Critical care management of the vascular patient

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Critical care management of the vascular patient

Pathophysiology Many vascular patients have atherosclerosis. Furthermore, risk factors for atherosclerosis (e.g. obesity, smoking) also contribute to hypertension, diabetes mellitus and chronic obstructive pulmonary disease. The collective impact of these factors is further exacerbated by: • the inflammatory response to surgery • cross-clamping of large vessels • haemorrhage.

Heather Morris Carlos M H Gomez

Cardiovascular

The principle of intensive care is to support organ function while awaiting recovery from insult. The challenge lies in identifying patients who can wait for recovery and those who cannot (and therefore need prompt intervention). Critical care involves a delicate balance between achievable and acceptable physiology. This precarious balance is different for each patient, for instance: • optimum intravascular volume may lead to excessive pulmonary, peripheral and cerebral oedema • a certain perfusion pressure can be achieved only at the expense of increased cardiac work and peripheral vasoconstriction • acceptable acid–base chemistry requires an increase in intrathoracic pressure (ventilation), cardiac work and tissue oedema.

Atherosclerosis of the aorta is associated with coronary artery disease. Myocardial infarction/ischaemia is the most common cause of death in patients undergoing vascular surgery. Atherosclerosis should be suspected if cardiovascular instability is marked and persistent; it can be confirmed by a combination of: • electrocardiography • echocardiography • angiography • serial presence of raised markers of myocardial necrosis. Treatment (e.g. anti-coagulation, fibrinolysis) is limited by surgery, though immediate coronary angioplasty and stenting are rapidly becoming the first-line treatments in the UK. Supportive management until recovery of cardiac function forms the cornerstone of treatment.

Stress response to surgery Surgery elicits protective neuroendocrine and inflammatory reactions. In general, recovery after surgery relates to the degree of tissue damage and inflammatory reaction, but not to the magnitude of neuroendocrine changes.

The systemic inflammatory response syndrome (SIRS) is the manifestation of excessive host response and leads to further tissue damage and dysfunction. SIRS is characterized by varying degrees of circulatory instability and end-organ insufficiency. In the ICU, SIRS is usually caused by infection.

The neuroendocrine response is characterized by a rapid increase in catecholamines and a more gradual rise in other catabolic hormones. Glycogen, fatty acids and amino acids are mobilized. The renin–aldosterone axis is activated, resulting in the retention of sodium and water.

Blood pressure (Figure 1): hypertensive patients with poorly compliant vessels and diabetics with autonomic neuropathy often have labile blood pressures. Hypertension carries the risk of ventricular distension and cardiac failure. Hypotension can reduce perfusion to the heart, brain and kidney.

Inflammation results in the activation of complement, coagulation and neutrophil–monocyte systems and production of cytotoxic chemicals. Some individuals produce an insufficient response and are overwhelmed by the injurious process; others mount an excessive inflammatory reaction which leads to widespread destruction of tissue. Hence, the benefits of modulating an excessive stress response must be weighed against risks of excessive immune suppression.

Respiratory Infections of the lower respiratory tract in the critically ill are often caused by multi-resistant organisms acquired in the hospital. They are particularly common and problematic in ventilated patients. Incidence and microbiology vary widely, but there are several common features. Mechanical ventilation makes normal defence mechanisms less efficient. Patients with chronic lung disease are at particular risk. Critically ill patients are generally immunocompromised and cross-infection is a major problem. Acute respiratory distress syndrome and acute lung injury encompass a clinical spectrum of elevated pulmonary alveolocapillary permeability characterized by: • refractory hypoxaemia • widespread alveolar infiltrate seen on chest radiograph • respiratory distress which is not caused by (but may coexist with) raised left atrial or pulmonary capillary pressure.

Heather Morris is a Specialist Registrar in Anaesthesia and Intensive Care at Northwick Park Hospital, London, UK. Carlos M H Gomezz is a Consultant in Intensive Care Medicine and Anaesthesia at St Mary’s Hospital, London, UK.

