Practical crisis management in the perioperative care of cardiac surgical patients

12 Practical crisis management in the perioperative care of cardiac surgical patients GEOFF CUTFIELD DON HARRISON FRANK JUNIUS

'Better a live problem than a dead certainty!' ContemporaryIrish (cardiac) surgicalproverb This chapter is intended to deal with practical measures to correct or to manage potential catastrophes, as they present to the anaesthetist, in the perioperative care of cardiac surgical patients. Where relevant to treatment, some aspects of the pathophysiology of the problems will be explored as well. Our aim is to focus on those problems peculiar to this group of patients. The reader is referred to other relevant chapters in this monograph or more general texts for discussion of crisis management of anaesthesia or intensive care problems outside these terms of reference. The three sections of the chapter will be devoted to problems during (1) anaesthesia, (2) cardiopulmonary bypass, and (3) immediate postoperative intensive care.

ANAESTHESIA A. PROBLEMS AT INDUCTION OF ANAESTHESIA Circulatory emergencies P r o b l e m 1: Cardiac arrest

Despite optimum management, cardiac arrest can and does occur during induction of anaesthesia in cardiac surgical patients. There are clearly defined groups of patients at risk, notably those presenting with left main coronary artery disease, the patients who develop severe myocardial ischaemia in the catheter laboratory whilst undergoing angiography or angioplasty procedures (balloon, stent, atherectomy, etc.), those with tight Bailli~re's ClinicalA naesthesiology--

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aortic stenosis or similar physiology from subaortic stenosis with hypertrophic obstructive cardiomyopathy, and patients with other cardiomyopathies in whom alterations in atrioventricular conduction and rhythm may occur without warning in response to minor stimuli. The cause of the arrest is related to the patient's pathology, for example:

9 Myocardial contractile failure as a result of acute severe myocardial ischaemia, such as might occur in association with hypotension in a patient with a critical (> 75%) left main coronary stenosis, or in the patient who has developed acute closure or dissection of a major coronary vessel while undergoing percutaneous transluminal angioplasty. 9 Combinations of myocardial contractile failure and arrhythmias may be seen in patients with tight aortic stenosis or hypertrophic obstructive cardiomyopathy when vascular resistance is lowered abruptly on induction. This causes profound hypotension, because of the limitation of stroke output caused by the aortic valvular 'choke', so that coronary perfusion pressure in vessels supplying hypertrophied myocardium is inadequate for perfusion. Of the reflex responses available to the patient, tachycardia is the only means of raising cardiac output, which further jeopardizes the myocardial oxygen supply-demand balance (Deutsch and Hantler, 1992). 9 Arrhythmias and conduction blocks alone may occur in patients with pre-existing conduction defects (e.g. bifascicular block, WolffParkinson-White syndrome, prolonged Q-T syndromes, etc.) or arrhythmias related to their underlying cardiac disease. They are also a major problem in patients who present with interstitial cardiac diseases, cardiomyopathies and inflammatory conditions. The range of rhythm disturbances seen is broad, from profound bradycardia (needing emergency external pacing (Kirschenbaum et al, 1989) with the development of complete heart block, to ventricular fibrillation. The authors have also noted problems with pancuronium accelerating atrioventricular conduction in patients with underlying supraventricular tachycardias and variable block. This has led to rapid supraventricular rhythms, compromised output and even caused cardiac arrest in ventricular fibrillation. Resuscitation of patients who suffer cardiac arrest during induction of anaesthesia is seldom easy. The most important strategy, inaddition to basic cardiopulmonary resuscitation, is the augmentation of aortic pressure to restore coronary perfusion. To delay administering pressors (adrenaline, metaraminol, etc.) in favour of antiarrhythmic drugs is to prejudice survival. Rapid institution of cardiopulmonary bypass and correction of the underlying lesion is the next step in assuring survival (Figure 1). Another important cause of collapse and cardiac arrest on induction of anaesthesia is anaphylaxis or other hypersensitivity reaction to drugs used in the induction sequence. The clinical features and emergency management of this situation are covered in depth in Chapter 10, however we believe that it is important to note some peculiarities in cardiac surgical patients afflicted with anaphylaxis:

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I Prevention:I Patient in high risk group? 9 left main coronary artery disease. 9 severe myocardial ischaemia in the Catheter Laboratory (angiography or angioplasty). 9 tight aortic stenosis, sub-aortic stenosis (HOCM). 9 cardiomyopathy, myocarditis.

c~-agonist prepared and available (e.g. Metaraminol 1 mg/ml) Cautious induction with continuous intra-arterial pressure monitoring, avoiding agents with known vasodilating actions (e.g. propofol), marked negative inotropic effects (e.g. thiopentone), or vagolytic effects (e.g. sufentanil/vecuronium): [consider high dose fentanyl and pancuronium] Beware of vicious cycle: ~

Hypotension ~ ' ~

L

i "n'oeme~ i

RV contractility

Dec re~SeeffdumyOcardial 1

J

*

Act early and decisively with: 9 pressor support if arterial pressure falls more than 20% from pre-induction values, 9 support of heart rate (atropine + isoprenaline + external pacing) if bradycardia

100% oxygen ventilation plus C.P.R. plus vasopressors plus heparinization

Cardiopulmonary bypass, urgently Figure 1. Decision path for cardiac arrest at anaesthetic induction.

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9 Preoperative [3-adrenergic blockade may confuse signs. For example, tachycardia is a consistent feature of anaphylaxis, but will be masked by [3 blockade. Profound hypotension may be the only initial response. [3 blockade will also render these patients apparently 'resistant' to the effects of adrenaline administered during resuscitation. 9 Volume resuscitation needs careful monitoring, particularly in patients presenting for valve surgery, for correction of congenital cardiac abnormalities, or those with poor left ventricular function. In these patients, while volume resuscitation is important, overloading may well jeopardize survival. 9 Life-threatening arrhythmias are more prevalent in anaphylaxis in patients with cardiac disease (Fisher, 1986). If anaphylaxis is diagnosed, whether or not to continue with the planned surgery is a matter for debate. There is little doubt, however, that a high proportion of patients suffering anaphylaxis develop a mediator-induced consumptive coagulopathy, and this can become a major problem in the post-bypass period.

Problem 2: Other haemodynamic problems Hypertension and hypotension are the most frequently encountered haemodynamic disturbances in cardiac anaesthesia, especially at induction of anaesthesia and during the pre-bypass period. Most frequently these disturbances are caused by changes in vascular tone in resistance and capacitance vessels, so affecting the loading of the heart. These changes occur in response to: (1) the combined central nervous system and peripheral cardiac and vascular effects of anaesthetic drugs; and (2) reflex responses to nociceptive stimuli. 9 Hypotension. It is more unusual for the cause of hypotension during the early phase of the operation to be related to depressed cardiac output, except where mechanical restriction of the heart's motion, hypovolaemia or myocardial ischaemia (see below) are implicated. Assessment of central venous or pulmonary capillary wedge pressure will give an indication of the state of filling. Assessment of peripheral perfusion, the contour of the arterial pressure waveform and urine flow will give an indication of cardiac output if it is not measured directly. An algorithm for the approach to management of hypotension in the postoperative period is given in Figure 9, and much of that decision path is relevant intraoperatively. 9 Hypertension and attendant increases in myocardial oxygen demand during induction and the pre-bypass period are best managed by assessing cause and using short-acting therapy. The cause generally relates to lightness of anaesthesia and reflex response to tissue manipulation, e.g. laryngoscopy, intubation, incision, sternotomy and other surgical stimuli. Appropriate and simple treatment includes deepening anaesthesia and inducing vasodilatation as indicated (see Myocardial ischaemia below).

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Respiratory emergencies Difficulty ventilating the patient at induction of anaesthesia is frightening, but should not engender panic. An algorithm for the approach to management of this problem is presented in Figure 2. There are several factors Anticipate! Always preoxygenate

Check upper airway for mechanical obstruction; oropharyngeal airway, assistance with jaw thrust

Review neuromuscular blockade; has relaxant been given and circulated? myotonus? opiate-induced chest wall rigidity?

Consider reactive bronchoconstriction; asthma? wheeze? anaphylaxis? skin discoloration or rash? (See Chapter 1O)" d ~ ' ' ' ' ~

Sustain assisted ventilation, monitoring Sao2, avoid high inflation pressures, short quick inflations

,/

\

Difficulty ventilating subsides

Proceed to intubation

Difficulty ventilating does not subside

/

Pulmonary oedema?

9 9 9 9

Intubation Ventilation PEEP Vasodilators

\

Tension pneumot~orax?

Wide-bore cannula into pleural space.

Figure 2. Decision path for difficultyventilatingpatient at anaesthetic induction.

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which might influence lung and chest wall compliance or airway resistance at induction in cardiac patients. Problem 1: Chest wall rigidity This problem is encountered frequently during induction of anaesthesia in cases where high doses of opioids, particularly fentanyl, are used (Jaffe and Ramsey, 1983). Experience suggests that this is predominantly a problem of increased expiratory muscle tone. The potentially deleterious effects on ventilation of this phenomenon can be overcome with: (1) generous preoxygenation; (2) a small preinduction dose of non-depolarizing relaxant, insufficient to cause distress to the patient, e.g. pancuronium 0.01 mg/kg; and (3) gentle manual assisted ventilation until full neuromuscular blockade is established. On occasions, where this advice is ignored and excessive inflation pressures are used, a situation analogous to cardiac tamponade may be produced, resulting in hypotension and compromising coronary peffusion. Problem 2: Acute pulmonary oedema Acute pulmonary oedema may be precipitated on induction in patients with very poor left ventricular function (left ventricular ejection fraction < 0.2) or those with severe valvular disease. This is aggravated by sudden changes in body position, e.g. lying flat from semirecumbent positions, or by injudicious fluid loading. For patients at high risk of developing pulmonary oedema, it is often better to induce anaesthesia with the patient in a comfortable semireclining position, securing the airway and mechanical ventilation before proceding to the supine position for the placement of central venous lines and preparation for surgery. Mishandled, this situation can rapidly multiply problems with hypoxaemia and desaturation, frank airway flooding making visualizing the larynx on laryngoscopy almost impossible, and compromise of cardiac output and tissue perfusion pressure. Problem 3: Tension pneumothorax This should be considered if a central venous line has been placed shortly before induction, or the patient is known to have emphysema with bullous disease (see Circulatory failure, below). Problem 4: Anaphylaxis (See Chapter 9, and comments above under Cardiac arrest above.) Distinguishing the cause of ventilatory difficulty in anaphylaxis, as distinct from the other causes above, is a matter of clinical judgement but the principles of management are similar: 1. 2.

Secure the airway. Oxygenate.

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3.

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Support the circulation as appropriate, while making the definitive diagnosis.

