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PubMed1996

5-hydroxydecanoate fails to attenuate ventricular fibrillation in a conscious canine model of sudden cardiac death.

The electrophysiologic and antifibrillatory properties of 5-hydroxydecanoate, a KATP channel antagonist, were studied in a conscious canine model of sudden cardiac death. After a surgically induced myocardial infarction, animals were subjected to programmed electrical stimulation to identify those at risk for sudden cardiac death. 5-Hydroxydecanoate was administered as a bolus (10 mg/kg i.v.) followed by an infusion, 10 mg/kg/h (group 1, n = 12) or 30 mg/kg bolus followed by an infusion, 30 mg/kg/h (group 2, n = 8) i.v., while vehicle treated animals received a 0.9% sodium chloride solution (group 3, n = 11). The administration of 5-hydroxydecanoate did not alter the ventricular effective refractory period or the QTc interval. Anterior wall myocardial infarcts, expressed as a percentage of the left ventricle, did not differ among groups. Infusions of 5-hydroxydecanoate did not confer significant protection from sudden cardiac death (death within 60 min of posterolateral ischemia) due to ventricular fibrillation: group 1, 50%; group 2, 38%; and group 3, 18%. The data demonstrate that a continuous infusion of 5-hydroxydecanoate (10 and 30 mg/kg/h, i.v.) does not provide protection from ischemia-induced ventricular fibrillation in the postinfarcted conscious canine.

Action Potentials↗
PubMed2002

ST-segment elevation and ventricular fibrillation without coronary spasm by intracoronary injection of acetylcholine and/or ergonovine maleate in patients with Brugada syndrome.

OBJECTIVES: The study examined whether patients with Brugada syndrome are sensitive to vagal stimulation or ischemia. BACKGROUND: Experimental studies have suggested that a prominent transient outward current (I(to))-mediated action potential notch and a subsequent loss of the action potential dome in the epicardium, but not in the endocardium, give rise to ST-segment elevation and subsequent ventricular fibrillation (VF). METHODS: We evaluated the frequency of coronary spasm, augmentation (> or =0.1 mV) of ST-segment elevation in leads V(1) to V(3), and induction of VF by intracoronary injection of acetylcholine (ACh) and/or ergonovine maleate (EM) in 27 symptomatic patients with Brugada syndrome and 30 control subjects. RESULTS: The coronary spasm was induced in 3 (11%) of the 27 patients with Brugada syndrome and in 13 (43%) of the 30 control subjects. ST-segment elevation was augmented by 11 (33%) of the 33 right coronary injections (ACh: 6/11 [55%]; EM: 5/22 [23%]), without coronary spasm, but not by any of the left coronary injections in patients with Brugada syndrome. Ventricular fibrillation was induced by 3 (9%) of the 33 right coronary injections (ACh: 2/11 [18%]; EM: 1/22 [5%]), but not by any of the left coronary injections. In contrast, neither ST-segment elevation nor VF was observed in any of the control subjects. CONCLUSIONS: Our results support the hypothesis that mild ischemia and vagal influences act additively or synergistically with the substrate responsible for the Brugada syndrome to elevate the ST-segment and precipitate VF. These observations suggest that Brugada patients may be at a higher risk for ischemia-related sudden death.

Acetylcholine↗
PubMed2006

Assessment of markers of thrombin generation in patients with acute myocardial infarction complicated by ventricular fibrillation.

