Tag Archives: cardiology

Thrombolysis in submassive PE – still equipoise?

The AHA has produced a comprehensive guideline on venous thromboembolic disease. Here are some excerpts pertaining to resuscitation room decision making, particularly: ‘should I thrombolyse this patient?’

Definition for massive PE: Acute PE with sustained hypotension (systolic blood pressure <90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or left ventricular [LV] dysfunction), pulselessness, or persistent profound bradycardia (heart rate <40 bpm with signs or symptoms of shock).

Definition for submassive PE: Acute PE without systemic hypotension (systolic blood pressure ≥90 mm Hg) but with either RV dysfunction or myocardial necrosis.
RV dysfunction means the presence of at least 1 of the following:

  • RV dilation (apical 4-chamber RV diameter divided by LV diameter >0.9) or RV systolic dysfunction on echocardiography
  • RV dilation (4-chamber RV diameter divided by LV diameter >0.9) on CT
  • Elevation of BNP (>90 pg/mL)
  • Elevation of N-terminal pro-BNP (>500 pg/mL); or
  • Electrocardiographic changes (new complete or incomplete right bundle-branch block, anteroseptal ST elevation or depression, or anteroseptal T-wave inversion)

Myocardial necrosis is defined as either of the following:

  • Elevation of troponin I (>0.4 ng/mL) or
    Elevation of troponin T (>0.1 ng/mL)

Odds ratio for short-term mortality for RV dysfunction on echocardiography = 2.53 (95% CI 1.17 to 5.50).

Troponin elevations had an odds ratio for mortality of 5.90 (95% CI 2.68 to 12.95).

Definition for low risk PE: those with normal RV function and no elevations in biomarkers with short-term mortality rates approaching ≈ 1%

Recommendations for Initial Anticoagulation for Acute PE
  • Therapeutic anticoagulation with subcutaneous LMWH, intravenous or subcutaneous UFH with monitoring, unmonitored weight-based subcutaneous UFH, or subcutaneous fondaparinux should be given to patients with objectively confirmed PE and no contraindications to anticoagulation (Class I; Level of Evidence A).
  • Therapeutic anticoagulation during the diagnostic workup should be given to patients with intermediate or high clinical probability of PE and no contraindications to anticoagulation (Class I; Level of Evidence C).


Patients treated with a fibrinolytic agent have faster restoration of lung perfusion. At 24 hours, patients treated with heparin have no substantial improvement in pulmonary blood flow, whereas patients treated with adjunctive fibrinolysis manifest a 30% to 35% reduction in total perfusion defect. However, by 7 days, blood flow improves similarly (≈65% to 70% reduction in total defect).

Thirteen placebo-controlled randomized trials of fibrinolysis for acute PE have been published, but only a subset evaluated massive PE specifically.
When Wan et al restricted their analysis to those trials with massive PE, they identified a significant reduction in recurrent PE or death from 19.0% with heparin alone to 9.4% with fibrinolysis (odds ratio 0.45, 95% CI 0.22 to 0.90).

Data from registries indicate that the short-term mortality rate directly attributable to submassive PE treated with heparin anticoagulation is probably < 3.0%. The implication is that even if adjunctive fibrinolytic therapy has extremely high efficacy, for example, a 30% relative reduction in mortality, the effect size on mortality due to submassive PE is probably < 1%. Thus, secondary adverse outcomes such as persistent RV dysfunction, chronic thromboembolic pulmonary hypertension, and impaired quality of life represent appropriate surrogate goals of treatment.

Data suggest that compared with heparin alone, heparin plus fibrinolysis yields a significant favorable change in right ventricular systolic pressure and pulmonary arterial pressure incident between the time of diagnosis and follow-up. Patients with low-risk PE have an unfavorable risk-benefit ratio with fibrinolysis. Patients with PE that causes hypotension probably do benefit from fibrinolysis. Management of submassive PE crosses the zone of equipoise, requiring the clinician to use clinical judgment.