Problem 5: Difficult intubation This subject has been covered in Chapter 4, however the message is the same in the cardiac patients: ' . . . adequate preoperative assessment and preparation, don't panic, maintain oxygenation with gentle manual ventilation whilst assembling appropriate assistance and equipment, keep an' eye on perfusion pressure and S-T segments, and avoid trauma.' The last point is particularly important when the patient is to be heparinized subsequently, with the attendant risk of further bleeding and haematoma formation. B. PROBLEMS DURING THE PRE-BYPASS PERIOD Circulatory failure

Problem 1: Myocardial ischaemia Lack of precision in recognizing myocardial ischaemia in the unconscious patient, and in measuring its effect on life afterwards, has hampered collection of data relating to success or failure of management and discouraged valid clinical trials. In day-to-day clinical practice, caring for the anaesthetized patient, signs of myocardial ischaemia include: 9 New S-T segment changes on diagnostic-mode ECG monitor traces. 9 Otherwise unexplained rises in pulmonary capillary wedge or right atrial pressures. 9 Unexplained decline in cardiac output or blood pressure. 9 Appearance of arrhythmias, conduction blocks or even asystole. These are all 'soft' signs, none having a high degree of sensitivity, nor of specificity. The diagnosis therefore rests very much on clinical suspicion and interpretation of patterns of response. Recognized myocardial ischaemia occurring during anaesthesia will have a cause, and a series of effects can be expected. There is clear evidence that repeated episodes of myocardial ischaemia contribute to myocardial necrosis (Braunwald and Kloner, 1982). Reasonable goals of management must therefore take into account removal of causative factors as well as treatment of the ongoing adverse effects. Specific therapy to remove causes of myocardial ischaemia requires identification of the initiating influences. In the clinical setting--until quite recently--we have focused almost entirely on the haemodynamic causes of myocardial ischaemia. The approach has been to try to determine whether the problem is one of demand-induced ischaemia or supply-induced ischaemia. Demand-induced ischaemia is associated with increased heart rate, ventricular wall stress or myocardial contractility. These are the so-called major determinants of myocardial oxygen demand (Merin, 1980). Supplyinduced ischaemia, on the other hand, may be caused by hypotension and

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resultant decreases in coronary perfusion pressure, or by reduced arterial oxygen content through combinations of anaemia and arterial hypoxaemia. Concerning the non-haemodynamic causes of intraoperative ischaemia, Leung and colleagues (1990) reported that 70% of new (ischaemic) regional wall motion abnormalities on echocardiography developed under stable haemodynamic conditions. There is now a large body of data, collected particularly by the participants in the Study of Perioperative Ischaemia (SPI) Research Group, which confirms the high incidence of ischaemic episodes which are not related to haemodynamic perturbations. The probable causes in these circumstances are changes in resistance to flow related to dynamic factors, such as: 9 Varying vessel calibre (spasm) and regional distribution of coronary perfusion (steal phenomenon). 9 Changing fluid viscosity of the blood. 9 Altering coagulability of the blood.

9 ST segment change 9 Rise in PCWP or right atrial pressures 9 Decline in cardiac output or blood pressure 9 Arrhythmia, conduction block

A I

Whichis the most likely cause?

/\ 'Haemodynamic'

1 'Non-haemodynamic' a) Vascular spasm b) Rheological c) Platelet-vessel wall interaction

'Supply'

Hypotension or hypoxaemia

I (Pressor + volume ,~?lnotrope ? [.Oxygen, red cells

or

'Demand'

Hypertension, tachycardia

I (Anaesthesia ~ Nitroglycerine 1,13-blockade

/

Nitroglycerine I Ca++ entry blockade Heparin

Figure 3. Decision path for myocardial ischaemia occurring in the pre-bypass period (see text for discussion and detail).

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A simplified algorithm for the management of perioperative myocardial ischaemia is given in Figure 3.

A. Management of demand-induced myocardial ischaemia The role of anaesthesia. The combination of light anaesthesia and surgical stimulation, particularly of suddenly varying intensity, results in marked sympathoadrenal activation. The consequences for circulatory haemodynamics hardly need elaborating to anaesthetists. The impact of systemic vasoconstriction and abrupt increases in heart rate on myocardial oxygen demand are significant, and in the presence of coronary artery disease, ischaemic myocardial dysfunction is readily provoked. Increasing depth of anaesthesia, particularly in anticipation of such responses outlined above, is a logical and effective strategy (O'Young et al, 1987). The most simple approach is through supplementation with inhalational agents with their benefits of (1) simplicity of administration (and removal), (2) relative predictability of haemodynamic effect, and (3) ease of titration to effect. Isoflurane has become much favoured in this context because of the advantage of its vasodilating ('unloading') property which is of greater potency than its negative inotropic action. Fears that isoflurane might cause coronary steal phenomenon in susceptible individuals with 'steal-prone' coronary disease anatomy have proved unfounded in clinical research and practice (Pulley et al, 1991; Slogoff et al, 1991). Nitroglycerine. By topical application to the nasal mucosa or (preferably) by intravenous infusion in the range 0.3-2.0 txg.g-1 .min -1, nitroglycerine is effective in both prevention and treatment of intraoperative demandinduced myocardial ischaemia (Gallagher et al, 1986; Bunt et al, 1988; Withington et al, 1988). We still await a clear exposition of the mechanism of action of nitroglycerine. There seems little doubt, however, that it relates to vascular smooth muscle relaxation through mimicking the action of the endogenous nitrovasodilator endothelium-derived relaxing factor (Angus and Cocks, 1989; Johns, 1991a, 1991b). The notion that nitroglycerine is predominantly a venodilator, perpetuated in textbooks of pharmacology, should now be dismissed. There is ample evidence that the vasodilating effects of nitroglycerine are widespread in the circulation, with a degree of selectivity for the coronary and pulmonary arteriolar vasculature (Pearl et al, 1983). Thus the beneficial effects in intraoperative myocardial ischaemia probably relate to the well-described reduction in pulmonary capillary wedge and left atrial pressures, as well as the effect in reducing aortic input impedance (Kelly et al, 1990), so lowering overall left ventricular wall tension. Any effect in vasodilating coronary arteriolar resistance would further benefit myocardial oxygen provision in these circumstances. There is need for caution in introducing nitroglycerine: 9 Patients with unrecognized or compensated hypovolaemia may become quite hypotensive, as with the addition of any form of vasodilator therapy. 9 The pulmonary vasodilatation of nitroglycerine will counter the hypoxic

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pulmonary vasoconstrictor response where it is active (Mookherjee et al, 1978). Thus, in patients with any ventilation-perfusion inequality, this will be aggravated, leading to venous admixture and the risk of hypoxaemia.

~-Adrenergic receptor blockade. This has an established place in the management of myocardial ischaemia. There are beneficial effects in restoring myocardial oxygen balance, reducing severity of myocardial 'stunning', and in limiting myocardial infarction size (Frishman, 1988). In the context of clinical anaesthesia, anticipated or recognized demand-induced myocardial ischaemia are good indications for the use of [3-adrenergic blocking drugs (Barnett, 1988; Merin, 1988; Runciman, 1989), particularly in the presence of: 1. Sinus tachycardia. Slowing of tachycardia to heart rates of 80 beats/rain may be accompanied by resolution of S-T segment changes. This strategy is particularly useful in the management of reflex tachycardia which results when nitrovasodilators (sodium nitroprusside or nitroglycerine) are administered to patients who have not previously received [3-adrenergic blocking drugs. 2. Supraventricular tachycardia. In addition to antagonizing the [31mediated chronotropic effect of catecholamines, all of the so-called cardioselective [3 blockers possess class II antiarrhythmic effects, i.e. they prolong the refractory period of the action potential. 3. Hypertension. [3-Blockers have a role in the management of acute hypertension associated with sympathetic activation, but never as firstline therapy. In these circumstances hypertension results from both oLand [3-receptor stimulation. Leaving oh-mediated vasoconstriction unblocked while reducing left ventricular contractility with [3 blockade risks aggravating ischaemia and heart failure, and is unwise and dangerous. In practice, care is also needed with [3 blockers for the following reasons:

1. 2.

3.

Cardiac failure may be exacerbated in susceptible patients because of the negative inotropic effect of [3 blockade. Reflex suppression. Normal reflex responses, mediated by sympathetic activity, may be suppressed by [3 blockade. Thus, important clinical signs that we monitor may be masked, particularly with regard to hypovolaemia, hypoglycaemia and hypercarbia. Bronchoconstriction. In susceptible patients, airways resistance may be increased by [3 blockade. In the asthmatic patient this can be very difficult to manage and [3 blockers, even the cardioselective drugs, are contraindicated.

The choice of drug to use will depend on a variety of factors, but chiefly the anaesthetist's experience and preference. We recommend repeated small doses, e.g. propranolol 0.5 mg or metoprolol 0.5 mg. Esmolol, with its ultrashort half-life is an alternative, where it is available.

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B. Managementof supply-induced myocardial ischaemia The gratuitous advice, encapsulated in the consultative gem 'This patient is fit for anaesthesia, provided that you do not let the blood pressure or the Po2 fall below 100', enshrines the principles (but not necessarily the values, or the sense) of management of supply-induced myocardial ischaemia. These principles, of course, imply the blending of common sense, clinical judgement and good clinical anaesthetic management. They do not need much further elaboration in this context.

Hypotension. The approach to the management of hypotension entails evaluation of likely cause, i.e. reduced cardiac output, reduced systemic vascular resistance, or both. The contribution of the anaesthetic technique needs to be taken into account (and appropriate modification made), then the choice between volume replacement and vasopressor or inotropic support will be dictated by the physiology (see Figure 9).

Hypoxaemia. Similar comments apply. The cause must be traced along the physiological cascade from inspired gas mixing on the anaesthetic machine to uncoupling from haemoglobin in the patient's capillaries! Urgent remedial action depends on identifying the cause and responding appropriately.

C. Managementof non-haemodynamically-mediatedmyocardial ischaemia This is a more difficult problem to manage during surgery. There are two reasons for this. Firstly, we do not have sufficiently sensitive methods to identify which of the aetiological factors is active: (1) spasm and maldistribution of coronary blood flow; (2) rheological changes; or (3) the plateletvessel wall interaction and alterations in both coagulability of the blood and reactivity of the vessel wall. Secondly, and related to this, we have as yet insufficient data available on which to base guidelines for treatment. Unfortunately there is no panacea. Each of the factors above entails its own particular pattern of management. For example there is evidence that where spasm is a problem, whether induced by noradrenergic mechanisms or by platelet activation and the subsequent cascade of vasoactive mediator release, nitroglycerine and the calcium channel antagonist drugs are effective in restoring normal patterns of flow distribution (Merin, 1987; Angus and Cocks, 1989; Horowitz and Powell, 1989; Johns, 1991b).

Aspirin. This has a significant role in the prevention and treatment of both the vasoactive and the thrombogenic effects of platelet activation. At present, many cardiothoracic surgical units recommend that preoperative aspirin therapy should be stopped 7-10 days before operation. In the authors' experience, however, excessive bleeding occurs only occasionally in patients who 'slip through' this recommendation, or who present for emergency surgery whilst still taking aspirin. Clinical trial data are needed to test the validity of the vogue for stopping aspirin therapy to prevent blood

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loss as against the potentially beneficial effects in prevention of perioperative myocardial ischaemia.

Heparin. This is used very effectively in the coronary care management of unstable angina where combinations of low flow and 'hypercoagulability' threaten viability of jeopardized myocardium. There may be problems however with increased bleeding if heparin is given during the dissection phase of 'redo' surgery.

