emergensi ppt

Heart Emergency According to Conscious State

• Conscious -> acute coronary syndrom• Unconscious -> cardiac arrest

Cardiac Arrest

• Abrupt cessation of cardiac pump function which may be reversible by a prompt intervention but will lead to death in its absence

• Rare spontaneous reversions• Likelihood of successful interventions relates to

mechanism of arrest, clinical setting, and prompt return of circulation

Epidemiology of Cardiac Arrest

• Between 77,000 and 174,000 patients -> treated for out-of-hospital cardiac arrest each year in the US

• The incidence of VF as the initial rhythm has declined over time -> 20-38% (now)

• ROSC -> 9 to 65% -> only 1 to 31% of patients survive to hospital discharge

Epidemiology of Cardiac Arrest

• Approximately 50% of cardiac arrest survivors -> comatose and treated with hypothermia

Common causes of Nontraumatic Cardiac ArrestGeneral Specific Disease/Agent

Cardiac CADCardiomiopathiesStructural abnormalitiesValve dysfunction

Respiratory Hypoventilation CNS dysfunctionNeuromuscular diseaseToxic and metabolic encephalopathies

Upper airway obstruction CNS dysfunctionForeign bodyInfectionTraumaNeoplasm

Pulmonary dysfunction Asthma,COPDPulmonary edemaPulmonary embolusPneumonia

Common causes of Nontraumatic Cardiac Arrest

General Specific Disease/Agent

Circulatory Mechanical obstruction Tension pneumothoraxPericardial tamponadePulmonary embolus

Hypovolemia Hemorrhage

Vascular tone SepsisNeurogenic

Metabolic Electrolyte abnormalities Hypokalemia or HyperkalemiaHypermagnesemiaHypomagnesemiaHypocalcemia

Toxic Prescription medications AntidysrhythmicsDigitalis beta-blockersCCBTricyclic antidepressants

Drug of abuse CocaineHeroine

Toxins CO, Cyanide

Common causes of Nontraumatic Cardiac Arrest

General Specific Disease/Agent

Enviromental LightningElectrocutionHypothermia or hyperthermiaDrowning/near-drowning

Etiology of Cardiac Arrest

• Primary respiratory failure -> initial HT and tachycardia -> followed by hypotension and bradycardia -> PEA, VF, or asystole

• Circulatory obstruction and hypovolemia -> initial tachycardia and hypotension -> bradycardia to PEA -> may deteriorate to VF or Asystole

• The Most common metabolic cause : hyperkalemia

Manifestation of Cardiac Arrest

• Unresponsiveness• Pulselessness• Shallow, gasping respirations may persist for a few

minutes• Occasionally preceded by:– Chest pain– Dyspnea


– Palpitations– Seizure activity

• Immediately prior to arrest:– Shock or hypotension– Impaired mentation


• Cardiopulmonary arrest -> triad :1.Unconsciousness2.Apnea3.Pulselessness (carotid or femoral artery)

Clinical Characteristics of Cardiac Arrest

• The onset of the clinical transition -> an acute change in cardiovascular status preceding cardiac arrest by up to 1 h

• ECG -> VF begin with a run of nonsustained or sustained VT

• Progression to biologic death -> depend on the mechanism of cardiac arrest, the length of the delay before interventions

Classification of Cardiac Arrest

• Primary cardiac arrest -> occur in the absence of hemodynamic instability

• Secondary cardiac arrest -> occur in patients in whom abnormal hemodynamics dominate the clinical picture before cardiac arrest

History of Cardiac Arrest

• Information surrounding the events1. Whether the arrest was witnessed2. The time of arrest3. What the pasien was doing (e.g., eating, exercising,

trauma)4. The possibility of drug ingestion, time of initial CPR5. Initial ECG rhythm

History of Cardiac Arrest

6. Interventions by EMS providers• Past medical history 1. baseline health and mental status2. Previous heart, lung, renal, malignant disease3. Hemorrhage, Infection4. Risk factors for CAD and pulmonary embolism• Current medications and allergies

