Risk Of Cardiovascular Collapse Research Articles

Acute fasting reduces tolerance to progressive central hypovolemia in humans.

Potential health benefits of an acute fast include reductions in blood pressure and increases in vagal cardiac control. These purported health benefits could put fasted humans at risk for cardiovascular collapse when exposed to central hypovolemia. The purpose of this study was to test the hypothesis that an acute 24-h fast (vs. 3-h postprandial) would reduce tolerance to central hypovolemia induced via lower body negative pressure (LBNP). We measured blood ketones (β-OHB) to confirm a successful fast (n = 18). We recorded the electrocardiogram (ECG), beat-to-beat arterial pressure, muscle sympathetic nerve activity (MSNA; n = 7), middle cerebral artery blood velocity (MCAv), and forearm blood flow. Following a 5-min baseline, LBNP was increased by 15 mmHg until -60 mmHg and then increased by 10 mmHg in a stepwise manner until onset of presyncope. Each LBNP stage lasted 5-min. Data are expressed as means ± SE β-OHB increased (β-OHB; 0.12 ± 0.04 fed vs. 0.47 ± 0.11, P < 0.01 mmol/L fast). Tolerance to central hypovolemia was decreased by ∼10% in the fasted condition measured via total duration of negative pressure (1,370 [Formula: see text] 89 fed vs. 1,229 ± 94 s fast, P = 0.04), and was negatively associated with fasting blood ketones (R = -0.542, P = 0.02). During LBNP, heart rate and MSNA increased similarly, but in the fasted condition forearm vascular resistance was significantly reduced. Our results suggest that acute fasting reduces tolerance to central hypovolemia by blunting increases in peripheral resistance, indicating that prolonged fasting may hinder an individual's ability to compensate to a loss of blood volume.NEW & NOTEWORTHY An acute 24 h fasting reduces tolerance to central hypovolemia, and tolerance is negatively associated with blood ketone levels. Compared with a fed condition (3-h postprandial), fasted participants exhibited blunted peripheral vasoconstriction and greater reductions in stroke volume during stepwise lower body negative pressure. These findings suggest that a prolonged fast may lead to quicker decompensation during central hypovolemia.

The use of ketamine as an induction agent for anesthesia in pulmonary thromboendarterectomy surgery: A case series.

Pulmonary thromboendarterectomy (PTE) surgery is the treatment of choice for patients with chronic thromboembolic pulmonary hypertension (CTEPH). The induction of anesthesia in patients with severe pulmonary hypertension (PHT) can be challenging, with a risk of cardiovascular collapse. The administration of ketamine in patients with PHT is controversial, with some recommendations contraindicating its use. However, ketamine has been used safely in children with severe PHT. We present a retrospective case series of adult patients with severe PHT presenting for PTE surgery, using intravenous ketamine as a co-induction anesthetic agent.

