Cardiac Effects of a Cocktail

Lawrence Gould, MD; Mohammad Zahir, MD; Anthony DeMartino, MD; and Robert F. Gomprecht, MD

The hemodynamic effects of a cocktail in cardiac disease have not been key to drink in less than ten minutes. previously studied, to our knowledge. Ten patients with cardiac disease Thirty minutes after the ingestion of and four normals underwent cardiac catheterization. Hemodynamic the whiskey, the pressures and car¬ diac were measured. measurements were obtained prior to and 30 minutes after oral ingestion output Left ventricular function was as¬ of 2 oz of Canadian With alcohol, all of the with cardiac whiskey. patients sessed to the de¬ disease demonstrated a fall in the cardiac index and stroke index. Alcohol according following terminations: produced in the normals an increase in these measurements. The cardiac rate, systemic , and pressure were LVSW = LVS LVd x SI X 1.36 x 1.050 - essentially unchanged in both groups. Small amounts of alcohol can 100 (1) cardiac function in with cardiac disease. impair patients LVSP = LVSW/SEP (2) MSER = SI/SEP (3) Alcohol is consumed in varying and 8 of the 12 subjects rarely took an TTIb = LVsxSEP (4) L\ amounts a alcoholic beverage. However four of by large segment TTIm = LVBXSEPxHR * *» of the population. It has even the patients admitted to excessive al¬ (5) been cohol prescribed by many physicians consumption. LVW = for their patients because of a pre¬ Procedures. -Catheterization of the CIX^^XBA (6) sumed cardiac stimulant effect. left was performed by retro¬ PR = BA„x 1,332 the a number arterial In last few years of grade catheterization CO (7) groups have investigated the cardiac through a brachial arteriotomy. A effects of alcohol in man. However, Cournand needle was placed into the Where LVSW signifies left ventricular most of these studies have been lim¬ opposite brachial artery. A No. 7 stroke work (g-m/beat/sq m of body sur¬ face stroke index (ml/beat/sq m ited to right ventricular catheter- Goodale-Lubin catheter was placed in area); SI, of body surface area); LV, mean left ven¬ izations1-5 so that left ventricular the pulmonary artery. tricular systolic pressure (mm Hg); LV„, function could not be ana¬ was determined in the precisely duplicate by left ventricular end-diastolic pressure (mm In the amount of eth- Fick and the results did lyzed. addition, technique, Hg); LVSP, mean left ventricular stroke anol administered over a short not differ more than 7%. period by Oxygen power (g-m/beat/sq m body surface of time was so excessive that it bore consumption was determined by mea¬ area/systolic sec); SET, mean systolic ejec¬ no relationship to the drinking habits suring ventilation with a spirometer, tion time (sec); MSER, mean systolic ejec¬ of most individuals.1-4" and analyzing the expired gas with a tion rate (ml/beat/sq m/systolic sec); TTI„, Micro-Scholander apparatus. Two to¬ tension time index per beat (mm Hg tension time index For editorial comment see page 1822. nometers were used for the gas collec¬ sec/beat), TTIm, per tions, and the results of the analysis minute (mm Hg/sec/min); HR, rate (beats/min); LVW, left ventricular work Thus, the cardiac effects of a cock¬ of the two gas samples had to agree (kg-m/min/sq m body surface area); BAm, tail in with cardiac disease 0.04%. Mixed venous blood was ob¬ patients by mean brachial tained from the artery pressure (mm Hg); are unknown. The following study pulmonary artery PR, systemic peripheral resistance (dynes- an¬ and arterial blood from the brachial was designed and performed to sec-cm '); CO, cardiac output (ml/sec); 1.36, swer this unresolved question. artery. Arterial and mixed venous conversion factor from mm Hg to cm HO; oxygen contents were determined by 1.050, whole blood specific gravity. Materials and Methods the method of Van Slyke and Neill. The statistical significance of the Selection ofPatients.—A group of 14 The blood samples were analyzed in differences (P values) in the normal hospitalized patients, 11 men and two different machines, and the re¬ and abnormal group prior to alcohol three women, underwent right and sults did not differ by more than 0.2 ingestion as well as the differences in left ventricular catheterizations, pri¬ vol/100 ml. the normal and abnormal group 30 marily as an aid to their clinical man¬ Left ventricular, pulmonary ar¬ minutes after the ingestion of alcohol agement. The conditions of the pa¬ terial, and systemic arterial pres¬ were calculated with the Student t- tients are listed in Table 1. A history sures, and cardiac output were mea¬ test. of alcohol consumption was obtained sured in the resting state. All Results pressures were obtained using the From the Department of Medicine, Mis- mid thoracic level as the reference Complete data on all 14 patients ericordia-Fordham Hospital Affiliation, Bronx, point. are in Table 1. In NY. presented addition, The were then 2 oz values before and after alco¬ Reprint requests to 600 E 233rd St, Bronx, NY subjects given average 10466 (Dr. Gould). of chilled 86.8-proof Canadian whis- hol ingestion in the normal and ab-

