Julita (Problem1-KGD) (01)

8/12/2019 Julita (Problem1-KGD) (01)

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Problem 1

Julita Suhardi

Emergency Medicine Block



Cardiac Arrest



Description

• Sudden death:

– Death within 24 hours of symptom onset

– Initial presentation in 50% of patients with

cardiovascular disease• Factors affecting survival:

– Initial rhythm

– Time to successful defibrillation

• Incidence of re-arrest in neurologically intactsurvivors:

– 30% at 1 year and 60% at 5 years



Etiology

• Acute coronary ischemia:

– Underlying etiology in 50% of arrests

– Myocardial irritability leads to ventricular

fibrillation• Primary dysrhythmia:

– Congenital and acquired electrical abnormalities

–

Hypertrophic/dilated cardiomyopathy – Myocarditis

• Cardiac rupture



• Pericardial tamponade

•

Metabolic abnormalities• Noncardiac etiologies:

– Consider especially in cases of pulseless electrical

activity

– Tension pneumothorax

– Hemorrhage

– Massive pulmonary embolus

– Sepsis

– Severe acidosis



• Drugs or toxins:

– Antidysrhythmics

– Digoxin

– Beta-blockers

– Calcium channel blockers

– Tricyclic antidepressants

– Cocaine

– Heroin



Signs and Symptoms

• Unresponsiveness

• Pulselessness

• Shallow, gasping respirations may persist for a fewminutes

• Occasionally preceded by: – Chest pain

– Dyspnea

– Palpitations

– Seizure activity• Immediately prior to arrest:

– Shock or hypotension

– Impaired mentation



Tests

Lab

• Indicated only when successful Return ofspontaneous circulation (ROSC) is achieved:

– Electrolytes – Blood urea nitrogen/creatinine

– Creatinine kinase with isoenzymes, cardiac troponin

– Arterial blood gas (avoid arterial puncture in

thrombolysis candidates). – CBC

– Therapeutic drug levels

– Toxicological testing



Imaging

• ECG:

– Establish or rule out acute coronary syndrome

• Chest radiograph:

– Endotracheal tube position

– Cardiac silhouette

– Pneumothorax

• ECG: – Pericardial effusion

– Wall motion abnormality

– Valvular dysfunction



Differential Diagnosis

• Syncope

• Seizure

•

Acute stroke• Hypoglycemia

• Acute airway obstruction

• Head trauma• Toxins



Treatment : Pre Hospital

• CPR or active compression-decompressionCPR (ACD-CPR)

• Confirm underlying rhythm

• Early defibrillation of ventricular tachycardia(VT) or ventricular fibrillation (VF):

– Automated external defibrillator

–EMT-D or layperson

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




• Secure airway and provide adequate

respirations:

– Endotracheal intubation

– Laryngeal mask airway

• Post-resuscitation care:

– Identify cause of arrest

– 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

• 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 threecountershocks: – 200 J

– 200“300 J

– 360 J• If defibrillation is unsuccessful:

– Epinephrine

– Vasopressin

•

If refractory to defibrillation and epinephrine: – Amiodarone

– Lidocaine

– Procainamide

– Magnesium for Torsades de Pointes



ED Treatment : Asystole

• Dismal prognosis if this is the presenting

rhythm

• Confirm in two or more leads

• Epinephrine

• Atropine

•

Consider transcutaneous pacing for severebrady-asystolic rhythm.



ED Treatment : Pulseless Electrical

Activity

• Epinephrine

• Atropine

• 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.

• Correct electrolyte abnormalities.

• Initiate volume resuscitation and provide

inotropic support as needed



Medication (Drugs)

• Amiodarone

• Atropine

•

Epinephrine• Lidocaine

• Magnesium

• Procainamide• Sodium bicarbonate

• Vasopressin





Adult basic life support (BLS)









PEA



PULSELESS ELECTRICAL ACTIVITY (PEA)

• Unresponsive state

• No respiration, pulse, or BP

•

Identifiable electrical rhythm on monitor butno pulse



Etiology

• failure of the normal cardiac pumping

mechanism

• obstruction to cardiac filling or output



Etiology

4H's

• Hypoxia

• Hypovolaemia

• Hyper/hypokalaemia/metabolic disorders

• Hypothermia

4T's

• Tension pneumothorax

• Tamponade (cardiac)

• Toxic substances (eg overdose)

• Thromboembolic/mechanical obstruction




1. Unresponsiveness,no respiration or pulse Call for help.

2. Begin CPR, provide oxygen and attach

manual monitor-defibrillator when availablewithout interrupting CPR.