BACKGROUND: In most cases, sudden cardiac death is triggered by ischemia-related ventricular tachyarrhythmias and accounts for 50% of deaths from cardiovascular disease in developed countries. Chronic elevation of indicators of coagulation activation has been found in patients with coronary heart disease, but a role of coagulation activation as a potential risk factor for ventricular fibrillation (VF) during acute myocardial infarction (MI) has not been investigated. METHODS: We enrolled 50 patients with a history of MI, of whom 26 presented with VF in the acute phase of myocardial ischemia; 24 patients had an acute MI without ventricular tachyarrhythmias. Levels of thrombin-antithrombin complexes (TAT), prothrombin fragment F1 + 2 (F1 + 2), fibrinopeptide A (FPA), plasmin-antiplasmin complexes (PAP), protein C, antithrombin, activated partial thromboplastin time (aPTT), thromboplastin time, D-Dimer, fibrinogen, and high-sensitivity C-reactive protein (hs-CRP) were measured in plasma samples of all patients. Blood collection was obtained sequentially in two separate settings. Patients were studied at a median of 351 days after the acute coronary event. RESULTS: Higher levels of TAT complexes (13.4 +/- 22.2 vs. 3.03 +/- 4.3 microg/l; p = 0.02), FPA (79.7 +/- 132.3 vs. 24.04 +/- 41.3 ng/ml; p = 0.04), and F1+2 (1.89 +/- 1.3 vs. 1.16 +/- 0.5 nmol/l; p = 0.01) were observed in patients with VF compared with patients without ventricular tachyarrhythmias during the acute phase of MI. D-Dimer levels displayed a trend without reaching statistical significance (0.69 +/- 0.48 vs. 0.48 +/- 0.24 mg/l; p = 0.06). No differences were found in hs-CRP (3.25 +/- 4.5 vs. 4.4 +/- 8.8 mg/l; p = 0.5) and fibrinogen (2.8 +/- 0.9 vs. 2.7 +/- 0.9 g/l; p = 0.6) measurements. Repeat assessment of markers of coagulation activation at a median of 847 days revealed a highly significant decrease in patients with VF. CONCLUSIONS: Markers of thrombin generation are transiently increased in patients with VF during the acute phase of MI. These findings have implications for risk assessment and genetic screening of patients prone to VF during acute myocardial ischemia.

Antithrombin III↗
PubMed2006

Ventricular fibrillation in pediatric cardiac arrest.

OBJECTIVES: After activating 9-1-1 for out-of-hospital cardiac arrest (CA), guidelines for children 1 year and older have evolved to include immediate automated external defibrillator (AED) use for witnessed arrest, and two minutes of cardiopulmonary resuscitation (CPR) followed by AED use for unwitnessed arrests. The best approach to resuscitation in a two-tiered emergency medical services (EMS) system depends in part on how likely the patient is to present with ventricular fibrillation (VF). Therefore, the authors evaluated the frequency of VF with respect to age and other characteristics to further elucidate the role of the AED among pediatric CAs. METHODS: The investigation was a retrospective cohort study of EMS-treated, nontraumatic, out-of-hospital CA among persons aged 1-18 years in King County, Washington, between April 1, 1976, and December 31, 2003. The primary goal was to identify the proportion of patients presenting to EMS in VF, according to age. The association between other characteristics and the likelihood of VF was also evaluated. Finally, hospital survival according to cardiac rhythm at EMS arrival was evaluated. RESULTS: Ventricular fibrillation was the presenting rhythm in 17.6% of cases (48/272). The proportion presenting with VF was 7.6% (10/131) among children aged 1-7 years and 27.0% (38/141) among children aged 8-18 years (p < 0.001). In multivariable models, VF was independently associated with age 8 years and older compared with 1-7 years (odds ratio, 3.19; 95% confidence interval [CI] = 1.46 to 6.97), witnessed arrest (odds ratio, 3.33; 95% CI = 1.63 to 6.82), and cardiac etiology (odds ratio, 2.89; 95% CI = 1.32 to 6.34). Survival was 31.3% (15/48) for VF and 10.7% (24/224) for nonshockable rhythm CAs. CONCLUSIONS: The proportion of children aged younger than 8 years presenting with VF is low compared with older children. The greatest increase in VF proportion occurs in children older than 12 years. Based on these results, the best approach for initial EMS resuscitation in a two-tiered EMS system, CPR versus AED use, is uncertain among younger children. Inclusion of witness status into the decision process for younger children may more efficiently allocate AED use, a finding in accordance with 2005 guidelines.

Adolescent↗
PubMed1981

Impact of prehospital cardiac algorithms on ventricular fibrillation survival rates.

