of 25 /25

kuliah kedaruratan kardiologi

Embed Size (px)

Text of kuliah kedaruratan kardiologi

Page 1: kuliah kedaruratan kardiologi
Page 2: kuliah kedaruratan kardiologi


and wheezing. X-ray : perihilar congestion, hypoxemia.

CARDIOGENIC SHOCK ; Hypotension; abnormal renal, hepatic and CNS function due to decreased perfusion and lactic acidosis.

Cardiomegaly, decreased VEF/abnormal ventricular wall motion, elevated PAWP, low cardiac output.

May have a previously known cause such as valvular heart disease/cardiomyopathy but may present also as a result of ischemia or secondary to severe systemic hypertension.

Page 3: kuliah kedaruratan kardiologi

Pneumonia, ARDS, fluid overload, COPD, asthma.

Pericardial effusion,

Cor pulmonale, pulmonary arteriopathy/PPH. Pulmonary emboli

Volume depletion, sepsis, pulmonary embolism

Page 4: kuliah kedaruratan kardiologi

1.Systolic dysfunction without hypotension.

Digoxin, diuretics, ACEI Metolazone/HCT Nesiritide ( a recombinant human BNP) Spironolactone Nitrate/hydralazine Ultrafiltration Mechanical ventilation

Page 5: kuliah kedaruratan kardiologi

2. Severe CHF with hypotension (Cardiogenic shock)

BP < 90 mmHg : Intravenous dopamine (titrated) Intravenous dobutamine/milrinone

BP = 90-100/>100 mmHg: Nitroprusside-drips (titrated) Intravenous Diuretics (Furosemide) Intravenous NTG Nesiritide (with caution) IABP (Intra aortic balloon pumping) PTCA/CABG/transplantation

After optimizing hemodynamic variables: ACEI, ARB, BB, hydralazine

Page 6: kuliah kedaruratan kardiologi

3. CHF with severe systemic hypertension

Initial therapy : Control of BP Intravenous nitroprusside/ NTG Intravenous enalaprilat

Continued treatment BB/ CCB (with caution)

4. High output or volume overload CHF

Treatment should be directed at the cause of high cardiac output (eg, anemia, B1 defficiency, sepsis, hyperthyroidism Volume overload state (renal failure, excessive Na intake) ---- ultrafiltration

Page 7: kuliah kedaruratan kardiologi

5. CHF with diastolic dysfunction

Beta adrenergic blockade Attention : aggressive diuretic therapy is counterproductive

6. Isolated right heart failure with pulmonary hypertension

Diuretics Oxygen therapy Digoxin NO/intravenous prostacyclin

Page 8: kuliah kedaruratan kardiologi


Evidence of elevated pericardial pressure manifested as elevated systemic venous pressure . Decreased cardiac output and hypotension; evidence of decreased peripheral perfusion.

Echocardiography : large pericardial effusion; RV early diastolic collapse, RA diastolic collapse, LA diastolic collapse; etc.

Right heart catheterization: Equalization of RA pressure, LA pressure, PCWP, and Ventricular EDP.

Page 9: kuliah kedaruratan kardiologi

Initial treatment / Medical therapy : Rapid intravenous fluid loading and dopamine Avoidance diuretics or vasodilators.

Priority of therapy (percutaneous or surgical therapy) : Drainage (Tapping)--- needle pericardiocentesis Surgical drainage : subxiphoid pericardioectomy, pericardial window, and subtotal pericardiectomy Percutaneous balloon pericardiotomy

Page 10: kuliah kedaruratan kardiologi


Hypertensive crisis : Systemic BP > 240/130 mmHg without symptoms, or elevated BP with chest pain, headache, or heart failure. May have intracranial hemorrhage, aortic dissection, pulmonary edema, myocardial infarction, or unstable angina. Hypertensive crisis traditionally has been classified as:

- Emergency and- Urgency

Malignant hypertension : Severe hypertension associated with encephalopathy, renal failure, or papiledema.

Page 11: kuliah kedaruratan kardiologi

In general, diastolic BP >120 mmHg Malignant htn with papiledema Hypertensive encephalopathy Severe htn in the setting of stroke, subarachnoid hemorrhage, head trauma Acute aortic dissection Htn and LV failure Htn and myocardial ischemia/infarction Htn after CABG operation Pheocromocytoma crisis Food and drug interactions with MAO inhibitors Cocain abuse Rebound htn after sudden drug withdrawal (clonidine) Idiosyncratic drug reactions ( atropin) Eclampsia

(Rapid decompensation of vital organ function)

Page 12: kuliah kedaruratan kardiologi

Diastolic BP > 120 mmHg, but no symptoms and sign of tissue damage Severe htn, accelerated htn Pheochromocytoma crisis Food and drug interactions with MAO inhibitors Rebound htn after sudden drug withdrawal Idiosyncratic drug reactions Preoperative htn Postoperative htn

(Marked elevations of BP without acute or progressive target organ )

Page 13: kuliah kedaruratan kardiologi

The goal therapy : immediate, controlled reduction in BP. BP initially be reduced by no more than 25% of MAP (diastolic pressure + 1/3 pulse pressure) over minutes to hours. (exception : aortic dissection, LV failure, and pulmonary edema.

Medical therapy : Nitroprusside (drug of choice), Glyceryl trinitrate, Labetalol ( contraindicated for patients with CHF, bradycardia, heart block, reactive airway disease), Nicardipine, Enalapril, Phentolamine, Hydralazine, Fenoldopam.

Page 14: kuliah kedaruratan kardiologi

Captopril (Fastest-acting oral ACEI) caution : marked renal insufficiency/ volume depletion



Nifedipine (Sublingual nifedipine should not be used in the treatment of patients with htn).

