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Pseudocholinesterase deficiency

Pseudocholinesterase deficiency is an inherited blood plasma enzyme abnormality. more...

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People who have this abnormality may be sensitive to certain anesthetic drugs, including the muscle relaxants succinylcholine and mivacurium as well as other ester local anesthetics (Maiorana & Roach, 2003). These drugs are normally metabolized by the pseudocholinesterase enzyme. When anesthetists administer standard doses of these drugs to a person with pseudocholinesterase deficiency, the patient experiences prolonged paralysis of his respiratory muscles, requiring an extended period of time during which the patient must be mechanically ventilated. Eventually the muscle-paralyzing effects of these drugs will wear off despite the deficiency of the pseudocholinesterase enzyme. If the patient is maintained on a mechanical respirator until normal breathing function returns, there is little risk of harm to the patient. This enzyme abnormality is a benign condition unless a person with pseudocholinesterase deficiency is exposed to the offending pharmacological agents (Alexander, 2002).


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Acute effects of intravenous cocaine on pulmonary artery pressure and cardiac index in habitual crack smokers
From CHEST, 1/1/97 by Eric C. Kleerup

Background: Some habitual crack cocaine smokers who deny IV drug abuse show decreased pulmonary transfer of carbon monoxide (Dco). We speculated that repeated elevations in pulmonary artery pressure (PAP) might cause pulmonary capillary damage and result in a lowered Dco, or that the reduction could be due to anoxic lung injury secondary to repeated episodes of cocaine-induced pulmonary vascular constriction.

Study Objective: Compare the acute effects of IV cocaine HCl and placebo on PAP, cardiac stroke volume, and cardiac output estimated indirectly by continuous Doppler echocardiography.

Design: A single-blind crossover study in which placebo always preceded the active drug.

Subjects: Ten current crack-smoking subjects, 32 to 47 years of age, with a history of limited previous IV cocaine use.

Methods: PAP, cardiac stroke volume, heart rate, and BP were measured continuously after injection of placebo followed by cocaine HCl (0.5 mg/kg).

Results: IV cocaine resulted in no significant change in PAP (-0.14 [+ or -] 3.3[SD] mm Hg, 95% confidence interval [CI] for difference -2.48, +2.21). Stroke volume index showed no significant change after cocaine ( -0.1 [+ or -] 2.0 mL; 95% CI, - 1.5, +1.3). Heart rate showed a significant increase (10.0 [+ or -] 7.2 [min.sup.-1]; p=0.0017, 95% CI, +4.9, +15.1). Cardiac index showed a significant increase (0.48 [+ or -] 0.32 L/min; p=0.0012, 95% CI, +0.25, +0.71). Pulmonary vascular resistance showed no significant change (-44 [+ or -] 101 dyne . s . [cm.sup.-5]/[m.sup.2], 95% CI, -116, +29).

Conclusions: IV cocaine HCl does not cause short-term increases in PAP or stroke volume index, but causes an increase in cardiac index due to its chronotropic effect.

(CHEST 1997,111:30-35)

Key words: cardiac output; cocaine HCl; pulmonary artery pressure

Abbreviations: AT/ET=acceleration time/ejection time; Ci=cardiac index; CI=confidence interval; Dco=diffusing capacity of the lung for carbon monoxide; HR=heart rate; mPAP=mean pulmonary artery pressure; NIDA=National Institute on Drug Abuse; PAP=pulmonary artery pressure; PVR=pulmonary vascular resistance; SVi=stroke volume index; VTI=velocity time integral