An algorithm is proposed:

Two criteria can be used to assist in determining whether a patient is more likely to benefit from fibrinolysis: (1) Evidence of present or developing circulatory or respiratory insufficiency; or (2) evidence of moderate to severe RV injury.

Evidence of circulatory failure includes any episode of hypotension or a persistent shock index (heart rate in beats per minute divided by systolic blood pressure in millimeters of mercury) >1

The definition of respiratory insufficiency may include hypoxemia, defined as a pulse oximetry reading < 95% when the patient is breathing room air and clinical judgment that the patient appears to be in respiratory distress. Alternatively, respiratory distress can be quantified by the numeric Borg score, which assesses the severity of dyspnea from 0 to 10 (0=no dyspnea and 10=sensation of choking to death).

Evidence of moderate to severe RV injury may be derived from Doppler echocardiography that demonstrates any degree of RV hypokinesis, McConnell’s sign (a distinct regional pattern of RV dysfunction with akinesis of the mid free wall but normal motion at the apex), interventricular septal shift or bowing, or an estimated RVSP > 40 mm Hg.

Biomarker evidence of moderate to severe RV injury includes major elevation of troponin measurement or brain natriuretic peptides.

Two trials are currently ongoing that aim to assess effect of thrombolysis on patients with submassive PE: PEITHO and TOPCOAT

Recommendations for Fibrinolysis for Acute PE
  • Fibrinolysis is reasonable for patients with massive acute PE and acceptable risk of bleeding complications (Class IIa; Level of Evidence B).
  • Fibrinolysis may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory insufficiency, severe RV dysfunction, or major myocardial necrosis) and low risk of bleeding complications (Class IIb; Level of Evidence C).
  • Fibrinolysis is not recommended for patients with low-risk PE (Class III; Level of Evidence B) or submassive acute PE with minor RV dysfunction, minor myocardial necrosis, and no clinical worsening (Class III; Level of Evidence B).
  • Fibrinolysis is not recommended for undifferentiated cardiac arrest (Class III; Level of Evidence B).
Recommendations for Catheter Embolectomy and Fragmentation
  • Depending on local expertise, either catheter embolectomy and fragmentation or surgical embolectomy is reasonable for patients with massive PE and contraindications to fibrinolysis (Class IIa; Level of Evidence C).
  • Catheter embolectomy and fragmentation or surgical embolectomy is reasonable for patients with massive PE who remain unstable after receiving fibrinolysis (Class IIa; Level of Evidence C).
  • For patients with massive PE who cannot receive fibrinolysis or who remain unstable after fibrinolysis, it is reasonable to consider transfer to an institution experienced in either catheter embolectomy or surgical embolectomy if these procedures are not available locally and safe transfer can be achieved (Class IIa; Level of Evidence C).
  • Either catheter embolectomy or surgical embolectomy may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory failure, severe RV dysfunction, or major myocardial necrosis) (Class IIb; Level of Evidence C).
  • Catheter embolectomy and surgical thrombectomy are not recommended for patients with low-risk PE or submassive acute PE with minor RV dysfunction, minor myocardial necrosis, and no clinical worsening (Class III; Level of Evidence C).


Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension
Circulation. 2011 Apr 26;123(16):1788-1830 (Free Full Text)

STEMI criteria vary with age and sex

On reading through the 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science – Part 10: Acute Coronary Syndromes, I found a reminder that the ECG criteria for diagnosing ST-elevation myocardial infarction (STEMI) vary according to age and sex. From the original article in the Journal of the American College of Cardiology:

The threshold values of ST-segment elevation of 0.2 mV (2 mm) in some leads and 0.1 mV (1 mm) in others results from recognition that some elevation of the junction of the QRS complex and the ST segment (the J point) in most chest leads is normal. Recent studies have revealed that the threshold values are dependent on gender, age, and ECG lead ([8], [9], [10], [11] and [12]). In healthy individuals, the amplitude of the ST junction is generally highest in leads V2 and V3 and is greater in men than in women.


