Gardar Sigurdsson

Hyperventilation-Induced Hypotension During Cardiopulmonary Resuscitation

Background—A clinical observational study revealed that rescuers consistently hyperventilated patients during out-of-hospital cardiopulmonary resuscitation (CPR). The objective of this study was to quantify the degree of excessive ventilation in humans and determine if comparable excessive ventilation rates during CPR in animals significantly decrease coronary perfusion pressure and survival. Methods and Results—In humans, ventilation rate and duration during CPR was electronically recorded by professional rescuers. In 13 consecutive adults (average age, 63±5.8 years) receiving CPR (7 men), average ventilation rate was 30±3.2 per minute (range, 15 to 49). Average duration per breath was 1.0±0.07 per second. No patient survived. Hemodynamics were studied in 9 pigs in cardiac arrest ventilated in random order with 12, 20, or 30 breaths per minute. Survival rates were then studied in 3 groups of 7 pigs in cardiac arrest that were ventilated at 12 breaths per minute (100% O2), 30 breaths per minute (100% O2), or 30 breaths per minute (5% CO2/95% O2). In animals treated with 12, 20, and 30 breaths per minute, the mean intrathoracic pressure (mm Hg/min) and coronary perfusion pressure (mm Hg) were 7.1±0.7, 11.6±0.7, 17.5±1.0 (P <0.0001), and 23.4±1.0, 19.5±1.8, and 16.9±1.8 (P =0.03), respectively. Survival rates were 6/7, 1/7, and 1/7 with 12, 30, and 30+ CO2 breaths per minute, respectively (P =0.006). Conclusions—Professional rescuers were observed to excessively ventilate patients during out-of-hospital CPR. Subsequent animal studies demonstrated that similar excessive ventilation rates resulted in significantly increased intrathoracic pressure and markedly decreased coronary perfusion pressures and survival rates.

Effects of Sleep Deprivation on Neural Circulatory Control

Effects of sleep deprivation on neural cardiovascular control may have important clinical implications. We tested the hypothesis that sleep deprivation increases heart rate, blood pressure, and sympathetic activity and potentiates their responses to stressful stimuli. We studied 8 healthy subjects (aged 40+/-5 years, 6 men and 2 women). Blood pressure, heart rate, forearm vascular resistance, and muscle sympathetic nerve activity were measured at rest and during 4 stressors (sustained handgrip, maximal forearm ischemia, mental stress, and cold pressor test). Measurements were obtained twice, once after normal sleep and once after a night of sleep deprivation. All measurements were obtained in a blinded, randomized manner. In comparison with normal sleep, sleep deprivation resulted in an increase in blood pressure (normal sleep versus sleep deprivation=82+/-8 versus 86+/-7 mm Hg, mean+/-SEM, P=0.012) and a decrease in muscle sympathetic nerve activity (normal sleep versus sleep deprivation=28+/-6 versus 22+/-6 bursts/min, P=0.017). Heart rate, forearm vascular resistance, and plasma catecholamines were not significantly changed by sleep deprivation, nor did sleep deprivation affect autonomic and hemodynamic responses to stressful stimuli. Sleep deprivation results in increased resting blood pressure, decreased muscle sympathetic nerve activity, and no change in heart rate. Thus, the pressor response to sleep deprivation is not mediated by muscle sympathetic vasoconstriction or tachycardia.

Interaction between a polymorphism of the apo A-I promoter region and smoking determines plasma levels of HDL and apo A-I.

Epidemiological studies have demonstrated that the risk of coronary artery disease (CAD) is increased in smokers but reduced in individuals with elevated plasma levels of high density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) A-I. In a sample of 315 men and women from Iceland, the mean levels of HDL-C and apo A-I in smokers were, respectively, 12% and 6% lower in men and 7% and 6% lower in women compared with nonsmokers. In the men who were nonsmokers, a guanine (G) to adenine (A) (G/A) substitution 75 bp upstream from the start of transcription of the apo A-I gene was associated with elevated levels of HDL-C and apo A-I, with those carrying the A allele having levels of HDL-C and apo A-I roughly 10% higher than those with only the G allele. This genotype effect was abolished in the men who smoked and absent in the sample of women. Based on the reported protective effect associated with elevated levels of apo A-I and HDL-C, men carrying the A allele would have roughly a 20% lower relative risk of CAD compared with those without the A allele, but only if they remained nonsmokers. This gene polymorphism would therefore be an important factor in determining those men who would most benefit from avoidance or cessation of smoking. Determining the mechanism of such interaction between genotype and environment will be important in understanding the etiology of CAD.

