Cardiac dysfunction and pulmonary edema following scorpion envenomation

Cardiac dysfunction with pulmonary edema following scorpion envenomation (SE) has been documented only in a few isolated case reports. We conducted a systematic hemodynamic study in five consecutive patients (mean age, 21.6 +/- 8 years) presenting with pulmonary edema occurring a few hours (9.6 +/- 5.2 hours) after SE. All patients had increased pulmonary capillary wedge pressure (mean, 25 +/- 1.8 mm Hg) while the systemic vascular resistance was elevated only in one. The stroke volume index was markedly depressed (21.7 +/- 3.6 ml/sq m) whereas cardiac index was normal or slightly decreased (2.5 +/- 0.4 L/min/sq m). Cerebral infarct and sudden cardiac arrest were the cause of death in two patients. In the three survivors, all the hemodynamic disturbances and respiratory abnormalities disappeared within a few days. We conclude that cardiac dysfunction was found in all five patients and this was reversible in the three surviving the acute episode.     

Hydrochlorothiazide-induced pulmonary edema with severe acute myocardial dysfunction

A 73-year-old woman presented with acute pulmonary edema and hypotension less than 1 h after taking hydrochlorothiazide 50 mg, a reaction which has been reported as a rare but classic adverse drug response. Though prior cases have supported a noncardiogenic pulmonary edema syndrome, hemodynamic monitoring in this patient demonstrated a refractory low cardiac output state for more than 24 h. In the absence of other etiologies, this represents a new finding.     

Acute pulmonary edema after cardioversion of cardiac arrhythmias

OBJECTIVE: To examine the occurrence of acute pulmonary edema after cardioversion of arrhythmias. METHODS: Cases, case series, and related articles on the subject identified through a comprehensive literature search were examined. RESULTS: Thirty cases (23 males) of post cardioversion acute pulmonary edema were identified. The mean age was 53.8 +/- 13 years (range, 18 to 75 years). Underlying arrhythmias were atrial fibrillation (69%), atrial flutter (24%), supraventricular tachycardia (4%), and ventricular tachycardia (4%). The duration of arrhythmia preceding cardioversion varied widely ranging from 1 day to 13 years. Twenty-six (87%) patients had concomitant cardiovascular disease comprising of coronary artery disease (38%), rheumatic heart disease (23%), cardiomyopathy (23%), and hypertension (8%). Direct current electrical cardioversion was used in 28 (93%) patients and pacing in two (7%) patients. Occurrence of pulmonary edema was independent of the amount of energy used for cardioversion (range 20 to 1280 Joules, mean 263 +/- 27 Joules). Short acting general anesthetic drugs were administered in 14 (47%) and sedation in eight (27%) patients. Sinus rhythm was established in 23 (77%) patients. Duration to develop pulmonary edema after cardioversion was available in 23 patients and ranged from immediately to 96 h. Pulmonary edema occurred within 15 min after cardioversion in 22%, within 3 h in 30%, within 24 h in 30%, within 48 h in 17% and within 96 h in remaining 4% of patients. Three patients required mechanical ventilation. CONCLUSION: The rare complication of acute pulmonary edema after cardioversion has been reported mostly in patients with underlying cardiac disease, and is independent of the amount of energy used for cardioversion.     

Acute pulmonary edema following pericardiocentesis for cardiac tamponade

Pericardiocentesis for therapeutic drainage of pericardial fluid may be associated with a variety of complications, including laceration of the right ventricle or coronary artery, arrhythmias, viscus perforation, hypotension, pneumothorax, adult respiratory distress syndrome and death. Hemodynamic derangements such as acute left ventricular failure, pulmonary edema and cardiogenic shock are infrequent and, hence, less well recognized. The present report describes a patient with pericardial effusion and tamponade who developed cardiogenic shock requiring inotropic support shortly following uncomplicated ultrasound-guided pericardial drainage.     

Effects of cardiac oscillations on acinar gas mixing during pulmonary edema.

We used a previously reported technique (Mackenzie et al., J. Appl. Physiol. 68: 2013-2018, 1990) to measure the effects of severe pulmonary edema on acinar cardiogenic gas mixing in anesthetized dogs. We also tested how increases in lung volume affected gas mixing in healthy lungs and during pulmonary edema. Cardiogenic gas mixing was evaluated by measurement of the rate of washout of xenon133 injected into an occluded pulmonary artery during apnea. The rate constant of xenon133 washout was 0.40 min-1 (+/- 0.06 SE) in the healthy lung at functional residual capacity. It decreased (P < 0.05) to 0.08 min-1 (+/- 0.03) when lung volume was raised 500 ml. Pulmonary edema was induced by injection of oleic acid (0.06 mg.kg-1) into the right atrium over a 4-min period; clinical signs of severe pulmonary edema were present after 90 min. The rate constant for xenon133 washout (0.07 +/- 0.03 min-1) was less than in the healthy lung (P < 0.05), and was not changed after lung volume was increased (P > 0.05). We conclude that, in the presence of severe pulmonary edema: (1) acinar resistance is increased and/or magnitude of cardiogenic oscillations is decreased; and (2) salutary effects of increased lung volume are not due to enhancement of cardiogenic gas mixing.     

