Category Archives: Ultrasound

Sonographic bits and bobs

Ultrasound-Guided Radial Artery Catheterization


In case you needed some evidence – a systematic review supports ultrasound guidance as a means of improving insertion success of radial artery catheters


BACKGROUND: Ultrasound guidance commonly is used for the placement of central venous catheters (CVCs). The Agency for Healthcare Research and Quality recommends the use of ultrasound for CVC placement as one of its 11 practices to improve patient care. Despite increased access to portable ultrasound machines and comfort with ultrasound-guided CVC access, fewer clinicians are familiar with ultrasound-guided techniques of arterial catheterization. The goal of this systematic review and meta-analysis was to determine the utility of real-time two-dimensional ultrasound guidance for radial artery catheterization.

METHODS: A comprehensive literature search of Medline, Excerpta Medica Database, and the Cochrane Central Register of Controlled Trials by two independent reviewers identified prospective, randomized controlled trials comparing ultrasound guidance with traditional palpation techniques of radial artery catheterization. Data were extracted on study design, study size, operator and patient characteristics, and the rate of first-attempt success. A meta-analysis was constructed to analyze the data.

RESULTS: Four trials with a total of 311 subjects were included in the review, with 152 subjects included in the palpation group and 159 in the ultrasound-guided group. Compared with the palpation method, ultrasound guidance for arterial catheterization was associated with a 71% improvement in the likelihood of first-attempt success (relative risk, 1.71; 95% CI, 1.25-2.32).

CONCLUSIONS: The use of real-time two-dimensional ultrasound guidance for radial artery catheterization improved first-pass success rate.

Ultrasound-Guided Catheterization of the Radial Artery
Chest. 2011 Mar;139(3):524-9

Open book fractures and ultrasound

For me, this is one of those ‘why didn’t I think of that?!’ studies… extending the FAST scan to measure pubic symphyseal widening to detect open-book pelvic fractures. A pubic symphysis width of 25 mm was considered positive; the authors state that this width is considered diagnostic for anterior-posterior compression fracture of the pelvis in the non-pregnant patient.
Since only four of the 23 patients studied had radiological widening, the authors’ conclusions make sense: Further study with a larger cohort is needed to confirm this technique’s validity for diagnosing PS widening in APC pelvic fractures.
A reasonable question might be: ‘so what?’, especially if pelvic binders are routinely applied to polytrauma patients and radiographs are rapidly obtained. However as a retrieval medicine doctor working in remote and austere environments I wonder whether this could be useful to us. Perhaps if combined with this intervention?

BACKGROUND: The focused abdominal sonography in trauma (FAST) examination is a routine component of the initial work-up of trauma patients. However, it does not identify patients with retroperitoneal hemorrhage associated with significant pelvic trauma. A wide pubic symphysis (PS) is indicative of an open book pelvic fracture and a high risk of retroperitoneal bleeding.

STUDY OBJECTIVES: We hypothesized that an ultrasound image of the PS as part of the FAST examination (FAST-PS) would be an accurate method to determine if pubic symphysis diastasis was present.

METHODS: This is a comparative study of a diagnostic test on a convenience sample of 23 trauma patients at a Level 1 Trauma Center. The PS was measured sonographically in the Emergency Department (ED) and post-mortem (PM) at the State Medical Examiner. The ultrasound (US) measurements were then compared with PS width on anterior-posterior pelvis radiograph.

RESULTS: Twenty-three trauma patients were evaluated with both plain radiographs and US (11 PM, 12 ED). Four patients had radiographic PS widening (3 PM, 1 ED) and 19 patients had radiographically normal PS width; all were correctly identified with US. US measurements were compared with plain X-ray study by Bland-Altman plot. With one exception, US measurements were within 2 standard deviations of the radiographic measurements and, therefore, have excellent agreement. The only exception was a patient with pubic symphysis wider than the US probe.

CONCLUSION: Bedside ultrasound examination may be able to identify pubic symphysis widening in trauma patients. This potentially could lead to faster application of a pelvic binder and tamponade of bleeding.