Physical Examination of Cardiac Arrest

• It is necessarily focused on a few key goals1. Ensure adequacy of airway maintenance and

ventilation2. Confirm the diagnosis of cardiac arrest3. Find evidence of cause4. Monitor for complications of therapeutic

interventions

Physical Examination Findings Indicating Potential Cause of Cardiac Arrest and Complications of Therapy

Physical Examination Abnormalities Potential CausesGeneral Pallor

Cold HemorrhageHypothermia

Airway Secretions, vomitus, or blood AspirationAirway obstruction

Resistance to positive-pressure ventilation

Tension PneumothoraxAirway obstructionBronchospasm

Neck Jugular venous distention Tension PneumothoraxCardiac tamponadePulmonary embolus

Tracheal deviation Tension Pneumothorax

Chest Median sternotomy scar Undelying cardiac disease


Physical Examination Abnormalities Potential CausesLungs Unilateral breath sounds Tension Pneumothorax

Right main stem intubationAspiration

Distant or no breath sounds or no chest expansion

Esophageal intubationAirway obstructionSevere bronchospasm

Wheezing Aspiration BronchospasmPulmonary edema

Rales AspirationPulmonary edemaPneumonia

Heart Audible heart tones HypovolemiaCardiac tamponadeTension PneumothoraxPulmonary embolus


Physical Examination Abnormalities Potential CausesAbdomen Distended and dull Ruptured abdominal aortic

aneurysm or ruptured ectopic pregnancy

Distended, tympanitic Esophageal intubationGastric insufflation

Rectal Blood, melena GI hemorrhage

Extremities Asymmetrical pulses Aortic dissection

AV shunt or fistula Hyperkalemia

Skin Needle tracks or abscesses IV drug abuse

Burns Smoke inhalationElectrocution

Supporting Examination of Cardiac Arrest

LabIndicated only when successful ROSC is achieved:

• Electrolytes• Blood urea nitrogen/creatinine• Creatinine kinase with isoenzymes, cardiac troponin• Arterial blood gas (avoid arterial puncture in

thrombolysis candidates)


Lab• CBC• Therapeutic drug levels• Toxicological testingImaging• ECG:– Establish or rule out acute coronary syndrome


Imaging• Chest radiograph:– Endotracheal tube position– Cardiac silhouette– Pneumothorax

• ECG:– Pericardial effusion


Imaging• ECG:– Wall motion abnormality– Valvular dysfunction

Differensial Diagnose of Cardiac Arrest

Differensial Diagnose of Cardiac Arrest

Sudden loss of consciousness with a palpable pulse:• Syncope• Seizure• Acute stroke• Hypoglycemia• Acute airway obstruction• Head trauma, Toxins

Management of Cardiac

Arrest

Treatment of Cardiac Arrest

• 5 stages: (1)initial evaluation and basic life support if

arrest is confirmed(2) public access defibrillation (when available)(3) advanced life support(4) postresuscitation care(5) long-term management

Treatment of Cardiac Arrest

• Pre Hospital• Initial Stabilization• ED Treatment• Medication (Drugs)• Follow-Up

The 5-Minute Emergency Medicine Consult (Rosen and Barkin-_s) 3ed

Pre Hospital

• Prompt initiation of standard CPR or active compression-decompression CPR (ACD-CPR)

• Confirm underlying rhythm• Early defibrillation of ventricular tachycardia

(VT) or ventricular fibrillation (VF):– Automated external defibrillator– EMT-D or layperson


Pre Hospital

• Consider CPR before defibrillation in cases of if arrest >5 minutes.

• Secure airway and provide adequate respirations:– Endotracheal intubation– Laryngeal mask airway

• Post-resuscitation care:– Identify cause of arrest


Pre Hospital

- 12-lead ECG, Monitor vital signs• Transport to the closest facility:– If return of spontaneous circulation, consider

transport to center equipped for interventional cardiac care.