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Patient RA, RV PA LV BA Rate SET SET No. Experimental Sex and Mean S/D S/D S/D S/D (Beats/ (Sec/ (Rate Condition State Age (yr) (mm Hg) (mm Hg) (mm Hg) Mean (mm Hg) (mm Hg) Mean Minute) Beat) Corrected) Control M 36 20/3 20/11 14 107/8 107/60 76 86 0.26 0.41 Normal Alcohol 19/10 13 110/8 110/65 80 84 .265 .40 2 Control 25/0 25/12 16 115/7 117/72 87 77 .28 .41 Normal Alcohol 24/10 15 115/7 118/68 84 84 .28 .42 3 Control M 21 16/0 15/0 115/6 120/70 87 68 .26 .36 Normal Alcohol 12/6 110/6 120/70 87 73 .32 .44 4 Control F 24 16/1 16/8 10 115/72 86 79 .30 .43 Normal Alcohol 15/7 9 110/70 84 79 .30 .43 5 Viral Control F 37 13/0 13/8 10 117/62 80 100 .27 .44 Alcohol 12/7 9 107/68 81 100 .26 .43

Pericarditis and chronic Control M 32 24/0 24/9 14 105/4 110/63 79 71 .30 .42 alcoholic Alcohol 20/8 12 112/5 128/80 96 75 .28 .41

Constrictive Control M 65 26/8 27/14 18 100/10 100/60 73 56 .28 .38 pericarditis Alcohol 18/12 14 98/11 98/58 72 64 .28 .38 8 Mitral Control F 52 35/5 35/16 23 135/10 135/60 85 68 .33 .45 stenosis Alcohol 27/12 17 130/10 137/58 85 54 .33 .42 9 Mitral Control M 53 82/7 82/30 47 90/18 100/67 78 100 .22 .39 insufficiency Alcohol 95/30 52 88/20 95/60 72 99 .22 .39 10 Hyperkinetic Control M 26 25/3 23/11 15 120/3 120/70 87 77 .31 .44 heart syndrome Alcohol 27/12 17 128/7 128/78 95 83 .30 .44 11 Mitral stenosis, aortic insufficiency, Control M 41 1 40/1 40/18 25 107/2 118/70 86 88 .24 .39 chronic alcoholic Alcohol 35/18 24 118/5 130/80 96 96 .24 .40 12 i Primary myo- cardial disease Control M 45 1 37/2 37/20 25 100/19 104/63 77 100 .23 .40 and chronic alcoholic Alcohol 43/23 29 94/20 100/60 73 100 .24 .41 13 Primary myo- cardial disease Control M 58 12 60/12 60/30 40 125/16 125/85 99 120 .20 .40 and chronic alcoholic Alcohol 60/28 39 130/18 130/80 96 104 .20 .37 14 Coronary heart Control M 56 6 25/5 25/13 16 130/9 138/78 98 67 .28 .39 disease Alcohol 30/17 21 130/13 142/80 100 71 0.27 0.39

*RA signifies ; S/D, systolic/diastolic; RV, right ventricular pressure; PA, pulmonary artery pressure; BA, brachial artery pressure; SET, systolic ejection time; LVSW, left ventricular stroke work; LVSP, left ventricular stroke power; MSER, mean systolic ejection rate; TTIb, tension time index per beat; TTIm, tension time index per minute; and LVW, left ventricular work.

