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Biomedical subjects

C W Zwillich

Publications and source records attributed to C W Zwillich.

At least 91 records · Page 5Linked to original sources
PubMed1978

Thyrotoxicosis: comparison of effects of thyroid ablation and beta-adrenergic blockade on metabolic rate and ventilatory control.

To elucidate the role of the beta-sympathetic system in thyrotoxicosis (THY), we examined cardiac sensitivity to infused beta-agonist and compared the effect of beta-blockade with that of resolution of the hyperthyroid state. Beta-sympathetic (beta-SYM) sensitivity was measured as the heart rate response to isoproterenol in THY patients and in normal subjects. The patients with THY showed both lower threshold (P less than 0.05) and increased slope (P less than 0.05) of the heart rate-isoproterenol response, suggesting beta-SYM hypersensitivity. The beta-SYM like features of THY were measured in 7 patients before and 7 days after beta-SYM blockade with propranolol (mean dose 411 +/- 32 mg/day [SEM]) which was shown to block the heart rate response to isoproterenol. These results were compared with those in a similar group of thyrotoxic patients rendered euthyroid with 131I. During beta-SYM blockade, heart rate decreased from 101 +/- 6.3 to 78 +/- 4.6 (P less than 0.01), but the elevated metabolic rate (V02), resting ventilation (VE), and increased hypoxic and hypercapnic ventilatory responses were not significantly affected. In the group rendered euthyroid with 131I, heart rate decreased from 110 +/- 3.5 to 76 +/- 7.8 (P less than 0.02), but in contrast to the result of beta-SYM blockade, a 28% decrease in VO2 (P less than 0.01), 41% decrease in VE (P less than 0.05), a 38% decrease in hypercapnic ventilatory response (P less than 0.05), and a 66% decrease in hypoxic response (P less than 0.03) occurred. During THY, beta-SYM mechanisms are responsible for part of the tachycardia, but the metabolic and ventilatory abnormalities are not beta-SYM mediated.

Adult↗
PubMed1978

Effects of progesterone on chemosensitivity in normal men.

Progesterone administration increase VE in man, but its effects on ventilatory response to hypercapnia and hypoxia have not been well documented. Accordingly, VE, HVR, and HCVR were measured during placebo and MPA administration in 11 normal men. The effect of MPA (20 mg orally q 8 hr for 32 hr) on T degrees, metabolic rate (VO2 and VCO2) was also determined. With MPA, T degrees, rose 0.4 degrees C +/- 0.0008 (S.E.M.) p less than 0.0001), VE increased 0.46 +/- 0.16 L/min (p less than 0.01), and VO2 and VCO2 did not change significantly. HCVR (measured under hyperoxic conditions during rebreathing) increased significantly (P less than 0.01) from 2.9 +/- 0.33 L/min/mm Hg (placebo) to 4.0 +/- 0.29 (MPA). HVR was measured as the shape parameter A, so that when A increased, HVR was augmented. During MPA, HVR increased from A = 132 +/- 19.1 to 179 +/- 20.5 (P less than 0.02). We conclude that 60 mg of MPA daily in normal men increases VE and chemosensitivity as measured by the ventilatory response to hypercapnia and hypoxia.

Adult↗
PubMed1978

The obesity-hypoventilation syndrome.

The triad of obesity, hypoventilation and inordinate hypersomnolence characterizes the obesity-hypoventilation syndrome. The reasons for daytime hypoventilation appear related to decreased chemical drives to breathe combined with the added physical impediment of extreme obesity. When the physiology of sleep was investigated in patients with this syndrome, intermittent nocturnal obstructive apneas were documented that produced blood gas abnormalities, arrhythmias and serious elevations of both pulmonary and systemic pressures. The obstructive apneas are due to intermittent loss of muscle tone of the tongue resulting in its prolapse against the posterior pharynx. The special importance of the obesity-hypoventilation syndrome lies in its being an example of a disorder of sleep and breathing that can appear in widely different clinical settings. Therapeutic measures include weight loss, progestational agents or permanent tracheostomy.