– Pediatric critical care center for children• Termination of resuscitative efforts:– Persistent, confirmed asystole, Prolonged arrest


Initial Stabilization

• Initiate advanced cardiac life support (ACLS).• Perform standard CPR as long as no pulse is

palpable.• Consider ACD-CPR:– Stop CPR only briefly to check cardiac rhythm or

intubate.• Secure the airway


Initial Stabilization

• Obtain IV access• Cardiac monitor• Therapy based on the underlying rhythm

according to ACLS protocols


ED Treatment

Pulseless VT or VF• Immediate defibrillation with up to three

countershocks:– 200 J– 200 - 300 J– 360 J


ED Treatment

• If defibrillation is unsuccessful:– Epinephrine– Vasopressin

• If refractory to defibrillation and epinephrine:– Amiodarone– Lidocaine


ED Treatment

- Procainamide– Magnesium for Torsades de Pointes

• Asystole• Dismal prognosis if this is the presenting

rhythm• Confirm in two or more leads• Epinephrine


ED Treatment

• Atropine• Consider transcutaneous pacing for severe

brady-asystolic rhythm.Pulseless Electrical Activity• Epinephrine• Atropine


ED Treatment

• Treat for reversible cause of pulseless electrical activity– Pneumothorax– Cardiac tamponade– Hypoxia– Pulmonary embolus– Hypovolemia (hemorrhage)


ED Treatment

Post-Resuscitation• Treat the underlying cause of the arrest.• ECG to establish presence of acute coronary

syndrome:– Immediate catheterization or thrombolysis for

ACS• Ventilatory support• Continue antidysrhythmic therapy.


ED Treatment

Post-Resuscitation• Correct electrolyte abnormalities.• Initiate volume resuscitation and provide

inotropic support as needed.


Medication (Drugs)

• Amiodarone: 300 mg (peds: 5 mg/kg) IVP• Atropine: 1 mg (peds: 0.02 mg/kg) IV tiap 15min up

to 0.04 mg/kg• Epinephrine: 1 mg (peds: 0.01 mg/kg) IVP tiap 15min• Lidocaine: 100 mg (peds 1 mg/kg) IVP, then 2x4

mg/min IV continuous infusion• Magnesium: 1x2 g slow IV


Medication (Drugs)

• Procainamide: 20 mg/min slow IV to a total of 1 g or until arrhythmia is suppressed; maintenance infusion 1x4 mg/min (peds: 15 mg/kg over 30 min IV)

• Sodium bicarbonate: 1 mEq/kg slow IV• Vasopressin: 40 U IVP (adults with VT/VF only)


Follow-Up

Disposition• Admission Criteria

Return of spontaneous circulation:1.Coronary care unit or intensive care unit2.Postresuscitation care


Indicators of Inadequate Blood Flow During Cardiopulmonary Resuscitation

Monitoring Technique Indicator

Carotid or femoral pulse Not palpable

CPP <15 mmHg

ETCO2 <10 mmHg (before vasopressor)

ScvO2 <40%

CPR

Tintinalli's Emergency Medicine 7th ed

Step 3: opening the air way

• Head Tilt–Chin Lift Maneuver -> gently extend the patient's neck, by placing one hand under the patient's neck and the other on the forehead and extending the head in relation to the neck. This maneuver should place the patient's head in the sniffing position, with the nose pointing up.


Step 3: opening the air way

• Jaw Thrust Maneuverthe safest method for opening the airway. This maneuver helps to maintain the cervical spine in a neutral position. The rescuer, who is positioned at the head of the patient, places the hands at the sides of the victim's face, grasps the mandible at its angle, and lifts the mandible forward.


Step 4 dan 5


Ventilation Technique


Step 6 dan 7

Prognose of Cardiac Arrest

• Depend on initial interventions -> if delayed (>4 or >6 minutes), it can be progressive biologic death because of progressive brain cell death

Complication of Cardiac Arrest

• Sudden cardiac death• Multi organ failure

Acute Coronary Syndrome: MI

• Imbalance in myocardial blood supply + O2 requirement• Acute cardiac ischemia encompasses a spectrum of

disease processes:– Unstable angina pectoris– Acute myocardial infarction (AMI)– ST elevation myocardial infarction (STEMI)– Non-STEMI

