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Yinvill
405120025
Kelompok 8
Klasifikasi
Heart Emergency According to Conscious State

Conscious -> acute coronary syndrom


Unconscious -> cardiac arrest
ACS
ACS: spectrum of clinical presentations ranging
from:
UAP
STEMI
UNSTEMI
Cardiac arrest
Abrupt cessation of cardiac pump function
which may be reversible by a prompt
intervention but will lead to death in its absence
Asystole
Pulseless ventricular tachycardia
Ventricular fibrillation
Pulseless electrical activity
ACS
Acute coronary syndrome
Imbalance in myocardial blood supply + O2
requirement MI
Acute cardiac ischemia encompasses a spectrum of
disease processes:
Unstable angina pectoris
Acute myocardial infarction (AMI)
ST elevation myocardial infarction (STEMI)
Non-STEMI
Patophysiology of ACS
ST-segment elevation myocardial
infarction
Etiology
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
Arteritis:
Lupus
Takayasu disease
Kawasaki disease
Rheumatoid arthritis
Prolonged hypotension
Anemia -> Hemoglobin <8 g/dL
Etiology
Hyperbarism or elevations in carboxyhemoglobin
Coronary artery gas embolus
Thyroid storm
Structural abnormalities of coronary arteries:
Radiation fibrosis
Aneurysms
Ectasia
Cocaine- or amphetamine-induced vasospasm
Risk Factor
Cardiac risk factors include:
Men, age >55 years
Postmenopausal women
Hypercholesterolemia
Diabetes mellitus
Hypertension
Smoking
Family history in a first-degree relative <55 years old
Signs and Symptoms of MI
Chest pain (most Anginal equivalents (MI
common) without chest pain):
Substernal pressure Abdominal pain
Heaviness Syncope
Squeezing Diaphoresis
Burning sensation Nausea or vomiting
Tightness Weakness

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


Signs and Symptoms of MI
Associated symptoms: eating, exposure to cold,
Dyspnea or emotional stress.
Syncope Symptoms commonly last
Fatigue 30 minutes or more.
Diaphoresis Symptoms may occur with
rest or during exertion.
Nausea
Blood pressure (BP) is
Vomiting usually elevated during
symptoms

Symptoms are usually


Differential Diagnosis of MI
Anxiety Mitral valve prolapse
Aortic dissection Myocardial infarction
Biliary colic Panic disorder
Costochondritis Peptic ulcer disease
Esophageal reflux Pneumonia
Esophageal spasm Psychogenic
Herpes zoster Pulmonary embolus
Hiatal hernia Unstable angina
Investigation
History & physical examination
substernal chest pain > 30 min (radiates to the neck, left shoulder,
and left arm) + diaphoresis
pale cool skin
sinus tachycardia
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
Electrocardiogram
ST-segment depression, transient ST-segment
elevation, and/or T-wave inversion 30-50%
Cardiac biomarkers
ECG of UAP/NSTEMI
ECG of
STEMI
Initial management
Prehospital care
Management strategies reperfusion therapy (PCI or
fibrinolytics)
Management in the emergency department
Aspirin, buccal absorption of a chewed 160325 mg
tablet
Hypoxemia O2 by nasal prongs or face mask (24
L/min) for the first 612 h reassessed
Control of discomfort
Sublingual nitroglycerin (three doses of 0.4 mg at about 5-min
intervals)
Morphine IV (24 mg every 5 min)
IV beta blockers
metoprolol, 5 mg every 25 min for a total of 3 doses
15 min oral regimen is initiated of 50 mg every 6 h for
48 h 100 mg every 12 h
Short term management
Placed at bed rest with continuous ECG
monitoring for ST-segment deviation and cardiac
rhythm
Ambulation is permitted if
Patient shows no recurrence of ischemia (discomfort or
ECG changes)
Does not develop a biomarker of necrosis for 1224 h

Medical therapy
Anti-ischemic & anti-thrombotic treatment
Anti-ischemic therapy
Include bed rest, nitrates, beta blockers
Nitrates
sublingually or by buccal spray (0.30.6 mg)
Persist after three doses given 5 min apart IV nitroglycerin
(510 ug/min using nonabsorbing tubing) may be
increased by 10 ug/min every 35 min pain relieved or
systolic arterial pressure <100 mmHg
pain-free for 1224 h Topical or oral nitrates replace the IV
nitroglycerin
Beta blockers
IV followed by oral beta blockers heart rate of 5060
beats/min
Invasive VS conservative strategy
Invasive strategy (high risk patients / class I indication)
anti-ischemic and antithrombotic agents
coronary arteriography is carried out within ~48 h of
admission
coronary revascularization (PCI or coronary artery bypass
grafting

