Successful management of the critically ill patient requires anticipation-not reaction.
"If the pathophysiology is not understood and monitoring is not appropriate, death will be attributed to the patient's disease rather than to the inappropriate therapy." W.C. Shoemaker
Successful management of the critically ill patient requires anticipation—not reaction. Anticipation of problems, based on knowledge of the pathophysiology of the disease process permits early detection and intervention. A thoughtful monitoring plan can then be individualized for each patient to document response to therapy and to anticipate complications.
In the current technological environment in which we live and practice, it is easy to become too dependent on monitoring equipment. A carefully performed physical exam remains the best monitoring tool available. Effective communication between the veterinarian and veterinary technician is important to successful monitoring of patients in the intensive care setting.
A written record of all observations, treatments and events is crucial. When multiple individuals are involved in providing patient care, written orders and records help to ensure consistency of care. The retrospective evaluation of data helps to identify and document trends of change in measured parameters.
The purpose of the cardiovascular system is to deliver adequate amounts of nutrients (oxygen) to each cell and to transport metabolic waste products from the cells. When cellular oxygen demands are not met, the cell switches to anaerobic metabolism. We cannot directly measure tissue oxygenation in the clinical setting and therefore rely on indirect indicators of adequate cardiac output and oxygen delivery. Lactate is produced in anaerobic metabolism. Elevations in serum lactate indicate inadequate oxygen delivery and anaerobic metabolism. Persistently elevated lactate levels have been shown to be correlated with patient mortality. Gastric mucosal pH and oxygen saturation of mixed venous blood are other global markers of adequate oxygen delivery. These measures are generally not available in the clinical setting and instead, the ability of the cardiovascular system to deliver adequate amounts of oxygen is evaluated indirectly by monitoring perfusion parameters (including mentation, mucous membrane color, capillary refill time, heart rate, pulse quality and extremity temperature) and blood pressure. In dogs, hypoperfusion is associated with tachycardia. In contrast, hypoperfused cats are often bradycardic. In retrospective study of cats with severe sepsis, Brady, et al. reported that 66% (19/29) of the cats evaluated had a heart rate < 140 bpm.
Global markers of anaerobic metabolism (base deficit, lactate) and of increased oxygen extraction (mixed venous oxygen saturation) have been shown to be more sensitive indicators of adequate perfusion. When these markers were evaluated in human patients treated for hypovolemic shock, more than 80% of the patients with normal heart rate, blood pressure and urine output were considered to be hypoperfused based on evidence of ongoing anaerobic metabolism and tissue acidosis.
Blood pressure can be measured by either direct or indirect methods. Direct blood pressure measurement requires placement of an arterial catheter, a transducer and an oscilloscope. Indirect techniques are less accurate but are non-invasive and more readily available. Indirect measurements can be obtained by either Doppler blood flow detection or oscillometric techniques. Normal values are listed below.
Blood Pressure-Normal Values
The systolic pressure should be maintained above 90 mmHg and the mean pressure should be above 60 mmHg. Cuff size is important for accurate measurement. The optimal width of the cuff bladder is 40-60% of the circumference of the extremity to which it is applied. The cuff should be long enough to encircle at least 60% of the limb. The cuff should be applied snugly with the bladder centered over the artery. Hypotensive animals should be treated with volume loading, cardiac support with dobutamine (dogs: 5-10 mcg/kg/min IV by constant rate infusion (CRI), cats 2.5-5 mcg/kg/min CRI) and vasopressors.
Heart rate and rhythm should be monitored. Tachycardia secondary to hypovolemia must be differentiated from elevated heart rates secondary to other causes of sympathetic stimulation such as pain and anxiety. Patients are at risk of arrhythmias secondary to hypovolemia and hypoxia. Anti-arrhythmic drugs should be considered only after eliminating extra-cardiac causes of arrhythmias (hypoxia, pain, electrolyte imbalances). Arrhythmias should be treated only if they are electrically unstable or adversely affecting perfusion.