Calcium channel antagon&ts. Of these drugs, the most convenient for use in the operating theatre is nifedipine (Barnett, 1988; Horowitz and Powell, 1989). There is no intravenous preparation of nifedipine readily available in the authors' region, but it is conveniently administered by piercing a 10 mg capsule and applying the liquid contents to either the sublingual or nasal mucosa of the anaesthetized patient. Clinical observations suggest that the pharmacodynamic profile of nifedipine used in this manner is better than that of intravenous verapamil, in that systemic vasodilatation and hypotension are less pronounced and there is little effect on heart rate. There are data to suggest that et-adrenergic responsiveness is impaired following administration of nifedipine (Merin, 1987; Massagee et al, 1987; Schulte-Sasse and Tarnow, 1987). For this reason, the anaesthetist should use nifedipine with caution, being alert for hypotension, particularly in patients who might be mildly hypovolaemic. D. Treating the effects of myocardial ischaemia The pathophysiological effects of untreated myocardial ischaemia may be summarized as 'afterload-work capability mismatch': 1. 2. 3. 4.

Depressed contractility. Impaired relaxation. Increased ventricular end-diastolic pressures. Accelerated oxygen debt.

Successful management of the cause might limit the severity of the adverse effects, nevertheless support of the circulation may well be required while reversible causative factors are being dealt with. On the left side of the circulation, the effects outlined above may culminate in the development of pulmonary oedema. This should be managed aggressively with: 1. Oxygen therapy. 2. Vasodilator therapy (especially nitroglycerine, see above). 3. Inotropic support together with mechanical support (e.g. intra-aortic balloon counterpulsation) if indicated. 4. Positive end-expiratory pressure or continuous positive airway pressure. There are theoretical advantages to continuous positive airway pressure in addition to augmenting alveolar expansion and oxygen uptake; these

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include contributions to restoring capillary hydrostatic pressure balance as well as a limiting effect on ventricular dilatation. In truth, we are relatively ineffective in treating intraoperative myocardial ischaemia, even when we do recognize it! To overcome these inadequacies the thrust of future research and development in the intraoperative management of myocardial ischaemia needs to proceed in several directions: 9 Developing monitoring with much greater sensitivity and specificity. 9 Enhancing clinicians' interpretative skills, enabling the cause to be found in the particular case. 9 Developing appropriate responses to the problem and its cause. 9 Identifying the effectiveness of the response. 9 Successfully interrupting the train of events linking periodic ischaemia and myocardial necrosis.

Problem 2: Arrhythmias and conduction defects Cardiac surgical patients are especially prone to the development of disturbances of cardiac impulse generation and conduction. Particular problems are encountered (and these should be anticipated by thorough preoperative assessment) as a consequence of: 9 Combinations of drugs and techniques used in anaesthesia, with varying effects on control of heart rate and conduction velocity; for examples, sufentanil and vecuronium contributing to sinus arrest in [3-blocked patients, pancuronium contributing to rapid supraventricular tachycardia in association with atrial flutter and variable block, inadvertent hypocarbia and conversion of conduction blocks to complete heart block, etc. 9 Direct stimulation of arrhythmogenic structures, e.g. right atrial 'tickling' with guidewires at central venous cannulation, right ventricular outflow tract stimulation by the passage of pulmonary artery flotation catheters. The consequences may be benign in many cases, but in the high-risk patient such arrhythmias may result in cardiac arrest. 9 The influence of preoperative cardiac drug therapy, notably [3-adrenoreceptor blockers and calcium channel antagonists (Merin, 1987). Although the risks of rebound phenomena militate strongly against withholding these drugs preoperatively, their potential interactions with anaesthesia and surgical stress must be recognized. Profound sinus bradycardia is an increasingly prevalent problem in modern practice, particularly with high-dose opioid supplementation techniques. These need active intervention if they compromise cardiac output or perfusion pressure, however atropine may not be the agent of choice if the problem is more one of sympathetic withdrawal. An isoprenaline infusion (1-3 ng.kg-l.min -1) may be more appropriate for rate control in these circumstances, or consideration may be given to temporary pacing. The authors' observation is that junctional rhythms (with loss of the atrial contribution to ventricular filling and resultant decline in cardiac output and arterial pressure) and supraventricular arrhythmias are more prevalent in the pre-bypass period. These are better managed by finding

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and correcting causes, and (in the case of atrial fibrillation) DC cardioversion, rather than resorting to antiarrhythmic drug therapy.

Rapid atrialfibrillation on atrial cannulation. It is not uncommon for patients to develop rapid atrial fibrillation when the purse-string suture is placed in the right atrial appendage, or the clamp is applied to it, to facilitate atrial cannulation for bypass. In patients with poor ventricular function, whose stroke volume is more than usually dependent on the atrial 'kick' to ventricular filling, this complication can precipitate circulatory failure. The options for management are: 1. 2.

Synchronized DC cardioversion, if further dissection is essential before it is possible to resort to cardiopulmonary bypass; or To institute bypass immediately.

Ventricular arrhythmias. When these occur, they are suggestive of deteriorating ventricular performance and warrant vigilance. Both types of arrhythmias are potentiated by acid-base and electrolyte disturbances, particularly respiratory alkalosis and hypokalaemia (excessive diuretic therapy preoperatively, or in association with inadvertent overventilation). The role of magnesium ions in the cause or management of arrhythmias at operation is not clearly defined.

Problem 3: Unrecognized tension pneumothorax This is a rare but frequently overlooked cause of circulatory failure encountered in the pre-bypass period. The signs are readily confused with those of progressive biventricular failure, gradual hypotension with low cardiac output, together with rising atrial and pulmonary arterial pressures. Capnography provides the differential diagnosis, however, with low endtidal carbon dioxide characterizing ventricular failure and high levels being more consistent with tension pneumothorax. The causes of this complication include rupture of bullous cysts with mechanical ventilation, and accidental visceral pleural injury at central venous cannulation. The problem is readily identified and managed once sternotomy is completed.

Monitoring glitches and iatrogenic problems Problem 1: Mishaps at line placement Placement of lines for monitoring central pressures entails risk. Inadvertent arterial puncture is the most vexing of these. In some units the scheduled operation is abandoned if this complication occurs, on the basis that further bleeding and structural compression by haematoma may develop with heparinization for bypass. This is an extreme stance and a more moderate view is to take each case on its merit, proceeding with caution where the arterial puncture has occurred with a needle smaller than 16 gauge, or exploring and repairing any laceration caused by larger devices.

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The problems peculiar to pulmonary artery catheters are discussed in Chapter 13.

Problem 2: Misinterpretation of data Practical difficulties arise with interpretation of data from monitoring equipment in the pre-bypass period. These can contribute to management errors and need to be borne in mind. Examples include variable diathermy interference with monitor preamplifiers and cardiac output computers, compression of limbs (e.g. during internal mammary artery dissection) and loss of arterial pressure waveforms, and effects of table tilt on transducer positions relative to reference levels.

Problem 3: The 'angioplasty crash'--making do Valuable time (in minimizing delay from injury to reperfusion) may be wasted with fraught attempts to cannulate peripheral arteries and veins in shocked patients presenting from the catheter laboratory after failed angioplastic procedures. A simple expedient in these circumstances is for the cardiologist to leave the systemic arterial catheter sheath in place for use for pressure measurement, and to place central lines from the patient's neck for venous access as the operation proceeds. In a number of cases arriving in the theatre undergoing cardiopulmonary resuscitation in these circumstances, it is far better just to make do with what is available in the interests of getting the patient on to bypass as quickly as possible.

Problem 4: Monitor failure--practical expedients In circumstances where central processing of monitoring fails, back-up techniques are invaluable. A finger on a superficial temporal artery and an eye on ear lobe perfusion--provided they are attached to an educated practitioner---offer first-line back-up. Continuous auscultation of heart sounds with an oesophageal stethoscope facilitates arrhythmia recognition. If the pulse oximeter is battery compatible, the pulse sound also allows recognition of rhythm disturbances if the ECG monitor is suddenly disabled. An old aneroid gauge can be made to double as a continuous mean arterial pressure monitor when the video screen display fails, and a makeshift fluid manometer can be constructed for monitoring central venous pressure. These are very unsophisticated solutions which can be enormously reassuring when one is faced with dataless cardiac anaesthesia!

Problem 5: Polypharmacy and misadventure Cardiothoracic anaesthesia is accompanied by an expanded pharmacopoea. Meticulous attention to detail is required in handling the additional drugs used--in their preparation, in their storage, and in their administration. The potential for misadventure related to polypharmacy is ever-present, for example a vasopressor administered in place of the prophylactic antibiotic,

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etc. Most syringe exchanges in the cardiac theatre will be associated with significant problems and the reader is urged to pay attention to this risk (see Chapter 14).

Problem 6: The wandering sternal saw As more and more patients outlive the life span of their prosthetic valves and coronary artery grafts, so the prevalence of the 'redo' is increasing. In some institutions this prevalence has reached 30% of the cardiothoracic surgical workload. Reopening old sternotomy wounds is associated with greater risk of damage to underlying-and often adherent--structures, i.e. coronary grafts, the right ventricle and the aorta. The risk is recognizable in some cases where lateral chest radiographs demonstrate the anatomy but lack of radiological evidence of proximity of vital structures to the old sternotomy is not grounds for complacency! From the anaesthetist's perspective, preparation for large volume transfusion, with adequate venous access, is important in such cases. Acute myocardial ischaemia can occur if any patent grafts become twisted or lacerated during surgical dissection, depending on the degree of graft-dependence of the patient's coronary circulation.

Problem 7: Ventricular fibrillation during reopening of sternotomy During 'redo' surgery, as indicated above, myocardial ischaemia may give rise to ventricular tachycardia or ventricular fibrillation. There is a period of vulnerability when the sternum is reopened but dissection is not sufficiently advanced to be able to apply internal defibrillator paddles to the ventricles to permit DC cardioversion. This difficulty may be overcome by internal/ external defibrillation, using an external plate (e.g. a modern adhesive indifferent electrode for diathermy) applied to the patient's back before induction of anaesthesia, and a single internal paddle, both connected to the defibrillator.

C. PROBLEMS DURING THE POST-BYPASS PERIOD Ventilation emergencies

Problem 1: Unrecognized apnoea It is surprising how easy it is to neglect to recommence mechanical ventilation in anticipation of weaning from cardiopulmonary bypass. There are a number of contributory factors, primarily inattention, but compounded by a plethora of tasks, lack of check-lists, and ventilator disconnection alarms which can be inactivated during apnoea on bypass. The problem is magnified when there are difficulties in weaning and the patient is repeatedly returned to bypass and ventilation suspended.

PERIOPERATIVE C A R E IN C A R D I A C S U R G E R Y

439

Problem 2: Unsuspected hypercarbia Hypercarbia is often observed early after separation from bypass, despite seemingly normal ventilation patterns. The mechanisms which contribute to this phenomenon include: (1) disparate increases in minute carbon dioxide production during rewarming on bypass; (2) the altered solubility of carbon dioxide in blood as rewarming occurs, so that carbon dioxide is driven from solution as blood temperature increases; (3) regional variations in tissue perfusion--hence carbon dioxide wash-out--which occur in the transition from total cardiopulmonary bypass to pulsatile spontaneous perfusion. Despite raising sweep gas flows through the oxygenator during rewarming, we consistently find high carbon dioxide output on capnography and arterial blood gas analysis in the early stages off bypass. If this is not recognized and attended to promptly, the acidaemia may contribute to unwanted effects on myocardial function and vasomotor stability. These considerations make capnography an invaluable, if not essential, aid to the cardiac anaesthetist.