3. When device is attached, stop CPR to assess

rhythm. If identifiable rhythm noted onmonitor, immediately resume CPR beginningwith compressions.




4. Consider and treat possible causes:

• Trauma Hypokalemia/hyperkalemia

•

Tension pneumothorax Hypovolemia• Thrombosis (pulmonary Hypoxia or coronary)

• Hypoglycemia

•Tamponade, cardiac Hypothermia

• Toxins Hydrogen ion (acidosis)




5.Continue CPR using five cycles of 30

compressions and 2 breaths; check the

rhythm every 2 minutes.

6.Consider insertion of an advanced airway

(ETtube, LMA, or Combitube) if basic airway

management is inadequate.

7.If PEA persists epinephrine 1 mg,

vasopressin 40 U IV/IO to replace epinephrine.




8.Atropine 1 mg IV/IO heart rate on the ECGis less than 60 bpm.

9.Continue CPR; check the rhythm every 2

minutes.10.If the rhythm is not shockable with no pulse,

resume CPR and repeat steps 4 –8.

12.Stable ECG rhythm returns with adequatebreathing and circulation, monitor andreevaluate.



ASYSTOLE

• Unresponsive state, no respiration, pulse, or

BP

• ECG shows flat line; no electrical activity





ASYSTOLE

4. Consider and treat possible causes:

• Trauma Hypokalemia/hyperkalemia

• Tension pneumothorax Hypovolemia

• Thrombosis (pulmonary Hypoxia or coronary)

• Hypoglycemia

•Tamponade, cardiac Hypothermia

• Toxins Hydrogen ion (acidosis)



ASYSTOLE

5.Continue CPR using five cycles of 30

compressions and 2 breaths; check the

rhythm every 2 minutes.

6.Consider insertion of an advanced airway

(ETtube, LMA, or Combitube) if basic airway

management is inadequate.

7.If asystole persists epinephrine 1 mg,

vasopressin 40 U IV/IO to replace epinephrine.



ASYSTOLE

8. Consider atropine 1 mg IV/IO if the ECG stillshows asystole.

9.Continue CPR; check the rhythm every 2

minutes.10.If the rhythm is not shockable with no pulse,

resume CPR and repeat steps 4 –8.

12. If asystole persists, consider resuscitationprotocols were followed and reversible causesidentified.



Acute Coronary Syndrome:

Myocardial Infarction



Description

• Imbalance in myocardial blood supply and

oxygen 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

• Atherosclerotic narrowing of coronary vessels

• Vasospasme 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

• Arteritis:

– Lupus

– Takayasu disease

– Kawasaki disease

– Rheumatoid arthritis

• Prolonged hypotension

• Anemia

– Hemoglobin <8 g/dL



Etiology

• Hyperbarism or elevations incarboxyhemoglobin

• Coronary artery gas embolus

• Thyroid storm• Structural abnormalities of coronary arteries:

– Radiation fibrosis

– Aneurysms – Ectasia

• Cocaine- or amphetamine-induced vasospasm



Etiology

• Cardiac risk factors include:

– Hypercholesterolemia

– Diabetes mellitus

– Hypertension – Smoking

– Family history in a first-degree relative less than55 years old

– Men, age >55 years

– Postmenopausal women



Signs and Symptoms

• Chest pain:

– Most common presentation of myocardial

infarction (MI)

– Substernal pressure

– Heaviness

– Squeezing

– Burning sensation – Tightness



Signs and Symptoms

• 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



Signs and Symptoms

• Associated symptoms:

