Hemodynamic unstable patient

following arrhythmia / dysrhythmia

 Introduction
• The term dysrhythmia denotes any abnormality in cardiac rhythm.
• Clinically, dysrhythmias are classified as stable or unstable based on the
presence or absence of adequate end-organ perfusion (ie, systemic
hypotension, cardiac ischemia, pulmonary edema, or mental status changes).
• Dysrhythmias  bradydysrhythmias(HR<60) or tachydysrhythmias(HR >100).
• First, determine the hemodynamic stability of the patient. Look for any signs
of hypoperfusion, including systemic hypotension, cardiac chest pain,
pronounced diaphoresis, altered mental status, or congestive heart failure.
• Second, quantify the rate of the dysrhythmia  as normal, slow, or fast.
• Third, identify the morphology of the rhythm ( eg, narrow vs wide complex
QRS ). Next, determine whether the observed dysrhythmia is irregular or
regular in cadence.
• Finally, assess for any evidence of an AV conduction block. AV blocks are
divided into first, second, and third degrees based on the PR interval and the
cardiac rhythm.
 Tachycardia
• tachydysrhythmias(HR >100).
• Sign and symptoms of unstable tachycardia are tachypnea,
intercostal retracions, suprasternal retracions, paradoxical
abdominal breathing with the signs of hypoperfusion.
• Rapidly determine patient stability, as unstable patients
require immediate electrical cardioversion or defibrillation.
• For cardioversion, ensure that the defibrillator is set to the
SYNC mode before delivering the shock to avoid
precipitating VF. Defibrillate patients in pulseless VT and VF
in the unsynchronized (default) mode.
 Bradycardia
• bradydysrhythmias(HR<60)
• Signs and symptoms of unstable bradycardia are tachypnea,
intercostal retracions, suprasternal retracions, paradoxical
abdominal breathing with the signs of hypoperfusion.
• Unstable patients require immediate intervention with IV
doses of atropine (0.5-1.0 mg) and epinephrine ( 0.3-0.5 mg
over 2-3 minutes) if refractive.
• Initiate transcutaneous pacing and consider placement of an
introducer catheter into the internal jugular or subclavian
vein for transvenous pacing in all patients who fail to
respond.
• Catecholamine infusions (eg, dopamine) may be necessary to
maintain an adequate HR and blood pressure.
 Pulseless Electrical Activity (PEA)
• PEA is defined as coordinated electrical activity of the heart
(other than VT/VF) without a palpable pulse.
• This group of dysrhythmias includes electromechanical
dissociation (EMD), in which no myocardial contractions
occur, and pseudo-EMD, in which myocardial contractions
occur but no pulse can be palpated.
• Usually primary PEA is a natural progression from
hypotension  pseudo-EMD  EMD.
• True EMD is the result of a primary disorder of
electromechanical coupling in myocardial cells associated
with global myocardial energy depletion and acidosis
resulting from ischemia or hypoxia.
• Typically occurs after defibrillation following prolonged VF
and is associated with hyperkalemia, hypothermia, and drug
overdose.
• Pseudo-EMD caused by global myocardial dysfunction is a transient
state in the progression to EMD and has the same cause.
• An additional cardiac cause of pseudo-EMD is papillary muscle and
myocardial wall rupture, in which the ventricle continues to contract,
but forward flow is greatly diminished.
• Pseudo-EMD also may be caused by primary SVT.
• Additional extracardiac causes of pseudo-EMD include hypovolemia,
tension pneumothorax, pericardial tamponade, and massive
pulmonary embolism.
• Initial assessment also should include vascular Doppler ultrasound,
echocardiography, or PETco2 monitoring to distinguish EMD from
pseudo-EMD.
• As volume loading or continuous vasopressor infusion may be helpful
in cases of pseudo-EMD but not in routine cardiac arrest
resuscitation.
• Treatment of PEA requires all general resuscitation measures,
including CPR, intubation with assisted ventilation, intravenous
access, and repeated administration of vasopressors.
 Asystole
• Asystole represents complete cessation of
myocardial electrical activity.
• Although asystole may occur early in cardiac
arrest as a consequence of progressive
bradycardia, asystole generally represents the
end-stage rhythm after prolonged cardiac arrest
caused by VF or PEA.
• Treatment of asystole requires all general
resuscitation measures, including CPR, intubation
with assisted ventilation, intravenous access, and
repeated administration of vasopressors.
ECG
 Drugs used in cardiac emergency
Vasopressors
• The current recommended dose of epinephrine is 1 mg initially,
with repeated doses every 3-5 min.
• "High-dose" epinephrine confers no benefit and may be harmful.
• When there is no IV access, epinephrine can be given in the
endotracheal tube at a dose 2-2.5 times the IV dose.
• Alternatively, vasopressin 40 units IV may be given once.
Antidysrhythmics
• Amiodarone, 300 mg IV push, repeated as a second dose of 1 50
mg IV push may be useful for defibrillation refractory VT /VF.
• Magnesium, 2 g IV, may be useful in patients with torsade de
points.
Management in cardiac arrest
 Quiz
Your patient is deteriorating quickly. He is becoming
dizzy, diaphoretic. His blood pressure has fallen
from 100/70 to 60/p. The monitor is showing a fast
irregular, wide complex tachycardia. He suddenly
loses consciousness. The shock you deliver should
be
a) Synchronized
b) Unsynchronized
c) Using only one paddle
d) You should not deliver shock
An elderly man is brought into the ED by his grandson. He is
not responding but he does have a faint carotid pulse. His heart
rate is estimated to be about 150 and his blood pressure is
50/24. His skin is cool, pale and damp. You request an ECG,
which shows the following rhythm:

a) Sinus tachycardia
b) Ventricular
fibrillation
c) Monomorphic
Ventricular
tachycardia
d) Polymorphic
Ventricular
tachycardia
 References
• Clinical Emergency Medicine (Lange Medical
Books) 1st Edition
• Rosens Emergency Medicine - Concepts and
Clinical Practice