Ultrasonographic determination of pubic symphyseal widening in trauma: the FAST-PS study
J Emerg Med. 2011 May;40(5):528-33

E-FAST for pneumothorax

Some further evidence of the superiority of ultrasound over chest x-ray for the detection of pneumothorax (although it’s not perfect):

INTRODUCTION: Early identification of pneumothorax is crucial to reduce the mortality in critically injured patients. The objective of our study is to investigate the utility of surgeon performed extended focused assessment with sonography for trauma (EFAST) in the diagnosis of pneumothorax.
METHODS: We prospectively analysed 204 trauma patients in our level I trauma center over a period of 12 (06/2007-05/2008) months in whom EFAST was performed. The patients’ demographics, type of injury, clinical examination findings (decreased air entry), CXR, EFAST and CT scan findings were entered into the data base. Sensitivity, specificity, positive (PPV) and negative predictive values (NPV) were calculated.
RESULTS: Of 204 patients (mean age–43.01+/-19.5 years, sex–male 152, female 52) 21 (10.3%) patients had pneumothorax. Of 21 patients who had pneumothorax 12 were due to blunt trauma and 9 were due to penetrating trauma. The diagnosis of pneumothorax in 204 patients demonstrated the following: clinical examination was positive in 17 patients (true positive in 13/21, 62%; 4 were false positive and 8 were false negative), CXR was positive in 16 (true positive in 15/19, 79%; 1 false positive, 4 missed and 2 CXR not performed before chest tube) patients and EFAST was positive in 21 patients (20 were true positive [95.2%], 1 false positive and 1 false negative). In diagnosing pneumothorax EFAST has significantly higher sensitivity compared to the CXR (P=0.02).
CONCLUSIONS: Surgeon performed trauma room extended FAST is simple and has higher sensitivity compared to the chest X-ray and clinical examination in detecting pneumothorax.

Extended focused assessment with sonography for trauma (EFAST) in the diagnosis of pneumothorax: experience at a community based level I trauma center
Injury. 2011 May;42(5):511-4

Central lines in coagulopathic patients

If a patient needs a central line, he/she needs one. Often low platelets or a deranged coagulation profile are cited as reasons for omitting or delaying the procedure, but this is not based on evidence of increased complications. A recent Best Evidence Topic Review concludes:

…insertion of CVC lines do not require correction of haemostatic abnormalities prior to intervention. Rates of haemorrhage are low in patients with elevated PT, APTT or low thrombocyte count and appear to be closely related to the level of experience of the physician … rather than the defects of haemostasis.

Links to the abstracts of a couple of relevant articles reviewed are included below.
Central line insertion in deranged clotting
Emerg Med J. 2011 Jun;28(6):536-7 Full text
Low levels of prothrombin time (INR) and platelets do not increase the risk of significant bleeding when placing central venous catheters.
Med Klin (Munich). 2009 May 15;104(5):331-5
US-guided placement of central vein catheters in patients with disorders of hemostasis
Eur J Radiol. 2008 Feb;65(2):253-6

FAST in kids has low sensitivity

The abstract says it all – don’t use FAST to rule out significant abdominal free fluid in kids with blunt abdominal trauma. Fine as a rule-in test (for free fluid) though.

Objectives:  Focused assessment of sonography in trauma (FAST) has been shown useful to detect clinically significant hemoperitoneum in adults, but not in children. The objectives were to determine test characteristics for clinically important intraperitoneal free fluid (FF) in pediatric blunt abdominal trauma (BAT) using computed tomography (CT) or surgery as criterion reference and, second, to determine the test characteristics of FAST to detect any amount of intraperitoneal FF as detected by CT.

Methods:  This was a prospective observational study of consecutive children (0–17 years) who required trauma team activation for BAT and received either CT or laparotomy between 2004 and 2007. Experienced physicians performed and interpreted FAST. Clinically important FF was defined as moderate or greater amount of intraperitoneal FF per the radiologist CT report or surgery.

Results:  The study enrolled 431 patients, excluded 74, and analyzed data on 357. For the first objective, 23 patients had significant hemoperitoneum (22 on CT and one at surgery). Twelve of the 23 had true-positive FAST (sensitivity = 52%; 95% confidence interval [CI] = 31% to 73%). FAST was true negative in 321 of 334 (specificity = 96%; 95% CI = 93% to 98%). Twelve of 25 patients with positive FAST had significant FF on CT (positive predictive value [PPV] = 48%; 95% CI = 28% to 69%). Of 332 patients with negative FAST, 321 had no significant fluid on CT (negative predictive value [NPV] = 97%; 95% CI = 94% to 98%). Positive likelihood ratio (LR) for FF was 13.4 (95% CI = 6.9 to 26.0) while the negative LR was 0.50 (95% CI = 0.32 to 0.76). Accuracy was 93% (333 of 357, 95% CI = 90% to 96%). For the second objective, test characteristics were as follows: sensitivity = 20% (95% CI = 13% to 30%), specificity = 98% (95% CI = 95% to 99%), PPV = 76% (95% CI = 54% to 90%), NPV = 78% (95% CI = 73% to 82%), positive LR = 9.0 (95% CI = 3.7 to 21.8), negative LR = 0.81 (95% CI = 0.7 to 0.9), and accuracy = 78% (277 of 357, 95% CI = 73% to 82%).