Treatment of hypotension in pigs with an inspiratory impedance threshold device: A feasibility study

Objective:An inspiratory impedance threshold device was evaluated in spontaneously breathing animals with hypotension to determine whether it could help improve systemic arterial pressures when fluid replacement was not immediately available. Design:Prospective, randomized. Setting:Animal laboratory. Subjects:Thirty-nine female farm pigs (weight, 28 –33 kg). Interventions:A total of 39 anesthetized spontaneously breathing pigs were treated with an impedance threshold device, with cracking pressures from 0 to −20 cm H2O. Four separate experimental protocols were performed: protocol A, in which the hemodynamics of seven pigs were examined during application of an impedance threshold device at various levels of inspiratory impedance (−5, −10, −15, and −20 cm H2O), both before and after a severe, controlled hemorrhage to a systolic blood pressure of 50 –55 mm Hg; protocol B, in which nine pigs bled to systolic blood pressure of 50 –55 mm Hg were treated with an impedance threshold device set at −12 cm H2O and were compared with nine others treated with a sham device; protocol C, in which the effects of the impedance threshold device on mixed venous gases were measured in seven hemorrhaged pigs; and protocol D, in which the effects of the impedance threshold device on cardiac output in seven hemorrhaged pigs were measured. Methods and Main Results:During initial studies with both normovolemic and hypovolemic pigs, sequential increases in inspiratory impedance resulted in a significant increase in systolic blood pressure, whereas diastolic left ventricular and right atrial pressures decreased significantly and proportionally to the level of impedance. When comparing the sham vs. active impedance threshold device (−12 cm H2O) in hypotensive pigs, systolic blood pressure (mean ± sem) with active impedance threshold device treatment increased from 70 ± 2 mm Hg to 105 ± 4 mm Hg (p < .01). Pressures in the control group remained at 70 ± 4 mm Hg (p < .01). Cardiac output increased by nearly 25% (p < .01) with the active impedance threshold device when calculated using the mixed gas equation and when determined by thermodilution. Conclusions:These studies demonstrate that it is feasible to use a device that creates inspiratory impedance in spontaneously breathing normotensive and hypotensive pigs to increase blood pressure and enhance cardiopulmonary circulation in the absence of immediate fluid resuscitation. Further studies are needed to evaluate the potential long-term effects and limitations of this new approach to treat hypovolemic hypotension.

Cardiorespiratory interactions and blood flow generation during cardiac arrest and other states of low blood flow.

Purpose of reviewRecent advances in cardiopulmonary resuscitation have shed light on the importance of cardiorespiratory interactions during shock and cardiac arrest. This review focuses on recently published studies that evaluate factors that determine preload during chest compression, methods that can augment preload, and the detrimental effects of hyperventilation and interrupting chest compressions. Recent findingsRefilling of the ventricles, so-called ventricular preload, is diminished during cardiovascular collapse and resuscitation from cardiac arrest. In light of the potential detrimental effects and challenges of large-volume fluid resuscitations, other methods have increasing importance. During cardiac arrest, active decompression of the chest and impedance of inspiratory airflow during the recoil of the chest work by increasing negative intrathoracic pressure and, hence, increase refilling of the ventricles and increase cardiac preload, with improvement in survival. Conversely, increased frequency of ventilation has detrimental effects on coronary perfusion pressure and survival rates in cardiac arrest and severe shock. Prolonged interruption of chest compressions for delivering single-rescuer ventilation or analyzing rhythm before shock delivery is associated with decreased survival rate. SummaryCardiorespiratory interactions are of profound importance in states of cardiovascular collapse in which increased negative intrathoracic pressure during decompression of the chest has a favorable effect and increased intrathoracic pressure with ventilation has a detrimental effect on survival rate.

