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Cardiac arrhythmias and sudden sniffing deaths
ABSTRACTS
optimal and the survived months These in acute agement
PAEDP for this patient was 18 to 22 mm Hg cardiac output 4.5-5.0 liters/min. The patient and underwent resection of an akinetic area 4 later. studies indicate that hemodynamic monitoring myocardial infarction is beneficial in the manof heart failure and shock.
Microscopy of Myocardium from the Left Ventricular Outflow Tract of Patients with Hypertrophic Obstructive Cardiomyopathy VICTOR J. FERRANS, MD, PhD; ANDREW J. MORROW, MD, FACC; WlLLlAM C. ROBERT’S, MD, FACC, Bethesda, Maryland
Electron microscopic studies of surgically resected myocardium from the left ventricular outflow tract in 11 patients with hypertrophic obstructive cardiomyopathy (idiopathic hypertrophic subaortic stenosis) disclosed severe hypertrophy and focal interstitial fibrosis in each patient. The nuclei of the muscle cells were enlarged, with marginated chromatin, prominent nucleoli and bizarre infoldings of the nuclear membranes. The sarcoplasmic reticulum was normal in many areas, slightly dilated in others. Increased numbers of ribosomes, both free and attached to membranes of sarcoplasmic reticulum, were present in perinuclear zones. The amount of glycogen in muscle cells varied greatly. Many muscle cells showed abnormal orientation of myofibrils, some of which followed irregularly oblique courses through the cells. In all patients the Z bands of myofibrils frequently showed abnormalities characterized by increased width and by the formation of extensions of Z band material into adjacent regions of the sarcomeres. These Z band abnormalities were similar to, but less advanced than, those observed by Bishop in right ventricular myocardium after constriction of the pulmonary trunk. Basophilic degeneration of muscle cells was found by light microscopy in 2 patients ; in 1, electron microscopy showed that the basophilic deposits consisted of fibrils, 50 A in diameter, associated with granules 200 A in diameter. No evidence was observed to support Pearse’s concept that muscle cells in the hypertrophied outflow tract resemble those of atria1 myocardium or sinoatrial node.
Cardiac Arrhythmias and Sudden Sniffing Deaths NANCY C. FLOWERS, Augusta, Georgia
MD,
FACC; LEO G. HORAN,
MD,
FACC,
Since 1960 there has been an increasing number of almost instantaneous deaths reported in teenagers sniffing various volatile hydrocarbons. It has become obvious that sudden deaths are not the result of suffocation but are far more likely to be due to cardiac arrhythmias. The following study was undertaken in an attempt to elucidate such mechanisms. Eleven mongrel dogs were anesthetized with 30 mg/ kg of intravenously administered pentobarbital and
VOLUME
26, DECEMBER
1970
intubated. From the beginning of each experiment high speed, high frequency electrocardiographic leads II, Vi-V, and 3 intracardiac leads were recorded on magnetic tape. The intracardiac leads were recordings from the bundle of His and right bundle branch. Arterial blood gases and respiration were monitored. The dogs were allowed to breathe 1 of 3 aerosols, 2 of which used halogenated hydrocarbons as their propellants. Significant hypoxia or acidosis was not allowed to occur. Of the 11 animals, ventricular fibrillation occurred in 1 from improper pacing ; 1 was allowed to inhale an agent from which the halogenated hydrocarbon had been removed, and it showed no rhythm disturbance except a mild sinus tachycardia. A third animal was hyperoxygenated deliberately; a ~0~ of 320 mm developed, but alterations of rhythm did not occur. In all of the 8 remaining animals evidence of sinus node suppression developed within seconds to minutes of aerosol inhalation. This was manifested by profound sinus bradycardia followed by a His bundle escape rhythm and subsequent atrioventricular (A-V) dissociation. In no instance was any degree of A-V block seen. Manifestations of hyperirritability in the form of premature beats were confined to terminal events and never were the initial mechanism.
Rapid Assessment of Cardiopulmonary Hemodynamics in Acutely III Patients Utilizing a Single Right Heart Catheter JAMESS. FORRESTER, MD; THOMAS J. MCHUGH, MD; GEORGE DIAMOND, MD; RAVI PRAKASH, MD; WILLIAM GANZ, MD; H. J. C. SWAN, MD, PhD, FACC, Los Angeles, California
Serial measurement of pulmonary capillary wedge pressure, pulmonary arterial pressure, mixed venous oxygen saturation, central venous pressure and cardiac output was accomplished in 12 critically ill patients, 10 with acute myocardial infarction, utilizing a triple lumen catheter with a thermistor embedded at its tip. This complete panel of measurements was obtained within 3 minutes and did not require use of fluoroscopy or catheter manipulation. In addition to establishing baseline hemodynamic values and evaluating the response to drugs, the catheter aided in the diagnosis of (1) unsuspected ventricular septal defect, by simultaneous measurement of right atria1 and pulmonary oxygen saturation; (2) severe mitral insufficiency, by presence of a giant V wave in the pulmonary capillary wedge pressure tracing; (3) absence of suspected pericardial effusion, by right atria1 CO, contrast study; (4) “preclinical left ventricular failure” by increased pulmonary capillary wedge pressure in the absence of rales or abnormal chest roentgenogram ; (5) hemodynamic response to cardioversion by cardiac output, pulmonary capillary wedge pressure and pulmonary arterial pressure determinations before and after conversion of atria1 fibrillation to normal sinus rhythm. The average time for passage of catheter from the right atrium to the pulmonary artery was less than 1 minute. Neither catheter passage nor long-term placement of the catheter resulted in any significant complications.