– Dyspnea

– Syncope

– Fatigue – Diaphoresis

– Nausea

– Vomiting

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



Signs and Symptoms

• 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 ornitroglycerin

• 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

• 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



• Tests

– ECG

• Lab

– CK-MB and troponin I or T

– Hematocrit

– Coagulation profile

– Creatinine

• Diagnostic Procedures/Surgery – See Cardiac Testing




• 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

• Pre Hospital

– IV access

– Aspirin

– Oxygen

– Cardiac monitoring

– Sublingual nitroglycerin for symptom relief

– 12-lead ECG, if possible, with transmission orresults relayed to receiving hospital



• 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

– Oxygen

– Cardiac monitoring

– Oxygen saturation

– Continuous BP monitoring and pulse oximetry



ED Treatment

• STEMI requires reperfusion therapy as soon as

possible:

– Thrombolytics should be used if percutaneous

coronary intervention is not readily availablewithin a 90-minute time frame (see Reperfusion

Therapy, Cardiac).

•

Patients with non-STEMI, if started onglycoprotein IIb/IIIa inhibitors and if they

subsequently receive a stent, benefit from a

PCI within a 48-hour time frame.



• Aspirin should be administered first to all

patients with suspected MI unless the patient

has a known allergy.

• If BP is >90â€“100 mm Hg systolic, administer

sublingual nitroglycerin, nitropaste, or IV

nitroglycerin assuming no ECG criteria of rightventricular infarct:

– Symptoms that persist after three sublingual

nitroglycerin tablets are strongly suggestive ofAMI 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.

• Clopidogrel may be of benefit acutely whenadded to standard therapy by reducing the

odds of AMI patients having another occluded

artery, or a second heart attack or death by36% after 1 week of hospitalization.



• 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).



• Bradydysrhythmia associated withhypotension 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 leftanterior branch block or left posterior fascicular

block, left bundle branch block plus first-degreeAV block may require a temporary transvenouspacemaker.



Medication (Drugs)

• Amiodarone

• Aspirin

• Clopidogrel (Plavix)

• Enoxaparin (Lovenox)

• Heparin

•

Lidocaine• Magnesium



• Glycoprotein IIb/IIIa inhibitors:

– Eptifibatide

– Irofiban (Aggrastat)

– Abciximab (ReoPro)

• Nitropaste:

• Thrombolyt

• Metoprolol

• Morphine

• Nitroglycerin

• Nitroglycerin



MI ( non ST ELEvation )



Description

• Non-ST-elevation myocardial infarction

(NSTEMI) is a part of a clinical syndrome that

includes unstable angina.

• Probable cause is the generation of a subtotalcoronary occlusion or functional collateral

circulation:

– Often indicates an incomplete ischemic event



Description

• Coronary plaque disruption:

– Endothelial disruption exposes subendothelial

collagen and other platelet-adhering ligands, von

Willebrand factor (vWF), and fibronectin. – Release of tissue factors activates factor VII and

extrinsic pathway



Description

• Thrombus generation:

– Platelet adhesion via glycoprotein (GP) Ia/IIa to

collagen:

• Platelet activation: release of ADP, thromboxane A2, andserotonin alters the platelet GP IIb/IIIa receptor

vasoconstriction

• Platelet aggregation: GP IIb/IIIa receptor binds fibrinogen

molecules, cross-links platelets

local platelet plug – Platelet stabilization: thrombin converts fibrinogen

to fibrin, provides fibrin mesh, stabilizes platelet

aggregate



Etiology

• Coronary thrombosis

• Coronary artery spasm, idiopathic or cocaine

induced

• In situ thrombosis/hypercoagulable states

• Embolic event

• Arteritis



Signs and Symptoms (Diagnosis)

History• Pain:

– Pressure or tightness or heaviness

– Substernal, epigastric

– +/- radiation to arm, jaw, back

• Nausea, vomiting

• Diaphoresis

• Cough

• Dyspnea

• Anxiety

• Light-headedness

• Syncope



Signs and Symptoms (Diagnosis)

Physical Exam

• Hypertension

• Hypotension

• Arrhythmias

• S4 heart sound



Essential Workup

• ECG,

• cardiac markers,

• chest radiograph



TEST

Lab• Cardiac markers:

– Troponins: specific indicators of myocardial infarction

– Creatine kinase (CK

–Myoglobin

– LDH

• CBC

• Serum electrolytes including magnesium

•ESR: nonspecific marker of inflammation, rises within 3days, elevated for several weeks