normal groups are listed in Table 2. (P<.001). Similarly, the cardiac in¬ Comment There was no statistical difference dex rose in the normal group and fell in any of the hemodynamic measure¬ in the abnormal group (P<.02). The The present study demonstrated ments prior to the ingestion of alcohol varying response of the cardiac index that alcohol administration produced in the normal and abnormal group. in the two groups was due primarily a decrease in the cardiac index and Comparison of the two groups after to a narrowing of the arteriovenous stroke index in all of the patients the ingestion of alcohol revealed no oxygen difference in the normal with cardiac disease. The arterial significant differences in the brachial group and a widening of this value in pressure was essentially unchanged, artery mean pressure, pulmonary ar¬ the abnormal group (P<.05). and therefore the peripheral resist¬ tery mean pressure, and left ventricu¬ The significant increase in the left ance rose in the abnormal group. This lar and diastolic pressure. The oxygen ventricular stroke power, mean sys¬ is contrary to the popular conception consumption, cardiac rate, systolic tolic ejection rate, and left ventricu¬ of alcohol as a peripheral vasodilator. ejection period, tension time index lar work as well as the fall in the sys¬ It has been shown recently by Gil- per beat, and tension time index per temic peripheral resistance in the lespie7 that its reputation in this re¬ minute also did not reveal any signif¬ normal group was due to the increase spect depends principally on an in¬ icant changes. in the cardiac index and stroke index. crease in skin flow; muscle flow in the However, an increase in the stroke These hemodynamic factors in the ab¬ limbs is always reduced. index was seen in the normal group normal group changed in the opposite The abnormal response in our pa¬ while a decline in this factor was ob¬ direction due to the decline in the tients contrasts with the hemo¬ served in the abnormal group stroke index and cardiac index. dynamic response of normal individ-

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Arteriovenous Oxygen Cardiac Stroke LVSW LVSP MSER Peripheral Oxygen Consumption Index Index (g-m/ (g-m/ (ml/Beat/ TTIb TTIm LVW Resistance Difference (ml/min/ (Liters/min/ (ml/Beat/ Beat/ Beat/Systolic Sq m/Systolic (mm Hg/ (mm Hg/ (kg-m/ (dyne-sec- (Vol/100ml) Sq m)_Sq m)_Sq m) Sq m)_Sec) Sec)_Sec/Beat) Sec/min) min/Sq m) Cm s) Ï7 165 3^52 41 58 223 158 28 2400 3.8 955 4.3 162 3.77 45 66 249 170 29 2450 4.3 940 Í8 146 3Ü2 39 60 214 139 32 2480 3Ä 1230 3.1 151 4.98 60 93 332 214 32 2700 6.0 728 ¿L2 143 3ÄÖ 50 78 300 192 30 2030 4^2 1070 2.5 141 5.60 77 115 360 240 35 2570 7.0 650 ~ 33 2860 Î23Ô 43 127 2^97 67 ~ 133 36

3.7 137 3.69 88 ...... 157 33 2600 4.4 975

5.0 129 2.58 26 ...... 96 31 3140 2.9 1520

6.1 154 2.53 25 ...... 96 28 2780 2.9 1570

4.0 136 3.42 48 69 230 160 31 2240 3.9 990 5.3 158 2.99 40 61 218 143 31 2350 4.1 1370

6.2 107 1.72 31 40 143 111 28 1570 1.8 1940 6.7 99 1.48 23 29 104 82 27 1760 1.5 2860

3.9 164 4.20 61 109 330 185 45 3020 5.1 1030 5.2 136 2.61 48 82 248 145 43 2320 3.2 1640

8.8 208 2.37 24 25 114 109 20 1980 2.6 1440 9.7 190 1.97 20 19 86 91 19 1915 2.0 1625

2.4 147 6.15 79 132 425 255 37 2860 7.6 665 2.9 152 5.22 63 109 364 210 38 3180 7.1 855

5.3 166 3.13 36 54 180 120 32 2820 3.8 1030 5.7 162 2.84 30 49 162 100 35 3400 3.9 1240

3.1 141 4.53 46 54 234 200 23 2320 5.0 800 4.7 159 3.39 34 36 150 142 23 2260 3.5 1010

6.0 160 2.68 22 34 174 113 24 2920 3.8 1470 9.1 165 1.82 17 27 139 87 26 2640 2.5 2090

