CARDIAC ARREST

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Causes & prevention of Cardio respiratory arrest

• Definition: A respiratory arrest is when breathing stops (apnea). A cardiac arrest is when the heart stops contracting & pumping blood.

• Causes: 1. Airway problems. 2. Breathing problems. 3. Cardiovascular problems.

Cardiovascular Emergencies

1. Unconscious Cardiac Arrest

- Ventricular Fibrillation / Pulseless Ventricular Tachycardia- Asystole- Pulseless Electrical Activity (PEA)

2. Conscious Acute Coronary Syndrome (ACS)

- Unstable Angina Pectoris (UAP)- Acute Non ST-Elevation Myocardial infarction (NSTEMI)- Acute ST-Elevation Myocardial infarction (STEMI)

Cardiac Arrest

• Cardiac arrest is characterized by abrupt loss of heart function

• Main sign of cardiac arrest : loss of consiousness + pulseless

• Can be resuscitated within few minutes (4-5m) if CPR is initiated

Why cardiac arrest is dangerous?

• 10-15 seconds : Loss of consciousness• 30 seconds : ECG become flat, respiration may

arrested• 60 seconds : Pupil dilates fully • 4-6 minutes : Brain damage• 8-10 minutes : Irreversible cerebral cortical damage

ETIOLOGY• Acute coronary ischemia:• Primary dysrhythmia(Cardiomyophaty and myocarditis)• Cardiac rupture• Pericardial tamponade• Metabolic abnormalities• Noncardiac etiologies(Tension pneumothorax, sepsis, etc):• Drugs(Cocaine and Heroin,etc)

Pathophysiology of Cardiac Arrest

3 basic mechanism : 1.Ventricular Fibrillation / Pulseless

Ventricular Tachycardia2.Asystole3.Pulseless Electrical Activity

* Asystole and PEA are not shockable.

ECG waveform characteristics and their corresponding positions in heart.

Ventricular Fibrillation • Occur in 30% of in-hospital cardiac arrest• More common in ischemic and infarction heart disease • More likely to respond to treatment

• ECG : bizarre irregular waveform, random in both frequency and amplitude

• Shows disorganized electrical activity in myocardium• The only effective treatment is early defibrillation

• Clinical Manifestations:– Pulse disappears with onset of VF– Collapse, unconsciousness– Agonal breaths apnea in <5 min➔– Onset of reversible death

• Etiologies:– Acute coronary syndromes leading to ischemic areas

of myocardium– Stable-to-unstable VT, untreated– PVCs with R-on-T phenomenon– Multiple drug, electrolyte, or acid-base abnormalities

Coarse VF

Fine VF

• Treatment:– Early defibrillation is essential– Agents given to prolong period of reversible death

(oxygen, CPR, intubation, epinephrine,vasopressin)– Agents given to prevent refibrillation after a shock

causes defibrillation (lidocaine, amiodarone, procainamide, β-blockers)

– Agents given to adjust metabolic milieu (sodium bicarbonate, magnesium)

ALGORITHMFOR

VF / VT

Harrison’s Principle of Internal Medicine 18th Ed14

Pulseless Electrical Activity (PEA)• Cardiac conduction impulses occur in organized pattern, but

this fails to produce myocardial contraction (former “electromechanical dissociation”); or insufficient ventricular filling during diastole; or ineffective contractions

• Occur 5% of in-hospital cardiac arrest

• ECG: Rhythm displays organized electrical activity (not VF/pulseless VT)

• Seldom as organized as normal sinus rhythm• Poor prognosis

• Clinical Manifestations:– Collapse; unconscious– Agonal respirations or apnea– No pulse detectable by arterial palpation

• Etiologies– Hypovolemia – “Tablets” (drug OD, ingestions)– Tamponade, cardiac

• Treatment:– Per PEA algorithm– Primary ABCD (basic CPR)– Secondary

• AB (advanced airway and ventilation);• C (IV, epinephrine, atropine if electrical activity <60

complexes per minute);• D (identify and treat reversible causes)

ASYSTOLE• Occur in 25% of in-hospital cardiac arrest• Occur 10% of out-side hospital cardiac arrest• Characterized by ventricular standstill due to

suppression of the cardiac peacemaker by myocardial disease, anoxia, electrolyte imbalance,or drugs

• ECG shows flat traces• Often represent massive heart damage • Survival less than 4%

• Clinical Manifestations:– Early may see agonal respirations; unconscious;

unresponsive– No pulse; no blood pressure– Cardiac arrest

• Etiologies:– End of life (death)– Ischemia/hypoxia from many causes– Acute respiratory failure (no oxygen; apnea; asphyxiation)– Massive electrical shock: electrocution; lightning strike– Postdefibrillatory shocks

• Treatment:– Always check for status– Primary ABCD survey (basic CPR)– Secondary ABCD survey

ALGORYTHMFOR

BRADYCARDIA OR ASYSTOLE

Harrison’s Principle of Internal Medicine 18th Ed21

ACUTE CORONARY SYNDROME

Initial Assessment

Acute myocardial infarction(STEMI)

• MI when arterial blood flow to the myocardium is suddenly decreased / interrupted.

