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Cardiac Arrest and Cardiopulmonary
Resuscitation in Hospital Setting
By
Prof. Ramadan Nafae
Professor and Head of Chest Diseases Department
Faculty of Medicine Zagazig University
History
Before the introduction of open-chest cardiac massage and electrical
reversal of ventricular fibrillation (VF), resuscitation was successful
primarily in victims of respiratory arrest.
 The combined procedures of positive-pressure ventilation, closed-
chest
precordial
compression,
and
electrical
defibrillation
were
introduced into clinical practice in 1960 by a retired Johns Hopkins
University Dean of Engineering, W. B. Kouwenhoven, who worked in
collaboration with a surgical resident, J. R. Jude, and graduate student
of biomedical engineering, G. G. Knickerbocker. This ushered in the
modern era of CPR.
Pathogenesis of cardiac arrest
Cardiac
arrest
is
characterized
by
abrupt
cessation of mechanical activity of the heart and
loss of spontaneous and effective circulation.
electrical
mechanism of
cardiac arrest
Pulseless
electrical
activity and
asystole (20%)
VF/VT(80%)
Etiology
Diagnosis
1. Unexpected loss of consciousness in the unmonitored
patient.
2. Loss of palpable central arterial pulse.
3. Respiratory arrest in a patient previously breathing
spontaneously.
Differential Diagnosis
1.
2.
3.
4.
Syncope or vasovagal reactions.
Coma.
“Collapse”.
Seizures.
Management
American Heart Association Chain of Survival
Initial management in the hospital setting
If ventricular fibrillation (VF) or ventricular tachycardia (VT) is
the first rhythm encountered, up to three DC shocks should be
delivered as soon as possible, at energy settings of 200 J, 200 J
and then 360 J .
If the rhythm is other than VF, immediately proceed to the nonVF/VT protocol.
If the rhythm cannot be identified immediately: Gain control of
th airway, commence basic CPR and establish intravenous (IV)
access while waiting for rhythm monitoring equipment to arrive.
Ventricular fibrillation
Ventricular tachycardia
Technique of CPR
Establish an effective airway
♦The three basic airway manoeuvres are head tilt, chin lift and jaw
thrust.
♦The
airway must be cleared of any foreign matter or obstruction
with finger sweeps (community) or suction (hospital) and positioning.
♦Initially use mouth-to-mask or bag-and-mask ventilation.
♦Intubation with a tracheal tube will give better control
of the
airway.
♦If
intubation is difficult, do not persevere – ensure adequate
ventilation and oxygenation with a simpler technique such as a
laryngeal mask.
Ventilation
Either via mouth mask or bag mask ventilation.
Use the most high Fio2 possible (100% O2).
Ventilations should be performed with a tidal volume
of 5–7 mL/kg of ideal body weight.
Single rescuer or two rescuer, nonintubated patient:
give two breaths after every 30 compressions.
Two rescuers, intubated patient: give breaths at a rate
of 8–10 breaths/min.
Do not pause in chest compressions for
ventilations.
Circulation
♦Check for a carotid or femoral pulse. If there is no pulse or only
a weak pulse and the blood pressure is too low to be measured,
start external chest compression.
♦Rescuer’s hand located in the lower margin of sternum.
♦Heel of one hand is placed on the lower half of the sternum
and the other hand is placed on top of the hand on the sternum
so that the hands are parallel.
♦Elbows are locked in position, the arms are straightened, and
the rescuer’s shoulders are positioned directly over the hands,
providing a straight thrust.
♦The sternum is depressed 11/2–2 in. in normal-sized adults
with each compression at a rate of 100/min..
Effective CPR, at best, will give a cardiac output that will be
25–30% of normal, a systolic blood pressure (BP) of 60–80
mmHg and a diastolic pressure of approximately 40 mmHg.
Cardiac output will decline with time. After 15 minutes, it will
be only 15% of normal.
The ‘chest thump’ as an initial manoeuvre to convert VF
may be used in monitored VF/pulseless VT arrests as it will
occasionally result in conversion. However, the ‘chest thump’
should not delay the administration of DC shock.
Cardiac monitoring and dysrhythmia recognition:
Defibrillation is the major determinant of survival in cardiac arrest
due to VF or pulseless VT.
Resume chest compressions after delivering one shock.
Relationship between the interval before attempted defibrillation
and hospital discharge after out-of-hospital cardiac arrest
Drug therapy during CPR may be
given by the following routes:
Peripheral vein (antecubital or external jugular are preferred).
Central venous line (subclavian or internal jugular
Intraosseous (IO) cannulation provides access that is safe and
effective for drug delivery, fluid resuscitation, and blood
sampling.
Endotracheal: Medications should be administered at 2–2.5
times the recommended intravenous (IV) dose and should be
diluted in 10mL of normal saline or distilled water, a catheter
should be passed beyond the tip of the endotracheal tube, and
the medication sprayed quickly followed by several quick
insufflations.