We have previously shown that heavy, habitual cocaine smoking is associated with a significant abnormality in gas transfer (diffusion) in the lung,[1] consistent with findings of other investigators.[2,3] The presence of an abnormality in diffusing capacity suggests structural lung damage. Clinical reports of acute noncardiogenic ("increased permeability") pulmonary edema[4] and diffuse alveolar hemorrhage in temporal association with cocaine use,[5,6] as well as autopsy evidence of frequent, clinically occult pulmonary hemorrhage[6-8] and interstitial pneumonitis and/or fibrosis[7] in lung specimens from cocaine users who die suddenly, provide support for the concept of cocaine-induced damage to the alveolar-capillary membrane. It has been suggested[9] that this damage could result from either (1) a direct toxic effect of the inhaled cocaine on the alveolar epithelium and/or capillary endothelium and/or (2) an intense vasoconstrictor effect of cocaine on the pulmonary circulation, causing a marked reduction in pulmonary capillary perfusion that leads to anoxic cellular damage. However, a vasoconstrictor effect of cocaine on the intact pulmonary circulation has not yet been demonstrated experimentally in man. The possibility of cocaine-induced pulmonary vasoconstriction is suggested by the following: (1) an autopsy report revealing medial hypertrophy and hyperplasia involving small or medium-sized pulmonary arteries in 20% of young cocaine users (without evidence of foreign-body microembolization) who died suddenly from acute cocaine intoxication;[10] (2) a report of biopsy specimen-proved symptomatic pulmonary vascular disease (intimal and medial hypertrophy of muscular pulmonary arteries) in a small group of crack-smoking women with borderline to severe pulmonary hypertension;[11] (3) in vitro studies of rabbit pulmonary artery segments with either intact or denuded endothelium;[12] (4) studies in animal models in which cocaine has been reported to accentuate pulmonary arterial pressor responses;[13] and (5) a recent clinical report of pulmonary arterial hypertension in asymptomatic IV cocaine users.[14] This latter finding, however, could be secondary to microembolization of particulate material injected IV, rather than to a toxic effect of cocaine itself on the pulmonary circulation.

In the absence of any reports of direct evidence of cocaine effects on pulmonary hemodynamics in man, we estimated pulmonary vascular pressures and resistance noninvasively by Doppler echocardiography in ten habitual crack users and examined the short-term effect of experimental administration of cocaine in the same subjects. We hypothesized that IV cocaine HCl would acutely produce pulmonary arterial/arteriolar vasoconstriction, as manifested by an increase in pulmonary artery pressure (PAP) out of proportion to the increase in cardiac output estimated by Doppler echocardiography.


Ten healthy current crack-smoking subjects, nine men and one woman, were recruited for experimental cocaine administration studies from chemical dependency treatment programs in the local community (after relapse) and from a cohort of crack smokers participating in ongoing studies of the pulmonary effects of habitual use of cocaine. Inclusionary criteria included age 25 to 50 years, current smoking of alkaloidal (crack) cocaine on a regular basis, and previous occasional use of IV cocaine (from 1 to 12 times per lifetime). Exclusionary criteria included the following: IV drug abuse more than 12 times per lifetime or within the previous year; history of smoking ( [is greater than] 20 times/lifetime) other illicit substances (eg, phencyclidine, heroin, opium, methamphetamine) except for cannabis; a history of chronic lung disease (eg, asthma, interstitial lung disease); history or clinical evidence of systemic or pulmonary hypertension; history of coronary artery disease, angina, arrhythmia, or congenital heart disease; abnormal 12-lead ECG; history or clinical evidence of hyperthyroidism or peripheral vascular disease; history of stroke, seizure disorder, or other neurologic abnormality; history of significant psychiatric disorder; or pseudocholinesterase deficiency. Women of child-bearing potential were not studied if they were pregnant, lactating, or not using a medically acceptable method of contraception. A urine pregnancy test was performed on all female subjects at the beginning of each study day to detect unsuspected pregnancy. Subjects without measurable tricuspid regurgitation by Doppler echocardiography (see below) were excluded from analysis. Eligible volunteers were studied after signing informed consent forms approved by the UCLA School of Medicine Human Subject Protection Committee and the West Los Angeles VA Medical Center Human Studies Committee.