Apnea↗
PubMed1977

Effects of hypermetabolism on ventilation and chemosensitivity.

Muscular exercise is associated with hypermetabolism and increased hypoxic ventilatory response (HVR). In order to dissociate mechanical and metabolic factors, the effect of hypermetabolism on hypoxic ventilatory response was evaluated at rest. Carbohydrate and protein feeding increases metabolic rate, and their effects on chemosensitivity, ventilation, and blood pH were evaluated in six normal subjects 2 h and 3 h after calorically equal test meals (1,000 cal). After carbohydrate, base-line oxygen consumption (Vo(2)) increased from 237+/-11.3 ml/min (SEM) to 302+/-19.4 (P < 0.001) and 303+/-18.5 (P < 0.001) at 2 h and 3 h, respectively. Hypoxic ventilatory response, measured as shape parameter A, increased from a control of 144+/-11.8 to 330+/-61.0 (P < 0.01) at 2 h and 286+/-57.0 (P < 0.05) at 3 h. These changes were associated with a mild metabolic acidosis as pH decreased from a control of 7.402+/-0.004 to 7.371+/-0.009 (P < 0.005) at 2 h and 7.377+/-0.008 (P < 0.005) at 3 h. After protein, Vo(2) increased from 241+/-6.7 to 265+/-6.2 (P < 0.02) and 270+/-5.4 (P < 0.001), an overall increase less than that which occurred after carbohydrate (P < 0.01). Hypoxic ventilatory response increased from 105+/-14.5 to 198+/-24.3 (P < 0.02) at 2 h and 219+/-17.3 (P < 0.01) at 3 h, which was not different from the increase with carbohydrate. After protein, no acidosis occurred. Thus, after protein, HVR increased despite the absence of a systemic acidosis. We conclude that both carbohydrate and protein feedings are associated with resting hypermetabolism and increased HVR compared with the fasting state. For both meals, increased metabolic rate was correlated with increased hypoxic response.

Adult↗
PubMed1977

Ventilatory response in myotonic dystrophy.

Patients with myotonic dystrophy often develop respiratory failure caused by alveolar hypoventilation. Abnormalities in the ventilatory response to hypoxia and hypercapnia may explain this phenomenon. Accordingly, hypoxic and hypercapnic responses were measured in seven patients with myotonic dystrophy who had only mild respiratory muscle weakness. Hypoxic response was significantly reduced, while hypercapnic response was affected more irregularly. It is possible that the high incidence of respiratory failure in such patients is related to decreased hypoxic ventilatory response, occurring because of an underlying neurogenic deficit.

Adult↗
PubMed1977

Effects of hyperthermia on hypoxic ventilatory response in normal man.

Increased body temperature stimulates hyperventilation in man but little is known about its effects on ventilatory responsiveness to hypoxia. Hence this study examined the effects of hyperthermia on hypoxic ventilatory response (HVR), hypercapnic ventilatory response (HCVR), and oxygen consumption (VO2). Six fasting subjects had these variables measured under basal conditions and at two levels of hyperthermia. Hypoxic ventilatory response was measured as the shape paramater A of the VE/PAO2 curves. Since hyperthermia produces hyperventilation and, therefore, hypocapnia, HVR was measured at the hyperthermic (hypocapnic alveolar CO2 tension (PACO2) and at the basal (normothermic) PACO2. Hypoxic ventilatory response (A) increased when measured at basal PACO2 levels, from 113 +/- 8.8 (S.E.M.) to 189 +/- 21.8 at 0.7 degrees C. and 240 +/- 34.0 at + 1.40 degrees C. (P less than 0.005). HVR measured during hyperthermic hypocapnia also increased at each temperature level but did not reach statistical significance (P = 0.1). Hypercapnic ventilatory response, as measured by the slope S of VE/PACO2 lines, increased significantly at each temperature elevation (P less than 0.025). We conclude that raising body temperature causes a significant augmentation of ventilatory responses to hypoxia (during normothermic PACO2 conditions) and to hypercapnia.