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Common vasoactive agents Agent

Effects

Indications

Disadvantages

Adrenaline

Receptor pharmacology Equipotent α/β

Tachycardia Raised cardiac output Raised blood pressure

Resuscitation Shock

Arrhythmias Acidaemia Hyperglycaemia

Noradrenaline

α1>β1

Raised blood pressure Reflex bradycardia

SIRS/sepsis

Vasoconstriction

Dobutamine

β1, β2

Tachycardia Raised cardiac output Vasodilation

Cardiac failure Sepsis

Arrhythmias Myocardial ischaemia

Dopamine

DA1, DA2, β1,α1

Renal vasodilation Tachycardia Raised blood pressure

Circulatory support

Arrhythmias Vasoconstriction

Dopexamine

β2>DA1>β1

Vasodilation Renal vasodilation Tachycardia

Circulatory support Cardiac failure Gut perfusion

Arrhythmias

Milrinone

Inhibition of phosphodiesterase III; raised levels of cyclic adenosine monophosphate

Cardiac contractility Vasodilation

Cardiac failure

Vasodilation

1

Dilutional and consumption coagulopathy often coexist. Treatment focuses on surgical control of the bleeding source (which can be difficult) together with transfusion of concentrated clotting products (guided by coagulation tests). Other issues related to blood and clotting product transfusions must also be considered: • temperature • electrolyte and oxygen transport deficiencies of stored products • risk of infection • anaphylaxis. In the absence of acute coronary ischaemia, critically ill patients are unlikely to derive significant benefit from blood transfusion that aims to increase haemoglobin concentration to >8 g/dl.

Acute repiratory distress syndrome and acute lung injury are lung manifestations of the endothelial dysfunction and hyperinflammatory response normally associated with SIRS.

Renal Renal impairment in vascular patients is common and abnormal renal function preoperatively is a significant risk factor for postoperative renal failure. Also, cardiovascular instability, haemorrhage, suprarenal cross-clamping and renal artery revascularization compromise kidney perfusion and increase the risk of acute renal failure. Death from acute renal failure remains alarmingly high, despite advances in critical care and renal replacement. Atherosclerosis can cause renovascular disease. Hypertension and diabetes contribute further to renal impairment (as does most of the medication used to optimize cardiac function). The combination of diuretics and preoperative fasting often leads to hypovolaemia.

Multiple organ dysfunction syndrome Vascular patients may develop multiple organ failure from which recovery may be prolonged. This is characterized by: • a combination of severe sepsis and SIRS • ventilator-associated pneumonia • ileus • inotrope dependence • wasting and malnutrition • renal failure • global central nervous dysfunction. A well-orchestrated and enthusiastic multidisciplinary approach with an emphasis on organ support is needed to ensure survival until physiological recovery ensues. Often, the main determinant of resolution of illness is freedom from infection.

Haematological Vascular surgery is often associated with haemorrhage and transfusion of large volumes of blood. Replacement is usually with packed red blood cells that are low in platelets and coagulation factors. The relationship between blood loss, quantity and quality of replacement, observed bleeding and measurable coagulation abnormalities is highly variable. Also, there is a complex interrelationship between surgery and activation of the inflammatory and coagulation cascades.

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Fluid balance

Ventilation

Careful fluid balance is essential because optimum volume for cardiac and respiratory function may have detrimental effects on renal function. Hypovolaemia (especially in sepsis or haemorrhage) can be underestimated, with severe consequences for end-organ perfusion. Hypervolaemia (particularly in left-heart dysfunction) can lead to oedema, which can overwhelm compensatory mechanisms. With capillary leak (a feature of sepsis), satisfactory intravascular volume replacement may cause serious peripheral and interstitial lung oedema. The balance between deleterious volume depletion and pulmonary oedema is critical and varies between patients. Therefore, accurate estimation of intravascular filling is very important, and can often be achieved by clinical examination and measurements of central venous pressure. However, central venous pressure may not reflect left ventricular filling accurately in right-heart dysfunction or pulmonary hypertension. Hence, a pulmonary artery catheter can be used.