Preliminary examination procedures included the following: a detailed respiratory and drug use questionnaire modified from the American Thoracic Society/National Heart, Lung and Blood Institute respiratory questionnaire[15] and National Institute on Drug Abuse (NIDA) National Survey on Drug Abuse[16]; medical history and physical examination; serum pseudocholinesterase determination; urine drug screen; 12-lead ECG; spirometry and single-breath diffusing capacity for carbon monoxide (Dco) measurement (adjusted for hemoglobin[17] and carboxyhemoglobin[18]); and a urine pregnancy test in female subjects. Eligible volunteers were advised to refrain from smoking cocaine or marijuana, taking any prescription or over-the-counter medication, or consuming any caffeine-containing beverage for at least 8 h prior to visiting the laboratory. They were also admonished not to smoke tobacco for at least 2 h before testing or to use any antihistamine preparation for at least 48 h. Studies were performed with a physician in attendance and emergency resuscitation equipment nearby.

At the beginning of each study, the amount of daily drug use (crack cocaine, marijuana, tobacco, and other drugs) during the preceding week and the time of last use were ascertained by questionnaire (self-report), and a urine sample was obtained for determination of cocaine metabolite (benzoyleogonine). A 12-lead ECG was performed. A catheter was inserted in an arm vein for injection of saline solution or cocaine HCl. A standard two-dimensional echocardiogram (Acuson 128XP; Mountain View, Calif) was performed to rule out structural malformations and to assess right ventricular outflow diameter. Finger arterial blood pressure was monitored continuously and noninvasively on the second or third finger of the left hand (Finapres 2300E; Ohmeda; Boulder, Colo). The sum of chest and abdominal wall excursions (proportional to tidal volume) measured by inductive plethysmography (Respitrace Plus; Non-Invasive Monitoring Systems; Miami Beach, Fla) was recorded directly on the echocardiographic recording tape. Doppler echocardiographic assessment of the right ventricular outflow tract was performed continuously from before administration of placebo until after return to baseline following cocaine administration.

The cocaine HCl was obtained from the NIDA in crystalline form. The dose of IV cocaine HCl (0.35 to 0.5 mg/kg) used was selected since it has been shown to yield euphoric effects comparable to those achieved during recreational use of cocaine[19] and to be below the dose levels associated with significant cocaine toxicity, according to unpublished NIDA guidelines for experimental cocaine administration. The subject was blinded to the administration of drug vs placebo. For each subject, the first injection consisted of a volume of 0.9% NaCl identical to that of the cocaine administered later, injected over 30 s, and followed by 6 mL 0.9% NaCl flush over 60 s. The second injection consisted of (1) cocaine HCl (7.67 mg/mL in 0.9% NaCl) at a dose of 23 mg (2 subjects, average dose 0.35 mg/kg lean body weight [body mass index of 22.0]) or (2) cocaine HCl (5 mg/mL in 0.9% NaCl) at a dose of 0.5 mg/kg lean body weight (8 subjects, average dose 36.5 [+ or -] 4.6 [SD] mg). This also was injected over 30 s and followed by a 6-mL flush of 0.9% NaCl over 60 s. The change in dose from 0.35 to 0.5 mg/kg was made after the first 2 subjects had been studied to assure a consistent chronotropic response based on the results of concurrent studies.

Individual beats from the Doppler spectral recordings obtained at end-expiration at approximately 1-min intervals were analyzed for acceleration time/ejection time (AT/ET), velocity time integral (VTI), and instantaneous heart rate (HR). Ectopic and postectopic beats were excluded from analysis. Mean pulmonary arterial pressure (mPAP) was estimated from AT/ET.[20] Stroke volume was calculated from the product of right ventricular outflow tract cross-sectional area and VTI.[21] Cardiac output was calculated as the product of HR and stroke volume. Right atrial pressure was estimated at 5 mm Hg (no subject had evidence of jugular venous distention). Pulmonary vascular resistance was calculated from the Doppler-estimated mPAP divided by the cardiac index (Ci). Stroke volume, cardiac output, and pulmonary vascular resistance (PVR) were indexed to body surface area for intersubject comparisons.

A physician was present at all times during the cocaine infusion experiments. Following cocaine administration, subjects were carefully monitored for evidence of acute cocaine toxicity such as systemic hypertension, tachycardia, clinically significant arrhythmia, chest pain, or headache.