  1. For men 40 years of age and older, the threshold value for abnormal J-point elevation should be 0.2 mV (2 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads.
  2. For men less than 40 years of age, the threshold values for abnormal J-point elevation in leads V2 and V3 should be 0.25 mV (2.5 mm).
  3. For women, the threshold value for abnormal J-point elevation should be 0.15 mV (1.5 mm) in leads V2 and V3 and greater than 0.1 mV (1 mm) in all other leads.
  4. For men and women, the threshold for abnormal J-point elevation in V3R and V4R should be 0.05 mV (0.5 mm), except for males less than 30 years of age, for whom 0.1 mV (1 mm) is more appropriate.
  5. For men and women, the threshold value for abnormal J- point elevation in V7 through V9 should be 0.05 mV (0.5 mm).
  6. For men and women of all ages, the threshold value for abnormal J-point depression should be −0.05 mV (−0.5 mm) in leads V2 and V3 and −0.1 mV (−1 mm) in all other leads.

What does establishment of abnormal J-point mean for STEMI diagnosis? The AHA/ECC guidelines state the following:

ST-segment elevation… is characterized by ST-segment elevation in 2 or more contiguous leads and is classified as ST-segment elevation MI (STEMI). Threshold values for ST-segment elevation consistent with STEMI are:
  • J-point elevation 0.2 mV (2 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men ≥40 years old);
  • J-point elevation 0.25 mV (2.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men <40 years old);
  • J-point elevation 0.15 mV (1.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (women).

So, in summary:

Older men – 2mm in V2/V3 and 1mm everywhere else
Younger men – 2.5 mm in V2/V3 and 1mm everywhere else
Women – 1.5 mm in V2/V3 and 1mm everywhere else

Shouldn’t be too difficult to remember.

Part 10: acute coronary syndromes: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation. 2010 Nov 2;122(18 Suppl 3):S787-817

AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part VI: acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology.
J Am Coll Cardiol. 2009 Mar 17;53(11):1003-11

‘Sensitive’ troponin assays do not rule out at ED presentation

An assessment of new ‘sensitive’ troponin assays at presentation of chest pain patients in a real-world ED setting showed that a single troponin I assay at ED presentation has insufficient sensitivity for clinical use to rule out MI. Author Anne-Maree Kelly discusses the current requirement for a minimum interval after an episode of chest pain to ensure adequate sensitivity: Currently in Australia the recommended minimum interval is 8 h after symptom onset. New evidence suggests that a shorter interval might be appropriate with the sensitive assays. Keller et al. reported 100% sensitivity at 3 h after ED presentation. Macrae et al. suggested that an assay 6 h from pain onset or serial assays 3 h apart with one at least 6 h from pain onset has high diagnostic accuracy. Although further research in an ED chest pain cohort is needed, the weight of evidence suggests a reduction in the minimum interval from pain onset to 6 h might be appropriate.

Aim: Troponin assays have high diagnostic value for myocardial infarction (MI), but sensitivity has been weak early after chest pain onset. New, so-called ‘sensitive’ troponin assays have recently been introduced. Two studies report high sensitivity for assays taken at ED presentation, but studied selected populations. Our aim was to evaluate the diagnostic performance for MI of a sensitive troponin assay measured at ED presentation in an unselected chest pain population without ECG evidence of ischaemia.
Methods: This is a sub-study of a prospective cohort study of adult patients with potentially cardiac chest pain who underwent evaluation for acute coronary syndrome. Patients with clear ECG evidence of acute ischaemia or an alternative diagnosis were excluded. Data collected included demographic, clinical, ECG, biomarker and outcome data. A ‘positive’ troponin was defined as >99th percentile of the assay used. MI diagnosis was as judged by the treating cardiologist. The outcomes of interest were sensitivity, specificity and likelihood ratios (LR) for positive troponin assay taken at ED presentation. Data were analysed by clinical performance analysis.
Results: Totally 952 were studied. Median age was 61 years; 56.4% were male and median TIMI score was 2. There were 129 MI (13.6, 95% CI 11.5-15.9). Sensitivity of TnI at ED presentation was 76.7% (95% CI 68.5-83.7%), specificity 93.6% (95% CI 91.7-95.1%), with LR positive 11.92 and LR negative 0.25.
Conclusion: Sensitive TnI assay at ED presentation has insufficient diagnostic accuracy for detection of MI. Serial biomarker assays in patients with negative initial TnI are required.

