pemicu 1a blok kgd - fk untar
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Materi pemicu 1A untuk blok kgd fk untar, preklinik.TRANSCRIPT
CARDIAC ARREST
3
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