Conclusion:  In this population of children with BAT, FAST has a low sensitivity for clinically important FF but has high specificity. A positive FAST suggests hemoperitoneum and abdominal injury, while a negative FAST aids little in decision-making

Test characteristics of focused assessment of sonography for trauma for clinically significant abdominal free fluid in pediatric blunt abdominal trauma
Acad Emerg Med. 2011 May;18(5):477-82

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)

Pre-hospital transcranial Doppler

The SAMU (Service d’aide médicale urgente) guys have had a run of interesting pre-hospital publications lately. In this study, one of their ultrasound-wielding physicians travelled in a car to meet comatose head injured patients in a large semi-rural territory area with up to a 120–160-min transport time to a hospital with emergency neurosurgical capability. Pre-hospital transcranial Doppler was done, the results of which appear to have influenced treatment decisions, including the pre-hospital administration of noradrenaline (norepinephrine). I think this study has answered the ‘can it be done?’ question, but further work is needed to determine whether it really makes a difference to outcome.

Background: Investigation of the feasibility and usefulness of pre-hospital transcranial Doppler (TCD) to guide early goal-directed therapy following severe traumatic brain injury (TBI).
Methods: Prospective, observational study of 18 severe TBI patients during pre-hospital medical care. TCD was performed to estimate cerebral perfusion in the field and upon arrival at the Level 1 trauma centre. Specific therapy (mannitol, noradrenaline) aimed at improving cerebral perfusion was initiated if the initial TCD was abnormal (defined by a pulsatility index >1.4 and low diastolic velocity).
Results: Nine patients had a normal initial TCD and nine an abnormal one, without a significant difference between groups in terms of the Glasgow Coma Scale or the mean arterial pressure. Among patients with an abnormal TCD, four presented with an initial areactive bilateral mydriasis. Therapy normalized TCD in five patients, with reversal of the initial mydriasis in two cases. Among these five patients for whom TCD was corrected, only two died within the first 48 h. All four patients for whom the TCD could not be corrected during transport died within 48 h. Only patients with an initial abnormal TCD required emergent neurosurgery (3/9). Mortality at 48 h was significantly higher for patients with an initial abnormal TCD.
Conclusions: Our preliminary study suggests that TCD could be used in pre-hospital care to detect patients whose cerebral perfusion may be impaired.

Pre-hospital transcranial Doppler in severe traumatic brain injury: a pilot study
Acta Anaesthesiol Scand. 2011 Apr;55(4):422-8

Kids tracheal tubes – formulas galore

An ultrasound study of paediatric airways showed sonographic measurement to be a better predictor of tracheal tube size (using a formula – derived and then validated – to estimate external tube diameter) than traditional formulae for selecting the internal tube diameter based on age. Since the measurements, taken at the lower edge of the cricoid cartilage, were made after patients were paralyzed, and were performed without ventilation or positive end-expiratory pressure to minimize fluctuation in tracheal diameter, taking about 30 seconds, this is not something I anticipate applying in critical care practice. However, the paper does provide a good opportunity to revise some of the existing formulae. They used:
(1) The Cole formula for uncuffed tubes: ID (intenal diameter) in mm= (age in years)/4 + 4
(2) The Motoyama formula for cuffed ETTs in children aged 2 yr or older: ID in mm = (age in years)/4 + 3.5
(3) The Khine formula for cuffed ETTs in children younger than 2 yr: ID in mm = (age in years)/4 + 3.0
The formula established in the study was:

  • cuffed ETT outer diameter (OD) = 0.46 x (subglottic diameter) + 1.56
  • uncuffed ETT OD = 0.55 x (subglottic diameter) + 1.16

Age in months also correlated with optimal ETT size in mm, although the correlation was weaker than for subglottic diameter:

