ACUTE PULMONARY EDEMA : Dyspnea, orthopnea, rales, 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.
1. Systolic dysfunction without hypotension. Digoxin, diuretics, ACEI Metolazone/HCT Nesiritide ( a recombinant human BNP) Spironolactone Nitrate/hydralazine Ultrafiltration Mechanical ventilation
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
5. CHF with diastolic dysfunction Beta adrenergic blockade Attention : aggressive diuretic therapy is counterproductive 6. Isolated right heart failure with pulmonary hypertension
CARDIAC TAMPONADE
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.
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
Malignant hypertension : Severe hypertension associated with encephalopathy, renal failure, or papiledema.
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
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
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.
Captopril (Fastest-acting oral ACEI) caution : marked renal insufficiency/ volume depletion Clonidine Labetalol Nifedipine (Sublingual nifedipine should not be used in the treatment of patients with htn).
Other atypical : fatigue, syncope, altered sensorium, stroke, nausea, vomiting and lethargy
Atypical presentations: More common in elderly, diabetics, women
Cardiac causes: ACS Syndrome X Pericarditis MVP Aortic stenosis Hypertrophic cardiomypathy Aortic causes: Aortic dissection Penetrating ulcer of aorta Pulmonary causes : Embolism Gastrointestinal causes: Esophageal spasm, reflux Gastritis, gastric ulcer Cholecystitis
UNSTABLE ANGINA PECTORIS (UAP) & NON ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION (NSTEMI)
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.
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.
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
ACE inhibitors
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)
CARDIOGENIC SHOCK
Diagnosis : 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
Non-mechanical causes of cardiogenic shock: 1. AMI (ACS-STEMI) 2. Low CO syndrome 3. RV infarction 4. End-stage cardiomyopathy Mechanical causes of cardiogenic shock : 1. Rupture of septum or free wall 2. Mitral or aortic insufficiency 3. Papillary muscle rupture or dysfunction 4. Critical aortic stenosis 5. Pericardial tamponade
A. Stage I (Compensated hypotension) B. Stage II (Decompensated hypotension) C. Stage III (Irreversible shock)
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.