To determine the value of algorithms in the field, a set of cardiac clinical algorithms was developed for and tested by the City of Philadelphia paramedics. A controlled test was carried out by revising the narrative standard operating procedure to reflect algorithm content and giving the algorithms, in pocket-size booklet form, to half the Fire Rescue platoons (43 men). Baseline data included paramedics' characteristics, arrhythmia recognition and management test scores, and data on the number of patients who were discharged alive from the hospital following successful treatment of ventricular fibrillation in the field. Platoons with and without the algorithms served identical areas of the city, did not differ in response times, and were treated similarly with regard to continuing education during the study period. Paramedics who received the algorithms were encouraged, but not required, to use them. Platoons using the algorithms experienced an increase in their ventricular fibrillation patient survival rates from 10.6% to 14.5%; those platoons not using the algorithms had a decrease in patient survival rates from 11.8% to 7.0% (P = 0.0732). There was no statistically significant difference in the paramedics' scores on arrhythmia recognition and management tests given before and after use of the algorithms. Only 39% of the paramedics used the algorithms during actual patient care, but 83% used them as a study guide or for reference between runs. The data suggest that algorithm use may minimize the rate of knowledge and skill decay.

Allied Health Personnel↗
PubMed2002

Detection of ventricular fibrillation and tachycardia from the surface ECG by a set of parameters acquired from four methods.

The recent development and increased application of automatic external defibrillators have prescribed very strong requirements towards ventricular fibrillation (VF) and fast ventricular tachycardia (VT > 180 bpm) detection from the surface electrocardiogram (ECG). We attempted to use informative parameters from several existing analysis methods and from a method developed in-house. A set of nine parameters was derived initially, with four of them being selected after statistical assessment. Detection of VF against non-shockable rhythms was obtained using the K-nearest neighbours classification method, with 98.6% specificity and 96.7% sensitivity. The detection accuracy remained high after inclusion of VT episodes above and below 180 bpm to shockable and non-shockable rhythms respectively and after the addition of noise. Test signals were taken from the well-known ECG signal databases of the American Heart Association and the Massachusetts Institute of Technology-Beth Israel Hospital (MIT-BIH-'cudb' and 'vfdb' files).

Electrocardiography↗
PubMed1997

Induction of ventricular fibrillation by T-wave field-shocks in the isolated perfused rabbit heart: role of nonuniform shock responses.

OBJECTIVES: Single electrical field shocks are able to induce ventricular fibrillation (VF) if applied during the vulnerable period. During this period, a shock can either prolong the action potential duration or induce a new action potential. Whether the occurrence of different shock responses contributes to the induction of VF has not been investigated directly in the intact heart. METHODS: In 12 isolated Langendorff-perfused rabbit hearts seven monophasic action potentials (MAPs) were recorded simultaneously during the application of 838 T-wave shocks. Post-shock repolarization was assessed by classifying the shock-induced response in each MAP recording either as a full action potential or an action potential prolongation. Heterogeneity of post-shock repolarization was defined if both response patterns were present in different MAP recordings at the same time. The heterogeneity of post-shock activation was measured as the dispersion of the post-shock activation time (PS-AT). The arrhythmogeneity of a shock was quantified as the number of rapid shock-induced repetitive responses. RESULTS: Shocks inducing nonuniform repolarization were associated with greater arrhythmogeneity than shocks inducing uniform repolarization (17.6 +/- 30.0 versus 1.6 +/- 1.1 shock-induced repetitive responses, p < 0.001). The severity of the induced arrhythmia increased gradually with increasing nonuniformity of repolarization (p < 0.01 for a 10% increase), being maximal when the shock initiated near equal numbers of both full action potentials and action potential prolongations. The induction of severe arrhythmias by T-wave shocks was also associated with a higher dispersion of PS-AT (29 +/- 14 ms for the induction of VF, 19 +/- 12 ms for non-sustained arrhythmia, and 12 +/- 8 ms for no arrhythmic response, all p < 0.001). For VF inducing shocks, an increase in shock strength towards the upper limit of vulnerability decreased the dispersion of PS-AT from 34 +/- 15 ms to 23 +/- 11 ms (p < 0.001). CONCLUSIONS: Nonuniform post-shock repolarization and dispersed post-shock activation contribute to the induction of VF by T-wave shocks. A decreasing dispersion of PS-AT towards higher shock strengths may contribute to the decreased or abolished inducibility by shocks above the upper limit of vulnerability.

Action Potentials↗
PubMed2001

Role of structural complexities of septal tissue in maintaining ventricular fibrillation in isolated, perfused canine ventricle.