4.6 114 2.47 37 64 229 132 36 2440 3.5 1690 6.1 120 1.97 28 45 165 104 35 2480 2.8 2180

uals to the oral administration of normal patients, the cardiac output is a myocardial depressant. The one alcohol. JuchemsJ administered 0.92 to increased with alcohol mainly due to patient with coronary heart disease 1.91 ml/kg of alcohol of 14 healthy an increase in the . in our study also responded to alcohol male volunteers. He observed that the These findings suggest that some with a decline in the cardiac index cardiac output increased with increas¬ normal individuals respond to alcohol and stroke index. ing blood levels of alcohol. The rise in with an increase in the cardiac rate There is considerable evidence sug¬ the cardiac output was mainly due to while other normals mainly increase gesting alcohol's depressant action on an increase in the . The sys¬ their stroke volume. cardiac contractility. Wendt and his temic peripheral resistance fell in all The hemodynamic effect of ethyl al¬ co-workers8 have recently demon¬ of their patients. Riff et al1 adminis¬ cohol in nonalcoholic patients with strated in chronic alcoholics a con¬ tered 6 oz of chilled 90-proof bourbon coronary heart disease has been re¬ sistently negative myocardiac bal¬ whiskey to ten normal subjects. Peak cently investigated by Conway.:i He ance of isocitric dehydrogenase and blood alcohol levels were reached administered three to four whiskeys malic dehydrogenase. These findings within 30 minutes in the majority of to eight patients with stable coronary suggested to these authors that intra- the subjects. A significant increase in heart disease. Hemodynamic observa¬ mitochondrial enzymes are affected the cardiac output was observed 30 tions were made at rest and for 45 by clinical alcoholism even in patients minutes after the ingestion of the minutes after the alcohol intake. He without clinical, hemodynamic, or beverage, mainly due to an increase observed that the cardiac output and other biochemical evidence of heart in the cardiac rate. No change was arterial pressure dropped progres¬ disease. Gimeno et al9 have studied noted in the arterial pressure, while sively at rest. No change was seen in the effects of alcohol in the isolated the calculated peripheral resistance the cardiac rate or peripheral resist¬ rat atrium and have found that an al¬ decreased after alcohol. In our four ance. He concluded that ethyl alcohol most linear relation exists between

