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Cardiac Arrest and Cardiopulmonary Resuscitation in Hospital Setting

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Presentation on theme: "Cardiac Arrest and Cardiopulmonary Resuscitation in Hospital Setting"— Presentation transcript:

1 Cardiac Arrest and Cardiopulmonary Resuscitation in Hospital Setting
By Prof. Ramadan Nafae Professor and Head of Chest Diseases Department Faculty of Medicine Zagazig University

2 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.

3 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 VF/VT(80%) Pulseless electrical activity and asystole (20%)

4 Etiology

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

6 American Heart Association Chain of Survival
Management American Heart Association Chain of Survival

7 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.

8 Ventricular fibrillation Ventricular tachycardia

9 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.



12 Do not pause in chest compressions for ventilations.
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.


14 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..



17 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.

18 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

19 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.

20 Drugs Vasopressor Agents

21 Adrenaline 1 mg IV every 3 minutes.
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.

22 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.

23 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

24 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.

25 Amiodarone Other inotropes
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.

26 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.

27 Check for and correct reversible causes
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

28 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.

29 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.

30 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.

31 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.

32 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.






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