Simultaneous transfemoral aortic and transseptal mitral valve replacement utilising SAPIEN 3 valves in native aortic and mitral valves

AIMS Concomitant severe calcific aortic and mitral stenosis is a relatively uncommon but very challenging valvular heart disease to manage. We sought to evaluate the feasibility of a fully percutaneous approach to replace both stenotic native mitral and aortic valves using SAPIEN 3 valves. METHODS AND RESULTS An 87-year-old woman with chronic kidney disease stage 3, pul-monary hypertension, chronic obstructive pulmonary disease, a permanent pacemaker, and atrial fibrillation was referred with Class III heart failure symptoms. Her echocardiogram showed a decreased ejection fraction at 45%, severe mitral stenosis (mean gradient 13 mmHg, area 0.8 cm2) with severe MAC, and severe AS (mean gradient 35 mmHg, area 0.6 cm2). Surgical risk was felt to be very high after evaluation by our cardiothoracic sur-gery group (Society of Thoracic Surgeons risk score of 19%). She underwent simultaneous and fully percutaneous trans-femoral TAVR and transseptal TMVR using SAPIEN 3 valves. Post-implant TEE showed trace paravalvular mitral regurgitation and a mean gradient of 4 mmHg and mean aortic gradient of 8 mmHg with trace paravalvular leak. There was no LVOT obstruction. The patient was discharged seven days after the intervention. CONCLUSIONS After careful evaluation by experienced Heart Teams, combined native stenotic mitral and aortic valves can be percutaneously replaced using transcatheter SAPIEN 3 valves via transfemoral access in carefully selected high surgical risk patients.

Prognostic Value of Coronary Artery Calcium Score in Acute Chest Pain Patients Without Known Coronary Artery Disease: Systematic Review and Meta-analysis

STUDY OBJECTIVE Coronary artery calcium score (CACS) is a well-established test for risk stratifying asymptomatic patients. Recent studies also indicate that CACS may accurately risk stratify stable patients presenting to the emergency department (ED) with acute chest pain; however, many were underpowered. The purpose of this systematic review and meta-analysis is to evaluate the prognostic value and accuracy of a zero (normal) CACS for identifying patients at acceptable low risk for future cardiovascular events who might be safely discharged home from the ED. METHODS We searched multiple databases for longitudinal studies of CACS in symptomatic patients without known coronary artery disease that reported major adverse cardiovascular events (MACEs), including death and myocardial infarction. Pooled risk ratios, sensitivity, specificity, and likelihood ratios were analyzed. RESULTS Eight studies evaluated 3,556 patients, with a median follow-up of 10.5 months. Pooled prevalence of zero CACS was 60%. Patients with CACS=0 had a significantly lower risk of cardiovascular events compared with those with CACS greater than 0 (MACEs: relative risk 0.06, 95% confidence interval 0.04 to 0.11, I2=0%; death/myocardial infarction: relative risk 0.19; 95% confidence interval 0.08 to 0.47, I2=0%). The pooled event rates for CACS=0 (MACEs 0.8%/year; death/myocardial infarction 0.5%/year) were significantly lower than for CACS greater than 0 (MACEs 14.6%/year; death/myocardial infarction 3.5%/year). Analysis of summary testing parameters showed a sensitivity of 96%, specificity of 60%, positive likelihood ratio of 2.36, and negative likelihood ratio of 0.07. CONCLUSION Acute chest pain patients without history of coronary artery disease, ischemic ECG changes, or increased cardiac enzyme levels commonly have a CACS of zero, with a very low subsequent risk of MACEs or death or myocardial infarction. This meta-analysis proffers the potential role of initial CACS testing for avoiding unnecessary hospitalization and further cardiac testing in acute chest pain patients with a CACS of zero.