Problem 3: Difficulty ventilating the lungs Difficulty in ventilation of the lungs at the termination of bypass is an uncommon but potentially serious problem. The anaesthetist should adopt the routine of achieving reinflation of the lungs by manual pressure on the reservoir bag before the termination of bypass. The first few inflations will feel more difficult than pre-bypass inflation but thereafter there should be no difficulty. Early recognition of the problem is facilitated by the anaesthetist's setting of the upper limit of the current pressure alarm approximately 0.5 kPa (5 cmH20) above the pre-bypass peak airway pressure. Once the difficulty of ventilation is recognized the patient should be maintained on bypass until the cause is found and ventilation is satisfactory (Figure 4). The most likely causes of the difficulty are mechanical obstruction of the endotracheal tube, acute pulmonary oedema, tension pneumothorax or bronchospasm.

9 Mechanical obstruction of the endotracheal tube can be excluded by the usual investigations, e.g. digital palpation of the tube in the pharynx, passage of a suction catheter through the tube. Equal movement of the lungs or pleurae in the operative field excludes inadvertent endobronchial intubation. If a small diameter bronchoscope is available, bronchoscopy is the best technique for the exclusion of mechanical obstruction and it permits the exclusion of secretions as the cause of difficulty. 9 Acute pulmonary oedema is a rare problem unless the left atrial pressure is extremely high. This requires that there be left ventricular failure and a precipitated termination of bypass with gross overload of the left ventricle. Acute mitral incompetence following inadequate mitral valve repair is another possibility. Acute pulmonary oedema in these settings is rarely bloody and only occasionally do secretions appear at the anaesthetist's end of the endotracheal tube. If a lung can be seen in the operative field it will appear smaller than usual and will rise poorly with manual inflation. It may be firmer than normal to the palpating finger.

440

G. CUTFIELD ET AL Remain on bypass. Bronchoscopy (fibre-optic)

Evidence of mechanical obstruction?

/

/

",,

No

Yes

Withdraw or replace tube

Check left atrial pressure and assess lung movement

/ Pulmonary oedema likely

Treat underlying cause: --? ischaemic dysfunction --? rnitral regurgitation --? acute aortic regurgitation ~ ? LV overdistension

",, Bronchospasm likely

Bronchodilators --systemic 62 agonists --try adrenaline (1 : 10 000) 2 ml instilled down ET tube

Figure 4. Decision path for difficulty ventilating lungs in preparation for weaning from cardiopulmonary bypass.

9 Tensionpneumothorax is easily excluded by inspection of the pleura in the sternotomy wound. If there is doubt, the surgeon can create a small hole in one or both pleurae. 9 Bronchospasm may occur in the absence of pre-bypass airway obstruction. There may be no history of previous asthma. With manual inflation the lungs balloon into the operative field and deflate slowly. The cause is usually not discovered but an anaphylactoid reaction and/or activation of the complement system by bypass are usually suspected. Conventional therapy with 132 agonists, antihistamines or steroids is usually effective but the response may be slow. The causes and management of perioperative bronchospasm occurring during cardiac surgery have been reviewed recently by Schwartz and Lell (1989).

Circulatory emergencies Problem 1: Major rhythm and conduction problems Crisis management of arrhythmias and conduction defects has been

PERIOPERATIVE CARE IN CARDIAC SURGERY

441

discussed in Chapter 5. A wide variety of arrhythmias may be seen after cardiopulmonary bypass. Recalcitrant ventricular arrhythmias are suggestive of ischaemic damage to the myocardium. The causes to be assessed for potential reversibility include: 9 Incomplete revascularization in coronary graft patients. 9 Coronary air embolism from air bubbles in the aortic root (valve surgery) or in grafts (coronary artery bypass graft). 9 Acute graft closure with low graft blood flow, kinking or thrombosis. 9 Incomplete myocardial protection, depending on the .technique used (cardioplegic arrest or intermittent cross-clamping and reperfusion). 9 Unrecognized overdistension of the ventricles on bypass. 9 'Trash' embolism (after 'redo' coronary surgery). 9 Unrecognized perioperative myocardial infarction, occurring either during cardiopulmonary bypass or in the pre-bypass period. If ventricular arrhythmias are refractory to simple measures such as correction of remediable causes of myocardial ischaemia (above), correction of hypokalaemia and acid-base disturbances, and the administration of lignocaine (bolus I mg/kg), return to bypass and reperfusion is indicated. Clinical trials with the use of bretylium in these circumstances have demonstrated some benefit (Kirlangitis et al, 1990). Much has been made recently of magnesium ion supplementation in the management of ventricular arrhythmia after bypass. This approach still needs scientific validation and caution is required to avoid the unwanted hypotensive effects of what is in effect a natural calcium antagonist. Varying degrees of heart block are also prevalent in coronary and valve surgery patients. These necessitate pacing in a number of cases, specifically where the ventricular response is slow and cardiac dilatation occurs, and where there is dependence on atrial filling for optimum ventricular performance (e.g. ischaemic cardiomyopathy or concentric left ventricular hypertrophy associated with aortic stenosis) (see below).

Problem 2: Hypotension with vasodilatation

Over the last decade there has been a subtle shift evident in the post-bypass haemodynamic profiles of coronary artery surgery patients. Whereas it was common in the 1970s to observe hypertension with high systemic vascular resistance, necessitating potent vasodilator infusion after bypass, a contrary picture of excessive vasodilatation and high cardiac output is being found in an increasing proportion of patients. In many cases, support of arterial pressure with pure vasopressor therapy is required for short periods. Epidemiological studies are needed to identify the causes of this shift, but the contenders may include changing patterns of cardioplegic management, residual effects of papaverine in the surgical field, heightened sensitivity to the effects of preoperative drugs with vasodilating actions per se, and interactions between anaesthetic techniques and preoperative cardiac drug

442

G. CUTFIELD ET AL

Before weaning:

I

Rhythm acceptable?

/

"No1

? perfusionpressure adequate? ? serum potassiumnormal? ? atrial or ventriculardefibrillation required? ? antiarrhythmicagent required?

Yes

\N\

Heart rate 80-100/min?

I

Yes

? response to atropine_?

During weaning:

.

I Optimum filling pressure? ~ , . 4 E ~ ~ (comparison with pre-bypass filling pressures) Iroo low Jl I" Transfusi~176 I I pump I /

Following weaning:

Too high .Takeoffbioodinto pump reservoir 9 Vasodilator infusion

Low output state not improved

Persisting low output state

_J

/

Return to cardiopulmonary bypass.

Check: 1. Aortic--~radial pressure gradient? 2. Filling pressures: 9 hypovolaemia--~transfuse 9 failure:--*inotropic support 3. Capillary perfusion or systemic vascular resistance; 9 excessive vasoconstriction --wasodilator infusion 9 inappropriate vasodilatation --*check vasodilator infusion ~vasopressor (metaraminol, adrenaline, noradrenaline)

I Consider mechanical support: 9 IABP (intra-aortic balloon counterpulsation) 9 VAD (ventricular assist device) Indications: 9 Ventricutar dysfunction (LA, RA > 20, SBP < 90, CI < 2.C 9 Refractory to inotropic support and IABP 9 Probability of recovery Contraindications: 9 Inability to control haemostasis 9 Severe preoperative LV dysfunction combined with presumptive evidence of perioperative infarction

Figure 5. Decision path for low output state on weaning from cardiopulmonary bypass.

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443

therapy. It is important not to overlook other possible causes of a hyperdynamic circulatory state, notably acute sepsis (e.g. contaminated intravenous or cardioplegic solutions), thyroid disorders with so-called hyperthyroid 'storm', or Addisonian crisis. Problem 3: Low output states

The causes of low cardiac output states after cardiopulmonary bypass include: 9 Acute left ventricular failure secondary to inadequate protection of the myocardium on bypass, causing myocardial stunning. 9 Perioperative myocardial infarction. 9 Coronary air or particulate embolism. 9 Reactions to protamine administration (see below). 9 Acute right ventricular dysfunction (see below). The response by the anaesthetist to cardiac failure with low output should be dictated by the physiology as measured at the time, optimizing cardiac filling, supporting inotropic state where indicated, and controlling vascular resistance to aid ventricular ejection, whilst striving to maintain adequate coronary perfusion pressure (Figure 5). It is important to bear in mind that in low output states measurement of arterial pressures from radial arterial lines may be affected by gradients and pulse wave transmission abnormalities (O'Rourke et al, 1992). It is the central aortic pressure that matters most during this phase, governing as it does the coronary perfusion pressure gradient and the impedance to left ventricular ejection. Aortic pressure may need to be measured directly while the patient's condition is assessed and stabilized. There is no simple 'cookery book' solution applicable to all cases, and some will be refractory to drug therapy. From time to time case reports appear reporting good responses to alternative agents after 'standard' techniques have failed, and these may be worth considering, e.g. glucagon, glucose-insulin-potassium, phosphodiesterase III inhibitors, somatostatin analogues, etc. In these extreme cases mechanical circulatory support with intra-aortic balloon counterpulsation or ventricular assist devices may well be required. Intraoperative echocardiography is achieving a significant role in aiding decision making, that is in determining whether there is a reversible component to the problem (regional wall motion abnormalities versus fullthickness infarction, etc.). Mechanical circulatory support is better undertaken early rather than as a last resort after several attempts to wean from bypass with high-dose inotropes, provided that there are grounds for believing that the ventricular failure has a potentially reversible cause (Kanter et al, 1988; Pennington et al, 1988; Miller et al, 1990; Wareing and Kouchoukos, 1991). Problem 4: Hypertensive crises

Hypertensive crises are rare in the post-bypass period in the operating

444

G. CUTFIELD ET AL

theatre, except perhaps following aortic valve replacement and coarctation repairs. These may be quite difficult to manage. Many such patients present with unmodified baroreceptor reflexes so that treatment with vasodilators alone is complicated by reflex tachycardia. A balanced approach with vasodilators and 13-blocking drugs (unless contraindicated) is to be preferred. Problem 5: Protamine reactions

There are at least three different reactions which have been studied and identified: 1.

Systemic hypotension from rapid injection. The mechanism remains unclear but probably involves arachidonic acid metabolites and mediators of arteriolar dilatation. The response is predictable and can be avoided by slow protamine infusion (e.g. 100 mg/min). 2. Anaphylactic or anaphylactoid response; idiosyncratic type I hypersensitivity reactions.

Atrial pacing (fixed rata):

I

Pacing spike evident on ECG? 9 Power off? 9 Batteries flat? 9 Short circuit: between wires, or contact between bared wires and retractors, etc? 9 Connecting cables broken?

Yes

QRS complexes and arterial pulse waves related to pacing spikes?