INTRODUCTION: It is unclear how the patterns of wavelet propagation during ventricular fibrillation (VF) vary between structurally different tissues. We hypothesized that the structural complexities of septal tissue influence the maintenance of reentrant wavelets in the ventricle. METHODS AND RESULTS: Endocardial activation patterns during VF were analyzed in the isolated, perfused canine right ventricular (RV) free wall (n = 9), interventricular septum (n = 5), and left ventricular (LV) free wall (n = 6) using a computerized mapping system (2-mm resolution) with 120-msec consecutive windows. Each tissue sample was cut progressively to reduce the tissue mass until the VF was terminated. More wavelets were seen in the septa than in the RV and LV free walls at baseline (P = 0.004), and VF in the septa displayed a shorter cycle length than in the RV and LV free walls (P = 0.017). As the tissue mass decreased, VF became successively more organized in all regions: the number of wavelets decreased and the cycle length of VF lengthened. Single and "figure-of-eight" stationary, reentrant wavelets often were mapped after tissue mass reduction in the RV free walls and rarely in the LV free walls, but they were not observed in the septa. Less critical mass was required to maintain VF in the septa than in the RV and LV free walls (P = 0.0006). Gross anatomic and histologic examinations indicated that the tissue structure of the septa is more complex than that of the RV and LV free walls. CONCLUSION: VF activation patterns with progressive reduction of tissue mass differ for the septum and the ventricular free walls. The structural complexities of the septal tissue influence the maintenance of fibrillation in the ventricle.

Animals↗
PubMed1981

Reduction in vulnerability to ventricular fibrillation by bromocriptine, a dopamine agonist.

The effect of a dopamine agonist, bromocriptine, on ventricular fibrillation (VF) threshold was studied in anaesthetised dogs. Bromocriptine produced an increase of 50% in VFT. Pretreatment with the dopamine antagonist haloperidol abolished the effects of bromocriptine on VF threshold as did pretreatment with the peripheral dopamine antagonist, domperidone. It is concluded that bromocriptine reduces vulnerability of the nonischaemic canine ventricle to fibrillation. This effect is most probably mediated by peripheral presynaptic stimulation of dopaminergic receptors, thereby inhibiting noradrenaline release.

Animals↗
PubMed2000

Ventricular fibrillation induced by rapid atrial rates in patients with hypertrophic cardiomyopathy.

AIMS: To describe the mechanisms of induction of ventricular fibrillation (VF) by rapid atrial rates in patients with hypertrophic cardiomyopathy (HCM). METHODS: Electrophysiological studies, management and follow-up in three patients with HCM with VF induced by atrial pacing. RESULTS: In one patient, spontaneous sinus tachycardia triggered VF. In another patient, VF occurred after verapamil infusion during rapid atrial fibrillation, and in the remaining patient there was no clinical VF. In all three patients, short runs of atrial pacing (cycle length 272-380 ms) induced VF, and QRS widening preceded fibrillation in all patients. Marked ventricular electrogram fragmentation was documented in one patient during atrial pacing and in another patient during late ventricular extra-stimuli. Hypotension was associated with sinus tachycardia in one patient. The two patients developing clinical VF underwent atrioventricular (AV) junctional ablation; a ventricular defibrillator was implanted in one, and a mode-switching dual-chamber pacemaker in the other. No arrhythmic events occurred during 34- and 35-month follow-up, respectively. In the other patient, postatrial fibrillation pauses caused syncope, and he is asymptomatic 52 months after implantation of a dual-chamber pacemaker. CONCLUSIONS: Rapid atrial rates can trigger VF in some patients with HCM, probably through a combination of electrophysiological and ischaemic mechanisms. AV junctional ablation may prevent VF in selected cases.

Adolescent↗
PubMedDate not supplied

The effect of cocaine on Ventricular fibrillation threshold in the normal canine heart.

We determined the effect of cocaine on ventricular vulnerability to fibrillation, as measured by ventricular fibrillation threshold (VFT), and cardiac electrophysiology in 20 anesthetized dogs with normal hearts. Animals were randomized in blinded fashion to receive a continuous 3-hour infusion of cocaine 0.11 mg/kg/minute (total dose 20 mg/kg) or placebo (lactose dissolved in normal saline). The VFT, systolic and diastolic blood pressures, ventricular effective refractory period (ERP), and electrocardiographic intervals were measured at baseline and every 30 minutes during infusion. Baseline mean +/- SE VFT in cocaine and placebo groups was 57.0 +/- 7.8 and 51.8 +/- 7.6 mA, respectively (p = 0.64). Cocaine did not significantly decrease VFT, but actually increased it (i.e., reduced ventricular vulnerability to fibrillation) compared with placebo (84.6 +/- 10.4 vs 55.8 +/- 7.2 mA, respectively, at 150 minutes, p = 0.04). Cocaine prolonged ERP and PR, QRS, QT, QTc, JT, and JTc intervals. Cocaine does not increase ventricular vulnerability to fibrillation in anesthetized dogs with normal intact hearts. Its electrophysiologic effects are similar to those of class I antiarrhythmic agents in this model.