Basic principles (see Glossary) Mechanical (positive-pressure) ventilation is predominantly inspiratory support together with some form of expiratory support. The objective of inspiratory support is to inflate the lungs to allow gas exchange without causing trauma to the airway or lung. Expiratory support aims to reduce end-expiratory airway closure without causing impaired exhalation and air-trapping. In spontaneous and in positive-pressure ventilation, expiration is passive and depends on elastic lung recoil and airway resistance. Elastic lung recoil is difficult to manipulate, whereas air resistance can be altered pharmacologically. Hence, mechanical ventilation should be beneficial when treating conditions associated with inspiratory abnormalities. In contrast, mechanical ventilation would not be expected to be nearly as useful in predominantly expiratory disease because it cannot alter elastic recoil. Weaning There are many weaning strategies, but no single strategy is better than another.

A pulmonary artery catheter measures pulmonary artery pressures, including pulmonary artery wedge pressure. Other haemodynamic indices can be measured (cardiac output) or calculated (vascular resistance, oxygen transport). Pulmonary artery wedge pressure often reflects left atrial pressure, which in turn is proportional to left ventricular end-diastolic pressure and filling. However, pulmonary artery wedge pressure may not reflect true left ventricular preload in mitral valve pathology or left-heart disease. Pulmonary artery catheters can have serious complications. Less invasive monitors have gained wide acceptance, especially if measurement of pulmonary artery pressure is not crucial.

Respiratory failure: to understand the principle of weaning, one must understand respiratory failure, of which there are three forms. Postoperativee respiratory failuree is characterized by a combination of: • pain • basal atelectasis • altered intravascular and extracellular volume • hypothermia • drowsiness • capillary leak leading to pulmonary and peripheral oedema. Correction of these abnormalities and/or physiological support until recovery or compensation is the mainstay of management. Obstructivee respiratory failuree is commonly seen in chronic obstructive airway disease and asthma (i.e. diseases of the airways characterized by abnormal expiration caused by airway narrowing and/or excessive secretions). When significant, expiratory disease leads also to inspiratory weakness. Mechanical ventilation in obstructive respiratory failure provides inspiratory assistance in order to reduce the work of breathing while the expiratory pathology is reversed and general condition, muscle weakness and nutrition improve. Ventilation parameters for obstructive respiratory failure are: • a low inspiratory pressure (because compliance and inspiration are not normally affected) • low expiratory pressure (sufficient to prevent airway collapse and to trigger inspiratory effort, but not so high as to cause air-trapping). Weaning is often slow and difficult because mechanical ventilation does not treat the principal abnormality in obstructive respiratory failure. Restrictivee respiratory failure is the physiological ‘hallmark’ in diseases of the chest wall and neuromuscular disorders marked by predominantly inspiratory difficulties. Parenchymal Infection (e.g. pneumonia) is a form of restrictive lung disease in that lung consolidation leads to:

Cardiovascular support Basic principles The heart perfuses itself and has a formidable cardiac output reserve (about five-fold). Extraction of coronary blood oxygen is always near maximal, so increased consumption of oxygen can be met only by an increased supply of oxygen. The aim of cardiovascular support is to maintain perfusion of the organs and tissues. The balance between the need to maintain end-organ perfusion and its consequent (but opposing) increase in myocardial work and oxygen consumption is very delicate. The intra-aortic balloon pump is introduced into the descending aorta via the femoral artery. It inflates during diastole, augmenting diastolic pressure, thereby improving coronary flow. The intraaortic balloon pump deflates just before end-diastole, so afterload is reduced. The intra-aortic balloon pump improves coronary perfusion, though the perfusion of organs distal to the balloon may be affected. Ventricular assist devices are used in selected patients with severe refractory primary heart failure as temporary support until recovery ensues or a heart transplant becomes necessary.

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• reduced compliance and airway collapse • difficulty in drawing air into the lung • fatigue. Therefore, mechanical ventilation has an important role in the setting of pneumonia. Ventilation parameters due to pneumonia are a: • high mean or plateau airway pressure (but sufficiently low to prevent trauma) • high expiratory pressure to prevent airway collapse and facilitate gas exchange. Cautious ventilation and acceptance of certain physiological derangement (permissive hypercapnia) is favoured in order to avoid excessively high pressure and volume (with consequent iatrogenic lung damage).