Acute Fasting Decreases Tolerance to Lower Body Negative Pressure

Potential health benefits of an acute fast include reductions in blood pressure and increases in vagal cardiac control. These purported health benefits could put fasted humans at risk for cardiovascular collapse when exposed to central hypovolemia. Intense lower body negative pressure (LBNP) induces reproducible and reversible central hypovolemia. The purpose of this study was to investigate the influence of an acute 24‐hour fast on tolerance to severe LBNP. We tested the hypothesis that fasting would reduce tolerance to severe LBNP. Ours was a randomized, crossover design with an LBNP tolerance test occurring 3‐hrs postprandial (fed) and 24‐hrs postprandial (fast). A standardized meal was provided for both conditions. Criteria for termination of LBNP was; 1) a drop in systolic pressure of 15 mmHg or greater for 10 s and/or 2) sudden bradycardia. Eighteen young (23±0.7 yrs), normotensive, non‐obese (25±0.8 BMI), participants were brought to presyncope. We measured blood glucose (GLU), ketones (β‐OHB), and triglycerides (TRG) to confirm a successful fast. With subjects in a supine position, we recorded the ECG, beat‐to‐beat arterial pressure (finger plethysmography), muscle sympathetic nerve activity (MSNA; N=7), and forearm blood flow via venous occlusion plethysmography (VOP; N=12). Following a 5‐min baseline, LBNP was increased in 15 mmHg increments every 5 min in a stepwise manner until onset of presyncope. LBNP levels eliciting presyncope were denoted as 100% tolerance, data were assessed relative to this normalized maximal tolerance by expressing LBNP as 80, 40, and 0% (baseline) of maximal tolerance. Data are expressed as means ± SE. P‐values ≤ 0.05 were considered statistically significant and indicated by an (*). Changes in TRG, GLU and β‐OHB with fasting were consistent with expectations: TRG and GLU decreased (TRG; 130±16 fed vs. 78±9* mg/dL fast) (GLU; 100±3 fed vs. 81±2* mg/dL fast), and β‐OHB increased (β‐OHB; 0.12±.04 fed vs. 0.47±.11* mmol/L fast). Our participants were similarly hydrated, measured via urine specific gravity, (1.0168±.002 fed vs. 1.0122±.003 a.u. fast) and weight stable (77.8±3.6 fed vs. 76.9±3.4 kg fast) between conditions. Tolerance to central hypovolemia was decreased by ~10% in the fasted condition measured via total duration of negative pressure (1370±89 fed vs. 1229±94* s fast). At each normalized time point, heart rate and MSNA increased similarly in both conditions. Additionally, systolic blood pressure and stroke volume decreased similarly in both conditions. Both forearm blood flow (FBF) and forearm vascular resistance (FVR) are expressed as a percent change from 0 to 100%. ΔFBF significantly decreased in the fed condition at 100% (‐45.8±4.8 fed vs. ‐23.5±8.1* % fast) and ΔFVR increased in the fed condition at 100% (141.6±34.5 fed vs. 67.1±24.8* % fast). Our results suggest that acute fasting reduces tolerance to central hypovolemia by blunting increases in peripheral vascular resistance, and could lead to earlier decompensation when compared to the normal, fed state.

A right para-tracheal mass extending into the anterior mediastinum

The anesthetic management of patients with a mediastinal mass represent a challenge due to the potential for difficult ventilation and intubation, as well as the risk of cardiovascular collapse upon induction of general anesthesia. Different strategies and alternatives have been described. We present the case of a 70-year-old man with a right para-tracheal mass extending into the anterior mediastinum with 90% mid-tracheal lumen obstruction who was successfully managed with venous-venous extra-corporeal membrane oxygenation (ECMO) during mass debulking and tracheal stent placement.

THERAPEUTIC MISADVENTURE WITH A BETA BLOCKER DURING A THYROID STORM

SESSION TITLE: Critical Care and Pediatrics SESSION TYPE: Global Case Reports PRESENTED ON: 10/10/2018 01:00 PM - 02:00 PM INTRODUCTION: Thyroid storm (TS) has a high mortality rates, whether treated 20% [2] or untreated 50%-90% [1,2]. Immediate goals are to decrease synthesis, prevent release, decrease peripheral action with beta blockers, support circulation and treat the precipitating condition (3). Caution against beta blocker is warranted in patients with heart failure, although it may be beneficial when tachycardia is a significant precipitant to decompensated cardiac function (4). We present a case of thyroid storm with right heart failure and exaggerated response to propranolol leading to circulatory collapse secondary to cardiogenic shock. CASE PRESENTATION: 48-year-old female with untreated hypertension presented to emergency for progressively worsening dyspnea, cough and diarrhea with elevated white count and fever. Treatment was initiated per sepsis protocol and PE was ruled out with contrasted CT. Shortly afterward, GCS deteriorated from 14 to 6 and she was intubated for airway protection. Lab work revealed an undetectable TSH with elevated free T4 and T3. Upon revaluation, her Burch-Wartofsky Point Scale was 95, elevated from 55 on arrival. She received glucocorticoids, propylthiouracil and oral propranolol. She developed bradycardia and cardiac arrest. Post ROSC echocardiogram showed right heart failure with flattened ventricular septum and EF of 45%. A second cardiac arrest ensued despite glucagon and transcutaneous pacing attempts. She was stabilized with crystalloids, vasopressors and bicarbonate drip. Central venous and bladder pressures were 34 and 26, minutes before a third cardiac arrest that ended with an emergency bedside laparotomy for decompression of abdominal compartment syndrome. Her hospital course was further complicated by coagulopathy, blood loss and renal failure requiring dialysis. DISCUSSION: The concept of thyrocardiac disease must be kept in mind when managing a TS. In long standing hyperthyroidism, the resulting cardiomyopathy is compensated by tachycardia and increased sensitivity to catecholamines [3]. This compensation depends on excess adrenergic drive to maintains adequate cardiac output. Failure to consider this led to our therapeutic misadventure. Current management of TS includes propranolol to lessen the adrenergic effect on the heart and to inhibit peripheral conversion of T4 to T3. This patient’s experience suggested that abrupt disruption of this compensatory state with beta blockade puts the body at risk for cardiovascular collapse. CONCLUSIONS: It is imperative to for clinicians to avoid beta blockers or use short acting beta blockers with extreme caution when managing TS Reference #1: Nayak B1, Burman K. Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin North Am. 2006 Dec;35(4):663-86, vii Reference #2: Richard Carroll and Glenn Matfin Endocrine and metabolic emergencies: thyroid storm Ther Adv Endocrinol Metab. 2010 Jun; 1(3): 139–145. Reference #3: Singhal, A., & Campbell, D. "Thyroid storm." 2003. www.emedicine.com/ped/topic2247.htm (16 Dec. 2004) DISCLOSURES: No relevant relationships by Emmanuel Addo-Yobo, source=Web Response No relevant relationships by Nanette Bentley, source=Web Response No relevant relationships by Diana Trofimovitch, source=Web Response No relevant relationships by Karthik Vijayan, source=Web Response No relevant relationships by Gabriel Zaietta, source=Web Response