/

YesJ

I ~ No QRS complexesor arterial pulse waves related to pacing spikes QRS complexes \ and arterial waves ~1~ present but not related Consider: to pacing spikes , ,, , Atrio-ventricular conduction block I ~ AV sequential pacing

'

Satisfactory atrial pacing

Inadequate stimulus

i

Elevated threshold ~ Check threshold increase output

1'

i

Consider i Atrial fibrillation I

i Underlying rhythm with rate faster than stimulus frequency ! ,

atnal wire to Vt lead of ECG monitor and check 'atrial' ECG.

Figure 6(a). Decision path for failure of atrial pacing after cardiopulmonary bypass.

PERIOPERATIVE CARE IN CARDIAC SURGERY

3.

445

Catastrophic pulmonary vasoconstriction; also idiosyncratic but more difficult to manage because of the degree of circulatory (predominantly right ventricular) failure.

All of these reactions contribute to hypotension and degrees of circulatory failure. The reactions have been reviewed recently by Lowenstein and Zapol (Lowenstein, 1989; Lowenstein and Zapol, 1990) and Horrow (Horrow, 1988). Management of the patient depends on recognition of the role of protamine (i.e. the temporal relationship to its admininstration) and

I

Ventricular pacing (fixed rate, d e m a n d , o r AM s e q u e n t i a l ) :

[

Pacing spike evident on ECG? ~

No

~

Remedy!

9 Power off? 9 Batteries flat? 9 Short circuit: between wires, or contact between bared wires and retractors, etc? 9 Connecting cables broken?

Yes

f

QRS complexes and arterial (and venous) pulse waves related appropriately to pacing spikes? (Examine ECG monitor frace, pulse wave on arterial pressure monitor or pulse oximeter, and CVP or RA waveform)

Yes

\

J

No QRS complexes or arterial pulse waves related to pacing spikes QRS complexes a n d arterial w a v e s

present but not related to pacin! spikes

\ ~1~ Check atrial and ventricular systems independently Consider:

| Epicardial insertion site of ventricular

stimulation

I

Satisfactory

....... d

pacing

output Switch polarity i.e. '+' and ' ' connections and reassess Resite epicardial leads

i Inadequate stimuli

I

....... outputs

i Elevated thresholds

| iln demand mode] 'Sense' sensitivity

I

II

Ohe~176 ~ Increase outputs

NOTE: Local myocardial ischaemia, at the insertion sites of wires or electrodes, is the most likely cause of increased impedance to pacing stimulation

Consider

i i Atrial Underlying rhythm with rate fibrillation faster than stimulus frequency I 1 Stop pacing briefly and verify; if in doubt, connect I atrial wire to V1 lead of ECG monitor and check 'atriar' ECG =

I

Figure 6(b). Decision path for failure of ventricular pacing after cardiopulmonary bypass.

446

G. C U T F I E L D ET AL

the exclusion of other causes of hypotension. Emergency management should follow guidelines presented here (see sections on anaphylaxis, right ventricular failure, low output, etc.). Problem 6: Untoward reactions to colloid plasma expanders Recent publications have highlighted the plethora of hypotensive reactions to colloid plasma expanders. Some of these reactions have an immunological basis with complement fixing anaphylactoid features (e.g. Haemaccel, dextran), and others a pharmacodynamic basis (e.g. Stable Plasma Protein Solution (SPPS) in Australasia--hypotensive response in patients treated with angiotensin converting enzyme inhibitors, ascribed to presence of kinins and kallikrein precursors in SPPS and inhibition of host kininases, resulting in unmodified peripheral arteriolar dilatation). Problem 7: Tricks with pacemakers Short-term pacemaker dependence after operations involving cardiopulmonary bypass has become increasingly prevalent in the last decade. Little has been published about this trend but the likely contributing factors include the more generous preoperative use of calcium channel blocking drugs and the trends in cardioplegic solution composition to incorporate membrane stabilizing agents with attendant inhibition of spontaneous pacemaker depolarization potentials. Failure to capture may be both irritating and dangerous. It is unwise to wean from bypass until satisfactory capture of rhythm is established. An algorithm for management of pacing problems is given in Figure 6. Problem 8: Acute right ventricular failure This complication carries high mortality, particularly if it arises in the context of right ventricular infarction. It is important to recognize, however, that right ventricular failure has multiple causes, brought about by imbalance of the normal matching between right ventricular load and work capability. Loading considerations include: (1) the blood flow and pressure dynamics of filling (preload) and of the pulmonary circulation (afterload); and (2) the constraints of the interventricular septum and the pericardium. Factors affecting work capability include the inotropic state of the right ventricular myocardium and all of its determinants, but most particularly myocardial perfusion. Understanding the aetiology and the pathophysiology of right ventricular dysfunction, which in turn governs appropriate therapy, depends on our recognition of influences which disturb this matching (Laver et al, 1979; Calvin, 1991). In the setting of cardiac surgery these comprise: 1. Factors affecting loading characteristics. Increased pulmonary vascular impedance: 9 Atelectasis after bypass and hypoxic pulmonary vasoconstriction.

PERIOPERATIVE CARE IN CARDIAC SURGERY

447

Pre-existing pulmonary hypertension, e.g. mitral valve replacement and the 'sick mitral' patient. 9 Reactions to drugs, especially protamine, also anaphylaxis and acute severe asthma. 9 Adult respiratory distress syndrome. 9

/-

Clinical features: 9 9 9 9

RA pressure increased (> 20 mmHg), 'Crossing' of atrial pressures (RA > LA) increased 'v' wave of tricuspid regurgitation on RA trace Right ventricular enlargement, with or without pulmonary hypertension 9 Progressive hypotension and reduction in cardiac output

Priorities in management are:

Protect right coronary perfusion pressure gradient Crudely, RCPP = Aortic pressure- RV cavity pressure

1.1. Maintenance of aortic blood pressure 9 Inotropic support of the left ventricle (if needed) 9 Arterial vasopressors, e.g. noradrenaline, metaraminol 9 Intra-aortic balloon counterpulsation 1.2. Reduction of right ventricular cavity pressures 9 Pulmonary vasodilators; nitroglycerine, PGI2, PGE1 9 Check mode of respiratory support

Reduce right ventricular 'afterload'

~-2.

2.1. Reduction of pulmonary vascular impedance 9 Pulrnonary vasodilators; nitroglycerine, PGI2, PGE1 9 Check mode of respiratory support

k..3.

Support right ventricular contractility 9 Inotropic support: (more (3 agonist) dobutamine, isoprenaline 9 Consider R.V. assist device or ECMO in extreme cases

~"

4. Optimize right ventricular filling

Figure 7. Decision path for managing acute right ventricular failure after bypass.

448

2.

G. C U T F I E L D ET A L

Factors affecting work capability. Impaired right ventricular contractility: 9 Inadequate myocardial protection, problems with delivery of cardioplegia, cooling, etc. 9 Incomplete revascularization of supply to right ventricle. 9 Inferior myocardial infarction, preoperatively or intraoperatively.

Frequently, in clinical situations, by the time right ventricular failure is recognized it combines sinister aspects of both series and parallel ventricular interaction, and a vicious cycle of circulatory failure ensues. Acute, sustained elevation of the resistance to right ventricular ejection results in elevation of right ventricular intracavity pressures during systole and diastole. If there is no relief (as occurs, for example, with the development of tricuspid regurgitation in some patients) then coronary perfusion is impeded by reduction of the effective coronary perfusion pressure to the right ventricle. In addition, leftward septal migration during diastole further impairs left ventricular filling. As left ventricular output and aortic pressure decline, so does coronary perfusion pressure, with the result that what started as a problem of afterload-work capability mismatch becomes compounded by the development of right ventricular ischaemia, even when coronary arteries are normal. The principles of management of this difficult problem are summarized in Figure 7.

CARDIOPULMONARY BYPASS EQUIPMENT FAILURE Prevention is without doubt the best way to handle heart-lung machine equipment failure. We can do well to model the handling of heart-lung machine procedures on the jet aircraft industry's safety standards. By setting up a system of intensive checks and double checks, by appropriate anticipation of possible errors, by maintenance and replacement of equipment when needed, and by provision of adequate back-up facilities, it is conceptually possible to eliminate pump-related incidents. In order to learn from any unwelcome incidents it is very helpful to keep a log in which these incidents are recorded and analysed and remedial measures documented. By their nature, pump incidents are often traceable to human error or omission, and they often threaten the health and well-being of patient and staff. Thus these incidents are extremely stressful to the staff concerned. Panic when incidents occur has to be resisted to prevent compounding any error. Perfusionists should make an effort to mentally rehearse and condition themselves for possible incidents. A helpful hint at the suggestion of an incident is to stop the pump, clamp the arterial and venous lines immediately and take stock of the situation. Suppress any rising feeling of panic, pretend there is no emergency but rather a situation in which one acts fast and deliberately.

PERIOPERATIVE CARE I N CARDIAC SURGERY

449

Specific problems Problem 1: Oxygenator failure Before circuit assembly, the oxygenator should be inspected for defects and damage; in particular, cracks or breaks near the venous and cardiotomy reservoir inlets and the arterial and cardioplegia outlets should be excluded, and the gas inlet inspected. Once the heat exchanger has been connected, water leaks into the blood circuit should be sought. Once properly titled, and having confirmed function before connection to the patient, oxygenation failure should be extremely rare. Although it needs extreme physical violence to break any reputable modern oxygenator, perfusion teams should have the timing and equipment to replace vital elements of the circuit quickly and efficiently (a comparision to tyre changing in Formula 1 car races may be appropriate). Should an oxygenator need replacing, the following practical steps should be taken in quick successsion: 1. 2. 3. 4. 5. 6.

Stop the arterial pump. Clamp the arterial, venous and cardiotomy return lines well away from the oxygenator and assess the situation as quickly as possible. Inspect for air in the arterial line, unclamp the arterial line and infuse as much blood into the patient as possible, effectively treating the patient as a temporary storage reservoir. If possible, put any remaining blood into the cardiotomy reservoir by lowering it below the oxygenator. Put line clamps close to the oxygenator, but leave enough room (some 5 cm) so that the lines can be cut and reconnected without difficulty. Unclamp the arterial line and allow blood back into oxygenator, either by gently winding back (if a roller pump is being used), or passively (if a centrifugal pump is in use). Open the venous line and recommence perfusion.

These steps suffice in bubble oxygenations and in membrane oxygenators where the membrane is on the venous side. Those oxygenators with the membrane on the pressure side of the pump will need recirculation to remove gas from the blood path. Units which use these latter oxygenators may well consider having a replacement oxygenator of the former type available for such emergencies because perfusion can be recommenced more quickly. A practised and versatile team should be capable of replacing the simpler type of oxygenator in less than 2 minutes. Regular practice is essential and can be achieved easily using used circuits. Occasionally a damaged oxygenator can be nursed through a pump run by using surgical bone wax.

Problem 2: Cardiotomy reservoir and filter problems Replacement is usually straightforward, only needing a brief stop of the suction pumps. Two points of caution are:

450 1. 2.

