J. Michael Criley

Coronary Perfusion Pressure During Experimental Cardiopulmonary Resuscitation

Systemic blood flow during cardiopulmonary resuscitation may result from alterations in intrapleural pressure (IPP), with the heart serving only as a passive conduit. Chest compression with simultaneous lung inflation (C + SI) or with abdominal binding may also increase vascular pressures and cerebral flow. Our study was done to evaluate the effects of C + SI with and without abdominal binding on coronary perfusion pressure (CPP) during CPR. Micromanometric pressures were recorded in 7 dogs during ventricular fibrillation (VF) and CPR to evaluate CPP (aortic minus right atrial pressure). During chest compression alone, aortic (AoP) and right atrial (RAP) pressures did not differ significantly. During relaxation, AoP (15 +/- 4 mm Hg) was greater than RAP (3 +/- 2 mm Hg; P less than 0.001) and diastolic CPP averaged 12 +/- 4 mm Hg. C + SI significantly increased AoP, RAP, and IPP, but did not improve systolic or diastolic CPP. Tight abdominal binding during chest compression alone or during C + SI also increased AoP and RAP and caused a slight but insignificant decrease in diastolic CPP. Extravascular resistance to coronary flow during VP has been shown to average 28 mm Hg in the in vitro heart. Our study indicates that CPPs calculated during CPR do not reach sufficient values to overcome the resistance offered by the fibrillating myocardium. Interventions which increase IPP, intravascular pressures, and carotid flow do not improve CPP or, by inference, coronary flow.

Mechanical “cough” cardiopulmonary resuscitation during cardiac arrest in dogs

Hemodynamic findings during ventricular fibrillation (VF) and closed-chest cardiopulmonary resuscitation (CPR) are similar to those described during VF and vigorous coughing. Interventions during CPR that mimic the physiologic events of coughing (high intrathoracic pressure and high intraabdominal pressure) improve perfusion during VF and CPR. An external circulatory assist apparatus was devised to emulate cough physiology, i.e., simultaneous pulsatile increases in intrathoracic pressure (pneumatic vest), intraabdominal pressure (abdominal binder) and airway pressure (high-pressure airway inflation). In this study, vest/binder CPR was compared with conventional CPR during 30 minutes of VF and artificial support in 18 randomized dogs. Defibrillation and long-term (more than 24 hours) survival were chosen as end points. During VF and artificial support, aortic and right atrial (RA) pressures, the instantaneous aortic-RA pressure difference (coronary perfusion pressure) and blood gas levels were measured. After 30 minutes of VF and administration of 1 mg of epinephrine, countershock was attempted. Systolic aortic and RA pressures, mean aortic-RA pressure difference and blood gas levels were not significantly different between dogs that were successfully resuscitated and those that were not. However, peak diastolic coronary perfusion pressure (peak diastolic aortic-RA pressure) for survivors averaged 23 +/- 6 mm Hg, but only 6 +/- 10 mm Hg for nonsurvivors (p less than 0.001). A peak diastolic coronary perfusion pressure 16 mm Hg or greater had a positive and negative predictive value for a successful outcome of 1.00. Only 1 of 9 conventional CPR dogs survived 24 hours; 7 of 9 dogs supported with the vest/binder device were alive and neurologically normal at 24 hours (p = 0.007).(ABSTRACT TRUNCATED AT 250 WORDS)

Asystole and its treatment: The possible role of the parasympathetic nervous system in cardiac arrest

Parasympathetic tone may be high during ventricular asystole because of reflex vagal stimulation from a number of sources. Eight patients in cardiac arrest were treated with cardiopulmonary resuscitation. All eight patients had ventricular asystole as the initial rhythm or as the result of defibrillation. Six patients failed to respond to 5 cc to 20 cc of 1:10,000 epinephrine intravenously (IV). In all eight cases a regular rhythm (sinus in seven, idioventricular in one) appeared within 30 seconds of administration of the last dose of atropine (1 mg to 2 mg IV). Five patients (62.5%) lived 12 hours, three (37.5%) were discharged from the hospital. These results suggest that atropine may be of value in the treatment of ventricular asystole.

Natural History of Tricuspid Valve Endocarditis: A Two Dimensional Echocardiographic Study

Sixteen patients with tricuspid valve endocarditis were studied to define (1) what clinical or echocardiographic subsets are at risk for complications or need for tricuspid valve surgery, and (2) the long-term two dimensional echocardiographic course of tricuspid vegetations. There were 18 episodes of tricuspid endocarditis in the 16 patients; 12 patients had a history of intravenous drug abuse. Staphylococcus aureus was the most common infecting organism (11 patients). Persistent infection, cardiomegaly or radiography and right-sided heart failure were present in all patients undergoing tricuspid valve surgery and in none of the medically treated patients. Echocardiographic studies demonstrated tricuspid vegetations in 10 patients by M mode and in all 16 by two dimensional technique. Vegetation size, right ventricular enlargement and abnormal septal motion were not of prognostic significance. Two dimensional echocardiographic measurements of vegetation size correlated with surgical pathologic measurements in the four patients who underwent surgery. Serial two dimensional echocardiographic studies were available in eight patients a mean of 10.6 (range 2 to 19.5) months after the initial study: Vegetations had decreased in size or disappeared in seven patients and were essentially unchanged in one patient. It is concluded that (1) two dimensional echocardiography increases the detection of tricuspid valve vegetations and accurately estimates their size; (2) persistent infection, cardiomegaly and right-sided heart failure identify a subgroup of patients with tricuspid endocarditis who may have increased risk; (3) no M mode or two dimensional echocardiographic feature is a predictor of outcome; and (4) tricuspid valve vegetations tend to resolve with time.