Performance of a sensitive troponin assay in the early diagnosis of acute myocardial infarction in the emergency department.
Emerg Med Australas. 2011 Apr;23(2):181-5

Triple marker panel for AMI

A large Asian/Australasian study examined a 2hr triple-marker test in patients presenting with chest pain.

BACKGROUND: Patients with chest pain contribute substantially to emergency department attendances, lengthy hospital stay, and inpatient admissions. A reliable, reproducible, and fast process to identify patients presenting with chest pain who have a low short-term risk of a major adverse cardiac event is needed to facilitate early discharge. We aimed to prospectively validate the safety of a predefined 2-h accelerated diagnostic protocol (ADP) to assess patients presenting to the emergency department with chest pain symptoms suggestive of acute coronary syndrome.

METHODS: This observational study was undertaken in 14 emergency departments in nine countries in the Asia-Pacific region, in patients aged 18 years and older with at least 5 min of chest pain. The ADP included use of a structured pre-test probability scoring method (Thrombolysis in Myocardial Infarction [TIMI] score), electrocardiograph, and point-of-care biomarker panel of troponin, creatine kinase MB, and myoglobin. The primary endpoint was major adverse cardiac events within 30 days after initial presentation (including initial hospital attendance). This trial is registered with the Australia-New Zealand Clinical Trials Registry, number ACTRN12609000283279.

FINDINGS: 3582 consecutive patients were recruited and completed 30-day follow-up. 421 (11.8%) patients had a major adverse cardiac event. The ADP classified 352 (9.8%) patients as low risk and potentially suitable for early discharge. A major adverse cardiac event occurred in three (0.9%) of these patients, giving the ADP a sensitivity of 99.3% (95% CI 97.9-99.8), a negative predictive value of 99.1% (97.3-99.8), and a specificity of 11.0% (10.0-12.2).

INTERPRETATION: This novel ADP identifies patients at very low risk of a short-term major adverse cardiac event who might be suitable for early discharge. Such an approach could be used to decrease the overall observation periods and admissions for chest pain. The components needed for the implementation of this strategy are widely available. The ADP has the potential to affect health-service delivery worldwide.

A 2-h diagnostic protocol to assess patients with chest pain symptoms in the Asia-Pacific region (ASPECT): a prospective observational validation study.
Lancet. 2011 Mar 26;377(9771):1077-84
Full text link available at time of writing

In an accompanying editorial, nicely entitled ‘Acute MI: triple-markers resurrected or Bayesian dice?’ Dr Rick Body notes that the point-of-care triple-marker test has a relatively low sensitivity, at just 82.9%, when used alone, and the sensitivity only increased to 99.3% in the current study because it was used in an already-selected low-risk population. He writes: “Most people will probably consider this net risk to be statistically acceptable. However, if properly informed, low-risk patients might feel differently about the relative merits of waiting for definitive six-hour laboratory-based troponin testing or going home after two hours on the basis of results from a test that correctly identifies serious coronary disease, when present, in just over eight of 10 occasions.”

Dr Body has a new blog at The Bodsblog where we’re likely to be informed other data relevant to emergency cardiology as they emerge.

Point-of-care panel assessment using a similar triple-marker test at presentation and 90 minutes was also examined in the RATPAC study, in which it increased successful discharge home and reduced median length of stay, but did not alter overall hospital bed use.

Vasoactive drugs in cardiogenic shock

I’m always on the look-out for evidence to guide vasoactive drug therapy, an area where much dogma is spouted by many who have not read the literature. Here’s a small (note: pilot) study comparing two strategies for cardiogenic shock. The higher heart rate and lactate with epinephrine (adrenaline) are consistent with the findings of the great CAT study; this is of interest, but not necessarily clinically significant nor practice changing.

