acute coronary syndrome


acute

 [ah-kūt´] 1. sharp.2. having severe symptoms and a short course. Some serious illnesses that were formerly considered acute (such as myocardial infarction) are now recognized to be acute episodes of chronic conditions.acute care the level of care in the health care system that consists of emergency treatment and critical care. Called also secondary care.acute coronary syndrome a classification encompassing clinical presentations ranging from unstable angina through myocardial infarctions not characterized by alterations in waves" >Q waves; the classification sometimes also includes myocardial infarctions characterized by altered Q waves.acute respiratory distress syndrome (ARDS) a group of symptoms accompanying fulminant pulmonary edema and resulting in acute respiratory failure; called also shock lung, wet lung, and many other names descriptive of etiology or clinical manifestations. Many etiologic factors have been associated with ARDS, including shock, fat embolism, fluid overload, oxygen toxicity, fluid aspiration, narcotic overdose, disseminated intravascular coagulation, multiple transfusions, inhalation of toxic gases, diffuse pulmonary infection, and systemic reactions to sepsis, pancreatitis, and massive trauma or burns.
ARDS is characterized clinically by dyspnea, tachypnea, tachycardia, cyanosis, and hypoxemia. PaO2/FIO2 remains low (below 2 cc) even with oxygen therapy at high oxygen concentrations. The lung compliance is decreased so that the lung is stiffer and more difficult to ventilate. Chest radiographs show signs of bilateral interstitial and alveolar edema. Cardiac filling pressures are normal, and the pulmonary capillary wedge pressure is below 18 torr.
Most authorities consider that the syndrome has three phases or stages that characterize its progression: the exudative stage, the fibroproliferative or proliferative stage, and the resolution or recovery stage. The exudative stage comes first, two to four days after onset of lung injury, and is distinguished by the accumulation of excessive fluid in the alveoli with entrance of protein and inflammatory cells from the alveolar capillaries into the air spaces. The fibroproliferative stage comes second and is characterized by an increase in connective tissue and other structural elements in the lungs in response to the initial injury. It begins between the first and third weeks after the initial injury and may last up to ten weeks. Microscopic examination reveals lung tissue that appears densely cellular. The patient is at risk for pneumonia, sepsis, and pneumothorax at this time. The third stage is the resolution or recovery stage. During this stage the lung reorganizes and recovers, although it continues to show signs of fibrosis. Lung function may continue to improve for as long as six to twelve months or even longer, depending on the precipitating condition and severity of the injury. It is important to remember that there are often different levels of pulmonary recovery in patients with ARDS.
Some authorities refer to a fourth phase or stage of ARDS, the period after the resolution or recovery stage. Some patients continue to experience health problems caused by the acute illness, such as coughing, limited exercise tolerance, and fatigue. Anxiety, depression, and flashback memories of the critical illness may also occur and be similar to posttraumatic stress disorder.Treatment and Patient Care. Mechanical ventilation must be begun at the first signs of hyperventilation and hypoxemia, before obvious signs of respiratory distress develop. A cuffed endotracheal tube or tracheostomy tube is used to maintain an airway. The patient is ventilated at the lowest oxygen concentration that maintains the arterial oxygen saturation (SaO2) at 90 per cent. positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) may be used to increase the number of alveoli that remain open at the end of exhalation and thus decrease pulmonary shunt. hemodynamic monitoring, using a swan-ganz catheter, is done to measure cardiac output, pulmonary capillary wedge pressure, and right atrial wedge pressure. An arterial line is placed to continuously monitor blood pressure and measure arterial blood gases. A diuretic such as furosemide (Lasix) may be administered to reduce fluid volume overload and pulmonary edema. If infection develops, antibiotics are administered. Hemodynamic parameters, arterial blood gas levels, intake and output, breath sounds, vital signs, inspiratory pressure, tidal volume, inspired oxygen concentration, and end-expiratory pressure are all continuously monitored.acute situational reaction a transient, self-limiting acute emotional reaction to severe psychological stress. See acute stress disorder, adjustment disorder, posttraumatic stress disorder, and psychosis" >brief reactive psychosis.acute stress disorder an anxiety disorder characterized by development of anxiety, dissociation, and other symptoms within one month following exposure to an extremely traumatic event, the symptoms including reexperiencing the event, avoidance of trauma-related stimuli, anxiety or increased arousal, and some or all of the following: a subjective sense of diminished emotional responsiveness, numbing, or detachment, derealization, depersonalization, and amnesia for aspects of the event. If persistent, it may become posttraumatic stress disorder.acute stress reaction acute situational reaction.

acute coronary syndrome

n. A sudden, severe coronary event, such as unstable angina, in which obstruction of a coronary artery interferes with blood flow to the heart muscle.

acute coronary syndrome

A term that encompasses the permutations of acute ischaemic heart disease, which is a heterogeneous constellation of clinical symptoms associated therewith.
 
Diagnosis
Careful clinical history, physical examination, resting 12-lead and serial EKG-marked symmetrical T-wave inversion in precordial leads, various cardiac markers. For patients unlikely to have coronary artery disease, AHRQ guidelines recommend a treadmill test without imaging, recording an EKG both during symptoms and after symptom relief; recurrent symptom or a change in clinical status; ST-elevation ACS, which requires immediate reperfusion, must be rapidly excluded.
 
