Cardiovascular complications in the intensive care patient

Chapter 21 Cardiovascular complications in the intensive care patient


Haemodynamic monitoring

Indirect techniques are the most accessible method for blood pressure measurement in conscious horses. The coccygeal artery is used most often in both foals and adult horses. The cuff width should be 0.2–0.26 times the tail circumference because blood pressure is underestimated if the cuff is too wide and overestimated if it is too narrow.4 The inflation bladder must be centred over the artery and the cuff fitted tightly5 to avoid inaccuracy in blood pressure measurement.6,7 The indirect blood pressure in healthy adult horses is 111.8 ± 13.3 mmHg in systole and 67.7 ± 13.8 mmHg in diastole.8 A number of studies have reported noninvasive blood pressures in healthy foals as around 80–125 mmHg in systole and 60–80 mmHg in diastole.9,10 However, the mean arterial pressure is the more important determinant of organ perfusion than the systolic or diastolic pressures and supportive intervention should be considered if the mean arterial pressures fall below 60,5,11 particularly if there are other clinical signs of poor perfusion such as abnormal mucous membranes, capillary refill time, heart rate, extremity temperature, pulse quality and urine output.12 Furthermore, while its simplicity and noninvasive nature are an undoubted advantage, the clinician should remain aware of limitations in the accuracy of indirect blood pressure measurement and therefore it is best applied as a means to identify trends within an individual patient, rather than to compare between horses.

In human ICUs, direct measurement of pulmonary artery and capillary wedge pressure is considered the most reliable means to document pulmonary hypertension and invasive measurements of cardiac output and other haemodynamic variables are widely used in monitoring and therapeutic planning. However, while technically feasible, cardiac catheterization to allow direct measurement of pulmonary artery pressure or facilitate cardiac output measurement is still rarely employed in equine patients. (image PH) Nevertheless, practical means to measure cardiac output and other haemodynamic indices, such as lithium dilution, are becoming more widely available and are likely to be used in equine critical patients with increasing frequency.13,14 Monitoring of the cardiac output, stroke volume and systemic vascular resistance can allow the clinician to distinguish whether the cardiovascular status is compromised by reduced circulating volume, vascular tone, cardiac output or a combination of these and in doing so, select the most appropriate treatment and monitor the effects of vasopressors, inotropes and volume expansion.5,11


Echocardiography is the most valuable diagnostic aid for assessment of cardiac structure in horses and thus is the technique of choice in horses presenting with cardiac murmurs, and it is useful in ruling in or out structural heart disease in horses presenting with cardiac dysrhythmias. In the ICU setting, although echocardiography has the potential to assess cardiac output and pulmonary hypertension (see Chapter 9), it is less accurate than the gold-standard direct methods. On the other hand, its noninvasive nature is particularly attractive. Due to limitations in their accuracy, echocardiographic measurements of haemodynamic indices should be used primarily to identify trends within patients rather than taken as absolute measurements. Furthermore, the distributive shock that occurs with endotoxaemia and SIRS is principally due to dysregulation of systemic vascular function and accompanied by microthrombosis and possibly a direct myocardial depressant mechanism. Echocardiography is not a particularly useful tool for identifying these haemodynamic alterations when compared to measurement of cardiac output by thermodilution or lithium dilution, although horses and foals with endotoxaemia or septicaemia often have nonspecific echocardiographic signs of global cardiac dysfunction such as reduced fractional shortening, spontaneous contrast and poor ventricular wall movement. Hypovolaemic patients can have reduced cardiac chamber size and in septicaemic patients mild pericardial effusions are fairly common.1


Cardiac dysrhythmias

In horses, dysrhythmias occurring secondary to other systemic diseases, particularly gastrointestinal disease,15,16 are encountered more frequently than rhythm disturbances associated with primary myocardial pathology. In a group of 67 horses with duodenitis/proximal jejunitis, six horses (9%) had dysrhythmias detected by auscultation and conventional electrocardiography.15 The prevalence of dysrhythmias in the postoperative period following abdominal surgery is not known but is likely to be higher than may be appreciated on auscultation alone: in one survey of horses with ventricular dysrhythmias, 4 of 21 cases had recently undergone colic surgery16 and ambulatory ECGs obtained from fifty horses within 3 days of exploratory celiotomy demonstrated that 11 horses (22%) had isolated supraventricular premature depolarizations while 8 horses (16%) had ventricular dysrhythmias, including 4 (8%) with idioventricular rhythms or paroxysmal monomorphic ventricular tachycardia.17 In all but one of these cases the dysrhythmias were self-limiting, no specific treatment was required and the dysrhythmia had not been recognized on auscultation. Occasionally, more clinically significant dysrhythmias are encountered in the postoperative period following colic surgery, and in this instance clinical signs of reduced cardiac output and marked tachycardias may be apparent. A high index of suspicion is required and the clinician should consider an ECG assessment in all horses that have heart rates that are higher than might otherwise be suspected given the degree of pain or in horses showing weakness, pallor and other signs of low cardiac output.

Causes of dysrhythmias secondary to gastrointestinal disease include the direct effects of endotoxin on the myocardium, autonomic imbalance resulting from gastrointestinal distension and metabolic, electrolytic or acid–base imbalances.15 Ideally, underlying and contributory factors should be addressed first. The decision to institute specific antidysrhythmic therapy is generally based on assessment of whether it is likely that the dysrhythmia will destabilize into a life-threatening state. In general, ventricular dysrhythmias are much more likely to require antidysrhythmic therapy than supraventricular dysrhythmias, and commonly applied guidelines suggest that antidysrhythmics should be considered where the heart rate is rapid (greater than 100 bpm), the dysrhythmia is polymorphic and R on T phenomenon is present (see Fig. 13.17). However, the most important thing to consider is the clinical status of the animal, and the decision of whether to utilize antidysrhythmics should be based on the presence or absence of signs of low cardiac output. Strong evidence to support decisions on which specific antidysrhythmic agents to use in equine patients is lacking but procainamide, lignocaine and quinidine gluconate are popular first choices in ventricular tachycardia. Magnesium sulphate has been successful, and can be used alone, or in combination with other antidysrhythmic agents. Further details of these and other antidysrhythmics are described in more detail in Chapter 13. (image VT)

The electrolytes that are most commonly associated with dysrhythmias are potassium, calcium and magnesium and the role of these electrolytes in arrhythmiogenesis is discussed in detail in Chapter 6. Hypokalaemia, hypocalcaemia and hypomagnesaemia are common in horses with sepsis and endotoxaemia,18 thus monitoring and addressing electrolyte imbalances in critically ill horses is an important priority.


Hypokalaemia is commonly found in ill animals and causes include endotoxaemia,18 anorexia, diarrhoea and starvation.19 It is frequently present in horses with heat exhaustion along with hypochloraemia, hypocalcaemia and metabolic alkalosis. Hypokalaemia leads to prolongation of the Q–T interval and both supraventricular and ventricular dysrhythmias can be seen in horses with hypokalaemia. Supraventricular tachycardia, ventricular tachycardia, torsades de pointes and ventricular fibrillation can all occur with severe hypokalaemia. If severe hypokalaemia is present, the calculated potassium deficit should be replaced slowly intravenously at a maximum rate of 0.5 mEq/kg/hour while monitoring serum potassium concentrations.

Jul 31, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Cardiovascular complications in the intensive care patient

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