OBJECTIVE: There is no study that has compared, in a randomized manner, which vasopressor is most suitable in optimizing both systemic and regional hemodynamics in cardiogenic shock patients. Hence, the present study was designed to compare epinephrine and norepinephrine-dobutamine in dopamine-resistant cardiogenic shock.
DESIGN: Open, randomized interventional human study.
SETTING: Medical intensive care unit in a university hospital.
PATIENTS: Thirty patients with a cardiac index of <2.2 L/min/m and a mean arterial pressure of <60 mm Hg resistant to combined dopamine-dobutamine treatment and signs of shock. Patients were not included in cases of cardiogenic shock secondary to acute ischemic events such as myocardial infarction. Noninclusion criteria also included immediate indication of mechanical assistance.
INTERVENTIONS: Patients were randomized to receive an infusion of either norepinephrine-dobutamine or epinephrine titrated to obtain a mean arterial pressure of between 65 and 70 mm Hg with a stable or increased cardiac index.
MAIN RESULTS: Both regimens increased cardiac index and oxygen-derived parameters in a similar manner. Patients in the norepinephrine-dobutamine group demonstrated heart rates lower (p<.05) than those in the epinephrine group. Epinephrine infusion was associated with new arrhythmias in three patients. When compared to baseline values, after 6 hrs, epinephrine infusion was associated with an increase in lactate level (p<.01), whereas this level decreased in the norepinephrine-dobutamine group. Tonometered PCO2 gap, a surrogate for splanchnic perfusion adequacy, increased in the epinephrine-treated group (p<.01) while decreasing in the norepinephrine group (p<.01). Diuresis increased in both groups but significantly more so in the norepinephrine-dobutamine group, whereas plasma creatinine decreased in both groups.
CONCLUSIONS: When considering global hemodynamic effects, epinephrine is as effective as norepinephrine-dobutamine. Nevertheless, epinephrine is associated with a transient lactic acidosis, higher heart rate and arrhythmia, and inadequate gastric mucosa perfusion. Thus, the combination norepinephrine-dobutamine appears to be a more reliable and safer strategy.

Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study
Crit Care Med. 2011 Mar;39(3):450-5

Which cardiac arrest survivors have a positive angio?

A retrospective study of out-of-hospital cardiac arrest patients attended by a French pre-hospital system was performed to assess the predictive factors for positive coronary angiography.

OBJECTIVES: Coronary angiography is often performed in survivors of out-of-hospital cardiac arrest, but little is known about the factors predictive of a positive coronary angiography. Our aim was to determine these factors.

METHODS: In this 7-year retrospective study (January 2000-December 2006) conducted by a French out-of-hospital emergency medical unit, data were collected according to Utstein style guidelines on all out-of-hospital cardiac arrest patients with suspected coronary disease who recovered spontaneous cardiac activity and underwent early coronary angiography. Coronary angiography was considered positive if a lesion resulting in more than a 50% reduction in luminal diameter was observed or if there was a thrombus at an occlusion site.

RESULTS: Among the 4621 patients from whom data were collected, 445 were successfully resuscitated and admitted to hospital. Of these, 133 were taken directly to the coronary angiography unit, 95 (71%) had at least one significant lesion, 71 (53%) underwent a percutaneous coronary intervention, and 30 survived [23%, 95% confidence interval (CI): 16-30]. According to multivariate analysis, the factors predictive of a positive coronary angiography were a history of diabetes [odds ratio (OR): 7.1, 95% CI: 1.4-36], ST segment depression on the out-of-hospital ECG (OR: 5.4, 95% CI: 1.1-27.8), a history of coronary disease (OR: 5.3, 95% CI: 1.4-20.1), cardiac arrest in a public place (OR: 3.7, 95% CI: 1.3-10.7), and ventricular fibrillation or ventricular tachycardia as initial rhythm (OR: 3.1, 95% CI: 1.1-8.6).

CONCLUSION: Among the factors identified, diabetes and a history of coronary artery were strong predictors for a positive coronary angiography, whereas ST segment elevation was not as predictive as expected.