• It’s usually due to atherosclerotic occlusion by thrombus / emboli.

• Complete occlusion (ST segment elevation) 80-90% because of the thrombus

Patophysiology

• Unstable plaque• Plaque rupture• Unstable angina• Microemboli• Occlusive thrombus

Clinical finding

• Chest discomfort typically substernal radiate to the neck / left arm

• Pain classically oppresive or squeezing• May associated with SOB(shortness of

breathing),dizziness, syncope/presyncope, , nausea, vomitting, dyspnea, and diaphoresis

ECG

• Hyperacute T waves• Flipped T waves• Elevated ST segment• Abnormal Q wavesNormal ECG does not rule out the possibility of MI / ACS.

Laboratory findings

• CK-MB less sensitive than Troponin• Troponin cTnt & cTni the most cardiac

specific biochemical marker.• Mioglobin marker for injured cardiac

sensitive early marker

Differential Diagnosis

• Aortic dissection• Aneurysm• Pericarditis• GI bleeding

Killip Classification

Unstable Angina Pectoris (UAP)& NSTEMI

• UA is defined as angina pectoris or equivalent ischemic discomfort with at least one of three features– it occurs at rest usually lasting >10 minutes– it is severe and of new onset (i.e., within the

prior 4–6 weeks); or– it occurs with a crescendo pattern

• NSTEMI is a result of an acute imbalance between myocardial oxygen demand and supply, most commonly due to a reduction in myocardial perfusion.

• Most often it is caused by a non-occlusive thrombus that develops in a disrupted atherosclerotic plaque.

• UA and nSTEMI the thrombus partially occludes blood flow down a coronary artery, starving the heart muscle of oxygen and nutrients.

• This can result in symptoms with or without ECG changes and cardiac enzyme release.

History and Physical Examination

• The clinical hallmark of UA/NSTEMI is– chest pain– typically located in the substernal region or

sometimes in the epigastrium, that radiates to the neck, left shoulder, and/or the left arm

– Anginal "equivalents" such as dyspnea and epigastric discomfort may also occur, and these appear to be more frequent in women

History and Physical Examination

• The physical examination– Diaphoresis– Pale– Cool skin– Sinus tachycardia– Hypotension

Cardiac Biomarkers

• Patients with NSTEMI who have elevated biomarkers of necrosis, such as CK-MB and troponin, are at increased risk for death or recurrent MI

• Patients with UA who haven’t elevated biomarkers of necrosiscardiac biomarkers not increased

Drugs Commonly Used in Intensive Medical Management of Patients with Unstable Angina and Non-ST Segment Elevation MI

Drug Category Clinical Condition Dosage

Nitrates Administer sublingually, and, if symptoms persist, intravenously

Topical, oral, or buccal 5–10 mikrogram/min

Beta blockers Unstable angina Metoprolol 25–50 mg by mouth every 6 h

Calcium channel blockers

Patients whose symptoms are not relieved by adequate doses of nitrates and beta blockers, or in patients unable to tolerate adequate doses of one or both of these agents, or in patients with variant angina

Dependent on specific agent

Morphine sulfate

Patients whose symptoms are not relieved after three serial sublingual nitroglycerin tablets or whose symptoms recur with adequate anti-ischemic therapy

2–5 mg IV dose May be repeated every 5–30 min as needed to relieve symptoms and maintain patient comfort

Acute Coronary Syndrome

Acute Coronary Syndrome

CARDIOGENIC SHOCK

Description

• Inadequate tissue perfusion due to cardiac dysfunction

• Underlying mechanisms in acute myocardial infarction (AMI):– Pump failure:

• left ventricle (LV) infarct• Infarct in pre-existing LV dysfunction• Reinfarction

Description

– Mechanical complications:• Acute mitral regurgitation• Ventricular septal defect• LV rupture• Pericardial tamponade

– Right ventricular (RV) infarction

Etiology

• AMI• Sepsis• Myocarditis• Cardiomyopathy• Drug toxicity:

– Beta-blocker– Calcium channel blocker– Adriamycin

• etc

Signs and Symptoms

• General:– Cyanosis– Pallor– Diaphoresis– Dulled sensorium– Decrease in body temperature– Urine flow of less than 20 mL/h

Signs and Symptoms

• Cardiac:– Ischemic chest pain– Systolic apical blowing murmur– Gallop rhythm:

