key: cord-0915739-9s7j07c3 authors: Powys-Lybbe, J.; Aron., J. title: Echocardiography for patients with COVID-19 in intensive care date: 2021-10-07 journal: BJA Educ DOI: 10.1016/j.bjae.2021.08.004 sha: cedc8bd576b3f44d9571804be1b9ffb912dc17d6 doc_id: 915739 cord_uid: 9s7j07c3 nan -Barrier protection and FFP3 masks during procedure. -Single-use sachets of ultrasound gel -Removal of gel and debris from the probes after use. -Appropriate disposable cleaning wipes that are viricidal and compatible with ultrasound probes -Adequate drying time for cleaning solutions. A pandemic is a difficult time to deliver additional services -resources are limited and demand is high. A full diagnostic echocardiography is time consuming, exposes staff to risks of infection or carriage, and is often superfluous -a burden that is increased by serial observation. The goal is to identify serious pathology in a timely manner without unduly burdening the service. An effective approach is one in which the scanning is performed by a trained intensive care clinician who understands the clinical context and treatment modalities available, is able to monitor the response to treatment and titrate any interventions initiated. A fundamental understanding of echocardiography physics is necessary, combined with a level of practical experience typically seen after FUSIC Heart or British Society of Echocardiography (BSE) Level 1 certification ii . In addition, a service requires supporting infrastructure: referral pathways, supervision, education and governance processes need to be implemented. In line with FUSIC heart and BSE Level 1 methodology, qualitative 'eye-balling' is sufficient in most cases and reliable quantitative assessment of right ventricular (RV) function and haemodynamic monitoring is desirable. This requires more advanced skills delivered by practitioners holding an advanced qualification, such as the newly released standard for the UK: FUSIC Haemodynamic protocol iii . The effects of Covid-19 on the heart can be subtle. The addition of measurements that can help identify RV pathology and monitor change on serial imaging is important for classifying disease and directing interventions. It is beyond the scope of this article to detail intervention protocols, but the relevant articles are referenced and resources detailing these approaches are widely available. Changes that occur with COVID-19 have been well documented and are consistent: RV dilatation in most patients, with or without impairment, and a normal, impaired or hyperdynamic left ventricle v,vi . During the early infection there is a significant inflammatory response that drives pyrexia and vasodilation, which typically produce a high cardiac output, low systemic vascular resistance (SVR) state. The left ventricle is hyperdynamic in the face of reduced preload and afterload, circulating catecholamines and inflammatory mediators, and a loss of intravascular tone. . In a typical scenario, the right ventricle would display a similar hyperdynamic response as the pulmonary vascular resistance (PVR) is also decreased in systemic sepsis. However, in COVID-19 pneumonitis profound hypoxaemia causes hypoxic vasoconstriction, which acts to oppose the vasodilation of the pulmonary circulation, resulting in a normal or increased PVR. In addition, RV perfusion may be decreased as this requires an adequate mean arterial pressure, which is dependent on the SVR. Excessive circulating catecholamines (stress cardiomyopathy) and inflammatory mediators may also cause RV systolic impairment, more evident because of the afterload effects of preserved or high PVR This combination of pathologies may cause dilatation of the right ventricle. Measures of RV systolic function -Tricuspid anular plane systolic excursion (TAPSE) and RV S prime (RVS')which are representative measures of longitudinal RV free wall contraction may be preserved, but in the context of an overall hyperdynamic circulatory state normal values may actually represent early systolic impairment, particularly if there is a discrepancy between the two ventricles. As disease severity progresses, the right ventricle is exposed to an increasing adverse environment from a combination of iatrogenic insults and progressive lung disease: J o u r n a l P r e -p r o o f -High mean airway pressure ventilation strategies to manage hypoxaemia, including APRV. In particular, during the compliant phase of the disease, alveolar hyperdistention may cause iatrogenic injury by increasing RV afterload. -Increased consolidation with progression of ARDS and low-compliance lung disease (requiring higher ventilation pressures to achieve adequate tidal