Adult↗
PubMed1976

Respiratory failure associated with familial depression of ventilatory response to hypoxia and hypercapnia.

Respiratory failure has been associated with depressed ventilatory responses to hypoxia or hypercapnia or both. The possibility that familial factors are responsible for decreased chemosensitivity prompted this study of a child with unexplained respiratory failure and normal lung function. We found his ventilatory response to hypoxia and hypercapnia to be virtually absent. Studies of six healthy immediate family members (parents and siblings) showed that hypoxic response, as measured by an index of the relation between ventilation and hypoxia (index A), was consistently reduced: 45 +/- 8.7 S.E.M. (normal, 127 +/- 8.7) (P less than 0.005). Response to hypercapnia, measured as the slope of the ventilatory response to hypercapnia, was lower than normal, averaging 0.95 +/- 0.16 liters per minute per millimeter of mercury (normal, 1.76 +/- 0.13) (P less than 0.01). The patient's respiratory failure seemed related to deficient ventilatory responses to hypoxia and hypercapnia. It seems likely that this depressed hypoxic response is of familial origin.

Adolescent↗
PubMed1976

Clinical semi-starvation: depression of hypoxic ventilatory response.

A decreased metabolic rate has been associated with decreased ventilatory response to hypoxia and hypercapnia, and also with starvation. We fed a 500-calorie carbohydrate diet with supplemental electrolytes, designed to simulate alimentation by usual intravenous fluids, to seven normal subjects for 10 days to determine the effect of semi-starvation on metabolic rate and ventilatory responses. By the 10th day metabolic rate was significantly decreased, and hypoxic ventilatory response decreased to 42% of control (P less than 0.05). In two subjects, hypoxic ventilatory response was virtually abolished at day 10. These changes reversed toward normal with refeeding. The decrease in hypoxic ventilatory response response was significantly (P less than 0.01) related to the decrease in metabolic rate. Hypercapnic ventilatory response, measured as the slope of the ventilatory response to hypercapnia, decreased slightly but not significantly. The decrease in hypoxic ventilatory response seen during semi-starvation may contribute to the hypoxemia and respiratory failure subsequent to caloric restriction.

Adult↗
PubMed1976

Effects of hypocapnia and hypocapnic alkalosis on cardiovascular function.

Cardiovascular effects of hypocapnia and hypocapnic alkalosis with and without a fluid load were studied in four groups of dogs (group I: fluid load control; group II: fluid load-isolated hypocapnia; group III: fluid load-hypocapnic alkalosis; group IV: no fluid load-hypocapnic alkalosis). Hypocapnic alkalosis was induced by mechanical hyperventilation, and isolated hypocapnia by the simultaneous administration of 0.1 N HCl. Respiratory alkalosis was also studied during administration of a saline fluid load. Cardiac output and stroke volume increased in all groups receiving a fluid load (including isolated hypocapnia and hypocapnic alkalosis groups), but both fell significantly during hypocapnic alkalosis without fluid load. Pulmonary artery wedge pressure rose in groups with hypocapnic alkalosis with fluid load and isolated hypocapnia with fluid load, but did not change significantly with hypocapnic alkalosis without fluid load or in the normocapnic group with fluid load. It is concluded that cardiac output and stroke volume fall in response to hypocapnic alkalosis but both are maintained with a fluid load at the expense of an increased left ventricular preload.

Alkalosis↗
PubMed1975

Intensive respiratory care unit. Review of ten years' experience.