Adequate oxygen delivery is also dependent on the oxygen content of the arterial blood. Oxygen content is dependent on the amount of functional hemoglobin, the degree of saturation of the hemoglobin and the amount of oxygen dissolved in the blood. Oxygen content can be calculated by the following equation:
CaO2 = (1.37 x Hb x SaO2) + (0.003 x PaO2)
Each component of the equation should be monitored and optimized to ensure adequate oxygen delivery to the cells. The most significant portion of the oxygen content of arterial blood is oxygen bound to hemoglobin. The optimal hematocrit value for oxygen transport has been found to be from 27-33%. Efforts should be made to maintain the PCV in this range. Transfusions of whole blood, packed red cells or hemoglobin containing solutions should be given as needed. Following administration of Oxyglobin, hemoglobin levels can no longer be extrapolated from packed cell volume and must be directly measured.
The degree of hemoglobin saturation can be estimated by measuring the PaO2 or directly measured by oximetry. Co-oximeters are not suitable for bedside monitoring. In the absence of dysfunctional hemoglobin, pulse oximetry provides a convenient, continuous and non-invasive measure of arterial oxygen saturation. Dissolved oxygen constitutes a very small portion of normal O2 content.
Patients should be monitored for changes in pulmonary function. Many trauma patients have pulmonary contusions. Aspiration pneumonia is a common sequelae in post-operative and recumbent patients. Lung failure is seen commonly in sepsis and diseases associated with systemic inflammation. Respiratory rate, breathing pattern and auscultation of lung sounds should be done at least two times per day. Any changes in observed patterns should be noted and investigated.
The arterial pO2 (PaO2) is a measure of the ability of the lungs to exchange oxygen. It can be measured directly with an arterial blood gas. Hemoglobin saturation is related to PaO2 by the sigmoidal hemoglobin-oxygen dissociation curve and can therefore be estimated by evaluation of oxygen saturation. PaO2 should remain above 70 mmHg and SaO2 should be above 90%.
If pulmonary function is normal, PaO2 is expected to be 4-5x the inspired oxygen concentration. The difference between the "expected " and measured PaO2 value can be used as a measure of pulmonary dysfunction. PaO2/FiO2 can be used as a bedside measure of pulmonary shunt fraction.
Carbon dioxide is also measured as an indication of ventilation and pulmonary function. Low CO2 values (<35 mmHg) indicate hyperventilation and can occur from either pulmonary or non-pulmonary causes. Animals with decreased levels of consciousness or central nervous system disease will have decreased ventilatory drive. Abnormalities of the chest wall or pleural space can interfere with normal ventilation. Lung failure is associated with elevated CO2 levels. If the underlying cause cannot be corrected, hypercapnic patients must be mechanically ventilated. Several recent reports in the veterinary literature highlight the importance of monitoring CO2 in anesthetized patients.
Carbon dioxide can be evaluated on arterial or venous blood gases. Venous CO2 is usually 3 to 6 mmHg higher than the arterial value. End-tidal carbon dioxide monitors provide a non-invasive method of continuously approximating arterial carbon dioxide partial pressure. These devises measure the partial pressure of CO2 in the expired air obtained at the end of expiration. End-tidal CO2 is a good estimation of arterial CO2 in normal lungs, but becomes less accurate in patients with significant pulmonary disease.
Many critically ill patients have alterations in capillary permeability and/or decreased levels of albumin. These changes alter the normal balance between the vascular and interstitial fluid compartments. Adequate or even increased fluid in the interstitial space does not assure normal vascular volume. Perfusion parameters (MM color, capillary refill time, heart rate, pulse quality, blood pressure, extremity temperature) must be evaluated to assess intravascular volume. Central venous pressure (CVP) provides an indirect measurement of vascular volume and should be used to guide fluid therapy. The bedside measurement of CVP has been previously described. To assure an accurate measurement, placement of the catheter at the level of the cranial vena cava or right atrium should be confirmed radiographically. Oscillation of the fluid column with the patient's respiration and heartbeat confirm a functional catheter. In the hypotensive animal, fluid resuscitation should be used to raise the blood pressure until the CVP is 8-10 cm H2O.