Conservative strategy
anti-ischemic and antithrombotic
watchfull waiting
coronary arteriography
If rest pain or ST-segment changes
recur
evidence of ischemia on a stress test
Follow-Up
Disposition
Admission 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.
Cardiac arrest
Cardiac arrest
Primary cardiac arrests
Occurs in the absence of hemodynamic instability
success rate for immediate resuscitation 90%
secondary cardiac arrests
Occur in patients in whom abnormal
hemodynamics dominate the clinical picture before
cardiac arrest
70% of patients with secondary cardiac arrest
succumb immediately or during the same
hospitalization
Common causes of Nontraumatic Cardiac Arrest
General Specific Disease/Agent
Cardiac CAD
Cardiomiopathies
Structural abnormalities
Valve dysfunction
Respiratory Hypoventilation CNS dysfunction
Neuromuscular disease
Toxic and metabolic
encephalopathies
Upper airway obstruction CNS dysfunction
Foreign body
Infection
Trauma
Neoplasm
Pulmonary dysfunction Asthma,COPD
Pulmonary edema
Pulmonary embolus
Pneumonia
Common causes of Nontraumatic Cardiac Arrest
General Specific Disease/Agent
Circulatory Mechanical obstruction Tension pneumothorax
Pericardial tamponade
Pulmonary embolus
Hypovolemia Hemorrhage
Vascular tone Sepsis
Neurogenic
Metabolic Electrolyte abnormalities Hypokalemia (most common) or
Hyperkalemia
Hypermagnesemia
Hypomagnesemia
Hypocalcemia
Toxic Prescription medications Antidysrhythmics
Digitalis beta-blockers
CCB
Tricyclic antidepressants
Drug of abuse Cocaine
Heroine
Toxins CO, Cyanide
Common causes of Nontraumatic Cardiac Arrest
General Specific Disease/Agent
Enviromental Lightning
Electrocution
Hypothermia or hyperthermia
Drowning/near-drowning
Ventricullar fibrillation
Irregular wave and amplitude
No QRS complex, ST segmen, T wave
VT VF
Pathophysiology
Ischemic/ trauma/MI of ventricle unsyncronixe
depolarisation and repolarisation Manifestasi
klinis
Etiology of VF:
ACS
Untreated stable/unstable VT
Premature ventricular complexes with R
fenomenone in T
Drugs
Electrolytes and acid-base imbalance
Prolonged QT (primary/secondary) Hypoxia
Electrical shock
Pulseless electrical activity
Presents of electrical activity on EKG without
pulsation of artery
Ventricle contraction is not enough to create
pulsation at blood vessels
Etiologi
H T
Hypovolemic Toxin (e.g drugs)
Hypoxia Cardiac tamponade
Acidosis Tension pneumothorax
Hypo/ hyperkalemia Coronary thrombosis
Hypothermia Lungs thrombosis
Asystole
No contraction of heart
Etiology
ischemia/ hypoxia
Acute respiratory failure (no
oxygen/apneu/asphyxia)
Electrical shock (e.g lightning strike)
Defibrillation (in management of VT and VF)
Manifestation of Cardiac Arrest
Unresponsiveness Palpitations
Pulselessness Seizure activity
Shallow, gasping Immediately prior to
respirations may persist arrest:
for a few minutes Shock or hypotension
Occasionally preceded Impaired mentation
by:
Chest pain
Dyspnea
Manifestation of Cardiac Arrest
Cardiopulmonary arrest -> triad :
1. Unconsciousness
2. Apnea
3. Pulselessness (carotid or femoral artery)
ECG of VF
Criteria of ECG :
Unrecognized QRS and other waves
Wave: 150-500x/ min
Irregular rhythm
Sharp up and down peak
Amplitude
Soft peak at 2 - <5mm
Medium 5 - <10mm
Rough 10 - <15mm
Very rough > 15mm
ECG of PEA
Criteria of ECG
Rhythm shows electrical activity/ ventricular
depolarisation (not VF/VT)
Usually, rhythm is not regular as sinus rhythm
QRS interval
Narrow <0,10s
Wide >0,12s
HR: (>100x/min) or (<60x/min)
EKG: wide QRS is low frequency (20-40x/min) or
<20x/min