G. C U T F I E L D ET A L

Make certain the reservoir cannot be pressurized if an arterial line filter is bled into the reservoir without a one-way valve. More insidious and less well known is the possibility of wetting the whole cardiotomy filter. If the arterial line filter is vented into the cardiotomy filter, pressure can build up inside the filter if it is completely wetted. If the bubble-point pressure of the wetted cardiotomy filter is higher than the bubble-point pressure of the arterial line filter, air can be blown into the patient if there is no one-way valve in the venting line.

Problem 3: Tubing circuit problems Meticulous care is needed to ensure correct circuiting. Special points are: 1. 2.

Do not vent arterial and suction lines in their pump heads because air can be blown into the patient in the absence of one-way valves. Double-check for contaminants such as slivers of ampoule glass in the pump heads.

Problem 4: Ruptured pump head tubing This is a concern for all perfusionists using roller pumps. The most vulnerable and dangerous spot is where the roller first contacts the tube. At this site the pressure is likely to be negative for at least part of the cycle, and air can be sucked in as small bubbles over a period of time. This represents one of the more compelling reasons for using an arterial line filter, which has the capacity to stop air until bubble-point pressure is exceeded. If carefully bled off, this pressure may not be reached. An alternative and rapid way of detecting this problem is to attach a plain ultrasonographic Doppler flow detector (10MHz) to the polycarbonate connector closest to the patient on the arterial line. Such monitors are effective in monitoring any foreign matter, such as gas bubbles, going through the arterial line. Perfusionists quickly learn to distinguish normal from abnormal sounds. It is also good practice to design the arterial pump head tubing in such a way that there is sufficient length to be able to advance a fresh segment into the pump head at regular intervals, or even to extend to an alternative pump head.

Problem 5: Obstruction of arterial line d&tal to the pump head It should be mandatory to monitor the arterial line pressure routinely. There are devices available which will stop the pump when excessive arterial line pressures are recognized. In principle it is better to have a system which is not able to reach damaging pressures. Use of centrifugal pumps is one method but such units are still beyond the financial resources of many cardiac surgical units. A cheaper and equally effective method is to use distensible pump h e a d t u b i n g such as 0.5 inch silicon tubing and leave some 10 cm outside of the pump head. This will distend and distort without blowing the line, causing a leak back past the rollers. This solution also has

PERIOPERATIVE CARE I N CARDIAC SURGERY

451

the advantage of being both audible and visible in operation. Perfusionists should experiment with their circuit designs to make them 'blow-out proof'.

Problem 6: Gas supply disruptions It is most important to monitor oxygen supplies so that any interruptions are rapidly detected. It is also necessary to have a completely independent oxygen supply which can be connected directly to the oxygenator. This can be done simply, by having an adequate length of appropriate plastic tubing with a connector to allow attachment to the anaesthetic machine with its flowmeters and cylinders.

Problem 7: Electrical supply disruptions Many perfusion units enjoy the security of having an emergency power point in the operating theatre which will supply electrical power from the hospital's emergency generator in the event of community supply failure. Regrettably, reality is less enchanting. The power supply may fail at any point from the power station right down to the motor that turns the pump head, so that the site of interruption may not be easily localized. It is also possible to have a power failure which does not give a signal to the local emergency generator to switch on to emergency supply. Perfusionists should consult the hospital's engineers so that everyone is aware of possible problems and actions to be taken. Alternative supplies should be available. Handles should be ready for manual operation of pumps for a short time. While it is desirable to have a battery back-up supply, it should not be forgotten that heat exchangers in bypass circuits are the major current consumers and rapidly deplete battery charge. An alternative is to have hoses and a mixing valve available so the heat exchangers can be run from the theatre's cold and hot water supply. Any power failure may be in the heart-lung machine itself. Operators should know how to cope with minor problems such as fuse changes, and mechanisms should be available to bypass more serious faults. Modular heart-lung machines are preferable in such circumstances. The faults may lie in the machine's power cable or transformer base so it is important to have completely separate emergency pumps with power supply available. The availability of staff and facilities for quick identification and repair should be considered.

Problem 8: Massive arterial air embolism This is probably the greatest fear amongst perfusionists. It is now possible to acquire reliable equipment which both warns of a low oxygenator reservoir level and stops the arterial pump. Because of the great--but preventable-danger of embolism, it is advisable to have a clearly audible and visible warning signal at the 500 ml level on the reservoir. Such a precaution is further enhanced by incorporating another independent signal/controller, with a different warning note, at the 200 ml level which also stops the arterial

452

G. C U T H E L D ET A L

pump. In addition, it is cheap and easy to connect a plain Doppler 10 MHz flow detector to monitor the arterial line continuously. Such flow detectors can be set to be unobtrusive but audible, and will give a loud crackling sound when macrobubbles go down the line. They will also produce an audible alteration in sound character with microbubbles. The management of massive air embolism involves the whole operating team. The crucial elements are: removing as much air as possible from the patient; minimizing the effects on the brain by routine cerebral injury management; and recirculating the pump. There is evidence that taking the patient to a hyperbaric chamber, even at a late stage such as 24 hours later, is beneficial. Problem 9: Real accidents

One should pay some attention to the possibility of misadventure, for example staff tripping over equipment, visitors fainting, equipment being dropped, or sudden movement of the heart-lung machine or operating table. It is possible to design the set-up so that vulnerability to such disruption is kept as low as possible. Design and safety concepts in cardiopulmonary bypass are very well reviewed by Reed and colleagues (1988).

POSTOPERATIVE INTENSIVE CARE Generally speaking, problems which occur in the immediate postoperative intensive care period are the product of: (1) preoperative disease states and drug therapy; (2) the physiological effects of cardiopulmonary bypass; and (3) the technical effectiveness of the surgical procedure. In most cases, one can anticipate events if the influence of each of these factors is known: ' . . . to be forewarned is to be forearmed'.

Circulatory emergencies Problem 1: New myocardial ischaemia

The development of new myocardial ischaemia in the early postoperative phase in the care of coronary graft patients represents an emergency. Perhaps the single most important indicator to be 'on the lookout' for is the surgeon's honest appraisal of the technical aspects of his or her performance at operation: the calibre of graft conduits, the calibre of arteries grafted and anastomoses fashioned, and the adequacy of revascularization achieved. Recognition of ischaemia in this period is complicated by many factors. Reliance on ECG changes--in particular the configuration of the S-T segment--is confounded by: 1. 2.

Conduction blocks and their effects on repolarization patterns. Pacing (similarly).

PERIOPERATIVE C A R E IN C A R D I A C S U R G E R Y

3. 4.

453

Effects of postoperative hypothermia and electrolyte disturbances on S-T and T wave configuration. Early effects of pericardial irritation.

Thus, a high index of suspicion must be maintained and myocardial ischaemia should be high on the list of differential diagnoses when coronary graft patients develop unexpected haemodynamic problems, notably: 9 Hypotension concomitant with bradycardia, which may progress rapidly to asystolic cardiac arrest despite pharmacological intervention. 9 Progressive low cardiac output state, or increasing inotrope requirement to maintain stability. 9 Ventricular arrhythmia and, particularly, refractory ventricular tachycardia. Causes of new myocardial ischaemia in the postoperative period are similar to those outlined for circulatory failure, but take into account the grafts as well as the native vessels. Although graft 'spasm' has been blamed for postoperative cardiac arrests and sudden death in the early hours after coronary graft surgery, there is very little clinical or experimental proof of the credibility of this assertion. Post-mortem examination of the heart in these cases often reveals patent grafts and patent arteries. It is much more likely that the explanation is a dynamic problem related to either twisting or kinking of grafts and anastomoses with changing geometry of the heart as loading conditions vary with the patient's emergence from anaesthesia, or compromise of the regional oxygen supply-demand balance created by inadequate graft calibre or flow to too large a territory of myocardium when the minute work of that territory is increased. Management of the patient with new myocardial ischaemia in the postoperative period clearly depends on the presentation (Figure 8). Immediate return to the operating theatre for re-exploration and regrafting is the most logical approach, particularly when circulatory stability is compromised (Raman et al, 1989). Subjecting the patient to emergency coronary angiography is fraught with risks in transfer and in instrumentation. This is rarely justified. Open operative inspection, together with the surgeon's knowledge of the operation, readily reveals the culprit graft and facilitates reinstitution of cardiopulmonary bypass, reperfusion of the ischaemic segment and reconstruction of the graft at fault.

Problem 2: Hypotension Hypotension is the most prevalent problem in the postoperative care of cardiac surgical patients. The approach to care comprises: 1. 2. 3. 4.

Recognizing hypotension, for its dangers. Assessing severity of hypotension and urgency of correction. Determining the cause of hypotension. Seeking the most appropriate therapy. The dangers of hypotension in these patients are:

454

G. CUTFIELD ET AL

Suspicion of new myocardial ischaemia in the postoperativerecovery area:

S

,)

9 diagnostic ST segment morphology 9 hypotension concomitant with bradycardia asystolic cardiac arrest 9 progressive low cardiac OUtputstate, or increasing inotrope requirement 9 ventricular arrhythmia, particularly refractory ventricular tachycardia

Emergency resuscitation:

~

m

m

m

~

~

Cardiac o hypotensive BP < 50 mmHg systolic)

Hypotensive (BP 60-90 mmHg systolic)

but Rhythm stable

Y Support of coronary (graft) perfusion pressure: 9 Judicious volume 9 Pressor support (a agonist, e.g. metaraminol, noradrenaline

Reopen sternotomy --,internal cardiac massage (with care for grafts)

by infusion) 9 Inotropic support if atrial pressures rising

Support of coronary (graft) flow: 9 Nitroglycerine infusion

/ No resolution of ischaemic changes I Re-heparinize urgently

\ I

Returnpatient to operating theatre I as soon as practicable, for re-exploration _+reperfusion _+regrafting

Figure 8. Decision path for management of new myocardial ischaemia in the immediate postoperative period.

PERIOPERATIVE C A R E I N C A R D I A C S U R G E R Y

455

1.

Impairment of vital organ system perfusion, especially in the coronary, cerebral and renal circulations, and particularly in older patients. 2. Reduction in new coronary artery graft blood flow and consequent risk of early graft failure in patients who have had coronary artery bypass grafts. 3. Hypotension may be a late sign of impending life-threatening complications (e.g. left or right ventricular failure, tamponade) after cardiac surgery. The optimal postoperative blood pressure is really determined by the patient's condition. For example, an elderly patient having combined coronary grafting and carotid endarterectomy, and who has cerebrovascular disease and long-standing hypertension, may require higher pressures for optimal cerebral perfusion. Conversely, in a patient with long-standing mitral valve disease, whose normal blood pressure is 90/60 mmHg, a similar pressure would be acceptable following valve replacement. Physiologically, postoperative hypotension is caused by either reduced cardiac output or reduced systemic vascular resistance, or both. Reduction in blood pressure may therefore be related to: 1. Reducedpreload, i.e. hypovolaemia; causes include inadequate volume replacement or active bleeding, loss of atrial 'kick' with conversion to atrial fibrillation or junctional rhythm. 2. Reduced contractility. Causes include: 9 Interstitial oedema in the myocardium, common after cardiopulmonary bypass. 9 Myocardial ischaemia (see above). 9 Substances with negative inotropic effects such as 13blockers, lignocaine, verapamil, or bacterial toxins. 9 Impaired relaxation of the ventricle, e.g. compression by excessive positive pressure during mechanical ventilation, or tension pneumothorax, or pericardial tamponade. 3. Reduced systemic vascular resistance. Causes include: 9 Excessive vasodilator therapy, e.g. too much sodium nitroprusside (SNP) or inadvertent bolus of SNP. 9 Reduced sympathetic outflow associated with administration of sedation. 9 Persisting effects of preoperative antihypertensive therapy. 9 Substances with systemic vasodilating effects such as histamine, kinins in SPPS, bacterial toxins in sepsis, hormones released during anaphylactic reactions, etc. Appropriate therapy for hypotension therefore requires identification of the cause of the fall in blood pressure, using clinical skills, supplemented by monitoring and trend charts, and investigations (Figure 9). Emergency measures to be taken while identifying the cause of hypotension are to: 2.