Predictive factors for positive coronary angiography in out-of-hospital cardiac arrest patients
Eur J Emerg Med. 2011 Apr;18(2):73-6

An easily missed cause of shock

A potentially reversible cause of haemodynamic shock in critically ill patients is left ventricular outflow tract obstruction (LVOTO). We are familiar with this phenomenon in conditions such as hypertrophic cardiomyopathy (HCM), but LVOTO can occur in the absence of HCM and result in hypotension that may be refractory to catecholamines. In fact, vasoactive drugs are often the precipitant.

A case is reported of an intubated elderly man with pneumonia and COPD who upon starting dopamine and furosemide for hypotension and anuria developed severe haemodynamic deterioration1. Echo revealed a hyperkinetic left ventricle with mild concentric hypertrophy, septal wall thickness of 12 mm (normal range up to 10mm), and a reduced end-diastolic diameter. Systolic anterior motion (SAM) of the anterior mitral leaflet causing a significant left ventricular outflow tract obstruction (LVOTO), with a peak gradient of 100 mmHg, was detected. The patient improved with discontinuation of vasoactive drugs and fluid loading. A follow up cardiac MR showed a structurally normal LV.

The authors describe the factors that combine to produce this syndrome:

  • Anatomical substrate – Left ventricular hypertrophy due to hypertension, mitral valve repair, previous aortic valve replacement, abnormalities of the mitral subvalvular apparatus, sigmoid septum and a steep aortic root angle.
  • Precipitating factors – Drug therapies such as catecholamine infusion or diuretics, which respectively enhance the contractility of the basal segments and reduce the left ventricular cavity, emotional stress (like described in the apical ballooning syndrome), hypovolaemia, dehydration, sepsis, and myocardial infarction; hypovolaemia and mechanical ventilation further exacerbate underfilling of the LV and dynamic LVOTO.

In a review article on the topic, Dr Chockalingam and colleagues describe structural and functional factors in this finely crafted explanation2:

The asymmetrically hypertrophied septum, progressive narrowing of the LVOT during systole, and direction of the bloodstream cause drag forces and a Venturi effect on the anterior mitral leaflet, which results in SAM of the anterior mitral leaflet. This movement results in the anterior mitral leaflet contacting the septum for a period of systole, effectively obstructing the path of ventricular outflow. Failure of the anterior mitral leaflet to coapt with the posterior leaflet in systole results in MR. The degree and duration of mitral SAM determine the severity of the dynamic LVOTO gradients and MR.

Although classically described with hypertrophic cardiomyopathy, SAM and LVOTO can independently result from various clinical settings such as LV hypertrophy (hypertension or sigmoid septum), reduced LV chamber size (dehydration, bleeding, or diuresis), mitral valve abnormalities (redundant, long anterior leaflet), and hypercontractility (stress, anxiety, or inotropic agents). Dynamic LVOTO may occur with acute coronary syndrome and often presents with shock and a new systolic murmur3. The presence of a new murmur in a shocked ACS patient should therefore prompt consideration of the following diagnoses:

  • Acute mitral valve dysfunction
  • Ventricular septal defect
  • Free wall rupture
  • Dynamic LVOTO

Treatment is aimed at alleviating the causes and should be individualised. Options include coronary revascularisation, volume therapy, beta blockade, removing afterload reduction (vasodilators and balloon pumps can exacerbate LVOTO), and alpha agonists such as phenylephrine.


In summary, dynamic LVOTO:
  • is a potentially reversible cause of haemodynamic shock in critically ill patients
  • should be considered in critically ill patients whose shock fails to improve or worsen with inotropic medication
  • should be considered in patients with ACS, shock, and a new systolic murmur
  • can result from combinations of LV hypertrophy, reduced LV chamber size (dehydration, bleeding, or diuresis), mitral valve abnormalities, and hypercontractility (stress, anxiety, or inotropic agents)
  • is yet another reason why the haemodynamic monitor of choice in shocked patients should be echocardiography!