Glossary Airway resistance relates pressure gradient required to generate a certain flow; increased in asthma. Compliance relates change in volume to change in pressure (dV/dP). Compliance is decreased in parenchymal or interstitial diseases (e,g. infection, oedema, airway collapse, fibrosis), but is increased in airway disease (e.g. emphysema, bronchitis). Shunt occurs when poorly ventilated alveoli are adequately perfused; causes hypoxaemia, the treatment for which necessitates recruitment of underventilated areas. Typical in pneumonia and lung collapse.

Conditions: in reality, there is a spectrum of conditions with varying degrees of inspiratory and expiratory abnormalities. For example, patients with asthma or chronic obstructive airway disease can develop serious pneumonia, and those with kyphoscoliosis can also have asthma. Acute respiratory distress syndromee poses a particular challenges for ventilation and weaning. Capillary leak leads to lifethreatening non-cardiogenic pulmonary oedema with increased lung water. This leads to decreased compliance and an altered alveolar–capillary membrane (which cause reduced alveolar ventilation and therefore ventilation/perfusion match, leading to shunt and hypoxaemia). Ventilation strategy is as for restrictive respiratory failure and pneumonia.

Deadspace occurs when adequately ventilated alveoli are insufficiently perfused; causes effective fall in alveolar ventilation with consequent hypoxaemia and hypercapnia. Positive end-expiratory pressure (PEEP) is applied to maintain alveoli open at the end of every breath. It increases intrathoracic pressure and can adversely reduce venous return and cardiac output. Continuous positive airway pressure (CPAP) is the equivalent term to PEEP when applied to spontaneous ventilation. Pressure support refers to ventilator-applied inspiratory pressure bursts triggered by a spontaneous effort. The tidal volume delivered depends on lung compliance.

Tracheostomies Tracheostomies are increasingly being performed early in patients likely to require ventilation for more than several days. The benefits of less sedation (improved care of the mouth and secretions) and less deadspace outweigh risks (early bleeding, pneumothorax, late development of tracheal infection and stenosis). Advantages of percutaneous tracheostomies at the bedside (e.g. logistics, reduction in tracheal infections) must be weighed against advantages of the traditional surgical technique (e.g. safety and access, especially in unfavourable anatomy of the neck and airway). Irrespective of technique, the experience of the operator and timing of the procedure are the most important factors related to complications, which can be catastrophic.

Pressure control is the equivalent term to pressure support when applied to mandatory or controlled ventilation. Tidal volume also depends on compliance. Volume support and volume control are equivalent terms to pressure support and pressure control, but in these cases the tidal volume is fixed and the pressure achieved is a function of compliance.

CROSS REFERENCES Reyal Y, Bellingan G. The basic science of acute lung injury. Surgery 2004; 22(6): 3–7. Vohra H A. The intra-aortic balloon pump. Surgeryy 2004; 22(6): i–ii. Zimbler N, Campbell A. Sepsis, SIRS and MODS. Surgeryy 2004; 22(4): 73–6.

Renal failure The key to prevention of renal failure is: • maintenance of circulating volume and perfusion pressure • early treatment of deteriorating renal function with an emphasis on identification and treatment of cause • avoidance of nephrotoxins. Renal failure is associated with fluid, electrolyte and acid–base imbalance, hence renal replacement therapy may be needed. A range of techniques are available, from peritoneal dialysis to haemofiltration (see ‘Access for dialysis’ page 277). Most common in the ICU is continuous veno–venous haemodiafiltration. Filtration techniques are associated with less cardiovascular instability than dialysis. ‹

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FURTHER READING Crane J, Cheshire N. Recent developments in vascular surgery. BMJJ 2003; 327: 911–15. Hillman K, Bishop G. Clinical intensive care. 2nd edition. Cambridge: Cambridge University Press, 2004. Rumbak M J, Newton M, Truncale T et al. A prospective, randomized study comparing early percutaneous dilated tracheotomy to prolonged translaryngeal intubation (delayed tracheotomy) in critically ill medical patients. Crit Care Med d 2004; 32: 1689–94.

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