• S3 reflects severe myocardial dysfunction• S4 is present in 80% patients in sinus rhythm with AMI

– Systolic click:• Suggests rupture of the chordae tendinae

Signs and Symptoms

• Neck:– Jugular venous distention

• Abdominal:– Epigastric pain– Nausea and vomiting

• Neurologic:– Obtundation

Test

Electrocardiogram• Normal ECG does not rule out AMI.• Findings of AMI (ST-elevations in two or more

contiguous leads)• May occur in non-ST-elevation acute coronary

syndrome• Dysrhythmias• LV hypertrophy

Test

Chest Radiography• Pulmonary congestion• Pleural effusion• Cardiomegaly• Pneumonia• Pneumothorax• Pericardial effusion

TestEmergent Echocardiography• Transthoracic echocardiography (TTE) with color

Doppler• LV contractility looking for hypokinesis, akinesis or

dyskinesis• Acute mitral regurgitation or septal defects• RV dilatation, tricuspid insufficiency, high pulmonary

artery and RV pressures suggest pulmonary embolism• RV hypokinesis or akinesis, RV dilatation, normal

pulmonary pressures suggest RV infarction• Pericardial effusion, right atrium or RV diastolic

collapse suggest cardiac tamponade

Lab

• B-type natriuretic peptide (BNP):– Diagnostic and prognostic value

• Creatine kinase (CK), CK-Mb, troponin• Electrolytes and renal function

– Acute renal failure is a strong predictor of mortality

• CBC:– Identify anemia or elevated WBC

• Drug levels (e.g., digoxin)

Differential Diagnosis

• Obstructive shock• Distributive shock• Hypovolemic shock

Treatment

Pre Hospital• ABCs, IV access, O2, monitor

• Consider fluid bolus if no crackles.• Aspirin• Nitroglycerin or morphine sulfate for chest

pain in absence of hypotension• Transport AMI patients to facility with 24-hour

cardiac revascularization capability.

Treatment

Initial Stabilization• ABCs• Two large bore peripheral IV lines• Cardiac monitor• Endotracheal intubation for airway compromise:

– Consider etomidate for induction (minimal effect on blood pressure)

• Fluid challenge (100–250 mL normal saline) in absence of pulmonary congestion

• Foley catheter to monitor urine output

Treatment

Medication (Drugs)• Dobutamine• Dopamine• Furosemide• Milrinone• Nitroglycerin• Nitroprusside• Norepinephrine

CPR

Definition• CPR is an organized, sequential response to

cardiac arrest, including– Recognition of absent breathing and circulation– Basic life support with chest compression and rescue

breathing– Advanced cardiac life support (ACLS) with definitive

airway and rhythm control– Postresuscitative care

• Prompt initiation of chest compression and early defibrillation (when indicates) are the key of success.

When to start CPRAnyone who initiate resuscitation knowledge and skills to initiate CPR when dealing with cases of cardiac arrest.

A.Incidence of cardiac arrest who witnessedIf we are witnessing the cardiac arrest, was should immediately started CPR. However, there are

circumstances like this some underlying unnecessary CPR started:

– There is evidence of demand for family– CPR efforts will harm people who helped– Possible CPR can restore spontaneous circulation is very small– Cardiac arrest happened on terminal illness who have been

treated to the maximum

B. Incidence of cardiac arrest was not witnessed•Helper ill cardiac know how long it's been going on. For something like this we do not need to start doing CPR if the state finds as follows:

– There is a sign that death does not change like rigor mortis / bruised corpse

– It's getting no signs of decay– Patients experiencing trauma that can not be saved,

such as charred, decapitation

When to stop CPRThere are several compelling reasons for rescuers to stop CPR among other things:•Helpers are doing basic and advanced life support optimal included:

• CPR, defibrillation in patients with VF / VT without a pulse, vasopressin / epinephrine IV, open the airway, ventilation and oxygenation using airway aid and all levels lanut rhythm after treatment performed.

•Helpers are considering whether there is a hypothermia patient. Helpers has established the presence / absence of hypothermia by measuring body temperature.

• Helpers have considered whether patients exposed to toxic materials or an overdose that inhibits CNS.

• Helper was recorded through a monitor systolic settled for 10 minutes or more.

• The time interval pd cardiac resuscitation efforts were unsuccessful witnessed restore spontaneous circulation was 25-30 minutes.

General Technique of CPR continued

• If alone, alternate 30 chest compressions and 2 ventilations for any age patient

• In two-rescuer CPR for infant/child, alternate 15 compressions and 2 ventilations– Chest-encircling method in infant

• Give each ventilation over 1 second• Follow local protocol regarding oxygen

Put hand(s) in correct position for chest compressions

Give 30 chest compressions at rate of 100 per minute

Then give 2 ventilations