Mg++, Ca++) imbalances alter potency.
DC cardioversions should be performed with extreme caution in patients with high digoxin levels.
Dose: IV loading dose of 15mcg/kg over 2 hours. Daily dose depends on renal function. Daily plasma levels are required (therapeutic range 0.5-2ng/ml).
Digoxin toxicity: often a UAT with variable AV block. Non-sustained and sustained VT can also develop. A malignant arrhythmia is best treated with the monoclonal antibody and Mg++ loading (to plasma level 2-2.5mmol/L). DC cardioversion can precipitate VF.
IV Heparin: Short acting (t1/2=1 hour) and reversible with protamine. Easy to monitor (via APTTR). Risk of heparin-induced thrombocytopenia. Most commonly used in ICU.
SC Low-molecular-weight heparin: Longer acting (t1/2= 4 hours), only partially reversed with protamine. Monitoring (by anti-Factor Xa activity) often not needed.
Heparinoids (danaparoid) and thrombin inhibitors (lepirudin and argatroban) are anticoagulants principally used in the presence of heparin-induced thrombocytopenia and intolerance to warfarin.
Warfarin: A drug rarely used in ICU due to its longer-term effects. Inhibits synthesis of Factors 2/7/9/10. Reversible quickly with factor concentrates and FFP and slowly with vitamin K.
5. Disease monitoring, follow-up and disposition
Special considerations for nursing and allied health professionals
What's the evidence?
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