Tag Archives: shock

All Updates, ICU, Resus, Ultrasound

An easily missed cause of shock

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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.

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  • 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

All Updates, Resus, Ultrasound

IVC collapse depends on breathing pattern

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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

All Updates, ICU, Resus

Propofol and the heart

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I don’t normally blog about animal studies, but on reading a review of recent(-ish) shock research I was interested in the following piece that describes the effect of diffrent induction agents on rat heart muscle:
Sedation is frequently necessary in patients with septic shock, and therefore Zausig and colleagues investigated the effects of dose-dependent effects of various induction agents (propofol, midazolam, s(+)-ketamine, methohexitone, etomidate) in a Langendorff heart preparation from rats rendered septic by CLP. Propofol exerted the most pronounced depressant effects on both the maximal systolic contraction and the minimal diastolic relaxation, and cardiac work. Furthermore, propofol only adversely deleteriously affected the myocardial oxygen supply- demand ratio. In contrast, s(+)-ketamine was associated with the best maintenance of cardiac function. Within the limits of the study – that is, the use of an ex vivo isolated organ model – the authors concluded that s(+)-ketamine may be an alternative to the comparably inert etomidate, the use of which is, however, limited due to its endocrine side effects.

Of course we should be cautious about extrapolating animal lab work to clinical practice, but this supports my position of vehement opposition to the injudicious use of propofol for RSI in critically ill patients!
Year in review 2009: Critical Care – shock
Critical Care 2010, 14:239 Full text

All Updates, Resus, Trauma

Flat IVC on CT associated with deterioration

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BACKGROUND: : We aimed to investigate the value of the diameter of the inferior vena cava (IVC) on initial computed tomography (CT) to predict hemodynamic deterioration in patients with blunt torso trauma.
METHODS: : We reviewed the initial CT scans, taken after admission to emergency room (ER), of 114 patients with blunt torso trauma who were consecutively admitted during a 24-month period. We measured the maximal anteroposterior and transverse diameters of the IVC at the level of the renal vein. Flat vena cava (FVC) was defined as a maximal transverse to anteroposterior ratio of less than 4:1. According to the hemodynamic status, the patients were categorized into three groups. Patients with hemodynamic deterioration after the CT scans were defined as group D (n = 37). The other patients who remained hemodynamically stable after the CT scans were divided into two groups: patients who were hemodynamically stable on ER arrival were defined as group S (n = 60) and those who were in shock on ER arrival and responded to the fluid resuscitation were defined as group R (n = 17).

RESULTS: : The anteroposterior diameter of the IVC in group D was significantly smaller than those in groups R and S (7.6 mm ± 4.4 mm, 15.8 mm ± 5.5 mm, and 15.3 mm ± 4.2 mm, respectively; p < 0.05). Of the 93 patients without FVC, 16 (17%) were in group D, 14 (15%) required blood transfusion, and 8 (9%) required intervention. However, of the 21 patients with FVC, all patients were in group D, 20 (95%) required blood transfusion, and 17 (80%) required intervention. The patients with FVC had higher mortality (52%) than the other patients (2%). CONCLUSION: : In cases of blunt torso trauma, patients with FVC on initial CT may exhibit hemodynamic deterioration, necessitating early blood transfusion and therapeutic intervention. Predictive Value of a Flat Inferior Vena Cava on Initial Computed Tomography for Hemodynamic Deterioration in Patients With Blunt Torso Trauma
J Trauma. 2010 Dec;69(6):1398-402

All Updates, ICU, PHARM, Resus

Passive leg raising during CPR

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Measuring end-tidal carbon dioxide (ET CO2 ) is a practical non-invasive method for detecting pulmonary blood flow, reflecting cardiac output and thereby the quality of CPR. It has also been shown to rise before clinically detectable return of spontaneous circulation (ROSC).
Passive leg raising (PLR) increases venous return and may therefore augment cardiac output and in a cardiac arrest this may be reflected by an elevation in ETCO2.
A Swedish observational study of 126 patients with out of hospital cardiac arrest due to a likely cardiac aetiology underwent tracheal intubation with standardised ventilation and chest compressions (either manually or using the LUCAS device, as part of larger study of mechanical chest compressions according to a cluster design). Patients were stratified to receive either PLR to 20 degrees or no PLR. ETCO2 was measured during CPR, either for 15min, or until the detection of ROSC.

Hang on I think that's overdoing it a bit

During PLR, an increase in ETCO2 was found in all 44 patients who received PLR within 15s (p=0.003), 45s (p = 0.002) and 75 s (p = 0.0001). Survival to hospital discharge was 7% among patients with PLR and 1% among those without PLR (p = 0.12). Among patients experiencing ROSC (60 of 126), there was a marked increase in ETCO2 1 min before the detection of a palpable pulse.
Passive leg raising during cardiopulmonary resuscitation in out-of-hospital cardiac arrest—Does it improve circulation and outcome?
Resuscitation. 2010 Dec;81(12):1615-20

All Updates, PHARM, Resus, Trauma

Evidence refutes ATLS shock classification

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I have always had a problem with the ATLS classification of hypovolaemic shock, and omit it from teaching as any clinical applicability and reproducibility seem to be entirely lost on me. I was therefore reassured to read that real physiological data from the extensive national trauma registry in the UK (TARN) of 107,649 adult blunt trauma patients do not strongly support this classification. A key observation we regularly make in trauma patients is the frequent presence of normo- or bradycardia in hypovolaemic patients, which is well documented in the literature.