633
optimal and the survived months These in acute agement
PAEDP for this patient was 18 to 22 mm Hg cardiac output 4.5-5.0 liters/min. The patient and underwent resection of an akinetic area 4 later. studies indicate that hemodynamic monitoring myocardial infarction is beneficial in the manof heart failure and shock.
Microscopy of Myocardium from the Left Ventricular Outflow Tract of Patients with Hypertrophic Obstructive Cardiomyopathy VICTOR J. FERRANS, MD, PhD; ANDREW J. MORROW, MD, FACC; WlLLlAM C. ROBERT’S, MD, FACC, Bethesda, Maryland
Electron microscopic studies of surgically resected myocardium from the left ventricular outflow tract in 11 patients with hypertrophic obstructive cardiomyopathy (idiopathic hypertrophic subaortic stenosis) disclosed severe hypertrophy and focal interstitial fibrosis in each patient. The nuclei of the muscle cells were enlarged, with marginated chromatin, prominent nucleoli and bizarre infoldings of the nuclear membranes. The sarcoplasmic reticulum was normal in many areas, slightly dilated in others. Increased numbers of ribosomes, both free and attached to membranes of sarcoplasmic reticulum, were present in perinuclear zones. The amount of glycogen in muscle cells varied greatly. Many muscle cells showed abnormal orientation of myofibrils, some of which followed irregularly oblique courses through the cells. In all patients the Z bands of myofibrils frequently showed abnormalities characterized by increased width and by the formation of extensions of Z band material into adjacent regions of the sarcomeres. These Z band abnormalities were similar to, but less advanced than, those observed by Bishop in right ventricular myocardium after constriction of the pulmonary trunk. Basophilic degeneration of muscle cells was found by light microscopy in 2 patients ; in 1, electron microscopy showed that the basophilic deposits consisted of fibrils, 50 A in diameter, associated with granules 200 A in diameter. No evidence was observed to support Pearse’s concept that muscle cells in the hypertrophied outflow tract resemble those of atria1 myocardium or sinoatrial node.
Cardiac Arrhythmias and Sudden Sniffing Deaths NANCY C. FLOWERS, Augusta, Georgia
MD,
FACC; LEO G. HORAN,
MD,
FACC,
Since 1960 there has been an increasing number of almost instantaneous deaths reported in teenagers sniffing various volatile hydrocarbons. It has become obvious that sudden deaths are not the result of suffocation but are far more likely to be due to cardiac arrhythmias. The following study was undertaken in an attempt to elucidate such mechanisms. Eleven mongrel dogs were anesthetized with 30 mg/ kg of intravenously administered pentobarbital and
VOLUME
26, DECEMBER
1970
intubated. From the beginning of each experiment high speed, high frequency electrocardiographic leads II, Vi-V, and 3 intracardiac leads were recorded on magnetic tape. The intracardiac leads were recordings from the bundle of His and right bundle branch. Arterial blood gases and respiration were monitored. The dogs were allowed to breathe 1 of 3 aerosols, 2 of which used halogenated hydrocarbons as their propellants. Significant hypoxia or acidosis was not allowed to occur. Of the 11 animals, ventricular fibrillation occurred in 1 from improper pacing ; 1 was allowed to inhale an agent from which the halogenated hydrocarbon had been removed, and it showed no rhythm disturbance except a mild sinus tachycardia. A third animal was hyperoxygenated deliberately; a ~0~ of 320 mm developed, but alterations of rhythm did not occur. In all of the 8 remaining animals evidence of sinus node suppression developed within seconds to minutes of aerosol inhalation. This was manifested by profound sinus bradycardia followed by a His bundle escape rhythm and subsequent atrioventricular (A-V) dissociation. In no instance was any degree of A-V block seen. Manifestations of hyperirritability in the form of premature beats were confined to terminal events and never were the initial mechanism.
Rapid Assessment of Cardiopulmonary Hemodynamics in Acutely III Patients Utilizing a Single Right Heart Catheter JAMESS. FORRESTER, MD; THOMAS J. MCHUGH, MD; GEORGE DIAMOND, MD; RAVI PRAKASH, MD; WILLIAM GANZ, MD; H. J. C. SWAN, MD, PhD, FACC, Los Angeles, California
Serial measurement of pulmonary capillary wedge pressure, pulmonary arterial pressure, mixed venous oxygen saturation, central venous pressure and cardiac output was accomplished in 12 critically ill patients, 10 with acute myocardial infarction, utilizing a triple lumen catheter with a thermistor embedded at its tip. This complete panel of measurements was obtained within 3 minutes and did not require use of fluoroscopy or catheter manipulation. In addition to establishing baseline hemodynamic values and evaluating the response to drugs, the catheter aided in the diagnosis of (1) unsuspected ventricular septal defect, by simultaneous measurement of right atria1 and pulmonary oxygen saturation; (2) severe mitral insufficiency, by presence of a giant V wave in the pulmonary capillary wedge pressure tracing; (3) absence of suspected pericardial effusion, by right atria1 CO, contrast study; (4) “preclinical left ventricular failure” by increased pulmonary capillary wedge pressure in the absence of rales or abnormal chest roentgenogram ; (5) hemodynamic response to cardioversion by cardiac output, pulmonary capillary wedge pressure and pulmonary arterial pressure determinations before and after conversion of atria1 fibrillation to normal sinus rhythm. The average time for passage of catheter from the right atrium to the pulmonary artery was less than 1 minute. Neither catheter passage nor long-term placement of the catheter resulted in any significant complications.
633