Idioventricular rhythm
ECG of asystole
Criteria of ECG
Classic flat line
No rhythm
No QRS complex
Treatment
Initial evaluation & basic life support
observations of the state of consciousness, respiratory
movements, skin color, and the presence or absence of
pulses in the carotid or femoral arteries call 911
severe stridor + persistent pulse aspiration Heimlich
maneuver
precordial blow, or "thump," delivered firmly occasionally
revert VT or VF, but there is concern about converting VT to
VF
only when monitoring and defibrillation are available
head is tilted back and the chin lifted
Mouth-to-mouth respiration
Chest compression
arms remaining straight, 100x per minute, depress sternum 4-5
cm
AED
ACLS
defibrillation/cardioversion and/or pacing
VF or VT is established monophasic 300 J /
biphasic 120150 J escalated to a maximum of
360 J monophasic (200 J biphasic)
if the first shock fails 5 cycles of CPR be carried
out before repeated shocks
if 5 min has elapsed between the onset of cardiac
arrest 6090 s of CPR before the first shock
intubation with an endotracheal tube
insertion of an intravenous line
MANAGEMENT
Shock
Cardiogenic shock & pulmonary
edema
life-threatening conditions that should be
treated as medical emergencies

Etiology
severe left ventricular (LV) dysfunction
pulmonary congestion and/or systemic
hypoperfusion
Cardiogenic shock
systemic hypoperfusion due to severe depression of
the cardiac index [<2.2 (L/min)/m2]
sustained systolic arterial hypotension (<90 mmHg)
elevated filling pressure [pulmonary capillary wedge
pressure (PCWP) > 18 mmHg]
Most common etiologies
acute myocardial infarction
cardiomyopathy or myocarditis
cardiac tamponade
Other etiologies
Post cardiac arrest RV failure
Refractory sustained Refractory sustained
tacchyarrhythmias bradyarrhythmias
Pulmonary embolus Toxic metabolic
Severe valvular heart Beta blocker/CCB
disease overdose
Severe acidosis &
Critical aortic / mitral
hypoxemia
stenosis
Acute severe aortic /
mitral regurgitation
Incidence
leading cause of death of patients hospitalized
with MI
LV failure accounts for ~80% of the cases of CS
complicating acute MI
fell from 20% in the 1960s but has plateaued at
~8% for >20 years
typically associated with ST elevation MI (STEMI)
Pathophysiology
Large infarctions and
shock SIRS
Inflammatory cytokines,
inducible nitric oxide
synthase shock
Pump failure
Poor tissue perfusion
lactic acidosis
Pulmonary edema
hypoxemia
vicious cycle of
worsening MI &
hypotension
Timing
Risk factors 1/4 of MI patients
acute MI develop CS rapidly
older age (within 6 hour of MI
onset)
female sex
3/4 later on the 1st
prior MI
day
diabetes
Subsequent onset of CS
anterior MI location
reinfarction soon after reinfarction,
MI marked infarct expansion,
a mechanical
complication
Clinical findings
Continuing chest pain & Tachypnea, Cheyne-
dyspnea Stokes respirations
Pale, apprehensive, jugular venous
diaphoretic distention
Altered consciousness S1 is usually soft, and an
weak and rapid pulse S3 gallop may be audible
90110 beats/min Acute, severe MR and
Systolic BP <90 mmHg + VSR systolic murmurs
narrow pulse pressure LV failure causing CS
(<30 mmHg) rales
quiet precordium + weak Oliguria
apical pulse urine output < 30 mL/h
Laboratory findings ECG
WBC count > with left acute MI with LV failure
shift Q waves and/or >2-mm
BUN & creatinin >> ST elevation in multiple
leads
Hepatic transaminase >> LBBB
Lactic acid > 1,5 of infarct anterior
Arterial blood gases severe left main stenosis
hypoxemia and metabolic global ischemia
acidosis
severe (e.g., >3 mm) ST
creatine phosphokinase, depressions in multiple
troponin I & T > leads
Chest X ray Echocardiogram
pulmonary vascular left-to-right shunt in
congestion patients with VSR
pulmonary edema Pulmonary embolism
CS results from a first MI Proximal aortic
hearts size is normal dissection with aortic
regurgitation or
tamponade
Pulmonary artery catheterization
Prognosis
wide range of expected death rates
age, severity of hemodynamic abnormalities, severity
of the clinical manifestations of hypoperfusion, and the
performance of early revascularization
Independent risk factors
advanced age; depressed cardiac index, ejection
fraction, and BP; more extensive coronary artery
disease; and renal insufficiency
Pulmonary edema
Etiology
Cardiogenic & non
cardiogenic
Pathophysiology (cardiogenic)
Cardiac abnormality pulmonary venous & hydrostatic
pressure > fluids exit the capillary interstitial &
alveolar edema pleural effusion breathing
discomfort

