Shock with myocardial infarction

Ivabradine is used in the treatment of angina in patients in normal sinus rhythm. It acts on the sinus node resulting in a reduction of the heart rate. It is contraindicated in severe bradycardia (heart rate lower than 60 beats/ minute), cardiogenic shock, acute myocardial infarction, moderate-to-severe heart failure, immediately after a cerebrovascular accident, second and third-degree heart block and patients with unstable angina or a pacemaker. Side-effects include bradycardia, first-degree heart block, ventricular extrasystoles, headache, dizziness and visual disturbances, including blurred vision. 

Renal disease or renal dysfunction (eg, as suggested by serum creatinine levels greater than or equal to 1.5 mg/dL [males], greater than or equal to 1.4 mg/dL [females], or abnormal Ccr) that may also result from conditions such as cardiovascular collapse (shock), acute myocardial infarction (Ml), and septicemia CHF requiring pharmacologic treatment hypersensitivity to metformin acute or chronic metabolic acidosis, including diabetic ketoacidosis, with or without coma. Treat diabetic ketoacidosis with insulin. 

The determination of lactate is becoming increasingly popular in the diagnosis of shock and myocardial infarction and in neonatology and sports medicine. Therefore, great efforts are being made to develop sensor-based lactate analyzers which may readily be used at the bedside. The first enzyme electrode-based lactate analyzer was developed in 1976 by La Roche (Switzerland) (see Thble 14-8). It contains cytochrome in a small reaction chamber in front of a platinum electrode polarized at +0.25-0.40 V. The lactate values measured with the analyzer correlate fairly well with those obtained with the spectrophotometric reference method using deproteinized blood ... 

One case of anaphylactic shock (27 ) and one of generalized exfoliative dermatitis (28 ) after the use of lidocaine as a local anaesthetic have been described. The intravenous administration of lidocaine in patients with myocardial infarction sometimes also leads to undesirable side effects, of which hypotension is the best known. The problem is mainly one for the cardiologist, but since inadvertent intravenous injection during local anaesthesia may occur, the anaesthetist must be aware of it. A case of sinusbradycar-dia after a bolus injection of 50 mg (29 -) and an atrioventricular block after 800 mg, given in the course of 12 hours (30 ) have been described. Two fatalities, one due to ventricular fibrillation after 50 mg and one to sinus arrest after 100 mg, have been re-... 

ET measured in the plasma appears to be a spillover of the ET that is (locally) released by the endothelium. It is known that low levels of ET (ranging from 0.25 to 5.0 pg/ml) are normally present in the circulation (B8, P12). These levels are increased by 3-10 times in patients with renal failure (S30), diabetes (V3), hypertension, bums (H32), myocardial infarction, primary pulmonary hypertension (N8), and cardiogenic shock (LI, L9, L10, PI, W8). ET is assumed to be released... 

Suggested Alternatives for Differential Diagnosis Acute respiratory distress syndrome, plague, congestive heart failure and pulmonary edema, HIV infection and AIDS, pneumonia, shock, phosgene, influenza, tularemia, phosphine toxicity, anthrax, silent myocardial infarction, and salicylate toxicity with pulmonary edema. 

Preexisting second- or third-degree AV block, right bundle branch block when associated with a left hemiblock (bifascicular block), unless a pacemaker is present to sustain the cardiac rhythm if complete heart block occurs recent myocardial infarction (Ml) presence of cardiogenic shock hypersensitivity to the drug. 

Barron HV, Every NR, Parsons LS, et al. The use of intra-aortic balloon counterpulsation in patients with cardiogenic shock complicating acute myocardial infarction data from the National Registry of Myocardial Infarction 2. Am Heart J 2001 141 933-939. 

Barron HV, Pirzada SR, Lomnitz DJ, Every NR, Gore JM, Chou TM. Use of intra-aortic balloon counterpulsation in patients with acute myocardial infarction complicated by cardiogenic shock. J Am Coll Cardiol 1998 31(Suppl A) 135A-135A [abstract]... 

Procainamide can decrease the occurrence of all types of active ventricular dysrhythmias in patients with acute myocardial infarction who are free from A-V dissociation, serious ventricular failure, and cardiogenic shock. About 90% of patients with ventricular premature contractions and 80% of patients with ventricular tachycardia respond to procainamide administration. 

Figure 3.1 Graph showing the ratio between inspired (FJ) and alveolar (FA) end-tidal concentrations of the agents shown. The least soluble agents approach equilibrium (FA/FI=1) the most rapidly. Also, since both inhalation and intravenous anaesthetic drugs tend to reduce cardiac output, they facilitate the uptake of volatile agents. It follows that any inhaled anaesthetic drug must be given with great caution to patients in shocked states, e.g. hypovolaemia, arrhythmias, myocardial infarction.

Dobutamine is widely used to increase myocardial contractility, cardiac output, and stroke volume in the peri-operative period. It is less likely to increase heart rate than dopamine. There is evidence that dobutamine can increase both myocardial contractility and coronary blood flow. This makes it particularly suitable for use in patients with acute myocardial infarction. Dobutamine is also suitable for treating septic shock associated with increased filling pressures and impaired ventricular function. Owing to the competing a and 3 activity there is usually little change in mean arterial pressure. 