Unreferenced dogma that became viral

An excellent discussion section in this paper states: ‘it is clear that the ATLS classification of shock that associates increasing blood loss with an increasing heart rate, is too simplistic. In addition, blunt injury, which forms the majority of trauma in the UK, is usually a combination of haemorrhage and tissue injury and the classification fails to consider the effect of tissue injury‘
Testing the validity of the ATLS classification of hypovolaemic shock
Resuscitation. 2010 Sep;81(9):1142-7

Acute Med, All Updates, ICU, Kids, Resus

Crystalloids vs colloids and cardiac output

It is said that when using crystalloids, two to four times more fluid may be required to restore and maintain intravascular fluid volume compared with colloids, although true evidence is scarce. The ratio in the SAFE study comparing albumin with saline resuscitation was 1:1.3, however.
A single-centre, single- blinded, randomized clinical trial was carried out on 24 critically ill sepsis and 24 non-sepsis patients with clinical hypovolaemia, assigned to loading with normal saline, gelatin 4%, hydroxyethyl starch 6% or albumin 5% in a 90-min (delta) central venous pressure (CVP)-guided fluid loading protocol. Haemodynamic monitoring using transpulmonary thermodilution was done each 30 min to measure, among other things, global end-diastolic volume and cardiac indices (GEDVI, CI). The reason sepsis was looked at was because of a suggestion in the SAFE study of benefit from albumin in the pre-defined sepsis subgroup.
Independent of underlying disease, CVP and GEDVI increased more after colloid than saline loading (P = 0.018), so that CI increased by about 2% after saline and 12% after colloid loading (P = 0.029).
Their results agree with the traditional (pre-SAFE) idea of ratios of crystalloid:colloid, since the difference in cardiac output increase multiplied by the difference in volume infused was three for colloids versus saline.
Take home message? Even though an outcome benefit has not yet been conclusively demonstrated, colloids such as albumin increase pre-load and cardiac index more effectively than equivalent volumes of crystalloid in hypovolaemic critically ill patients.
Greater cardiac response of colloid than saline fluid loading in septic and non-septic critically ill patients with clinical hypovolaemia
Intensive Care Med. 2010 Apr;36(4):697-701

All Updates, ICU, Resus

The right antibiotic in septic shock makes a massive difference

A retrospective review of appropriate vs inappropriate antimicrobial therapy was undertaken in over four thousand septic shock patients from multiple centres. In terms of definitions, the authors state:
“Appropriate antimicrobial therapy was considered to have been initiated if an antimicrobial with in vitro activity appropriate for the isolated pathogen or pathogens (or in the case of culture-negative septic shock, an antimicrobial or antimicrobial agent concordant with accepted international norms for empiric therapy and modified to local flora) was either the first new antimicrobial agent with which therapy was started after the onset of recurrent or persistent hypotension or was initiated within 6 h of the administration of the first new antimicrobial agent. Otherwise, inappropriate therapy was considered to have been initiated.”
The results are striking: survival rates after appropriate and inappropriate initial therapy were 52.0% and 10.3%, respectively (odds ratio [OR], 9.45; 95% CI, 7.74 to 11.54; p < 0.0001).
A multivariable logistic regression analysis of possible factors that may affect outcome showed the appropriateness of the initial antimicrobial therapy remained most strongly associated with outcome (OR, 8.99; 95% CI, 6.60 to 12.23; p < 0.0001) among all the risk factors assessed.
Initiation of Inappropriate Antimicrobial Therapy Results in a Fivefold Reduction of Survival in Human Septic Shock
Chest. 2009 Nov;136(5):1237-48
N.B. This work was done by the same authors who brought us the study that showed the earlier antibiotics were given to hypotensive septic patients, the better the outcome:
Kumar A, Roberts D, Wood KE, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med 2006; 34:1589-1596

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Low PPV can still be fluid responsive

Pulse pressure variation with respiration (PPV) predicts fluid responsiveness in mechanically ventilated patients. Because this is due to transmission of airway pressures to the vasculature, it is hypothesised that low tidal volume ventilation (or non compliant lungs, or both) results in less PPV even in fluid-responsive patients. This was confirmed in a study looking at the effect of airway driving pressure (Pplat – PEEP) on PPV. The study confirmed the positive predictive value of a high PPV, but some of those patients with a ‘low’ PPV (below a commonly accepted cut-off of 13%) were still fluid responsive, which was defined as a 15% or more increase in stroke index after a fluid challenge. In fluid responders with a low PPV, (Pplat – PEEP) was less than or equal to 20 cmH20.
Take home message: In mechanically ventilated patients, PPV values <13% do not rule out fluid responsiveness, especially when (Pplat – PEEP) was less than or equal to 20
The influence of the airway driving pressure on pulsed pressure variation as a predictor of fluid responsiveness
Intensive Care Med. 2010 Mar;36(3):496-503

All Updates, Ultrasound

Collapsible IVC predicts 'low' CVP

The IVC undergoes a change in diameter during the respiratory cycle. Investigators compared the degree of sonographic IVC respirophasic diameter change with CVP in 73 patients and found >= 50% change in diameter predicted a CVP< 8 mmHg with 91% sensitivity (95% CI 71% to 99%) and 94% specificity (95% CI 84% to 99%). The positive predictive value was 87% (95% CI 66% to 97%), and the negative predictive value was 96% (95% CI 86% to 99%). Presumably the rather arbritrary CVP of 8 was chosen because of its importance as a target for goal directed therapy in sepsis guidelines. A more meaningful endpoint such as a fluid responsive cardiac output might be a more clinically relevant application of this technique, which had been demonstrated previously. Emergency Department Bedside Ultrasonographic Measurement of the Caval Index for Noninvasive Determination of Low Central Venous Pressure
Ann Emerg Med. 2010 Mar;55(3):290-5