Etiology of MI

• Atherosclerotic narrowing of coronary vessels• Vasospasm although this is usually at rest and

considered unstable if new onset• Microvascular angina or abnormal relaxation of

vessels with diffuse vascular disease• Plaque disruption• Thrombosis

Etiology of MI

• Arteritis:– Lupus– Takayasu disease– Kawasaki disease– Rheumatoid arthritis

• Prolonged hypotension• Anemia -> Hemoglobin <8 g/dL

Etiology of MI

• Hyperbarism or elevations in carboxyhemoglobin• Coronary artery gas embolus• Thyroid storm• Structural abnormalities of coronary arteries:– Radiation fibrosis– Aneurysms– Ectasia

Etiology of MI

• Cocaine- or amphetamine-induced vasospasm• Cardiac risk factors include:– Hypercholesterolemia– Diabetes mellitus– Hypertension– Smoking– Family history in a first-degree relative <55 years old

Etiology of MI

• Cardiac risk factors include:– Men, age >55 years– Postmenopausal women

Signs and Symptoms of MI

• Chest pain:– Most common presentation of MI– Substernal pressure– Heaviness– Squeezing– Burning sensation– Tightness


• Anginal equivalents (MI without chest pain):– Abdominal pain– Syncope– Diaphoresis– Nausea or vomiting– Weakness


• May localize or radiate to arms, shoulders, back, neck, or jaw

• Associated symptoms:– Dyspnea– Syncope– Fatigue– Diaphoresis


– Nausea– Vomiting

• Symptoms are usually reproduced by exertion, eating, exposure to cold, or emotional stress.

• Symptoms commonly last 30 minutes or more.• Symptoms may occur with rest or during exertion.


• Often preceded by crescendo angina• May be improved or relieved with rest or nitroglycerin• Symptoms generally unchanged with position or

inspiration• Positive Levine sign or clenched fist over chest is

suggestive of angina.• Blood pressure (BP) is usually elevated during symptoms

Physical Exam of MI

• Physical exam is usually unrevealing.• Occasional physical findings include:– S3 or S4 due to left ventricular systolic or diastolic

symptoms– Papillary muscle dysfunction resulting in mitral

regurgitation– Diminished peripheral pulses

Supporting Exams of MI

• ECG• Lab1.CK-MB and troponin I or T2.Hematocrit3.Coagulation profile4.Creatinine

Differential Diagnosis of MI

• Anxiety• Aortic dissection• Biliary colic• Costochondritis• Esophageal reflux• Esophageal spasm• Herpes zoster


• Hiatal hernia• Mitral valve prolapse• Myocardial infarction• Panic disorder• Peptic ulcer disease• Pneumonia• Psychogenic


• Pulmonary embolus• Unstable angina

Treatment of MI

Pre Hospital• IV access• Aspirin, Oxygen• Cardiac monitoring• Sublingual nitroglycerin for symptom relief• 12-lead ECG, if possible, with transmission or

results relayed to receiving hospital

Treatment of MI

Alert• All chest pain should be treated and transported as a

possible life-threatening emergency.• Do not administer thrombolytics or heparin if aortic

dissection is suspected.Initial Stabilization• IV access

Treatment of MI

• Oxygen• Cardiac monitoring• Oxygen saturation• Continuous BP monitoring and pulse oximetry

ED Treatment• STEMI requires reperfusion therapy as soon as

possible:

Treatment of MI

– Thrombolytics should be used if percutaneous coronary intervention is not readily available within a 90-minute time frame (see Reperfusion Therapy, Cardiac).

• Patients with non-STEMI, if started on glycoprotein IIb/IIIa inhibitors and if they subsequently receive a stent, benefit from a PCI within a 48-hour time frame.

Treatment of MI

• Aspirin should be administered first to all patients with suspected MI unless the patient has a known allergy.