Echo showing systolic anterior motion of the mitral valve

1. Pathophysiology of Dynamic Left Ventricular Outflow Tract Obstruction in a Critically Ill Patient Echocardiography. 2010 Nov;27(10):E122-4

2. Dynamic Left Ventricular Outflow Tract Obstruction in Acute Myocardial Infarction With Shock Circulation. 2007 Jul 31;116(5):e110-3 Free Full Text 3. Dynamic left ventricular outflow tract obstruction in acute coronary syndromes: an important cause of new systolic murmur and cardiogenic shock Mayo Clin Proc. 1999 Sep;74(9):901-6

Supplemental oxygen decreases LV perfusion in volunteers

Oxygen therapy in normoxic acute coronary syndrome patients is controversial, and a previous systematic review cautioned against it in uncomplicated MI. A volunteer study using cardiac imaging demonstrates the effects of supplemental oxygen on coronary blood flow.


OBJECTIVES: Oxygen (O2) is a cornerstone in the treatment of critically ill patients, and the guidelines prescribe 10-15 l of O2/min even to those who are initially normoxic. Studies using indirect or invasive methods suggest, however, that supplemental O2 may have negative cardiovascular effects. The aim of this study was to test the hypothesis, using noninvasive cardiac magnetic resonance imaging, that inhaled supplemental O2 decreases cardiac output (CO) and coronary blood flow in healthy individuals.

METHODS: Sixteen healthy individuals inhaled O2 at 1, 8 and 15 l/min through a standard reservoir bag mask. A 1.5 T magnetic resonance imaging scanner was used to measure stroke volume, CO and coronary sinus blood flow. Left ventricular (LV) perfusion was calculated as coronary sinus blood flow/LV mass.

RESULTS: The O2 response was dose-dependent. At 15 l of O2/min, blood partial pressure of O2 increased from an average 11.7 to 51.0 kPa with no significant changes in blood partial pressure of CO2 or arterial blood pressure. At the same dose, LV perfusion decreased by 23% (P=0.005) and CO decreased by 10% (P=0.003) owing to a decrease in heart rate (by 9%, P<0.002), with no significant changes in stroke volume or LV dimensions. Owing to the decreased CO and LV perfusion, systemic and coronary O2 delivery fell by 4 and 11% at 8 l of O2/min, despite the increased blood oxygen content.

CONCLUSION: Our data indicate that O2 administration decreases CO, LV perfusion and systemic and coronary O2 delivery in healthy individuals. Further research should address the effects of O2 therapy in normoxic patients.

Effects of oxygen inhalation on cardiac output, coronary blood flow and oxygen delivery in healthy individuals, assessed with MRI
European Journal of Emergency Medicine 2011, 18:25–30

Furosemide infusion in acute decompensated heart failure

A randomised controlled trial of 308 patients with acute decompensated heart failure compared continuous furosemide infusion with ‘low’ dose (equal to their total daily oral loop diuretic dose in furosemide equivalents) or high dose furosemide boluses. There was no outcome difference between infusion and bolus, although the high dose (2.5 times previous oral diuretic dose 12 hourly for 48 hours) improved patients’ symptoms while causing transient elevations in serum creatinine. Editorialist Dr G Fonarow states:

‘..these findings should change current practice. Since a high-dose regimen may relieve dyspnea more quickly without adverse effects on renal function, that regimen is preferable to a low-dose regimen. Administration of boluses may be more convenient than continuous infusion and equally effective.’


BACKGROUND: Loop diuretics are an essential component of therapy for patients with acute decompensated heart failure, but there are few prospective data to guide their use.

METHODS: In a prospective, double-blind, randomized trial, we assigned 308 patients with acute decompensated heart failure to receive furosemide administered intravenously by means of either a bolus every 12 hours or continuous infusion and at either a low dose (equivalent to the patient’s previous oral dose) or a high dose (2.5 times the previous oral dose). The protocol allowed specified dose adjustments after 48 hours. The coprimary end points were patients’ global assessment of symptoms, quantified as the area under the curve (AUC) of the score on a visual-analogue scale over the course of 72 hours, and the change in the serum creatinine level from baseline to 72 hours.