Drugs
Vasopressor Agents
Adrenaline
Its alpha vasoconstrictor action diverts the blood flow, increasing the flow
to vital organs and increasing coronary and cerebral perfusion pressures.
Adverse effects include increased myocardial oxygen consumption (VO2),
subendocardial ischemia and arrhythmia.
Adrenaline is still the first line drug for use in patients who have VF/VT
unresponsive to defibrillation, a systole and pulseless electrical activity
(PEA).
It must be emphasized that adequate chest compression is critical if one
is to gain the full beneficial effects of vasoconstrictors.
1 mg IV every 3 minutes.
Vasopressin
naturally occurring antidiuretic hormone vasopressin is a
vasoconstrictor at high doses via theV1 receptor.
It is recommended by some to be used in VF/VT refractory to
shock and adrenaline.
 One dose only at 40 units. The half-life of vasopressin is
10–70 minutes.
Sodium bicarbonate
The indications for the use of sodium bicarbonate in CPR are few:
pre-existing metabolic acidosis.
hyperkalaemia .
overdosage with tricyclic drugs. It may also be useful in prolonged CPR
(e.g. more than 20 minutes).
Give sodium bicarbonate (50 mmol) IV as a bolus dose and then use
regular arterial blood gas determinations to guide further treatment
Calcium chloride
Calcium is indicated for hyperkalaemia and hypocalcaemia and in
cases in which it is suspected that there is toxicity due to calcium
channel blocking drugs.
Give calcium chloride (10%) 2–4 mg/kg. Repeat after 10 minutes if
necessary.
Atropine
Atropine may reverse extremes of bradycardia and even ventricular
asystole after intense vagal stimulation, especially during anesthesia or
surgical proceduresIn these instances, 1 mg of atropine sulfate is injected
intravenously and repeated in 3 to 5 minutes if bradyarrhythmia persists.
Amiodarone
Amiodarone is useful in both supraventricular and ventricular
arrhythmia, particularly in patients with impaired left ventricular function.
150 mg IV over 10 minutes then an infusion of 1 mg/min for 6 hours.
Other inotropes
Combinations of other drugs, such as dobutamine, dopamine,
noradrenaline and isoprenaline, may have a place in ‘fine-tuning’
cardiovascular function after spontaneous circulation has been re-
established.
Defibrillation
Defibrillation depolarizes the myocardium and allows the most rapid
natural pacemaker, the sinoatrial node, to drive the heart’s rhythm.
Immediate defibrillation is the treatment of choice for VF or Vt .
 If VF or VT without an output is the first rhythm encountered, up to
three sequential countershocks of 200 J, 200 J and then 360 J should
be delivered, with no CPR in between.
The defibrillator operator is responsible for determining that staff
members are clear of the bed at the time of defibrillation.
Staff members must familiarise themselves with their hospital’s
defibrillators and have some basic knowledge about troubleshooting.
Further management
Check for and correct
reversible causes
5 H’s:
Hypoxaemia
Hypovolaemia
Hypothermia
Hydrogen ion – acidosis
Hyper/hypokalaemia and
metabolic disorders
5 T’s:
Tamponade
Tension pneumothorax
Toxins/poisons/drugs
Thrombosis – coronary
Thrombosis – pulmonary
embolism
Continue CPR: when conducting tests, procedures or reviewing an ECG,
do not interrupt the CPR for more than a few seconds.
A spontaneous palpable pulse is the best evidence that cardiac output
has returned. Immediately resume CPR if the pulse is not detected.
Brain resuscitation
The most effective way to maintain cerebral function is to
provide efficient CPR.
Inducing hypothermia following successful resuscitation is
currently being studied. Initial studies show improved neurologic
outcome.
Poor Prognostic indicators after CPR
The purpose of CPR is to prevent sudden,
unexpected death, not to prolong meaningless life.
Brainstem signs such as pupil size and reaction to
light are unreliable indicators of neurological status
during CPR.
Post-cardiopulmonary resuscitation
It is important to correct as many ‘correctables’ as possible.
Obtain a post-resuscitation chest x-ray to exclude pulmonary
barotrauma, aspiration pneumonia, gastric dilatation and check the position
of the ETT and invasive monitoring devices in the thorax (e.g. temporary
pacemakers, central venous catheters).
Regarding neurological damage, most studies have shown that if there
is to be full neurological recovery, it will occur within the first 48 hours after
cardiac arrest, Otherwise there will be varying degrees of permanent
damage resulting from the global ischaemia at the time of arrest.
Prevention of cardiopulmonary arrests
Because of the increased monitoring and awareness in ICUs, it
probably is no coincidence that patients in intensive care rarely
experience unexpected cardiorespiratory arrest.
It is therefore important that the entire staff of a hospital become
better educated in how to recognise patients who are rapidly
deteriorating.
There is some evidence that the cardiac arrest team would be more
successful being rapidly deployed to patients who were at high risk of
having an arrest, rather than to those who had actually arrested.
Medical emergency teams