Data Analysis

Paired t tests were used to compare measurements obtained following placebo with (1) those obtained in the first 5 min following cocaine, and (2) all measurements following cocaine until returned to baseline. A Hotelling [T.sup.2], a multivariant analogue of the t-statistic, was used to assess differences in mPAP, HR, stroke volume index (SVi), Ci, and PVR index given their correlation structure.[22] A repeated-measures model using the variance of each subject during the measurement period was used to derive 95% confidence intervals (CIs) for the difference between cocaine and placebo values.[23]


Mean age, smoking history, and diffusing capacity of the study participants are shown in Table 1. Subjects were young to middle-aged adults who, on the average, were heavy smokers of cocaine base (mean of 0.93 g/wk). Most were also current smokers of tobacco and marijuana. Dco was mildly reduced ( [is less than] 75% predicted) in 4 of the 10 subjects.

Previous reports of echocardiographic measurements in asymptomatic IV cocaine users have shown elevations in estimated PAP (systolic PAP [is greater than] 30 in 8 of 13 subjects).[14] The pulmonary hypertension has been hypothesized to be due to granulomatous inflammation from injected insoluble agents (talc, corn starch, microcrystalline cellulose). However, an autopsy study demonstrated pulmonary artery medial hypertrophy in the absence of foreign particle microembolization in 4 of 20 deaths from cocaine overdose,[10] raising the possibility that repeated episodes of cocaine-induced acute pulmonary vasoconstriction might eventually produce pulmonary hypertension and medial hypertrophy. However, acute administration of intranasal cocaine, 2 mg/kg, results in an increase in HR and Ci, but no change in mPAP or SVi assessed at 15, 30, or 45 min by pulmonary artery catheterization.[38]

Since cocaine-induced subjective effects and tachycardia are of short duration, we postulated that any change in mPAP might be transient. Noninvasive measurement of mPAP using the AT/ET at the right ventricular outflow tract has a good correspondence to pressures measured by pulmonary artery catheterization (r=0.94)[39] and also allows almost continuous measurements that can be gated to end-expiration. Using a moderate dose of cocaine, this study shows no change in mPAP compared with placebo. We also establish a 95% CI for the group mean that narrowly defines the change in mPAP and makes it unlikely that a clinically significant change in mPAP occurred in this group. This lack of change is present in the first 5 min after infusion of cocaine and for all measurements following cocaine.

It is possible that higher doses of cocaine or a different route of administration might provoke a significant increase or decrease in mPAP. However, higher doses also would make acute untoward side effects more likely in this volunteer subject population. Although it is possible that some subjects are responders and some are nonresponders to pulmonary vasomotor effects of cocaine, the outlying subjects with either high or low initial mPAP did not respond differently from the remainder of the group in our study. In dogs, tachyphylaxis to the hypertensive and myocardial oxygen consumption effects occurs at higher doses of cocaine (0.8 mg/kg) administered at 1-h intervals, but lower doses result only in an elevation of the baseline hemodynamic variables.[40] Although our subjects stated that they had refrained from smoking cocaine in the 8 h prior to the study day, it is possible they did not abstain or that the duration of abstinence was insufficient. However, we did observe the expected chronotropy and systemic BP increases after cocaine, so that it is less likely that our failure to demonstrate acute pulmonary vasoconstriction following cocaine was due to the development of tolerance as a result of recent cocaine use.

The marked difference in response to cocaine between the systemic and pulmonary vasculature may be due to several factors. First, the greater compliance of the pulmonary vasculature may prevent rises in PAP through the recruitment of additional, previously collapsed vessels, even though all the vessels might be constricted secondary to cocaine administration (excess capacitance). Second, the pulmonary vascular system may be unable to respond to a given constrictor stimulus to the same degree as the systemic vasculature due to decreased or absent smooth muscle in the pulmonary arteries and arterioles (decreased responsivity). Finally, the pulmonary vascular smooth muscle may have a lower density of adrenergic receptors for stimulation by catecholamines causing less constriction in response to local increases in norepinephrine and dopamine than in the systemic circulation (decreased sensitivity).