Synthetic colloids are given to many critically ill patients with increased capillary permeability. Increasing the number of osmotically active particles in the blood helps to hold fluid in the vascular space. The ability of a fluid to "hold" water is termed colloid oncotic pressure (COP). Normal COP is approximately 20 mmHg. COP values <15 put patients at risk of the development of peripheral edema. The stimulus for hepatic production of albumin is the COP of the blood. Therefore, colloid administration producing elevated COP values may decrease endogenous albumin production. The correlation between the refractive index of infused hetastarch or dextran and COP is not known. Therefore, changes in refractive index cannot be used to monitor colloid administration. Measurements of COP can help guide colloid therapy and may help in the diagnosis of some edematous states.
Electrolytes should be measured at least daily. Serum sodium, chloride, potassium and calcium should be maintained within the normal range. Many animals on IV fluids require potassium supplementation. Clinical signs of hypokalemia include muscle weakness. Ventroflexion of the head and neck is an early sign of hypokalemia. Magnesium depletion has been identified as a common electrolyte abnormality in critically ill veterinary patients. Less than 1% of total body magnesium is found in the serum. Therefore, serum levels may not accurately reflect total body magnesium status. A low serum level indicates magnesium deficiency and the need for supplementation, however a normal serum level can occur in the presence of a total body magnesium deficiency. Magnesium deficiency should be suspected and empirically treated in patients with refractory hypocalemia or hypokalemia. Magnesium is available as a sulfate or chloride salt for IV supplementation. The intravenous dose is 0.5-1.0 mEq/kg/day. The dose should be administered slowly over 2-4 hours or by constant rate infusion. Rapid IV administration may result in hypocalcemia, hypotension, atrioventricular and bundle-branch blocks, and respiratory muscle weakness.
Hypoglycemia can occur rapidly and unexpectedly in critically ill patients, therefore blood glucose should be monitored. The development of hypoglycemia in a critically ill adult patient should prompt the consideration of sepsis.
The measurement of acid base status has become routine with the development of portable, affordable blood gas monitors. Venous samples are useful for evaluation of the metabolic, acid base status. Bicarbonate and base excess are used to evaluate metabolic status. Metabolic alkalosis (HCO3> 24) is seen in patients with gastric outflow obstruction from either mechanical or functional causes. Metabolic alkalosis is also seen following the administration of loop diuretics such as furosemide. Metabolic acidosis (HCO3 < 24) is seen in diseases such as diabetes mellitus, ingestion of ethylene glycol and renal failure. Inadequate oxygen delivery to tissues causes a shift to anaerobic metabolism and increased production of lactic acid. A metabolic acidosis secondary to accumulation of lactic acid suggests inadequate tissue oxygen delivery. Base excess has been used as an indirect marker of lactate and has been shown to be a powerful predictor of survival in human trauma patients.
Patients who have experienced hypotension during anesthesia or secondary to their underlying disease process are at risk of acute renal failure. In addition, these patients are often receiving potentially nephrotoxic drugs. Urine output should be carefully monitored in "at risk" patients. Normal urine output is 1-2 ml/kg/hr. In both oliguric and polyuric patients measurement of fluid "ins and outs" should be used to manage fluid therapy. Patients should receive insensible loses (10 ml/lb/day) in addition to measured urine output.
"Ins and outs" requires the placement of a urinary catheter and closed collection system. Although placement of an indwelling urinary catheter is associated with risk of infection, the benefit of having an accurate measurement of urine output often outweighs this risk in this patient population. Creatinine and/or BUN should be monitored daily during a crisis period. Urine should be evaluated daily for evidence of renal tubular casts or glucosuria.
If urine production is inadequate, an evaluation of intravascular volume and blood pressure should be made before administration of any drugs. The use of "low dose" dopamine to increase urine output has come under scrutiny. Wohl was unable to demonstrate the presence of dopamine receptor activity in feline kidneys making the use of "low dose" dopamine of no value in cats. Mannitol (0.25 gm/kg) may be helpful in the early stages of acute renal failure.