Clinical findings
rapid onset of dyspnea at rest, tachypnea, tachycardia, and
severe hypoxemia
Rales and wheezing
due to airway compression from peribronchial cuffing
Hypertension
due to release of endogenous catecholamines
Other examinations
Echocardiography
systolic and diastolic ventricular dysfunction and valvular lesions
Electrocardiography
ST elevation and evolving Q waves is usually diagnostic of acute MI
Brain natriuretic peptide levels > heart failure as the
etiology
X ray
peribronchial thickening, prominent vascular markings in the
upper lung zones, and Kerley B lines
patchy alveolar filling (in perihilar distribution) diffuse alveolar
infiltrates
Swan-Ganz catheter
high pressure PCWP
Treatment
Oksigen therapy
Positive pressure ventilation
Diuretics
Furosemide <=0.5 mg/kg
Nitrates
Sublingual nitroglycerin (0.4 mg x 3 every 5 min) IV
nitroglycerin, commencing at 510 ug/min
Morphine
2- to 4-mg IV boluses
ACE-I
A low dose of a short-acting agent may be initiated and
followed by increasing oral doses
Other Preload-Reducing Agents
IV recombinant brain natriuretic peptide (nesiritide)
potent vasodilator + diuretic (refractory patients & not
recommended in ischemia or MI)
Physical Methods
Patients without hypotension should be maintained in
the sitting position with the legs dangling along the side
of the bed
Inotropic and Inodilator Drugs
dopamine and dobutamine
bipyridine phosphodiesterase-3 inhibitors (inodilators)
milrinone (50 g/kg followed by 0.250.75 ug/kg per min)
stimulate myocardial contractility + peripheral and pulmonary
vasodilation
Digitalis Glycosides
rarely used at present
Intraaortic Counterpulsation
IABP
Treatment of Tachyarrhythmias and Atrial-
Ventricular Resynchronization
a primary tachyarrhythmia may require cardioversion
patients with reduced LV function and without atrial
contraction / with lack of synchronized atrioventricular
contraction atrioventricular sequential pacemaker
Stimulation of Alveolar Fluid Clearance
IV Beta-adrenergic agonist treatment decreases
extravascular lung water
BCLS and ACLS
CPR

Tintinalli's Emergency Medicine 7th ed


Step 3: opening the air way
Head TiltChin 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.

Tintinalli's Emergency Medicine 7th ed


Step 3: opening the air way
Jaw Thrust Maneuver
the 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.

Tintinalli's Emergency Medicine 7th ed


Step 4 dan 5

Tintinalli's Emergency Medicine 7th ed


Ventilation Technique

Tintinalli's Emergency Medicine 7th ed


Step 6 dan 7
All rescuers should, at a minimum, provide
chest compressions.
If bystander not trained (adult arrest): Hands-
Only CPR
If bystander trained and able: perform
compressions and ventilations at rate of 30:2
Healthcare provider: perform compressions
and ventilations at rate of 30:2
Compression Depth
AT LEAST 2 inches (2005 rec : 1 to 2 inches)
Without effective chest compressions
Oxygen flow to brain stops
Oxygen flow to heart stops
Drugs go nowhere
Compression rate AT LEAST 100x/min
Eliminations of Look Listen and Feel
Why? Minimizes delay to action
Cricoid pressure is NOT reccomended in
routine use
Why? Interfere with ventilation and advanced
airway placement
Team resuscitation
Minimizes interuptions in compression
Complication and prognosis
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