Downloaded From: http://jama.amarc.silverchair.com/ by a American Medical Association User on 04/10/2014 dence or Table 2.—Average Changes of Hemodynamic Factors Before and After Alcohol of heart liver disease. No sig¬ nificant change in the cardiac output, Control After Alcohol stroke and vascu¬ ,-A_^ t_A_ volume, peripheral Normal Abnormal Normal Abnormal P lar resistance was observed 30 min¬ _Factor_Group Group Group Group Value Oxygen consumption (ml/min/sq m) 145 147 148 150 NS utes after the ingestion of alcohol. Stroke index (ml/beat/sq m) 49 41 68 33 < .001 The four chronic alcoholic patients Systematic peripheral resistance with cardiac disease in our study 823 (dynes-sec-cm-!) 1,124 1,258 1,644 < .05 demonstrated a decline in the cardiac Brachial artery mean pressure index and stroke index after the in¬ (mm Hg) 84 84 84 87 NS of Fur¬ Arteriovenous oxygen difference gestion Canadian whiskey. (Vol/100ml) 4.5 4.9 3.4 6.2 < .05 ther, this abnormal hemodynamic re¬ Pulmonary artery mean pressure sponse was observed in the two (mm Hg) 12 23 11 23 NS patients with primary myocardial dis¬ Cardiac index m) 3.2 4.5 2.7 .02 (liters/min/sq 3.3 < ease. Thus, the alcoholic patient, with rate 79 85 80 85 NS (beats/min) and without overt cardiac disease, re¬ Left ventricular stroke work in a (g-m/beat/sq m) 65 65 91 51 NS sponds different hemodynamic Left ventricular stroke power manner to the administration of alco¬ (g-m/beat/sq m/systolic sec) 246 229 314 182 < .05 hol. Mean systolic ejection rate It would appear that the chronic al¬ (ml/beat/sq m/systolic sec) 156 148 195 120 < .01 coholic and the nonalcoholic patient Left ventricular work with cardiac disease can dele- kg-m/min/sq m) 3.9 4.0 5.4 3.4 < .05 respond Tension-time index per minute teriously to the administration of (mm Hg/sec/min) 2,442 2,531 2,580 2,580 NS small amounts of alcohol. This is re¬ Tension-time index per beat flected hemodynamically by the de¬ (mm Hg/sec/beat) 31 31 32 31 NS cline in the stroke index and cardiac Systolic ejection time index. Since acts as a (sec/beat) 0.28 0.27 0.29 0.26 NS alcohol myocar¬ Systolic ejection time dial depressant, the advisability of its (corrected rate) 0.40 0.41 0.42 0.40 NS use in patients with cardiac disease Left ventricular end-diastolic o can be questioned. pressure (mm Hg) 7 10 7 _12 NS References 1. Riff DP, Jain AC, Doyle JT: Acute hemo- the concentration of alcohol and the lary muscle. The effects of alcohol dynamic effects of ethanol on normal human vol- unteers. Amer Heart J 78:592-597, 1969. in were similar in decline . quantitatively papil¬ 2. Juchems R: Hemodynamic effects of ethyl Regan and his associates'" adminis¬ lary muscles from cats with right alcohol in man. Amer Heart J 78:133-135, 1969. tered 15% ethanol intravenously to ventricular failure. 3. Conway N: Hemodynamic effects of ethyl alcohol in patients with coronary heart disease. dogs at a rate of 0.1 ml/kg/min for The hemodynamic response of alco¬ Brit Heart J 30:638-644, 1968. two hours, and observed a progressive hol in alcoholic patients without car¬ 4. Blomqvist G, Saltin B, Mitchell JH: Acute effects of ethanol of the to decline in the stroke and a rise diac disease is different from ingestion response output entirely submaximal and maximal exercise in man. Cir- in the left ventricular end diastolic the previously described response of culation 42:463-470, 1970. pressure. Recently Mendoza and his the normal group and the non¬ 5. Wendt VE, Ajluni R, Bruce TA, et al: Acute associates" have in alcoholic with cardiac dis¬ effects of alcohol on the human myocardium. demonstrated patients Amer J Cardiol 17:804-812, 1966. dogs that a mean alcohol blood level ease. Regan and his co-workers" 6. Regan TJ, Levinson GE, Oldewurtel HA, et of 195 mg/100 cc is associated with a studied two groups of alcoholic pa¬ al: Ventricular function in non-cardiacs with al- cardiac disease after coholic fatty liver: Role of ethanol in the produc- marked diminution in the velocity of tients without tion of cardiomyopathy. J Clin Invest 48:397-407, left ventricular contraction. Spann moderate and low dose levels of alco¬ 1969. and co-workers'- have studied the hol Twelve ounces of scotch 7. Gillespie JA: Vasodilator properties of alco- his ingestion. hol. Brit Med J 2:274-277, 1967. acute effects of alcohol on the con¬ were fed over a two-hour period to 11 8. Wendt VE, Wu C, Balcon R, et al: Hemo- tractile state of papillary muscles for alcoholic subjects, and a similar group dynamic and metabolic effects of chronic alcohol- of alcoholic 6 ism in man. Amer J Cardiol 15:175-184, 1965. both normal and failing cat . In seven subjects received 9. Gimeno AL, Gimeno MF, Webb JL: Effect a normal papillary muscle prepara¬ oz of scotch. The low-dose group of ethanol on cellular membrane potential and of isolated rat atrium. Amer J an alcohol concentration of 100 showed no significant changes in the contractility tion, Physiol 203:194-200, 1962. mg/100 ml caused a 9% decrease in stroke index or left ventricular end 10. Regan TJ, Karoxenidis G, Moschos CB, et contractile element velocity at a con¬ diastolic pressure over a four-hour pe¬ al: The acute metabolic hemodynamic responses of the left ventricle to ethanol. J Clin Invest stant of 0.5 a concen¬ riod. After 12 there was a load mg/sq mm; oz, progres¬ 45:270-280, 1966. tration of 300 mg/100 ml, a decrease sive rise in the left ventricular end 11. Mendoza LC, Hellberg K, Rickart A, et al: of and a concentration of 500 diastolic pressure and a decrease of The effect of intravenous ethyl alcohol on the 18%; circulation and toward con¬ coronary myocardial contractility mg/100 ml, a decrease of 38%. In ad¬ stroke output, reverting of the human and canine heart. J Clin Pharma- dition, alcohol decreased both the trol values by four hours. Wendt and col 11:165-176, 1971. peak tension developed and the max¬ his associates' administered 6 oz of 12. Spann JF Jr, Mason DT, Beiser GD, et al: four alco¬ Actions of ethanol on the contractile state of the imal rate of tension development of chilled vodka by mouth to normal and failing cat papillary muscle, ab- the isometrically contracting papil- holic patients without clinical evi- stracted. Clin Res 16:249, 1968.

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