In ten years' experience in the respiratory care units serving both medical and surgical patients, 18,077 consecutive patients received ventilatory support for 24 hours or more. The overall survival rate including all patients was 75.2%. Survival rate has not changed appreciably during the past five years. The respiratory care unit provides technical assistance and consultation to primary physicians of the medical and surgical services. This system of intensive respiratory care is flexible and applicable to general hospitals that treat large numbers of patients with acute respiratory respiratory failure.

Acute Disease↗
PubMed1975

Ventilatory control in myxedema and hypothyroidism.

Alveolar hypoventilation is known to occur in myxedema. To clarify the role of hypoxic ventilatory drive and hypercapnic ventilatory drive in thyroid hormone insufficiency states, 10 patients with myxedema and seven with hypothyroidism (thyroid ablation) were studied before and after thyroid replacement. An index developed for hypoxic ventilatory drive was markedly reduced in myxedema: 17 plus or minus 4.7 (S.E.M.) (normal, 126 plus or minus 8.7) (P smaller than 0.01) and increased to 78 plus or minus 12.6 (p = 0.02) with thyroid hormone replacement. In the hypothyroid group this index was also depressed as compared to normal at 67 plus or minus 20 (p smaller than 0.01) and increased to 114 plus or minus 19 (p smaller than 0.02) with replacement. An index for hypercapnic ventilatory drive was depressed in myxedema, 0.69 plus or minus 0.01), but was not significantly depressed in hypothyroidism. With thyroid hormone replacement this index did not significantly increase in either group. We conclude that both myxedema and hypothyroid states produce depression of hypoxic ventilatory drive that is responsive to replacement therapy. This alteration in ventilatory control may contribute to the hypoventilation seen in myxedema.

Adult↗
PubMed1975

Decreased hypoxic ventilatory drive in the obesity-hypoventilation syndrome.

Most patients with extreme obesity do not exhibit alveolar hypoventilation, but an intriguing minority do. The mechanism(s) of this phenomenon remain unknown. A disorder in ventilatory control has been suggested as a major factor in the pathogenesis of the obesity-hypoventilation syndrome. Accordingly, hypoxic and hypercapnic ventilatory drives were measured in 10 patients with the typical symptoms of the syndrome: obesity, hypersomnolence, hypercapnia, hypoxemia, polycythemia and cor pulmonale. Hypoxic ventilatory drive, measured as the shape parameter A, averaged 21.9 +/- 5.35, approximately one-sixth that in normal controls, A = 126 +/- 8.6 (P less than 0.01). The ventilatory response to hypercapnia also was markedly reduced, the slope of the response averaging 0.51 +/- 0.005, or about one-third the normal value of 1.83 +/- 0.13 (P less than 0.01). This decreased responsiveness in hypoxic and hypercapnic ventilatory drive was consistent throughout the group. The depression in ventilatory drive found in the obesity-hypoventilation syndrome may be causally related to the alveolar hypoventilation manifested by these patients.

Adult↗
PubMed1975

Theophylline-induced seizures in adults. Correlation with serum concentrations.

Eight patients developed grand mal seizures during intravenous theophylline therapy. None had a history of neurologic disorder, and all were acutely ill with severe pulmonary or cardiovascular disease, or both. Serum theophylline concentrations obtained within 1 hour of the seizure ranged from 25 mug/ml to 70mug/ml, with a mean value (53 plus or minus 4.8 mug/ml) more than twice the upper limit of the recommended therapeutic concentration. This serum theophylline concentration was greater than the concentration found in a group of patients with less severe drug-related symptoms (35 plus or minus 1.8 mug/ml, P less than 0.01). A third group of patients without drug-related symptoms had a mean theophylline serum concentration of 19 plus or minus 2.0 mug/ml, which was less than that found in either group with toxicity symptoms (P less than 0.05). Factors predisposing to the high serum concentrations in the patients with seizures were both higher drug dosage, compared with the other groups (P less than 0.01), and hepatic dysfunction, which was more common in both groups with drug-related symptoms.

Adult↗