  • cuffed ETT OD = 0.027 x (age) + 5.2
  • uncuffed ETT OD = 0.030 x (age) + 5.4

BACKGROUND: Formulas based on age and height often fail to reliably predict the proper endotracheal tube (ETT) size in pediatric patients. We, thus, tested the hypothesis that subglottic diameter, as determined by ultrasonography, better predicts optimal ETT size than existing methods.
METHODS: A total of 192 patients, aged 1 month to 6 yr, who were scheduled for surgery and undergoing general anesthesia were enrolled and divided into development and validation phases. In the development group, the optimal ETT size was selected according to standard age-based formulas for cuffed and uncuffed tubes. Tubes were replaced as necessary until a good clinical fit was obtained. Via ultrasonography, the subglottic upper airway diameter was determined before tracheal intubation. We constructed a regression equation between the subglottic upper airway diameter and the outer diameter of the ETT finally selected. In the validation group, ETT size was selected after ultrasonography using this regression equation. The primary outcome was the fraction of initial cuffed and uncuffed tube sizes, as selected through the regression formula, that proved clinically optimal.
RESULTS: Subglottic upper airway diameter was highly correlated with outer ETT diameter deemed optimal on clinical grounds. The rate of agreement between the predicted ETT size based on ultrasonic measurement and the final ETT size selected clinically was 98% for cuffed ETTs and 96% for uncuffed ETTs.
CONCLUSIONS: Measuring subglottic airway diameter with ultrasonography facilitates the selection of appropriately sized ETTs in pediatric patients. This selection method better predicted optimal outer ETT diameter than standard age- and height-based formulas.

Prediction of Pediatric Endotracheal Tube Size by Ultrasonography
Anesthesiology. 2010 Oct;113(4):819-24

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

IVC collapse depends on breathing pattern

A high degree of sonographically-visualised collapse of the inferior vena cava (IVC) during inspiration suggests a volume-responsive cardiac output. This inspiratory collapse is said to be due to a fall in intra-thoracic pressure. However, the IVC traverses the abdominal compartment and is therefore under the influences of hepatic weight, intra-abdominal pressure, and venous return of pooled splanchnic and lower extremity blood.
Diaphragmatic descent, which increases intra-abdominal pressure, may contribute to the respiratory change in IVC diameter. This was borne out in a volunteer study in which diaphragmatic breathing was compared with chest wall breathing. With diaphragmatic breathing there was a trend for a larger IVC collapse index (median 0.80, range 0.48–1.00 vs. 0.57, range 0.13–1.00, P = 0.053). The authors state:
These findings suggest that during inspiration the IVC, in addition to responding to falling intra-thoracic pressure, may also be compressed with diaphragmatic descent and have implications regarding the use of IVC diameters to estimate the central venous pressure without knowing the manner of breathing, intra-abdominal pressure, or magnitude of diaphragmatic excursion.”
The take home message for me is that there is probably a more complex mechanism of IVC behaviour during respiration than is often taught, and that breathing pattern and abdominal issues may influence the IVC diameter and degree of collapse seen on ultrasound. This might not however negate the correlation between a high degree of collapse and fluid-responsiveness, which is what I’m looking for in my patients with shock or hypotension.
Incidentally the first author of this study is Bruce Kimura, a pioneer of focused echo in the emergency setting and author of a fantastic little book all about the parasternal long axis approach, which seems to be impossible to source on the web at the moment.

AIMS: Although the inspiratory ‘collapse’ of the inferior vena cava (IVC) has been used to signify normal central venous pressure, the effect of the manner of breathing IVC size is incompletely understood. As intra-abdominal pressure rises during descent of the diaphragm, we hypothesized that inspiration through diaphragmatic excursion may have a compressive effect on the IVC.
METHODS AND RESULTS: We measured minimal and maximal intrahepatic IVC diameter on echocardiography and popliteal venous return by spectral Doppler during isovolemic inspiratory efforts in 19 healthy non-obese volunteers who were instructed to inhale using either diaphragmatic or chest wall expansion. During inspiration, the maximal diaphragmatic excursion and popliteal vein flow were compared between breathing methods. The IVC ‘collapsibility index,’ IVCCI, was calculated as (IVC(max)-IVC(min))/IVC(max). The difference in diaphragmatic excursion between diaphragmatic and chest wall breaths in each subject was correlated with the corresponding change in IVCCI. Diaphragmatic breathing resulted in more diaphragmatic excursion than chest wall breathing (median 3.4 cm, range 1.7-5.8 vs. 2.2 cm, range 1.0-5.2, P= 0.0003), and was universally associated with decreased popliteal venous return (19/19 vs. 9/19 subjects, P< 0.004). The difference in diaphragmatic excursion correlated with the difference in IVCCI (Spearman’s rho = 0.53, P= 0.024).
CONCLUSION: During inspiration of equivalent tidal volumes, the reduction in IVC diameter and lower extremity venous return was related to diaphragmatic excursion, suggesting that the IVC may be compressed through descent of the diaphragm.

The effect of breathing manner on inferior vena caval diameter
Eur J Echocardiogr. 2011 Feb;12(2):120-3