RESULTS: In the comparison of bolus with continuous infusion, there was no significant difference in patients’ global assessment of symptoms (mean AUC, 4236±1440 and 4373±1404, respectively; P=0.47) or in the mean change in the creatinine level (0.05±0.3 mg per deciliter [4.4±26.5 μmol per liter] and 0.07±0.3 mg per deciliter [6.2±26.5 μmol per liter], respectively; P=0.45). In the comparison of the high-dose strategy with the low-dose strategy, there was a nonsignificant trend toward greater improvement in patients’ global assessment of symptoms in the high-dose group (mean AUC, 4430±1401 vs. 4171±1436; P=0.06). There was no significant difference between these groups in the mean change in the creatinine level (0.08±0.3 mg per deciliter [7.1±26.5 μmol per liter] with the high-dose strategy and 0.04±0.3 mg per deciliter [3.5±26.5 μmol per liter] with the low-dose strategy, P=0.21). The high-dose strategy was associated with greater diuresis and more favorable outcomes in some secondary measures but also with transient worsening of renal function.

CONCLUSIONS: Among patients with acute decompensated heart failure, there were no significant differences in patients’ global assessment of symptoms or in the change in renal function when diuretic therapy was administered by bolus as compared with continuous infusion or at a high dose as compared with a low dose. (Funded by the National Heart, Lung, and Blood Institute; ClinicalTrials.gov number, NCT00577135.).

Diuretic strategies in patients with acute decompensated heart failure
N Engl J Med. 2011 Mar 3;364(9):797-805

Delayed door-to-balloon even with helicopters

For a whole bunch of reasons, patients with ST-elevation myocardial infarction who undergo interhospital transfer for primary percutaneous coronary intervention may not meet the required 90 minute door-to-balloon time. In a new study of patients transferred by helicopter, only 3% of STEMI patients transferred for reperfusion met the 90-minute goal. Should this result in an increase in the use of fibrinolysis at non–percutaneous coronary intervention hospitals?

Opportunity for gratuitous helicopter shot never knowingly declined

STUDY OBJECTIVE: Early reperfusion portends better outcomes for ST-segment elevation myocardial infarction (STEMI) patients. This investigation estimates the proportions of STEMI patients transported by a hospital-based helicopter emergency medical services (EMS) system who meet the goals of 90-minute door-to-balloon time for percutaneous coronary intervention or 30-minute door-to-needle time for fibrinolysis.

METHODS: This was a multicenter, retrospective chart review of STEMI patients flown by a hospital-based helicopter service in 2007. Included patients were transferred from an emergency department (ED) to a cardiac catheterization laboratory for primary or rescue percutaneous coronary intervention. Out-of-hospital, ED, and inpatient records were reviewed to determine door-to-balloon time and door-to-needle time. Data were abstracted with a priori definitions and criteria.

RESULTS: There were 179 subjects from 16 referring and 6 receiving hospitals. Mean age was 58 years, 68% were men, and 86% were white. One hundred forty subjects were transferred for primary percutaneous coronary intervention, of whom 29 had no intervention during catheterization. For subjects with intervention, door-to-balloon time exceeded 90 minutes in 107 of 111 cases (97%). Median door-to-balloon time was 131 minutes (interquartile range 114 to 158 minutes). Thirty-nine subjects (21%) received fibrinolytics before transfer, and 19 of 39 (49%) received fibrinolytics within 30 minutes. Median door-to-needle time was 31 minutes (interquartile range 23 to 45 minutes).

CONCLUSION: In this study, STEMI patients presenting to non-percutaneous coronary intervention facilities who are transferred to a percutaneous coronary intervention-capable hospital by helicopter EMS do not commonly receive fibrinolysis and rarely achieve percutaneous coronary intervention within 90 minutes. In similar settings, primary fibrinolysis should be considered while strategies to reduce the time required for subsequent interventional care are explored.

Reperfusion Is Delayed Beyond Guideline Recommendations in Patients Requiring Interhospital Helicopter Transfer for Treatment of ST-segment Elevation Myocardial Infarction.
Ann Emerg Med. 2011 Mar;57(3):213-220