Risk factors
Diabetes, smoking, hypertension, increased cholesterol.
 
Types
ST-elevation ACS is essentially the same as Q-wave infarction; non-ST-elevation ACS encompasses a broader range of disease—e.g., rest angina, new-onset angina, increasing angina, postinfarction angina, variant angina, and non-Q-wave infarction.
 
Early management
Bed rest, control of precipitating factors, initiation of medical therapy with IV access.
 
Prognosis
Most ACS patients stabilise; 10% suffer in-hospital MI; some patients die suddenly; patients with cardiomegaly and non-responders to initial medical therapy have a higher risk for subsequent cardiac events.
Clinical trials
Randomised clinical trials have provided data on the incidence of subsequent cardiac events in non-ST-elevation ACS patients with unstable angina: ESSENCE, GUSTO II, PARAGON, PURSUIT trials reported death rates between 2.9% and 4.7%, reinfarction rates of 5% to 12%, and stroke rates of 0.4% to 0.9%; other risk factors associated with adverse outcomes include male sex, older age, HTN, left ventricular hypertrophy, poor performance on exercise stress testing, and extensive disease on angiography or nuclear testing.
Antagonists
Thrombogenic stimuli (i.e., ulcerated plaques and intimal tears) can persist for prolonged periods, and the haemostatic system may remain activated for months after ACS decreased in patients treated with GP IIb/IIIa inhibitors (abciximab, eptifibatide, tirofiban, lamifiban); agents that directly inhibit thrombin, including hirudin and bivalirudin, are being explored as alternatives to unfractionated heparin in ACS and during percutaneous coronary interventions.
Theoretical advantages
Inhibit clot-bound thrombin, decreased variability in dosing, eliminate risk of HIT and thrombocytopenic purpura.
Next generation treatments
IV VEGF (vascular endothelial growth factor), fibroblast growth factor; laser revascularisation, external counterpulsation; gene therapy with various molecules, IV GP IIb/IIIa (efficacy of these last agents has not been strong).

acute coronary syndrome

Cardiology A term that encompasses the permutations of acute ischemic heart disease, which is a heterogeneous constellation of clinical symptoms associated therewith Diagnosis Careful clinical Hx, PE, resting 12-lead and serial EKG–marked symmetrical T-wave inversion in precordial leads, various cardiac markers; for Pts unlikely to have CAD, AHRQ guidelines recommend a treadmill test without imaging, recording an EKG both during Sx and after Sx relief; recurrent Sx or a change in clinical status; ST-elevation-ACS–which requires immediate reperfusion–must be rapidly excluded Risk factors DM, smoking, HTN, ↑ cholesterol Types ST-elevation ACS is esentially the same as what was formerly termed Q-wave infarction, non-ST-elevation ACS encompasses a broader range of disease–eg, rest angina, new-onset angina, increasing angina, postinfarction angina, variant angina, and non-Q-wave infarction Early management Bed rest, control of precipitating factors, initiation of medical therapy Prognosis Most ACS patients stabilize; 10% undergo in-hospital MI; some Pts die suddenly; Pts with cardiomegaly and non-responder to initial medical therapy have a higher risk for subsequent cardiac events; randomized clinical trials have provided data on the incidence of subsequent cardiac events in non-ST-elevation ACS patients with unstable angina; ESSENCE, GUSTO II, PARAGON, PURSUIT trials reported death rates between 2.9% and 4.7%, reinfarction rates of 5% to 12%, and stroke rates of 0.4% to 0.9%; other risk factors associated with adverse outcomes include male sex, older age, HTN, left ventricular hypertrophy, poor performance on exercise stress testing, and extensive disease on angiography or nuclear testing; antagonists–thrombogenic stimuli–ie, ulcerated plaques and intimal tears can persist for prolonged periods, and the hemostatic system may remain activated for months after ACS ↓ M&M in Pts treated with GP IIb/IIIa inhibitors–abciximab, eptifibatide, tirofiban, lamifiban; agents that directly inhibit thrombin, including hirudin and bivalirudin, are being explored as alternatives to unfractionated heparin in ACS and during percutaneous coronary interventions Theoretical advantages Inhibit clot-bound thrombin, ↓ variability in dosing, eliminate risk of HIT and thrombocytopenic purpura Next generation treatments VEGF, fibroblast growth factor; laser revascularization, external counterpulsation; gene therapy with various molecules, IV GP IIb/IIIa. See GUSTO 2, Myocardial infarction, Reperfusion-eligible acute MI.

a·cute cor·o·nar·y syn·drome

(ACS) (ă-kyūt' kōr'ŏ-nar-ē sin'drōm) A general term for clinical syndromes due to reduction of blood flow in coronary arteries (e.g., unstable angina, acute myocardial infarction).
Synonym(s): acute myocardial infarction, preinfarction angina, unstable angina.

a·cute cor·o·nar·y syn·drome

(ACS) (ă-kyūt' kōr'ŏ-nar-ē sin'drōm) A general term for clinical syndromes due to reduction of blood flow in coronary arteries.
Synonym(s): preinfarction angina, unstable angina.