Analysis of Variance↗
PubMed1994

Effect of bystander initiated cardiopulmonary resuscitation on ventricular fibrillation and survival after witnessed cardiac arrest outside hospital.

OBJECTIVE: To describe the proportion of patients who were discharged from hospital after witnessed cardiac arrest outside hospital in relation to whether a bystander initiated cardiopulmonary resuscitation. PATIENTS: All patients with witnessed cardiac arrest outside hospital before arrival of the ambulance and in whom cardiopulmonary resuscitation was attempted by the emergency medical service in Gothenburg during 1980-92. RESULTS: Cardiopulmonary resuscitation was initiated by a bystander in 18% (303) of 1,660 cases. In this group 69% had ventricular fibrillation at first recording compared with 51% in the remaining patients (P < 0.001). Among patients in whom cardiopulmonary resuscitation had been initiated by a bystander 25% were discharged alive versus 8% of the remaining patients (P < 0.001). Independent predictors of survival were in order of significance: initial arrhythmia (P < 0.001), interval between collapse and arrival of first ambulance (P < 0.001), cardiopulmonary resuscitation initiated by a bystander (P < 0.001), and age (P < 0.01). Among patients who were admitted to hospital alive 30% of patients in whom cardiopulmonary resuscitation had been initiated by a bystander compared with 58% of remaining patients (P < 0.001) had brain damage and died in hospital. Corresponding figures for death in association with myocardial damage were 18% and 29% respectively (P < 0.01). CONCLUSIONS: Cardiopulmonary resuscitation initiated by a bystander maintains ventricular fibrillation and triples the chance of surviving a cardiac arrest outside hospital. Furthermore, it seems to protect against death in association with brain damage as well as with myocardial damage.

Age Factors↗
PubMed1983

Prevention of ventricular fibrillation by bretylium in a conscious canine model of sudden coronary death.

In anesthetized dogs, a silver wire electrode was inserted into the lumen of the circumflex coronary artery (LCX) and myocardial infarction was produced by a temporary 90-minute occlusion of the left anterior descending coronary artery (LAD) followed by reperfusion. Four days later while in the ambulatory state, a 150 microA current was applied to the intimal surface of the LCX of saline (n = 10) and bretylium (n = 10) treated animals. Intimal injury and coronary thrombosis produced ST segment changes at 138 +/- 39 minutes (chi +/- SEM), followed by premature ventricular beats (at 142 +/- 37 minutes), ventricular tachycardia (at 156 +/- 49 minutes), and ventricular fibrillation (at 163 +/- 51 minutes) in 9 of 10 saline-treated animals. In bretylium-treated animals, ST segment changes appeared at 128 +/- 35 minutes, with six animals surviving for 24 hours (p less than 0.03 vs saline). LAD infarction was present in both saline (14.1 +/- 2.3%) and bretylium (15.1 +/- 2.1% of left ventricle) treated animals with only bretylium-treated animals developing LCX infarcts (16.1 +/- 2.1%). Bretylium prevents ventricular fibrillation (VF) resulting from ischemia at a site distant to prior myocardial infarction in the conscious dog and deserves further attention as a potential antifibrillatory agent for prevention of sudden coronary death in man.

Animals↗
PubMed1995

QT dispersion does not predict early ventricular fibrillation after acute myocardial infarction.