volumes) -Refractory hypoxia worsening pulmonary vasoconstriction and increasing RV afterload. -Reduced CO2 clearance causing worsening pulmonary vasoconstriction. -Superimposed pulmonary infection and systemic infections, which alter the delicate pressure-flow relationships in systems with no physiological reserve. -Micro-and macro-pulmonary thromboembolic disease. -Synergistic effects of existing pulmonary disease such as COPD or obesity vii . As RV distention progresses, venous congestion may cause multiorgan dysfunction and failure. In addition to restrictive fluid therapy protocols and a hyperinflammatory state, thrombotic risk is significantly increased. The inferior vena cava (IVC) may be dilated with limited variability due to high pulmonary and RV pressures or may show a degree of variability. Significant variability is seen in preload responsive states when RV function is normal but can also be seen in non-responsive states when the RV is failing. In established RV failure, features of congestion worsen with decreased or absent IVC variability -with the potential for increasing hypotension and reduced organ perfusion with consequent dysfunction. Possible therapeutic options to optimise the right side of the circulation include giving cautious monitored fluids; fluid removal; lower ventilatory pressures; prone positioning (which may allow lower ventilatory pressures to be used as lung bases recruit); higher ventilatory pressures to recruit dependent lung and lower pulmonary vascular resistance; vasoconstrictor therapy to optimise RV perfusion; inotropic drugs to augment RV contractility; pulmonary vasodilator therapy (oral, inhaled or intravenous); and thrombolysis. Identification of predominating pathophysiology allows correct therapeutic options to be initiated, monitored and titrated viii . For the most part the left ventricle is spared from direct damage, although cases of COVID-19-induced myocarditis are not uncommon ix . However, there are numerous causes of indirect effects. Inadequate left ventricular (LV) filling may occur because of: inadequate LV preload (from RV dysfunction, hypovolaemia, pulmonary emboli, high ventilatory pressures); reduced diastolic filling time due to tachycardia; or compression by septal bowing from a dilated RV. Low LV output could occur because of ventricular interdependence or high afterload states caused by excessive vasoconstrictor therapy to manage hypotension resulting from hypovolaemia). Impaired contractility may be caused by circulating catecholamines (stress cardiomyopathy) and/or inflammatory mediators, ischaemic injury (global due to imbalance between demand and supply; territorial due to existing coronary artery disease) or high dose sedative agents that exert negative inotropic effects. Pleural and pericardial effusions may be observed and intervention should be guided by their size and potential lung or cardiac dysfunction, against the risks of drain insertion. Lung ultrasound may be simultaneously performed when assessing for effusions. Echocardiography in this setting should be focused and used repeatedly as a haemodynamic monitor. Understanding the disease process and clinical context is vital, however, to make management decisions based on the finding from the scan. The primary goal is to provide therapy that is successful at managing ventilatory failure whilst preserving RV function as much as possible. This decision tree below suggests an approach to integration between ultrasound imaging and decision management in ICU patients with COVID-19. Of note BSE guidelines for impairment of the RV are as follows: COVID-19 causes profound changes to the right ventricle through multiple different mechanisms. Focused echocardiography is a quick and useful bedside investigation that provides invaluable insight into the multiple overlapping pathologies that can exist. An awareness of these enable the physician to provide directed and individualised patient care to support the heart whilst the lung damage is given appropriate time to recover. The authors declare no conflict of interests A Complex Multisystem Disorder The impact of focused echocardiography using the Focused Intensive Care Echo protocol on the management of critically ill patients, and comparison with full echocardiographic studies by BSE-accredited sonographers Spectrum of Cardiac Manifestations in COVID-19' Yishay Szekely et al. 29 vii 'Potential pathophysiology of COVID-19 in patients with obesity' B Lui et al. Comment on Myocarditis in a patient with COVID-19: a cause of raised troponin and ECG changes' Denis Doyen, MD et al. The Lancelet, Clinical picture J o u r n a l P r e -p r o o f