Page 443 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 38: Acute Right Heart Syndromes 313

disturbances leading to further RH dysfunction and potentially AV dys- Mechanical ventilation in the prone position (PPV; reviewed in
synchrony. 49,50 Afferent vagal stimulation and baroreceptor stimulation Chap. 52) has consistently been demonstrated to improve gas exchange
in ischemic myocardial tissue lead to enhanced parasympathetic tone in adults with ARDS. However, whether PPV improves survival in
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and the cardioinhibitory Bezolde-Jarisch reflex. Reperfusion thera- unselected ARDS patients is unresolved. PPV has been demonstrated
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pies can paradoxically exacerbate this response resulting in severe but to exert it’s salutary effects by reducing antero-posterior pleural pres-
transient bradycardic hypotension. sure gradients, reducing the pro-atelectatic pressure effects of the heart
Meta-analysis of 22 studies involving 7136 patients with AMI iden- and ventral trans-diaphragmatic pressures and reducing heterogeneity
tified 27.5% with RV myocardial involvement. The pooled relative of regional lung V/Q relationships. As a consequence of these mecha-
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risk mortality increase for RVI patients was 2.59 (95% CI, 2.02–3.31; nisms, PPV has also been demonstrated to unload the RV in patients
Z = 7.57; p <.00001) compared with non-RV MI. The mortality risk with ARDS and acute cor pulmonale. In 21 patients with severe ARDS
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was consistent across studies where RVI was diagnosed by ECG alone or and acute pulmonary hypertension with RV dysfunction, 18 hours of
supplemented by echocardiographic confirmation. RVI was significantly PPV significantly decreased end-inspiratory plateau pressure and Pa CO 2
more frequently complicated cardiogenic shock, ventricular arrhythmias, despite unchanged tidal volumes. Additionally PPV was associated
and mechanical complications including papillary muscle rupture. with a significant improvement in RV function compared with SPV
The focus of management in RV infarction is on maintenance of as assessed by right ventricular enlargement and septal dyskinesia at
optimal RV preloading to avoid worsened RV distension, preservation transesophageal echocardiography.
of RV synchrony, reduction in RV afterload (particularly when LV dys-
function is present), and inotropic and mechanical support of the RV. 53 Sepsis: Sepsis itself is probably capable of causing pulmonary hyperten-
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Early reperfusion with fibrinolytics or direct coronary intervention sion, even in the absence of acute lung injury, based on animal models
has been advocated based on clear evidence of early reperfusion, func- and limited human studies. 61,62 Although common in patients with severe
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tional RV performance improvement and improved hospital mortality. sepsis, it is our experience that acute pulmonary hypertension is only of
However, even delayed efforts at reperfusion with fibrinolytic or clinical importance when ARDS (or another clear precipitant) is present.
directed PCI are indicated for most patients. Echocardiography can Sepsis-associated proinflammatory cytokines particularly tumor necrosis
be highly useful in confirming RV infarction and in determining the factor-α have been demonstrated to induce caspase-mediated apoptosis
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response to therapeutic interventions. and myocyte dysfunction as well as having negative inotropic effects on
the ventricular myocardium. It seems likely that the systemic hypotension
Acute Lung Injury/Acute Respiratory Distress Syndrome: As many as one of septic shock also renders the RV more vulnerable to ischemic systolic
quarter of patients with ARDS develop significant pulmonary hyperten- dysfunction when combined with modest increases in afterload. It has
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sion and RV dysfunction 45,46 although the frequency of this complica- been argued that this right ventricular perfusion gradient accounts for the
tion in an era when Pa catheters are infrequently inserted is likely to be differentially impaired perfusion and contractility of the RV compared
clinically underappreciated. Contributors to Pa hypertension in ARDS with the LV in sepsis. 62
include hypoxic pulmonary vasoconstriction, mediator release, high alve- A notable insight into the complex role of endogenous nitric oxide
olar pressure during mechanical ventilation, and microthrombi in situ. in regulating pulmonary vascular tone in septic shock patients was