• PT/PTT/INR for patients on warfarin



TEST

Imaging

• ECG:

– ST-segment depression or transient elevation

indicates increased risk – T-wave inversion in regional patterns does not

increase risk but helps differentiate cardiac pain fromnon cardiac pain

•

Chest radiograph: – To assess heart size, pulmonary edema/congestion or

identify other causes of chest pain



TEST

Imaging

• Echocardiography:

– To identify wall motion abnormalities and assess

left ventricular function• Radionuclide studies:

– Thallium or sestamibi scanning: identifies viablemyocardium

– Technetium 99: identifies recently infarctedmyocardium




• ST-elevation myocardial infarction• Pulmonary embolus

• Aortic dissection

•

Acute pericarditis• Pneumothorax

• Pancreatitis

• Pneumonia

• Esophageal spasm/gastroesophageal reflux• Esophageal rupture

• Musculoskeletal pain (diagnosis of exclusion)



Treatment

Pre Hospital

• IV access

• Oxygen administration

• Cardiac monitoring and treatment of

arrhythmias

• Aspirin, analgesia, anxiolytics



Treatment



• IV access


arrhythmias



Treatment



• IV access


arrhythmias



Medication

• Aspirin

• Beta-blockers:

– Atenolol

– Esmolol

– Metoprolol

– Propranolol

• Clopidogrel



Medication

• Calcium channel blockers

– Diltiazem

– Verapamil

• GP IIb/IIIa inhibitors:

– Abciximab

– Eptifibatide

– Tirofiban



Medication

• Heparins:

– Enoxaparin

– Unfractionated heparin

• Lorazepam

• Morphine sulfate

• Nitroglycerin



Shock kardiogenik



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

i i



Description

– Mechanical complications:

• Acute mitral regurgitation

• Ventricular septal defect

• LV rupture

• Pericardial tamponade

– Right ventricular (RV) infarction

E i l



Etiology

• AMI• Sepsis

• Myocarditis

• Myocardial contusion

• Valvular disease• Cardiomyopathy

• Left atrial myxoma

• Drug toxicity: – Beta-blocker – Calcium channel blocker

– Adriamycin

Si d S



Signs and Symptoms

• ABCs and vital signs: – Patent airway (early)

– Labored breathing and tachypnea (early); respiratoryfailure (late)

–Diffuse crackles or wheezing

– Hypoxia

– Hypotension:• Systolic blood pressure <90 mm Hg

• Decline by at least 30 mm Hg below baseline level

– Tachycardia

– Weak pulses

Si d S



Signs and Symptoms

• General:

– Cyanosis

– Pallor

– Diaphoresis

– Dulled sensorium

– Decrease in body temperature

– Urine flow of less than 20 mL/h

Si d S t



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

Si d S t



Signs and Symptoms

• Neck:

– Jugular venous distention

• Abdominal:

– Epigastric pain

– Nausea and vomiting

• Neurologic:

– Obtundation

T t



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

T t



Test

Chest Radiography

• Pulmonary congestion

• Pleural effusion

• Cardiomegaly

• Pneumonia

•

Pneumothorax• Pericardial effusion

T t



TestEmergent Echocardiography

• Transthoracic echocardiography (TTE) with colorDoppler

• LV contractility looking for hypokinesis, akinesis ordyskinesis

• Acute mitral regurgitation or septal defects

• RV dilatation, tricuspid insufficiency, high pulmonaryartery and RV pressures suggest pulmonary embolism

• RV hypokinesis or akinesis, RV dilatation, normalpulmonary pressures suggest RV infarction

• Pericardial effusion, right atrium or RV diastolic collapsesuggest cardiac tamponade

L b



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)

Diff ti l Di i




• Obstructive shock

• Distributive shock

• Hypovolemic shock

Treatment



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



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 (100â€“250 mL normal saline) inabsence of pulmonary congestion

• Foley catheter to monitor urine output

Treatment



Treatment

Medication (Drugs)• Dobutamine

• Dopamine

• Furosemide• Milrinone

• Nitroglycerin

• Nitroprusside• Norepinephrine

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Julita (Problem1-KGD) (01)

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