Effects of aging on left ventricular structure and function.

To better characterize the cardiac structural and functional changes that are associated with aging, Doppler-echocardiography was performed on 23 young (mean age, 25 years) and 30 old (mean age, 70 years) healthy normotensive subjects. Left ventricular cavity dimensions and wall thickness were determined and left ventricular mass index was calculated from M-mode echocardiograms. Stroke volume was calculated from Doppler-measured aortic flow. Diastolic filling was evaluated by pulsed Doppler echocardiography of mitral inflow. Posterior wall thickness (1.0 vs 0.8 cm, p less than 0.05) and relative wall thickness (0.42 vs 0.35, p less than .05) were significantly greater in the elderly subjects compared with the younger subjects. Left ventricular mass index increased on average 0.25 gm/m2/yr but was not significantly increased in the elderly compared with the younger subjects (89 vs 77 gm/m2). Shortening fraction and stroke volume did not differ between the two groups. Diastolic filling was dramatically altered with aging, and the elderly subjects demonstrated a doubling of percent atrial contribution (37% vs 19%, p less than 0.0001) and halving of peak early-to-peak atrial velocity ratio (0.85 vs 1.77, p less than .01).

Increases in coronary vein CO2 during cardiac resuscitation.

We investigated the aortic, mixed venous, and great cardiac vein acid-base changes in eight domestic pigs during cardiac arrest produced by ventricular fibrillation and during cardiopulmonary resuscitation (CPR). The great cardiac vein PCO2 increased from a control value of 52 +/- 2 to 132 +/- 28 (SD) Torr during CPR, whereas the arterial PCO2 was unchanged (39 +/- 4 vs. 38 +/- 4). The coronary venoarterial PCO2 gradient, therefore, increased remarkably from 13 +/- 2 to 94 +/- 29 Torr. The simultaneously measured great cardiac vein lactate concentrations increased from 0.24 +/- 0.06 to 7.3 +/- 2.34 mmol/l. Much more moderate increases in the lactate content of aortic blood from 0.64 +/- 0.25 to 2.56 +/- 0.27 mmol/l were observed. Increases in great cardiac vein PCO2 and lactate were highly correlated during CPR (r = 0.91). After successful CPR, the coronary venoarterial PCO2 gradient returned to normal levels within 2 min after restoration of spontaneous circulation. Lactate content was rapidly reduced and lactate extraction was reestablished within 30 min after CPR. These studies demonstrate marked but reversible acidosis predominantly as the result of myocardial CO2 production during CPR.

Mechanism of blood flow generated by precordial compression during CPR. I. Studies on closed chest precordial compression.

The mechanism of forward flow produced by precordial compression during CPR was investigated with the aid of echocardiographic and hemodynamic measurements in anesthetized, mechanically ventilated domestic pigs. Both mitral and tricuspid valves opened during compression diastole and closed during compression systole. Valve motion persisted throughout resuscitation in 17 of 22 animals which were hemodynamically resuscitated. There was a 25 percent reduction in left ventricular area during compression systole. Maximum pressure generated during compression systole in the aorta exceeded that of the right atrium throughout the 12-min interval of precordial compression in successfully resuscitated animals. These observations provide evidence of direct cardiac compression as the mechanism accounting for effective forward blood flow during CPR. The persistence of valve function, chamber compression, and pressure gradients during precordial compression was predictive of successful resuscitation. The absence of these factors prognosticates failure of resuscitation and explains, in part, the inconsistency of prior reports.

Impaired coronary vasodilator reserve in the immediate postcoronary angioplasty period: analysis of coronary artery flow velocity indexes and regional cardiac venous efflux.

