Myocardial infarction inhaled

Tetrafluoroethane has been tested in metered-dose inhalers for the treatment of respiratory diseases. Test subjects included adult and pediatric asthmatic patients as well as individuals with severe COPD. No adverse effects were reported (Smith et al. 1994 Taggart et al. 1994 Ventresca 1995 Woodcock 1995). Structurally related compounds, including 1,1,1-trichloroethane and trichlorofluoromethane, were also tested for cardiac sensitization in dogs with experimentally induced myocardial infarctions. In these experiments cardiac sensitization occurred at the same concentration as in healthy dogs (Trochimowicz et al. 1976). Thus, no sensitive or particularly susceptible populations can be identified for HFC-134a. 

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.

A healthy 33-year-old man with prior cocaine use had a small myocardial infarction and, 36 hours later, having inhaled cocaine, developed a dissection of the left main coronary artery, extending distally to the left anterior descending and circumflex arteries. There was marked anterolateral and apical hypokinesis. 

Carder JR, Fuerst RS. Myocardial infarction after toluene inhalation. Pediatr Emerg Care 1997 13(2) 117-9. 

Morbidity and mortality associated with wildfires include burns, inhalation injuries, respiratory complications, and stress-related cardiovascular events (exhaustion and myocardial infarction while fighting or fleeing the fire). 

A 22-year-old man snorted an 8 mg crushed tablet of buprenorphine and 2 hours later had crushing chest pain, which resolved within a few minutes (4). The symptom recurred 3 weeks later after another inhalation of buprenorphine. An electrocardiogram suggested an acute anterior myocardial infarction caused by buprenorphine-induced coronary artery spasm. 

Repetitive abuse can cause crusting skin lesions and telangiectasis (angioma or hyperemic spots). Tracheobronchial irritation with dyspnea and hemoptysis has been reported. Withdrawal from industrial exposure has resulted in respiratory failure, left ventricular hypertrophy, and myocardial infarctions. Damage to the lungs, liver, kidneys, bone marrow, and brain is possible. Nitrite inhalants are thought to be carcinogenic and immunosuppressive. Tolerance occurs. 

It is well established that many of the toxic effects of inhaling environmental (second hand) tobacco smoke (ETS) are identical to those of active smoking. ETS is associated with increased risk of lung cancer, 15 respiratory disease (including asthma in children), 16 anc[ cardiovascular disease (including acute myocardial infarction). 17 ... 

Intentional inhalation, or huffing, of volatile organic chemicals for the purpose of inducing euphoria can bring on cardiac arrhythmia, ventricular fibrillation, myocardial infarction, cardiac arrest, and dilated cardiomyopathy, a condition in which the heart becomes enlarged and weakened, thereby limiting its ability to pump bloodJ4 15l Table 29.2 contains a list of cardiotoxic chemicals frequently, intentionally inhaled and the common sources of these chemicals. 

Heart rate (HR), heart rate variability and blood pressure are regulated, in part, by the sympathetic and parasympathetic nervous systems. Changes in one or more may inerease the risk of cardiovascular events (e.g. arrhythmias, myocardial infarction). Decreases in heart rate variability have been associated with cardiovaseular mortality/morbidity in older adults and those with significant heart disease. Eine particles in ambient concentrations have recently been implicated in deereases of heart rate variability (Timonen et al. 2006), increased risk of arrhythmias (Metzger et al. 2004 Lanki et al. 2006) and increased blood pressure (Timonen et al. 2006) in particular in older subject with compromised health. Additionally inhaled particles seem to enhance blood coagulation (Riickerl et al. 2007a, b). 

EPA/6000t-08/139. Environmental Protection Agency, Research Triangle Park, NC, USA Vedal S, Petkau J, White R et al (1998) Acute effects of ambient inhalable particles in asthmatic and nonasthmatic children. Am J Respir Crit Care Med 157 1034-1043 von Klot S, Wolke G, Tuch T et al (2002) Increased asthma medication use in association with ambient fine and ultrafine particles. Eur Res J 20 691-702 von Klot S, Peters A, Aalto P et al (2005) Ambient air pollution is associated with increased risk of hospital cardiac readmissions of myocardial infarction survivors in five European cities. Circulation 112 3073—3079... 

In a large observational study (n = 507966) patients who had recently started asthma medication (SABA, LABA, inhaled glucocorticoids) were at an initial increased risk of myocardial infarction, particularly in the first 3 months, which then fell there was no significant difference in the risk between treatments (RRs SABA = 2.4, LABA = 1.5, inhaled glucocorticoids = 1.5) [39 ]. Heavy long-term use (more than 13 prescriptions in 1 year) of an inhaled glucocorticoid and a SABA was also associated with an increased risk of myocardial infarction. Limitations of this study included potential confounders and the possibility that inhalers are sometimes incorrectly given for cardiac asthma (i.e. pulmonary edema). 

In a meta-analysis of 30 placebo-controlled trials of duration 4 weeks to 4 years, the analysis involved 19 545 individuals who were randomized to tiotropium (n = 10 846) as a dry powder inhaler (Handihaler) or a soft mist generating inhaler (Respimat) [95 ]. There was lower ad-cause mortality in the tiotropium group (RR = 0.88 Cl = 0.77,1.0). The main cardiovascular end-point was combined cardiovascular deaths, non-fatal myocardial infarctions, non-fatal strokes, and deaths (sudden death, sudden cardiac death, or cardiac death). The incidence of cardiovascular events was 2.15 per 100 patient-years in the treatment group versus 2.67 in the placebo group. The apparent reduction in events with tiotropium was siffiificant (RR = 0.83 Cl — 0.71, 0.98). The risk of myocardial infarction, cardiac failure, or stroke showed a trend towards reduction with tiotropium. 

Two other studies have concluded that inhalation of nanosized particulates is associated with increased rates of myocardial infarction (MI). In the first study, carried out in southern Germany, the authors concluded that transient exposure to traffic (which contaminates air with nanosized particulates) may increase the risk of MI in susceptible individuals [17]. 

In normal volunteers, inhalation of Ento-nox (a 50 50 mixture of nitrous oxide and oxygen) leads to depression of cardiac output (SED VIII). Caution in its use in patients with myocardial infarction is therefore necessary, but recently Kerr et al. (12 ) have reported that after the use of Entonox they did not find any change in cardiac rhythm or haemodynamic status . 

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