Cardiac Arrest and Cardiopulmonary Resuscitation in Hospital Setting

ByProf. Ramadan Nafae

Professor and Head of Chest Diseases DepartmentFaculty 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 arrestCardiac arrest is characterized by abrupt

cessation of mechanical activity of the

heart and loss of spontaneous and

effective circulation.electrical mechanism of cardiac

arrest

VF/VT(80%)

Pulseless electrical

activity and asystole

(20%)

Etiology

Diagnosis1. 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. Syncope or vasovagal reactions.2. Coma.3. “Collapse”.4. Seizures.

ManagementAmerican 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

non-VF/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 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.

Atropine

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.

DefibrillationDefibrillation 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:HypoxaemiaHypovolaemiaHypothermiaHydrogen ion – acidosisHyper/hypokalaemia and metabolic disorders

5 T’s:TamponadeTension pneumothoraxToxins/poisons/drugsThrombosis – coronaryThrombosis – 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 arrestsBecause 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

Medical emergency teams (METs) were

developed in Australia and consist of doctors and

nurses trained in advanced resuscitation

skills.

The idea is that seriously abnormal vital signs

trigger an emergency call, rather than waiting for

cardiopulmonary arrest.