Back from the dead: reanimation following severe hypothermic cardiac arrest

background Hypothermia is clinically defined as a drop in core body temperature below 35°C in a previously healthy individual in the absence of pre-existing inherent underlying thermoregulatory pathology. Classification of hypothermia below 35°C is described as mild (32°C to 35°C) and moderate (28°C to 32°C). A temperature below 28°C is classified as severe. At 28°C cardiopulmonary function is likely to become compromised. The myocardium becomes vulnerable to arrhythmia, ventricular asystole and subsequently complete cardiovascular collapse. Concomitant cognitive impairment is most commonly associated with severe hypothermia and cold injury. These patients tend to be individuals with mental illness, homelessness, and alcohol and illicit drug use. Recreational accidents such as skiing comprise the second most common group for hypothermic injury.1 There has been much academic debate and speculation regarding the optimal approach to rewarming any patient suffering from hypothermia.2 Mild hypothermia responds well to external rewarming techniques like forced heated air blankets.3 Moderate hypothermia is more precarious from a physiological standpoint. The myocardium is exceptionally vulnerable at these temperatures. Consequently, rapid rewarming techniques are favoured. This includes warmed intravenous (IV) fluids and warm peritoneal lavage in those who have not demonstrated overt signs of cardiac instability.4 Less commonly, these modalities can be augmented with airway warming and pleural irrigation.4,5 If patients with severe hypothermia have a sustainable cardiac rhythm, they are at increased risk for cardiovascular collapse.6 The optimal modality for rewarming a patient with severe hypothermic cardiac arrest remains a highly controversial topic.7 The most recent retrospective comparative study in 68 patients demonstrated cardiopulmonary bypass (CPB) rewarming to be far superior to conventional methods of rewarming, with mortality rates of 15.8% and 53.3%, respectively. Reanimation on CPB allows for several advantages, including rapid rewarming, but most importantly oxygenation and perfusion are preserved. A retrospective study analyzed the long-term neurological outcomes of survivors who reported normal neuropsychological findings in 93.3% of cases and normal brain magnetic resonance imaging in 86.7% of cases.8

Patient with Posterior Mediastinal Mass Requiring Urgent Cardiopulmonary Bypass

T HE literature on anesthetic concerns and perioperative care of patients with mediastinal masses has focused almost exclusively on anterior mediastinal masses. Posterior mediastinal masses traditionally have been suggested to carry a low risk of anesthetic implications. We present the case of a patient with a posterior mediastinal mass who experienced hemodynamic and respiratory decompensation upon induction of general anesthesia and required urgent transition to cardiopulmonary bypass (CPB). Our case illustrates the importance of real-time imaging provided by transesophageal echocardiography (TEE) in explaining the etiology of intractable hemodynamic instability and a new finding of significant pericardial and left pleural effusion not seen on preoperative imaging. TEE made clear the urgent need to initiate CPB because it revealed a near total compression of the left atrium, which was obstructing delivery of volume to the left ventricle. In addition, this case demonstrates the inadequacy of “stand-by” CPB and the need for every institution to establish an interdisciplinary team to develop, before surgery, a formal plan for the perioperative care of patients with mediastinal masses.