Reexpansion pulmonary edema.

A case of pulmonary edema following reexpansion of a collapsed lung due to pneumothorax is described and illustrated. The importance of recognizing this relatively uncommon phenomenon is stressed. The development of such edema can be prevented by avoiding application of sudden and excessive negative pleural pressures during the evacuation of a pneumothorax or a pleural effusion. The edema generally occurs in a lung that has been collapsed for more than three days. The importance of the duration of pulmonary collapse in the causation of edema is demonstrated in this patient.     

Scintigraphic diagnosis of pulmonary embolism

The ventilation-perfusion scintigram, as the pivotal noninvasive diagnostic aid in detection of pulmonary embolism, is interpreted with respect to regional comparison of ventilation, perfusion and chest radiographic findings. Two segmental mismatched defects in areas with normal ventilation and no associated radiographic abnormalities are required for the diagnosis. Scintigraphic findings can be classified into four major categories: normal, low probability, intermediate probability and high probability for pulmonary embolism (Table 1). Subsequent diagnostic measures can be derived from a flow chart accordingly (Figure 1). Patients with low probability have favorable outcomes without treatment; in those with high probability anticoagulants should be used unless specific contraindications exist. In the case of indeterminate results, further imaging evaluation is necessary.     

Contributions of pulmonary hypertension to HIV-related cardiac dysfunction

Background/Aim

To evaluate the prevalence of pulmonary hypertension among patients living with HIV/AIDS and to determine its contribution to cardiac dysfunction.

Method

A hospital based cross sectional study was carried out over a 6-month period at the Jos University Teaching Hospital. The subjects were 200 confirmed HIV positive patients, ≥18 years of age who consented to the study. Physical examination, laboratory investigations, 2 dimensional and Doppler echocardiography were conducted on the subjects.

Results

The mean age of the patients was 38 ± 9 years, and there were 142 females (71%).Females were younger, mean age 36 ± 8 years versus 41 ± 10 years for males (p-value <0.01). The median CD4 cell count was 312 cells/μl, there were no homosexual or intravenous drug user among the subjects.Eight of the subjects had pulmonary hypertension, with a case prevalence of 4%, and this had no relationship to CD4 cell count. Both systolic and diastolic functions were worse in subjects with pulmonary hypertension, with a negative correlation between mean pulmonary arterial systolic pressure (mPASP) and parameters like ejection fraction (r = −0.28, p-value 0.0003), fractional shortening (r = −0.21, p-value 0.003), deceleration time (r = −0.13. p-value 0.09).

Conclusion

Immune-suppression affects the cardiac function adversely and coexisting pulmonary hypertension contributes to poor systolic and diastolic function in affected patients. The subtle nature of presentation of pulmonary hypertension and other cardiac dysfunctions in HIV/AIDS patients demand a high-index of suspicion and early intervention if detected, to ensure better care for these emerging threats to our patients.     

Non-cardiogenic pulmonary edema after pericardial drainage for cardiac tamponade

We report a patient who developed adult respiratory distress syndrome following relief of pericardial tamponade. Because of increasing recognition of pulmonary edema in this situation, we recommend gradual removal of pericardial fluid with hemodynamic monitoring to limit the massive fluid shifts which appear to herald this dire complication.     

Scintigraphic assessment of regional cardiac adrenergic innervation

To assess the feasibility of noninvasively imaging the regional distribution of myocardial sympathetic innervation, we evaluated the distribution of sympathetic nerve endings, using 123I metaiodobenzylguanidine (MIBG), and compared this with the distribution of myocardial perfusion, using 201Tl. Twenty dogs were studied: 11 after regional denervation, and nine as controls. Regional denervation was done by left stellate ganglion removal, right stellate ganglion removal, and application of phenol to the epicardial surface. Computer-processed functional maps displayed the relative distribution of MIBG and thallium in multiple projections in vivo and excised heart slices in all animals. In six animals, dual isotope emission computed tomograms were acquired in vivo. Tissue samples taken from innervated and denervated regions of the MIBG images were analyzed for norepinephrine content to validate image findings. Normal controls showed homogeneous and parallel distributions of MIBG and thallium in the major left ventricular mass. In the left stellectomized hearts, MIBG was reduced relative to thallium in the posterior left ventricle; whereas in right stellectomized hearts, reduced MIBG was in the anterior left ventricle. Phenol-painted hearts showed a broad area of decreased MIBG extending beyond the area of phenol application. In both stellectomized and phenol-painted hearts, thallium distribution remained homogeneous and normal. Norepinephrine content was greater in regions showing normal MIBG (550 +/- 223 ng/g) compared with regions showing reduced MIBG (39 +/- 44 ng/g) (p less than 0.001), confirming regional denervation. Combined MIBG-thallium functional maps display the regional distribution of sympathetic innervation. This new ability to noninvasively map the distribution of sympathetic nerves with simultaneous comparison to regional perfusion may provide important new insights into mechanisms, whereby an imbalance in sympathetic activity may relate to clinical disorders.