Check airway, ventilation, cardiac rhythm.

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Check accuracy of blood pressure measurement with sphygmomanometer. Tilt patient head down if blood pressure less than 80 mmHg systolic. Scan infusions: bolus of vasodilator? inotrope infusion suspended inadvertently or reduced too rapidly? Check central venous pressure (left atrial pressure or pulmonary artery wedge pressure if available). Check peripheral perfusion and capillary return (ear lobes, fingers, toes). Check urine flow and level of consciousness.

Problem 3: Low cardiac output states

Refer to the section on circulatory emergencies above, and Figure 5. Problem 4: Hypertensive crises

Hypertension is common after cardiac surgery, especially coronary artery surgery. It is probably due to a combination of elevated levels of circulating catecholamines in response to the trauma of surgery and reflexes arising from the coronary arteries and aorta. This phenomenon remains active for 12-24 hours but seems to persist longer in patients with underlying essential hypertension. A similar pattern of approach to that recommended for the hypotensive patient is recommended, i.e.: 1. 2. 3. 4.

Recognizing hypertension, for its dangers. Assessing severity of hypertension and urgency of correction. Determining the cause of hypertension. Seeking the most appropriate therapy.

Hypertension represents a threat to the cardiac patient because of the inherent dangers: 1. 2. 3. 4.

Increased afterload on the left ventricle so that myocardial oxygen requirement is increased. Left ventricular failure may occur. Increased stress on operative suture lines. Hypertension and associated vasoconstriction may decrease tissue perfusion. Increased risk of cerebral haemorrhage.

Blood pressure may increase dramatically during transfer from the theatre to the postoperative intensive care area, and it is important to attend to such hypertension promptly (Figure 10). Problem 5: Haemorrhage

Postoperative bleeding is an everyday problem in most cardiac surgical units. The extent of blood loss depends on many factors, but untoward losses

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THE PRINCIPLES OF BLOOD PRESSURE REDUCTION: 1.

Assess the patient for level of awareness or sedation. Hypertension may be caused by agitation or inadequate pain control. Determine the cause: Agitation may be due to hypoxia or hypercarbia--check ventilation. Inadequate pain control---give narcotics.

2,

Arteriolar dilators~these are the preferred agents for lowering blood pressure acutely, N.B. If using arteriolar dilators, hypovolaemia may be 'unmasked'. It is important to note atrial pressures when using these drugs. Beware too of worsening ventilation: perfusion mismatch. The arteriolar dilators include: (i) Sodium nitroprusside (SNP). (ii) Glyceryl trinitrate (GTN). (iii) Hydralazine. (iv) Nifedipine--a calcium channel antagonist. Control of tachycardia: This may be troublesome, either contributing to hypertension, or as a reflex response from the baroreceptors to the use of arteriolar dilators. (i) Sedation? (ii) Metoprolol--with caution (see below).

4.

Pre-existing hypertension: Recommence patient's routine antihypertensive treatment as soon as possible.

Figure 10. Decision path for the management of hypertension in the immediate postoperative period.

(i.e. in excess of lOOml/h) are usually related to one or more of the following: 9 Problems with surgical haemostasis at operation. Ligating clips may spring from vein graft branches during closure of the chest; small bleeding points may remain unnoticed at lower arterial pressures post-bypass, only to become problems as arterial pressure rises during emergence from anaesthesia; vascular structures may be inadvertently lacerated during chest closure; or pacing wires and drains in the mediastinum may lacerate or erode vascular structures or cardiac chambers. 9 Problems with incomplete neutralization ofheparin effect. The mechanism of 'reheparinization' remains obscure. Laboratory data may confirm adequate reversal of the heparin effect following the initial protamine dose, but investigation of bleeding occurring within an hour frequently identifies heparin activity. This may be attributable to the administration of heparin-containing 'pump blood' or to wash-out of heparin seemingly sequestered in poorly perfused vascular beds as cardiac output is better distributed during recovery. 9 Problems with impairedplateletfunction. Abnormalities of platelet function measurable with the conventional bleeding time test are relatively common after open heart surgery and correlate with losses (Harker et al, 1980). The list of aetiological factors is large (George et al, 1991) and includes thrombocytopaenia (from loss of platelets due to adhesion to

PERIOPERATIVE C A R E I N C A R D I A C S U R G E R Y

459

circuit surfaces on bypass, or through inhibition of production caused by heparin), inhibition of platelet function (mediated by drugs, e.g. aspirin use preoperatively, heparin administration, some antibiotics) or consumption caused by platelet activation. 9 Coagulopathies. A variety of coagulopathies distinct from the actions of heparin occur after cardiothoracic surgery. More often these reflect consumption of clotting factors through activation of the coagulation and the fibrinolytic systems, secondary to complement activation or to the liberation of thromboplastins, for example in shed mediastinal blood. Iatrogenic factor-deficiency coagulopathies may be seen in cases where there has been major blood loss in the operating theatre and incomplete replacement transfusion therapy. More rarely encountered are patients with hitherto unrecognized congenital factor deficiencies (von Willebrand's, Christmas, haemophilia, etc.) or those who present with disseminated intravascular coagulation triggered by mediators of inflammation or sepsis. Continuously falling atrial pressures or reflex tachycardia, especially when neither respond to volume infusion, should engender a search for concealed bleeding. This may occur with drainage through communications between the pericardium (and mediastinum) and the peritoneal or pleural cavities. It is possible for bleeding of up to 2000 ml to be accommodated in either pleural cavity with seemingly little embarrassment to ventilation, and review of the postoperative chest radiograph of the supine patient may show only generalized haze in the lung field. A plan for the management of postoperative bleeding is given in Figure 11. Problem 6: Cardiac tamponade Postoperative tamponade is a well-recognized complication of cardiac surgery. The classical features are of gradually worsening hypotension with signs of poor peripheral perfusion and rising central venous pressure. However, there is considerable variation in the clinical features. The severity of the impairment of ventricular filling depends on the rate of bleeding into the intrapericardial space, the integrity of the pericardium and the impedance to drainage of blood from the pericardial sac through the drains. The rapidity of the deterioration of left ventricular output and organ perfusion varies with the end-diastolic volume presented to the ventricle and any compromise of sympathoadrenal reflex responses as a consequence of drug-induced blockade. The picture may vary from catastrophic hypotension proceeding quickly to cardiac arrest on the one hand, to an insidiously developing fall in organ perfusion mimicking left ventricular failure on the other. Oliguria is a characteristic feature, attributable equally to: (1) 'fooling' atrial stretch receptors (because of extrinsic pressure of clot on the atrial walls, thereby reducing transmural pressure gradients and wall tension), which in turn inhibits the release of atrial peptides and stimulates antidiuretic hormone output; and (2) to falling cardiac output and renal

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G. CUTFIELDET AL

perfusion. Paradoxically perhaps, cardiac tamponade is most likely to develop as coagulation of the blood reverts to normal, at which time 'surgical' bleeding may continue while drainage is compromised by clots in the drain. The classic picture of four chamber tamponade may be distorted if Excessive blood loss:

>400 ml in first hour > 100 ml/h in subsequent hours

Bright red blood, or pulsatile loss, or bleeding 'uphill' against gravity in drains:

Steady ooze, little obvious clot in drainage tubes, stable haemodynamic function and atrial pressures:

Consider bleeding from atrium, ventricle or major vascular (PA or systemic arterial) source

/

Review recent transfusion history, protamine administration, negative pressure on drains, Unit coagulation test (Hemochron ACT, SCT) results

Excessive j drainage suction?

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Resuscitation, transfusion, Urgent re-exploration

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Figure ll. Decisionpath for managing postoperativebleeding.

PERIOPERATIVE C A R E I N C A R D I A C S U R G E R Y

461

there is only a single chamber tamponaded by clot, for example around the right or left atrium. The other classical signs of muffled heart sounds and widened mediastinum on chest radiography are often absent. Pulsus paradoxus is a rare sign of postoperative tamponade. Precordial echocardiography is often not helpful in the immediate postoperative period because of technical difficulties caused by mediastinal collections of air, blood and clot--all with differing ultrasonographic impedances. The major diagnostic conundrum is to distinguish between tamponade and left or right ventricular failure. It is essential to remember that postoperative ventricular failure is extremely uncommon if the patient did not have ventricular impairment preoperatively or intraoperatively. The exceptions are those patients who develop postoperative myocardial ischaemia (see above) or a tension pneumothorax. Both of these conditions are readily diagnosed. A decision path for the differential diagnosis (and management) of cardiac tamponade is presented in Figure 12. When the haemodynamic deterioration is rapid, urgent reopening of the sternotomy is mandatory. If the deterioration is so rapid that the patient is unlikely to survive the time taken to move to the operating theatre, the sternotomy should be reopened in the intensive care unit. It is easier to manage bleeding through the opened wound than to manage tamponade with the chest closed. The infection rate of reopening is low. The traditional milking of intrapericardial drains is rarely successful in dislodging obstructing clots, and may promote myocardial drainage if high subatmospheric intrapericardial pressure is created, particularly if the drains are, in fact, patent. In the case of more slowly developing four chamber tamponade, insertion of a pulmonary artery catheter may show equalization of the right atrial, right ventricular end-diastolic and pulmonary capillary wedge pressures. In isolated right atrial tamponade and right ventricular failure, and some cases of left ventricular failure, there will be differences in these pressures (Skacel et al, 1991). While waiting for reopening of the sternum, the anaesthetist should continue to administer intravenous fluids in an attempt to maintain the stroke volume. The grossly elevated right-sided pressures which result do not usually produce other than short-term consequences.

Problem 7: Major rhythm and conduction problems The management of arrhythmias in the postoperative intensive care phase differs little from the perioperative approach (see Chapter 5 and p 440 above).

Problem 8: Untoward reactions to colloid plasma expanders Refer to p 446.

Problem 9: Problems with pacemakers The reader is referred to the section on circulatory emergencies above, as

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o. CUTFIELD ET AL

the presentation of these problems, and their management, are essentially similar, whether they occur in the operating theatre or the intensive care unit.

Problem 10: Acute right ventricular failure The pathophysiological features of this problem have been outlined in the 'post-bypass' section above (see circulatory emergencies, above). The Progressive hypotension, or signs of inadequate tissue perfusion with 'adequate' CVP

ECGchangessuggestiveof ~

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myocardial ischaemia?