In the absence of apparent change in the mPAP during acute administration of cocaine, it is difficult to postulate microvascular damage due to repeated vasoconstriction as an explanation for low Dco observed in some crack cocaine users. Moreover, the lack of a marked elevation in mPAP either acutely following experimental cocaine administration or chronically in habitual crack cocaine smokers argues against redistribution of blood flow to upper lung zones resulting from pulmonary hypertension with compensatory recruitment of capillaries from upper lung zones as an explanation for pseudonormalization of Dco in crack smokers with cocaine-related lung injury.

ACKNOWLEDGMENTS: The authors thank Ruth Barre, Enoch Y. Lee, and Becky Lopez for their technical assistance and James Sayre for his statistical expertise.


[1] Tashkin DP, Khalsa M-E, Gorelick D, et al. Pulmonary status of habitual cocaine smokers. Am Rev Respir Dis 1992; 145:92-100

[2] Weiss RD, Tilles DS, Goldenheim PD, et al. Decreased single breath carbon monoxide diffusing capacity in cocaine freebase smokers. Drug Alcohol Depend 1987; 19:271-76

[3] Itkonen J, Schnoll S, Glassroth J. Pulmonary dysfunction in `freebase' cocaine users. Arch Intern Med 1984; 144:2195-97

[4] Cucco RA, Yoo OH, Cregler L, et al. Nonfatal pulmonary edema after `freebase' cocaine smoking. Am Rev Respir Dis 1987; 136:179-81

[5] Forrester JM, Steele AW, Waldron JA, et al. Crack lung: an acute pulmonary syndrome with a spectrum of clinical and histopathologic findings. Am Rev Respir Dis 1990; 142: 462-67

[6] Murray RJ, Albin RJ, Mergner W, et al. Diffuse alveolar hemorrhage temporally related to cocaine smoking. Chest 1988; 93:427-29

[7] Bailey ME, Fraire AK, Greenberg SD, et al. Pulmonary histopathology in cocaine abusers. Hum Pathol 1994: 25: 203-07

[8] Laposata EA, Mayo GL. A review of pulmonary pathology and mechanisms associated with inhalation of freebase cocaine (`crack'). Am J Forensic Med Pathol 1993; 14:1-9

[9] Ettinger NA, Albin RJ. A review of the respiratory effects of smoking cocaine. Am J Med 1989; 87:664-68

[10] Murray RJ, Smialek JE, Golle M, et al. Pulmonary artery medial hypertrophy in cocaine users without foreign particle microembolization. Chest 1989; 96:1050-53

[11] Russell LA, Spehlmann JC, Clarke M, et al. Pulmonary hypertension in female crack users [abstract]. Am Rev Respir Dis 1992; 145:A717

[12] Beauchamp HD, Kundra N, Aranson R, et al. Cocaine induced vasoconstriction of pulmonary vascular smooth muscle [abstract]. Am Rev Respir Dis 1991; 143:A776

[13] Hyman AL, Nandiwada P, Knight DS, et al. Pulmonary vasodilator responses to catecholamines and sympathetic nerve stimulation in the cat. Circ Res 1981; 48:407-15

[14] Yakel DL Jr, Eisenberg MJ. Pulmonary artery hypertension in chronic intravenous cocaine users. Am Heart J 1995; 130: 398-99

[15] Ferris BG, Speizer F, Gaensler E, et al. Epidemiology standardization project. Am Rev Respir Dis 1978; 118:1-120

[16] Fishburne PM, Abelson HI, Cisin I. National survey on drug abuse: main findings. Rockville, Md: National Institute on Drug Abuse, 1980

[17] Cotes JE, Dabbs JM, Elwood PC, et al. Iron-deficiency anaemia: its effect on transfer factor for the lung (diffusing capacity) and ventilation and cardiac frequency during submaximal exercise. Clin Sci 1972; 42:325-35

[18] Mohsenifar Z, Tashkin DP. Effect of carboxyhemoglobin on the single breath diffusing capacity: derivation of an empirical correction factor. Respiration 1979; 37:185-91

[19] Foltin RW, Fischman MW. Smoked and intravenous cocaine in humans: acute tolerance, cardiovascular and subjective effects. J Pharmacol Exp Ther 1991; 257:247-61

[20] Kitabatake A, Inoue M, Asao M, et al. Noninvasive evaluation of pulmonary hypertension by a pulsed Doppler technique. Circulation 1983; 68:302-09