Hemodynamic effects of continuous abdominal binding during cardiac arrest and resuscitation

Abdominal binding improves arterial pressure and flow during cardiopulmonary resuscitation (CPR). This study was undertaken to assess the mechanisms of improved hemodynamics during cardiac arrest and CPR with continuous abdominal binding in a canine model (n = 8). Carotid and inferior vena caval (IVC) flow probes and cineangiography were used to observe magnitude and direction of blood flow. CPR with binding significantly increased (p < 0.001) systolic aortic (Ao) (49 ± 11 vs 34± 12mm Hg), right atrial (RA) (49 ± 11 vs 31 ± 10 mm Hg) and IVC pressure (50 ± 7 versus 31 ± 11 mm Hg) and common carotid flow (1.1 ± 0.4 vs 0.7 ± 0.4 ml/min/kg, p < 0.05) compared with CPR without binding. Aortic, RA and IVC diastolic pressures increased similarly. Binding decreased the diastolic Ao-IVC pressure difference by 8 ± 12 mm Hg and decreased net IVC flow (0.5 ± 1.4 vs 1.4 ± 1.2 ml/min/kg, p < 0.05). Binding also decreased coronary perfusion pressure (Ao-RA) in 5 of 8 dogs. Cineangiograms showed tricuspid incompetence and reflux from the right atrium to the inferior vena cava during chest compression and IVC-to-right heart inflow during relaxation, which was confirmed by the flowmeter data. Abdominal binding during CPR decreased the size of the perfused vascular bed by inhibiting subdiaphragmatic flow and increased intrathoracic pressure for a given chest compression force, leading to preferential cephalad flow. However, coronary perfusion pressure was often adversely affected. Further studies should be undertaken before the widespread clinical application of continuous abdominal binding during CPR.

Intermittent Severe Mitral Regurgitation

Abstract Cardiac catheterization in a patient with episodic pulmonary edema, a systolic murmur of varying intensity and normal heart size revealed a transient precipitous elevation of left atrial and ventricular pressures. The magnitude and contour of the left atrial and diastolic left ventricular pressure tracings resembled those seen in acute severe mitral regurgitation. The pressures returned to normal, and the murmur disappeared after sublingual administration of isosorbide dinitrate. Left ventricular cineangiography, performed when the patient was asymptomatic and pressures were normal, revealed minimal mitral regurgitation, left ventricular dyskinesis and no angiographic evidence of structural derangement of the mitral valve. The patient was concluded to have intermittent severe functional mitral regurgitation (papillary-muscle dysfunction) related to ischemic heart disease. On medical management, consisting of digitalis and isosorbide dinitrate, he has remained essentially asymptomatic over the sub...

Main pulmonary artery distention: A potential mechanism for acute pulmonary hypertension in the human newborn infant

Balloon-induced distention of the main pulmonary artery causes acute pulmonary hypertension and reflex pulmonary vasoconstriction in animals. Pulmonary artery pressure responses caused by MPA balloon inflation were measured in ten human newborn infants with cardiac failure (n = 5) or persistent fetal circulation (n = 5). During balloon inflation distal mean PAP increased significantly while cardiac rate remained unchanged. MPA distention caused greater increases of PAP in those infants with lower resting PAP. The greatest balloon-induced increases of PAP were observed in infants recovering from PFC. The existence of a pulmonary artery reflex and its possible role in the regulation of the human fetal and neonatal pulmonary circulation is discussed.

Postmyocardial infarction angina and coronary spasm

Coronary spasm can cause chest pain, and may even culminate in a myocardial infarction, but it is not often considered a cause of chest pain in the early postinfarction period. Three patients who had chest pain early (1 day to 3 weeks) after myocardial infarction were shown to have coronary spasm with ergonovine maleate provocation. Two patients had spasm in the coronary artery associated with the acute infarction; the third had spasm in a remote vessel. Two required intracoronary nitroglycerin to establish patency in the affected vessel. It is concluded that coronary vasospasm can result in postinfarction angina.

The Crescendo Presystolic Murmur of Mitral Stenosis with Atrial Fibrillation

Abstract A crescendo presystolic murmur was recorded in four patients with mitral stenosis and atrial fibrillation. Hemodynamic and cineangiographic data support the contention that this crescendo ...

Evaluation of left ventricular function (ejection fraction and segmental wall motion) by single pass radioisotope angiography

Changes in ejection fraction (EF) and segmental wall motion (SWM) have been shown to be sensitive indicators of left ventricular (LV) function. This information is only obtainable by contrast angiography or gated blood pool scans. Gated studies assume a fixed geometry for the LV for EF determinations, are lengthy and limited primarily to the LAO projection. We correlated contrast and Tc-99m pertechnetate angiograms by singl pass radioisotope angiography (immediately preceding the contrast study) in 12 patients. EF was calculated from the LV time/activity curve and values ranged from .21 to .72. Angiographic correlation yielded r = 0.97. Regional LV wall motion was evaluated by dividing a summated cardiac cycle into 16 frames and dynamically and sequentially displaying these frames. Regional wall motion evaluation of four LV quadrants correlated well with angiography (r = 0.97). For quantitation these images were divided into four anterior and four inferior segments and the areas of respective segments were compared and expressed as a shortening fraction. SWM compared favorably with angiographic determinations (r ranged from 0.70 to 0.99). Thus, single pass radioisotopic determinations of EF and SWM in the RAO projection correlated well with the angiographic values and provide essential quantitative information of LV function otherwise unobtainable at the bedside.