Ventricular arrhythmias may be associated with increased QT dispersion (difference between maximum and minimum QT on standard 12-lead ECG). We performed a case control study to determine if QT dispersion on the admission ECG could predict early VF after acute myocardial infarction. The cases were 24 patients with acute myocardial infarction (14 inferior, 8 anterior, and 2 lateral) with VF within 12 hours of admission. There were 24 control patients without VF matched for site of infarction and ST segment score (sum of ST segment elevation). VF occurred a median of 153 minutes (interquartile range 93-245) after onset of chest pain and 33 minutes (range 7-104) after initial ECG. QT (399 +/- 37 and 394 +/- 37), QT corrected (440 +/- 38 and 429 +/- 29), and QT dispersion (68 +/- 20 and 66 +/- 27) were similar in patients and controls. By design, ST score was similar (11 +/- 9 vs 9 +/- 5 mV), although a good match could not be obtained for three patients with extreme ST elevation. Patients with VF presented to the hospital earlier after the onset of chest pain (median 95 min [range 65-188] compared to 150 min [range 80-270], P = 0.05) and had a lower serum sodium (138 +/- 2.4 vs 140 +/- 2.5, P = 0.05) than controls. Thus, QT interval and QT dispersion, measured on the presenting ECG, did not predict early VF after myocardial infarction.

Aged↗
PubMed1987

Increased release of brain serotonin reduces vulnerability to ventricular fibrillation in the cat.

Brain serotoninergic neurons are known to participate in cardiovascular regulation. Administration of the serotonin precursor 5-l-hydroxytryptophan in conjunction with the monamine oxidase inhibitor phenelzine and the selective peripheral l-amino acid decarboxylase inhibitor carbidopa has been shown to raise the repetitive extrasystole threshold in the canine heart. The present investigation demonstrates that this drug regimen increases the cerebrospinal fluid concentration of serotonin and its major metabolite, 5-hydroxyindoleacetic acid, by 330 and 830%, respectively. By contrast, cerebrospinal fluid concentrations of norepinephrine and its major brain metabolite, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate, and of dopamine's metabolite, 3, 4-dihydroxyphenylacetic acid, were not significantly altered. Concomitantly, the ventricular fibrillation threshold was elevated by 42% and the effective refractory period prolonged by 7%. Efferent sympathetic neural activity was suppressed in the normal heart (from 7.9 +/- 1.3 to 3.9 +/- 1.1 impulses/s). The surge in sympathetic activity associated with acute myocardial ischemia was markedly attenuated. These results indicate that enhancement of central serotoninergic neurotransmission can reduce the susceptibility to ventricular fibrillation mediated through a decline in sympathetic neural traffic to the heart.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1992

Treatment of intractable ventricular fibrillation with prompt circulatory support using a biventricular assist device in pigs--an experimental study.

Refractory ventricular fibrillation (VF), intractable to conventional therapy, can be converted into a stable cardiac rhythm by immediate ventricular volume unloading using a form of mechanical circulatory assist (MCA). We investigated the efficacy of MCA in a controlled animal study in which 20 pigs were subjected to intermittent occlusions (5 times) of the left descending coronary artery (5 min. occlusion + 10 min. reperfusion). 12 of the 20 animals (60%) developed 14 events of VF. 64% of VF developed during reperfusion (p less than 0.05). Countershock was attempted up to eight times and was successful in 5 of the 14 events (36%) (primary defibrillation, PD). When conversion was not achieved, total biventricular bypass was instituted. Mean perfusion time between countershock attempts was 24.4 +/- 15.3 min. All animals (n = 9) with cardiac assistance were successfully defibrillated (secondary defibrillation, SD), (p less than 0.05). Hemodynamic parameters after SD were not significantly different from those after PD (p greater than 0.05). Survival rate following PD was 66.6%. Six animals were ultimately weaned from cardiac assistance following SD. Three others died of progressive cardiogenic shock in the six hour follow-up period following SD. These non-survivors had a significantly longer VF time than the survivors (41.7 +/- 10.4 vs. 15.8 +/- 8.0, p less than 0.05). Overall survival after SD was the same as that for PD: 66.6% (p greater than 0.05). These results show that prompt conversion of VF into a stable cardiac rhythm is a prerequisite to recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Sustained consciousness during ventricular fibrillation: case report of cough cardiopulmonary resuscitation.

A 54-year-old male developed ventricular fibrillation during right coronary angiography. Cough cardiopulmonary resuscitation was performed for 30 sec allowing the patient to remain alert and hemodynamically stable. Cough cardiopulmonary resuscitation is a simple, often overlooked technique that can be utilized during resuscitation in the cardiac catheterization laboratory.

Cardiac Catheterization↗