[21] Wong M, Matsumura M, Omoto R. Left and right ventricular flows by Doppler echocardiography: serial measurements in patients with aortic regurgitation during exercise, cold pressor stimulation, and vasodilation. J Am Soc Echocardiogr 1990; 3:285-93

[22] Morrison DF. Multivariate statistical methods. 3rd ed. New York: McGraw-Hill, 1990; 148

[23] Crowder MJ, Hand DJ. Analysis of repeated measures. 1st edition. New York: Chapman & Hall, 1990; 60

[24] Pinsky MR, Dhainaut J-FA. Pathophysiologic foundations of critical care. Baltimore: Williams & Wilkins, 1993; 15

[25] Wilson JD, Braunwald E, Isselbacher KJ, et al. Harrison's principles of internal medicine. 12th ed. New York: McGrawHill, 1991; A-7

[26] Gilman AG, Goodman LS, Rall TW, et al. Goodman and Gilman's the pharmacological basis of therapeutics. 7th ed. New York: MacMillan Publishing, 1985; 309

[27] Koivunen DG, Johnson JA. Effect on pressor and vascular responsiveness in rabbits of drugs that decrease norepinephrine uptake. Proc Soc Exp Biol Med 1994; 206:375-83

[28] Javaid JI, Fischman MW, Schuster CR, et al. Cocaine plasma concentration: relation to physiological and subjective effects in humans. Science 1978; 202:227-28

[29] Lange RA, Cigarroa RG, Yancy CW Jr, et al. Cocaine-induced coronary-artery vasoconstnction. N Engl J Med 1989; 321: 1557-62

[30] Lange RA, Cigarroa RG, Flores ED, et al. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med 1990; 112:897-903

[31] Albertson TE, Walby WF, Derlet RW. Stimulant-induced pulmonary toxicity. Chest 1995; 108:1140-49

[32] Perper JA, Van Thiel DH. Respiratory complications of cocaine abuse. Recent Dev Alcohol 1992; 10:363-77

[33] Chakko S, Myerburg RJ. Cardiac complications of cocaine abuse. Clin Cardiol 1995; 18:67-72

[34] Nademanee K. Cardiovascular effects and toxicities of cocaine. J Addict Dis 1992; 11:71-82

[35] Uszenski RT, Gillis RA, Schaer GL, et al. Additive myocardial depressant effects of cocaine and ethanol. Am Heart J 1992; 124: 1276-83

[36] Bedotto JB, Lee RW, Lancaster LD, et al. Cocaine and cardiovascular function in dogs: effects on heart and peripheral circulation. J Am Coll Cardiol 1988; 11:1337-42

[37] Kolbeck RC, Speir WA Jr. Regional contractile responses in pulmonary artery to alpha- and beta-adrenoceptor agonists. Can J Physiol Pharmacol 1987; 65:1165-70

[38] Boehrer JD, Moliterno DJ, Willard JE, et al. Hemodynamic effects of intranasal cocaine in humans. J Am Coll Cardiol 1992; 20:90-3

[39] Stevenson JG. Comparison of several noninvasive methods for estimation of pulmonary artery pressure. J Am Soc Echocardiogr 1989; 2:157-71

[40] Pagel PS, Tessmer JP, Warltier DC. Systemic and coronary hemodynamic effects of repetitive cocaine administration in conscious dogs. J Cardiovasc Pharmacol 1994; 24:443-53

(*) From the Divisions of Pulmonary and Critical Care Medicine UCLA School of Medicine, Los Angeles (Drs. Kleerup, Marques-Magallanes, and Tashkin) and VAMC West Los Angeles (Drs. Wong and Goldman).

Supported by NIH/NIDA grant RO1 DA08254. Manuscript received June 14, 1996; revision accepted July 11. Reprint requests: Dr. Kleerup, Div of Pulmonary and Critical Care Medicine, UCLA School of Medicine CHS 37-131, Box 951690, Los Angeles, CA 90095-1690

COPYRIGHT 1997 American College of Chest Physicians
COPYRIGHT 2004 Gale Group

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