Carotid β-stiffness index is associated with slower processing speed but not working memory or white matter integrity in healthy middle-aged/older adults

Aging is associated with increased carotid artery stiffness, a predictor of incident stroke, and reduced cognitive performance and brain white matter integrity (WMI) in humans. Therefore, we hypothesized that higher carotid stiffness/lower compliance would be independently associated with slower processing speed, higher working memory cost, and lower WMI in healthy middle-aged/older (MA/O) adults. Carotid β-stiffness (P < 0.001) was greater and compliance (P < 0.001) was lower in MA/O (n = 32; 64.4 ± 4.3 yr) vs. young (n = 19; 23.8 ± 2.9 yr) adults. MA/O adults demonstrated slower processing speed (27.4 ± 4.6 vs. 35.4 ± 5.0 U/60 s, P < 0.001) and higher working memory cost (-15.4 ± 0.14 vs. -2.2 ± 0.05%, P < 0.001) vs. young adults. Global WMI was lower in MA/O adults (P < 0.001) and regionally in the frontal lobe (P = 0.020) and genu (P = 0.009). In the entire cohort, multiple regression analysis that included education, sex, and body mass index, carotid β-stiffness index (B = -0.53 ± 0.15 U, P = 0.001) and age group (B = -4.61 ± 1.7, P = 0.012, adjusted R2 = 0.4) predicted processing speed but not working memory cost or WMI. Among MA/O adults, higher β-stiffness (B = -0.60 ± 0.18, P = 0.002) and lower compliance (B = 0.93 ± 0.26, P = 0.002) were associated with slower processing speed but not working memory cost or WMI. These data suggest that greater carotid artery stiffness is independently and selectively associated with slower processing speed but not working memory among MA/O adults. Carotid artery stiffening may modulate reductions in processing speed earlier than working memory with healthy aging in humans.NEW & NOTEWORTHY Previously, studies investigating the relation between large elastic artery stiffness, cognition, and brain structure have focused mainly on aortic stiffness in aged individuals with cardiovascular disease risk factors and other comorbidities. This study adds to the field by demonstrating that the age-related increases in carotid artery stiffness, but not aortic stiffness, is independently and selectively associated with slower processing speed but not working memory among middle-aged/older adults with low cardiovascular disease risk factor burden.

Coronary artery calcium score as a predictor for incident stroke: Systematic review and meta-analysis

BACKGROUND Coronary artery calcium score (CACS) is a well-established test for risk stratifying asymptomatic patients for overall cardiovascular or coronary events. However; the prognostic value for incident stroke remains controversial. The objective of this study was to investigate the predictive value of CACS obtained by non-contrast electrocardiogram-gated computed tomography for incident stroke. METHODS We searched PubMed, EMBASE, Cochrane databases for prospective longitudinal studies of CACS which reported the incidence of stroke. Incidence of stroke was compared in patients with and without coronary calcification. RESULTS Three studies evaluated 13,262 asymptomatic patients (mean age=60years, 50% men) without apparent cardiovascular diseases. During a follow-up of 7.2years (median 5years, range 4.4-9.5years, 95,434patient-years), the overall pooled incidence of stroke was 0.26%/year. The pooled risk ratio of CACS>0 for incident stroke was 2.95 (95% CI: 2.18-4.01, p<0.001) compared to CACS=0. The heterogeneity among studies was low (I2=0%). The pooled incidence rate of stroke categorized by CACS was 0.12%/year for CACS 0, 0.26%/year for CACS 1-99, 0.41%/year for CACS 100-399 and 0.70%/year for CACS ≥400. CONCLUSIONS In asymptomatic patients without apparent cardiovascular diseases, the incidence of stroke was overall low. The presence and severity of coronary artery calcification were associated with incident stroke over mid-long term follow-up.

Atrial Flutter Ablation and Risk of Right Coronary Artery Injury

Radiofrequency ablation (RFA) of atrial flutter (AFL) is a commonly performed procedure with low risk of complications. Several case reports and animal studies cautioned about the risk of right coronary artery (RCA) injury following AFL ablation. This risk is due to the anatomic proximity of the RCA to the cavo-tricuspid isthmus where ablation is performed. We present a case report that demonstrates postmortem evidence of RCA injury following RFA of AFL.