In retrospective analysis of 145 patients from the French Pa Catheter derived from a randomized, placebo-controlled, double-blind study of
study, Osman and coworkers identified right ventricular failure in 9.6% the nitric oxide synthase inhibitor 546C88. Patients who were ran-
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of patients defined as a mean PAP >25 mm Hg, CVP > PAOP and domized to the treatment arm had a 10% absolute higher mortality rate
stroke volume index <30 mL/m , although there was no independent at 28 days than patients in the placebo arm. 546C88-treated patients
2
association with 90-day survival in that study. Right ventricular dysfunc- had a greater incidence of pulmonary hypertension, with an initial
tion characterized by PRA > Ppao has been established to be an early increase in the pulmonary vascular resistance and a sustained reduc-
independent predictor of mortality in ARDS (OR 5.1 95% CI 1.5-17.1; tion in the pulmonary venous admixture, possibly through augmented
P = 0.009). The large prospective European ARDS Collaborative Study hypoxic pulmonary vasoconstriction. Three patients in the treatment
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evaluated pulmonary hemodynamic variables in 424 of 586 ARDS arm developed right heart failure. It has been suggested that sepsis-
patients. In most patients, mean Pa pressure was modestly elevated on associated NO production may have a partially protective effect on the
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admission (26.1 ± 8.5 mm Hg) and was persistently elevated at 48 hours pulmonary vasculature by optimizing pulmonary ventilation-perfusion
in nonsurvivors compared with survivors (28.4 ± 8.5 mm Hg vs 24.1 ± relationships.
6.7 mm Hg). The ratio of RV to LV stroke work was also significantly
elevated in all patients, and along with the ratio of partial oxygen pres- Acute Sickle Chest Syndrome: Acute pulmonary hypertension compli-
sure to the fraction of inspired oxygen (OR 0.96-0.98), was identified as cates vaso-occlusive sickle cell crises and can present as the acute
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an independent predictor of survival (OR 20-85; p = 0.0001). In a ret- sickle chest syndrome (ACS). ACS results from pulmonary micro-
rospective analysis of the ARDS Network, Fluid and Catheter Treatment vascular in situ thrombosis, pulmonary fat embolism from infarcted
Trial dataset, Bull, et al identified a high frequency of pulmonary vascu- long bone marrow, and hypoxic vasoconstriction. Recurrent episodes
lar dysfunction and a strong association between an increased transpul- result in secondary chronic pulmonary hypertension and cor pul-
monary gradient at enrollment (TPG; Pa mean pressure—Pa occlusion monale. Amongst 70 patients experiencing 84 ACS crises, acutely
pressure ≥12 mm Hg) with increased 60-day mortality rate (30% vs 19%; elevated pulmonary arterial pressures (estimated by echo tricuspid
P = 0.02). Notably if the TPG failed to normalize by day 5, this too was regurgitant jet velocity, TRV) was present in 60% (37% of patients had
associated with increased likelihood of death (36% vs 19%; P = 0.01). a TRV >3.0 m/s) and was associated with RV dilation in most patients
Shunting through a patent foramen ovale as a consequence acute pul- and RV systolic failure (cor pulmonale) in 13%. Acute Pa hyperten-
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monary hypertension with RV dysfunction in ARDS is common and is sion generally resolved after ACS resolution (PASP decreased from
associated with prolonged ventilator dependence. 39 out of 116 sequential 51 [47-67] mm Hg during severe ACS to 25 [35-40] mm Hg [P < 0.01]).
ARDS patients in one French prospective cohort had PFO-associated However, severe pulmonary hypertension (TRV >3.0 m/s) during
shunt demonstrated by bubble-contrast TEE. 46 ACS was associated with a dramatic reduction in long-term survival;
These findings would suggest an aggressive approach to lowering only 50% of those patients survived to 36 months versus 100% of
RV afterload in patients with ARDS by reducing alveolar pressures and patients with TRV <3.0 m/s; P = 0.007.
administering inhaled nitric oxide or prostacyclin. However, despite Inhaled NO, in addition to supplemental oxygen, blood transfusions,
reproducible reductions in Pa pressure and improvements in oxygen- and bronchodilators, may provide some additional benefit for general-
ation indices, randomized controlled studies using this approach have ized vaso-occlusive crises, but has not been systematically studied for
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repeatedly failed to demonstrate a survival benefit, as discussed below. sickle-associated ACS or pulmonary hypertension. 69

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