• If BP is >90-100 mm Hg systolic, administer sublingual nitroglycerin, nitropaste, or IV nitroglycerin assuming no ECG criteria of right ventricular infarct:– Symptoms that persist after three sublingual

nitroglycerin tablets are strongly suggestive of AMI or noncardiac etiology

• Beta-blockers should be administered if no contraindications (e.g., bradyarrhythmias, heart rate <60, congestive heart failure, hypotension, or obstructive pulmonary disease) are present.

• Morphine may be given to relieve pain and increase oxygen carrying capacity.

• Enoxaparin or heparin is generally appropriate as the next line of therapy.

• Angiotensin-converting enzyme inhibitors may effect a small decrease in mortality when given acutely.

• If non-STEMI is clearly the clinical diagnoses, a glycoprotein IIb/IIIa inhibitor should be started.

• Clopidogrel may be of benefit acutely when added to standard therapy by reducing the odds of AMI patients having another occluded artery, or a second heart attack or death by 36% after 1 week of

• Statin therapy reduces clinical events in patients with stable coronary artery disease., this may also extend to patients experiencing an acute ischemic coronary event.

• If patient is in cardiogenic shock, patient should be transported to a cardiac catheterization laboratory for angioplasty and intra-aortic balloon pump as soon as possible (see Congestive Heart Failure).

• Ventricular dysrhythmias:– See Ventricular Tachycardia

• Bradydysrhythmia associated with hypotension should be treated with atropine or external pacing:

• Conduction disturbances:– First-degree aortic valve (AV) block and Mobitz I

(Wenckebach) are often self-limited and do not require treatment.

– Mobitz II, complete heart block, new right bundle branch block (RBBB) in anterior MI, RBBB plus left anterior branch block or left posterior fascicular block, left bundle branch block plus first-degree AV block may require a temporary transvenous pacemaker.

Medications for MI

• Amiodarone: 150 mg IV over 5 minutes then 0.5 mg/min

• Aspirin: 160-325 mg PO• Clopidogrel (Plavix): 300 mg PO load, 75 mg PO per

day• Enoxaparin (Lovenox): 1 mg/kg SC q12h• Glycoprotein IIb/IIIa inhibitors:

Medications for MI

– Eptifibatide (Integrilin) 180 µg/kg IV over 1-2 minutes, followed by continuous infusion of 2 µg/kg/min up to 72 hours

– Irofiban (Aggrastat) 0.4 µg/kg/min for 30 minutes, then 0.1 µg/kg/min for 48-108 hours

– Abciximab (ReoPro) for use prior to PCI only: 0.25 mg/kg IV bolus

Medications for MI

• Heparin 80 units/kg IV bolus, then 18 units/kg/h

• Lidocaine: 1.5 mg/kg IV bolus, infusion of 2-4 mg/kg/min

• Magnesium: 2 g bolus IV• Metoprolol: 5 mg IV q5min-15min followed by

25-50 mg PO starting dose as tolerated

Medications for MI

(note: beta-blockers contraindicated in cocaine chest pain)

• Morphine: 2 mg IV, may titrate upward in 2-mg increments for relief of pain assuming no respiratory deterioration and SBP >90 mm Hg

• Nitroglycerin: 0.4 mg sublingual• Nitroglycerin: IV drip at 5-10 µg/min

Medications for MI

Nitropaste: 1-2 inches transdermal• Thrombolytics: see Reperfusion Therapy,

Cardiac, for dosing

Follow-Up

DispositionAdmission Criteria

• Patients with an AMI require hospital admission.• If the diagnosis is unclear, admission to the hospital

or an ED observation unit may be useful for serial cardiac enzymes, ECGs, and exercise stress testing and/or cardiac catheterization.

Follow-Up

Discharge Criteria• No patient with an AMI should be discharged from

the ED.Issues for Referral

• If PCI is unavailable in the treating institution, and particularly if the patient is in cardiogenic shock, patients should be transported to another hospital if PCI can be underway in less than 90 minutes.

References

• Harrison’s Principles of Internal Medicine. 18ed

• Tintinalli's Emergency Medicine 7th ed• The 5-Minute Emergency Medicine Consult

(Rosen and Barkin-_s) 3ed• Oxford Handbook of Accident and Emergency

Medicine-2nd Edition

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