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(Urgencydictatedby ctinicalconditionof the patient,) 9 Definitive diagnosis, 9 Evacuation of haematoma. 9 Secure haemostasis

Figure 12. Decision path for differential diagnosis and management of suspected cardiac tamponade in the immediate postoperative period (see text for discussion)_

PERIOPERATIVE C A R E IN C A R D I A C S U R G E R Y

463

clinical features in the intensive care context--where the chest is closed and the heart is not visible--include indirect signs of right ventricular enlargement, or pulmonary hypertension, i.e. precordial heave, loud P2, fixed splitting of heart sounds, etc. The principles of management have been presented in Figure 7.

Respiratory emergencies Problems with ventilation, whether related to difficulties with maintaining airway patency or with management of mechanical ventilation, have been reviewed earlier in this chapter. These discussions are equally pertinent in the immediate postoperative period. There are a few problems unique to the postoperative phase, and chief among these is the development of the adult respiratory distress syndrome (ARDS).

Problem 1: Adult respiratory distress syndrome This is a rare but troublesome complication. The Seattle ARDS Registry data suggest that ARDS develops, with variable severity, in about 6% of patients after surgery with cardiopulmonary bypass. Clinical features necessary for establishing the diagnosis include: 9 Deteriorating alveolar-arterial oxygen tension gradients in the absence of pre-existing pulmonary disease. 9 New panlobar infiltrates in lung fields on chest radiology. 9 Pulmonary capillary wedge pressures less than 18 mmHg. The pathophysiology is interstitial pulmonary oedema caused by high capillary permeability (secondary to endothelial injury) in the face of low hydrostatic pressures. Frank alveolar oedema with proteinaceous exudation occurs in severe cases. Subsequent resolution occurs--in those patients who survive--with proliferation of pneumocytes. We still have no means of predicting which patients might develop ARDS; furthermore, its aetiology is complicated, and there are no methods which have been adequately validated for use in prevention of the syndrome in cardiac patients. Of the known trigger factors, complement activation seems to be the dominant one. This may occur de novo, initiated by contact of blood and cells with foreign surfaces during extracorporeal circulation, or in response to reactions to colloid plasma substitutes (e.g. Haemaccel), to drugs (amiodarone has been implicated, as have hypersensitivity reactions to antibiotics), to transfused blood products, or to bacterial endotoxins. Management consists of support of organ system function, care with mechanical ventilation to avoid high inflation pressures (resorting to extracorporeal techniques for carbon dioxide removal and oxygenation in extreme eases) and patience (with vigilance) whilst the 'inflammatory storm' resolves.

The innocent bystanders---organ system failure While malfunctions of organ systems, other than the cardiovascular and

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G. C U T F I E L D ET A L

respiratory systems, seldom cause crises in postoperative care of the cardiac surgical patient, they deserve brief mention in a monograph such as this. Indeed, anticipation of problems (based on the knowledge of pre-existing disease) and their early recognition may have a significant effect on the patient's survival and quality of life after cardiac surgery. Life-threatening complications of cardiac surgery, related to diminished functional reserve of other organ systems, are disciassed below. Later problems with sepsis, which are beyond the scope of this chapter, further compound the list of complications. Problem 1: Oliguria and acute renal failure Given the effects of major surgery and surgical stress on renal blood flow distribution and glomerular filtration, it is hardly surprising that deterioration in renal function is a common postoperative problem in cardiac surgical patients. Patients who present with pre-existing renal disease, hypertension, diabetes or widespread vascular disease are particularly at risk. The aetiology of acute renal failure in such patients is multifactorial, comprising low renal blood flow, changes in distribution of blood flow in the kidneys (both inducing ischaemic damage), toxic effects of complement activation and drug effects. Intensive support, avoiding dehydration and optimizing renal perfusion pressures offer the best chance of preventing further damage. There is little comparative data and less outcome study data on which to base 'protective' strategies; nevertheless, most units employ variations of low-dose dopamine infusions, frusemide and/or mannitol therapy in supportive care. Crises which precipitate more aggressive measures (haemodialysis or continuous veno-venous haemodiafiltration (CVVHD)) comprise hyperkalaemia, progressive metabolic acidaemia, gross fluid overload, and uraemia with bleeding diathesis or depression of consciousness. Problem 2: Cerebrovascular accidents and spinal cord ischaemia These complications are often difficult to diagnose in the immediate postoperative period before the patient would be expected to have regained consciousness. The aetiology is also muttifactorial, but the majority of strokes are ischaemic or embolic (atheroma, mural thrombus, microbubbles of air, microaggregates, etc.) in nature, rather than caused by intracranial bleeding. Management is, again, supportive. Computed tomography scanning is of little benefit in the first 36 hours as the changes caused by reactive cerebral oedema wax and wane, and the potential for disaster in moving patients to the radiology suite outweighs the benefit. Efforts to minimize intracranial pressure are recommended, but outcome studies are few and difficult to perform because of the enormous variability in the nature of lesions and their natural propensity for recovery of function. Crisis management, as such, is seldom required.

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465

Problem 3: The acute abdomen and elusive diagnoses Brief discussion of these conditions is warranted here because they may give rise to serious cardiovascular and respiratory problems in the immediate postoperative period, and because their occurrence may jeopardize the benefit to the patient of having undergone cardiac surgery in the first place. In general, intra-abdominal mischief is difficult to diagnose in the unconscious or heavily sedated, partially paralysed patient recovering after open heart surgery. Furthermore, fever and leukocytosis are observed frequently in these patients, generally related to recovering thermoregulation, and atelectasis and stress, respectively. Thus regular examination of the patient, and a high index of suspicion, are needed to detect these problems early. Any unusual abdominal signs in the immediate postoperative period should be taken seriously and investigated. Specialist surgical consultation is recommended--the sooner, the better. Gut ischaemia. This complication carries a very high mortality, depending on extent and resectability. Recognition of gut ischaemia is difficult in the unconscious patient; frequently the diagnosis is not made until late in the progress of the disease. Early signs include unexplained acidaemia, often occurring long before abdominal signs. Abdominal signs are not consistent and range from none, through mild distension with absence of bowel sounds to frank peritonitis. Offensive smelling, bloody diarrhoea (when it occurs) is characteristic. Possible causes of bowel infarction include; 1.

2. 3.

Embolism: 9 Thromboembolism from fragmentation of mural thrombus from: left atrium, e.g. with changes in cardiac rhythm; left ventricle, as a consequence of surgical manipulation. 9 Fragments from valvular vegetations in endocarditis. Excessive use of a-adrenergic agonists in patients with pre-existing atheromatous vascular disease in the splanchnic circulation, and Atheroma embolism, now reckoned to be more prevalent than previously recognized (Lie, 1992).

Survival depends on speed of recognition, on the extent of resection that is possible, and on the associated complications: sepsis and endotoxaemia (from release of gut flora) and acute renal failure in particular. Peptic ulceration and perforation or haemorrhage. Although the incidence of stress ulceration in critically ill patients has been much modified by the introduction of drugs designed to diminish gastric acid production and to enhance splanchnic (and particularly gastric) capillary blood flow, these complications are still seen in the early postoperative period after cardiac surgery. The risks are compounded by several factors, notably the use of aspirin, the unwanted effects of catecholamines to cause enhanced splanchnic vasoconstriction, and a degree of residual anticoagulation. Crisis management of the patient with gastrointestinal ulceration hinges on supporting the circulation while making the diagnosis (with endoscopy), and preparation for urgent surgery where indicated.

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G. C U T F I E L D ET A L

Adrenal haemorrhage. This is a rare event, but important to recognize because of its preventable mortality. Unrecognized and untreated cases die, and the diagnosis is not made in most cases until post-mortem examination. The pathophysiology of adrenal haemorrhage is not understood. It is associated with major trauma and vascular and cardiac surgery. Pancreatitis. The development of acute pancreatitis after cardiac surgery occurs sporadically. Estimates of incidence vary from 1 to 12%. Predisposing factors include pre-existing conditions (alcoholism, previous pancreatitis, gallstone disease, etc.), perioperative events (systemic embolism in particular), the duration of cardiopulmonary bypass, and (curiously) the administration of calcium ions post-bypass. Recognition of the condition may be delayed in the ventilated patient because of the inconsistency of physical signs. Prognosis depends on the extent of necrosis and the response to the injury. Simple prognostic criteria, such as Ranson's, have been devised but these have not been specifically validated for cardiac patients. Ascending cholangiitis and acalculous cholecystitis. These conditions are difficult to diagnose in the unconscious patient because signs may be concealed; nevertheless, they represent a threat to survival because of the risk of overwhelming sepsis. Acute hepatic failure. Fortunately, this complication occurs rarely after cardiac surgery. It seems to be confined to patients already suffering with hepatic congestion as a consequence of advanced valvular heart disease, or with hepatobiliary disease and portal hypertension. Mortality of postoperative hepatic failure is very high and post-mortem histology is consistent with an acute ischaemic injury. Natural history data is sparse but we theorize that the ischaemic injury may be the result of very low hepatic artery blood flow during cardiopulmonary bypass in high-risk patients. Presentation is with catastrophic hyperkalaemia and lactic acidosis, initially puzzling because they occur in the setting of seemingly normal or even supernormal cardiac output and renal function. Support with dialysis or CVVHD may offset hyperkalaemia temporarily until the other clinical features of fulminant hepatic failure (jaundice, coagulopathy, coma, etc.) and liver function tests confirm the clinical diagnosis. Urgent hepatic transplantation has been suggested as a heroic measure to save life in such cases, but very little outcome data is available to justify this approach. Problem 4: Other metabolic derangements Type H lactic acidosis with adrenaline. Lactate overproduction, particularly secondary to inadequate cardiac output and tissue perfusion, should be the first cause considered when metabolic acidaemia is encountered in the cardiac surgical patient. The authors' experience suggests, however, that other causes of metabolic acidosis are frequently overlooked in the postoperative acute care area. Many patients receiving inotropic support (notably with adrenaline) develop acidaemia with elevated serum lactate

PERIOPERATIVE CARE IN CARDIAC SURGERY

467

levels despite having normal or even supernormal tissue perfusion. This may represent maldistribution of perfusion, but is more likely to be related to reduction in hepatic lactate extraction as a consequence of intense splanchnic vasoconstriction, thus an underclearance rather than overproduction of lactate. In either case, management should be altered to enhance splanchnic perfusion rather than correcting base deficit with sodium bicarbonate alone. Insulin resistance. Perioperative morbidity and mortality rates are higher in

diabetic patients, whether or not they normally require insulin. Hyperglycaemia is associated with enhanced infection risk, accentuated ischaemic organ dysfunction and impaired wound healing. For these reasons careful control of blood glucose levels is important and is most easily achieved with short-acting insulin infusions. It is important to recognize, however, that the peripheral actions of insulin are antagonized by hypothermia and by high circulating levels of catecholamines (exogenous or endogenous). As both of these influences occur commonly after cardiac surgery, extra vigilance is required to avoid rebound hypoglycaemia. As a general rule, insulin infusion rates in excess of 5 units/h should be required very rarely. Insulin requirements will decline in most cases in the first 6 hours postoperatively. Sustained insulin resistance in otherwise stable patients suggests other complications, notably sepsis.

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