The cardiac output or flow of blood normally is so rapid that the distribution of a drug or poison throughout the body is complete within a short period of time. An entire 6 liter supply of blood is pumped through the body at the rate of about once per minute. Some organs and tissues are more highly perfused with blood than others, such as the brain, heart, liver, and kidneys. Adipose (fat) tissue is not as richly endowed. Should a person be in shock or have suffered a myocardial infarction (heart attack), however, the cardiac output can be sharply diminished and a route of drug administration normally used may be circumvented because of poor... 

A review of trials has suggested that vasopressin is more likely to cause adverse effects at doses of 0.04 U/minute or more when it is used to treat septic shock mesenteric ischemia and cardiac dysfunction and ischemia were particularly associated with high doses (30). The authors suggested that limiting the dosage to 0.03 U/minute may minimize these effects. This suggestion has been supported by a retrospective audit of the effects of continuous vasopressin infusion in septic shock in 102 men and women, mean age 53 years (31). There were adverse events that may have been linked to vasopressin in 18 patients cardiac arrest (n = 9) ischemic/mottled digits (n = 8) myocardial infarction (n = 1) and hyponatremia (n = 1). Adverse events occurred with doses of vasopressin of 0.04 units/minute and over, except in one patient (dose not stated). 

Severe sepsis and septic shock are common and are associated with a mortality rate which is still around the 50% mark. There are an estimated 751,000 cases of sepsis or septic shock in the United States each year, and they are responsible for as many deaths as acute myocardial infarction [63]. The transition from a systemic inflammatory response syndrome, typical of the initial onset of a septic shock, to severe sepsis, multi-organ failure, and irreversible shock, involves a multitude of pathogenic changes. 

All cardiac glycosides are best avoided in patients with acute myocardial infarction, since they increase oxygen demand in ischemic tissue, increase peripheral vascular resistance, and carry an increased risk of dysrhythmias, especially in the presence of tissue hypoxia and acidosis. Furthermore, there is evidence that digitalis is of little value in patients with acute myocardial infarction and either left ventricular failure or cardiogenic shock (150). The evidence that mortality in patients who take digitalis after an acute myocardial infarction is increased is discussed in the section Death in this monograph. 

Non-cardiogenic pulmonary edema has been seen several times after contrast media in patients with a prior history of myocardial infarct (SEDA-16, 531) it can also be a component of anaphylactic shock. Non-cardiogenic pulmonary edema has been reported as a complication of intravenous injection of iomeprol (71). 

A 42-year-old woman suffered an acute anterior myocardial infarction, initially associated with pulmonary edema. After hemodjmamic stabilization she was given lisinopril 10 mg oraUy. Two hours later she developed circulatory failure in conjunction with acute renal insufficiency. Right heart catheterization showed markedly reduced systemic vascular resistance but a normal cardiac index. After the usual causes of cardiogenic shock had been ruled out, repeated fluid challenges and intravenous noradrenaline failed to improve her hemodynamic status. She was therefore given angiotensin II intravenously (5-7.5 pg/minute), which immediately and markedly raised the systematic vascular... 

Bergeron GA, Goldsmith R, and Schiller NB (1988) Myocardial infarction, severe reversible ischemia, and shock following excess thyroid administration in a woman with normal coronary arteries. Archives of Internal Medicine 148 1450-1453. 

The general metabolic response to shock includes the normal response to stress with mobilization of lipids, although the serum triglyceride concentration is not usually affected. Following acute myocardial infarction and other cardiac events there tend to be notable decreases in LDL and HDL cholesterols, and apolipoprotein B and A-I concentrations with an increase in the triglyceride concentration. Surgical procedures and intercurrent iUnesses produce similar... 

Atherosclerosis is a chronic inflammation of the arterial vessel wall resulting in plaque formation that eventually may cause cardiovascular events, such as myocardial infarction or cerebral vascular accidents. The presence of autoimmune components in atherosclerosis is well established. Autoantibodies to heat-shock proteins and oxidized low-density lipoproteins (oxLDL) are prevalent in the circulation of patients with atherosclerosis, but the role of these autoantibodies is debated. While anti-oxLDL IgG antibodies may facilitate uptake of oxLDL by foam cells in the lesions, natural IgM antibodies directed to oxLDL may even protect from atherosclerosis. Atherosclerotic plaques also contain some T cells that are considered to be autoreactive, although the respective autoantigens have not yet been identified. These T cells are probably not involved in the plaque formation as such, but they may cause plaque instability, rupture, and subsequent clinical events. 

Dopamine also stimulates cardiac Pi-receptors through both direct and indirect mechanisms. It is used to correct hemodynamic imbalances induced by conditions such as shock, myocardial infarction, trauma, or congestive heart failure. As a catechol and primary amine, dopamine is rapidly metabolized by COMT and MAO and, similar to dobutamine, has a short duration of action with no oral activity. It is administered as an intravenous infusion. 

Antoniucci D, Valenti R, Migliorini A, Moschi G, Trapani M, Dovellini EV, Bolognese L, Santoro GM. Abciximab therapy improves survival in patients with acute myocardial infarction complicated by early cardiogenic shock undergoing coronary artery stent implantation. Am J Cardiol 2002 90 353-357. 

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