Page 15: kuliah kedaruratan kardiologi


Chest pain : substernal pressure, squeezing, or sensation of suffocation. Some patients describe aching, burning, tightness. The pain radiate to the shoulder, neck, jaw, left or right arm and the fingertips. Occasionally the pain predominantly epigastric or intrascapular.

Dyspnea may also be the only major presenting symptom in about 10% patients wit AMI (atypical presentation)

Other atypical : fatigue, syncope, altered sensorium, stroke, nausea, vomiting and lethargy

Atypical presentations: More common in elderly, diabetics, women

Page 16: kuliah kedaruratan kardiologi

Cardiac causes:• ACS

• Syndrome X• Pericarditis

• MVP• Aortic stenosis

• Hypertrophic cardiomypathy

Aortic causes:• Aortic dissection

• Penetrating ulcer of aorta

Pulmonary causes :• Embolism

Costochondritis :• Tietze’s syndrome

Neurologic causes :• Cervical spondylosis

• Other compression neuropathy• Herpes

Psychological causes :• Panic disorder

• Anxiety• Depression

• Hysteria

Gastrointestinal causes:• Esophageal spasm, reflux

• Gastritis, gastric ulcer• Cholecystitis

Page 17: kuliah kedaruratan kardiologi


Biochemical markers : CK/CKMB, Myoglobin, Troponins BNP, hsCRP

Imaging studies : Echocardiography, Radionuclide perfusion imaging (Thalium/Technetium)

Early exercise stress testing (Treadmill)

Page 18: kuliah kedaruratan kardiologi

Depend on the causes of the chest pain

ACS Pericarditis

Aortic dissection Pulmonary embolism

Page 19: kuliah kedaruratan kardiologi



Upon diagnosis of UAP or NSTEMI, level of risk for death & nonfatal cardiac ischemic events must be assessed. Treatment is based on this risk level.

Patients considered HIGH RISK if one or more of the following are present: 1. Recurrent ischemia (ST-depression/ST elevation). 2. Ongoing chest pain at rest >20 min. 3. Elevated cardiac marker levels (CK-MB, Troponin T, CRP). 4. Developing hemodynamic instability. 5. Major arrhythmias (VF, VT) or LV dysfunction. 6. Early post-infarction UAP 7. Thrombus on angiography.

Page 20: kuliah kedaruratan kardiologi

Low risk patients : 1. No recurrent chest pain 2. No evidence of angina at rest 3. No elevation of troponin or other biochemical markers 4. Norma or unchanged ECG during chest discomfort

• Aspirin & clopidogrel/ticlopidine• Nitrates (sublingual/spray or IV)• Oral beta-blocker (if not contraindicated)• Calcium antagonists (diltiazem)• Lipid lowering agent (statin/ fibrate/niacin)• Heparin (Low molecular weight heparin-LMWH)• Stress test (Treadmill test) recommended either during hospitalization or within 72 hr.

Page 21: kuliah kedaruratan kardiologi

Bed rest with continuous ECG monitoring Supplemental O2 to maintain O2 saturation>90%

Treatment of ischemic pain• Nitrates (sublingual/spray/IV) :

- contraindicated in patients who have taken sildenafil within the past 24 hr - Use with caution in patients with RV failure

• Beta-blockers• Morphine sulfate - May be administered with nitrates. - may need concomitant administration of anti emetic • Calcium antagonists (CCB)• ACE inhibitors

Page 22: kuliah kedaruratan kardiologi

Antiplatelet & anticoagulant therapy :• Aspirin & Clopidogrel (should be initiated promptly)• Heparin (LMWH) sc / UFH• GP IIIa/IIb receptor antagonist.

Risk modification: • Lipid lowering agents: statin/ fibrate/ niacin

Invasive procedures :• Intra aortic balloon counterpulsation (IABP).• Percutaneous coronary intervention (PCI) or• Coronary artery bypass graft (CABG)

Page 23: kuliah kedaruratan kardiologi


Decreased urine output(<30 mL/h) Impaired mental function Cool extremities Distended neck vein (jugular vein) Hypotension with evidence of peripheral and pulmonary venous congestion.(Syst.BP <80 mmHg, or syst.BP <90 mmHg with medication/IABP) Cardiac index <2,2 L/min/m2 Pulmonary artery wedge pressure (PCWP) >18 mmHg

When more than 45% of the LV myocardium is necrotic, cardiogenic shock becomes evident clinically. Bradycardia and arrhythmias may underlie cardiogenic shock

Page 24: kuliah kedaruratan kardiologi

Non-mechanical causes of cardiogenic shock:1. AMI (ACS-STEMI)2. Low CO syndrome3. RV infarction4. End-stage cardiomyopathy

Mechanical causes of cardiogenic shock :1. Rupture of septum or free wall2. Mitral or aortic insufficiency3. Papillary muscle rupture or dysfunction4. Critical aortic stenosis5. Pericardial tamponade

Page 25: kuliah kedaruratan kardiologi

A.Stage I (Compensated hypotension)B.Stage II (Decompensated hypotension)C.Stage III (Irreversible shock)

If the the cause CS is AMI, controlling the infarct size. Oxygen ( 4 L-6L/min)/ Intubation may be required Fluid resuscitation (monitoring CO and PCWP) Pharmacologic support : 1. Inotropes:

• Dobutamine, Dopamine , Digoxin• Isoproterenol , Norepinephrine , Amrinone• Glucagon

2. Vasodilators : Nitroprusside , Nitroglycerin Other modalities : Thrombolytic therapy, PCI, IABP, etc.