The ratio of peak hyperemic/basal mean coronary flow velocity, an index of coronary vasodilator reserve, immediately after coronary angioplasty normalizes in less than 50% of patients. To evaluate other indexes of coronary vasodilator capacity, both intracoronary arterial velocity and cardiac venous efflux were measured at rest and during vasodilator-induced coronary hyperemia (intracoronary nitroglycerin and papaverine) before and after angioplasty in 27 patients; 17 patients had measurements of intracoronary velocity alone and 10 had thermodilution measurements of great cardiac vein flow. Coronary flow velocity responses were also measured in 6 angiographically normal segments in patients undergoing angioplasty and in 10 normal left coronary artery segments in patients with normal coronary arteries or isolated right coronary artery disease. Despite significant angiographic (72 +/- 12 to 23 +/- 11% diameter narrowing) and hemodynamic (49 +/- 12 to 19 +/- 12 mm Hg aortocoronary gradient) improvement, coronary vasodilator reserve ratios for both arterial velocity and venous flow after angioplasty were only minimally affected. Angioplasty did not significantly increase rest coronary vein flow or artery flow velocities, but did result in significantly higher papaverine responses after angioplasty. Mean and phasic coronary velocity, diastolic coronary flow velocity integral and measured great cardiac vein flow ratios were significantly lower when compared with those in 16 angiographically normal coronary artery segments. These data indicate that maximal hyperemic coronary flow velocity is increased after angioplasty, but the reserve ratios, calculated by any of several flow velocity indexes, remain minimally improved. Angiographic correlations (percent coronary diameter, absolute diameter or cross-sectional area) with variables of coronary blood flow or velocity suggest that no single variable is useful in assessing angioplasty results. However, postangioplasty arterial mean velocity and diastolic flow velocity integral are nearly normalized in most patients, whereas relative changes remain attenuated. These findings are important in studies assessing coronary vasomotor responses in patients with atherosclerotic coronary disease, especially after angioplasty.

Systolic and diastolic flow abnormalities in elderly patients with hypertensive hypertrophic cardiomyopathy.

Seventeen patients with clinical and echocardiographic features of hypertensive hypertrophic cardiomyopathy of the elderly were studied to more completely characterize left ventricular systolic and diastolic function in this group. Measurements of left ventricular structure and systolic and diastolic function were made in the study patients and compared with those of age-matched control subjects. The study group had significantly greater left ventricular mass, wall thickness, shortening fraction and relative wall thickness than did the control subjects. Left ventricular end-diastolic dimension was smaller and left atrial size was not different in study patients compared with control subjects. Left ventricular filling was characterized by an increased peak atrial velocity and reduced ratio of peak early to peak atrial velocity in the study group. Left ventricular outflow velocities were elevated in 14 of the 17 study patients with peak velocities ranging from 1.2 to 5.0 m/s corresponding to a peak intraventricular gradient of 16 to 100 mm Hg. The velocity waveforms in these patients were late-peaking, similar to those described in hypertrophic obstructive cardiomyopathy. The elevated velocities were localized to the left ventricular outflow tract. These findings imply a pathophysiologic state in these elderly patients with long-standing hypertension, very similar to that in hypertrophic obstructive cardiomyopathy, and provide further support for the use of pharmacologic agents with negative inotropic properties or positive lusitropic properties in this group.

Expired carbon dioxide: a noninvasive monitor of cardiopulmonary resuscitation.

End-tidal CO2 concentration (ETCO2) may serve as a simple noninvasive measurement of the blood flow generated by precordial compression during cardiopulmonary resuscitation (CPR). In a mechanically ventilated porcine preparation of ventricular fibrillation, onset of fibrillation was associated with a rapid decrease in ETCO2 from 4.0 +/- 0.2% to less than 0.7 +/- 0.2%. With precordial compression, it increased to 1.9 +/- 0.3%. Animals that were successfully defibrillated after 12 min of CPR demonstrated an immediate increase in ETCO2. The ETCO2 increased from 1.9 +/- 0.3% to 4.9 +/- 0.3% over an interval of between 30 and 60 sec. These changes in ETCO2 were closely related to proportionally similar decreases and increases in cardiac output (CO), and a close correlation between ETCO2 and CO was demonstrated (r = .92). A similar highly significant correlation between ETCO2 and CO was also demonstrated during open-chest cardiac massage (r = .95). ETCO2 therefore serves as a noninvasive measure of pulmonary blood flow and therefore CO. In 17 successfully resuscitated animals. ETCO2 during precordial compression averaged 1.7 +/- 0.2%, whereas it was only 0.5 +/- 0.1% in five animals in whom resuscitation procedures were unsuccessful (p less than .001). Accordingly, ETCO2 prognosticates outcome during CPR and immediately identifies restoration of spontaneous circulation.