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Patient assessment and monitoring (Proceedings)
The ability to accurately assess your patient is a key feature of success for a veterinarian. Although the importance of proper patient assessment is applicable to all fields of veterinary medicine, it is most apparent for the emergency/critical care clinician who may need to make rapid decisions based on observations obtained in a very short period of time.
The ability to accurately assess your patient is a key feature of success for a veterinarian. Although the importance of proper patient assessment is applicable to all fields of veterinary medicine, it is most apparent for the emergency/critical care clinician who may need to make rapid decisions based on observations obtained in a very short period of time. Proper patient assessment is based on both 'the big picture' and subtle details that can be identified with careful observation and a thorough physical examination.
Animals presenting through the emergency room should be assessed immediately to determine if they are hemodynamically stable or if they require emergent therapy. Helpful indicators of cardiovascular instability include altered mentation, collapse, tachycardia, tachypnea, weak or thready femoral pulses, and lactic acidosis. Once therapy has been initiated, it is also critical to re-assess the critical pet for response to therapy. If these parameters fail to normalize following treatment for shock, then diagnostics need to be performed on an emergent basis in order to identify the underlying disease process. If the hemodynamic status improves in response to therapy, it is also important to be vigilant and re-assess the patient regularly. If therapy for shock is successful, for example, it is imperative that the clinician decide on a treatment plan, then re-assess the animal regularly to see if the plan is adequate. Ongoing tachycardia and the development of tachycardia are both early signs of impending cardiovascular decompensation. Early detection of these changes and subsequent interventions will increase the likelihood of a positive outcome
The purpose of the heart is to deliver oxygenated blood from the heart to the peripheral tissues. Oxygen delivery (DO2) is a function of cardiac output (CO), and arterial oxygen content (CaO2).
DO2 = CO x CaO2
Although oxygen delivery and cardiac output are difficult to measure clinically, evaluation of certain parameters such as heart rate, arterial blood pressure and central venous pressure can help assess the state of the cardiovascular system.
Heart rate can be monitored by palpating the chest wall, feeling the arterial pulse, by auscultation, or by performing an electrocardiogram (ECG). Since CO = HR x SV, it is clear that changes in heart rate can affect oxygen delivery to tissues. Causes for tachycardia are many and include hypovolemia, shock, pain, anxiety, primary cardiac disease, and cardiac arrhythmias. Bradycardia may occur with high vagal tone, cardiac diseases including sick sinus syndrome, in cats with shock, and in animals in which cardiac arrest is imminent. Animals that present to the emergency room with tachycardia should be connected to a continuous ECG machine to identify the type of arrhythmia (such as ventricular tachycardia), and to observe response to therapy. If an arrhythmia is documented while connected to an ECG machine, a 6-lead ECG should be printed for further categorization of the arrhythmia. In many instances, continuous ECG monitoring is implemented in hospitalized animals with critical illness, severely depressed mentation, diseases known to predispose to arrhythmias, such as the post operative dog with gastric torsion and in dogs with cardiac arrhythmias necessitating anti-arrhythmic therapy.
Palpation of the arterial pulse during auscultation of the heart can be helpful in identifying arrhythmias (i.e. pulse deficits). The arterial pulse is most commonly palpated using the femoral and dorsal pedal arteries, and in the anesthetized patient, the lingual artery. The arterial pulse strength corresponds to the pulse pressure which is the difference between systolic and diastolic blood pressures and as such is not a direct indicator of blood pressure. A weak arterial pulse is suggestive of cardiovascular collapse or shock, while a pulse quality described as hyperkinetic or bounding may be consistent with anemia, the hyperdynamic phase of sepsis, or cardiac abnormalities such as patent ductus arteriosus and aortic insufficiency. Serial evaluation of the arterial pulse quality can be helpful in assessing response to therapy.
Arterial blood pressure
Arterial blood pressure is defined as the force exerted by flowing blood on the vessel walls. Determinants of blood pressure reflect the relationship with the cardiovascular status as described by the equation BP = CO x PR where CO is cardiac output and PR is peripheral resistance. Although cardiac output plays an important role in blood pressure during exercise, peripheral resistance is the major determinant at rest. Arterial resistance is controlled by many factors including sympathetic stimulation, the renin-angiotensin system, and renal regulation of blood volume. Blood pressure is tightly controlled in animals as the cardiovascular system will maintain adequate blood pressure at all costs. The information gathered through arterial blood pressure measurement must be correctly interpreted in order for appropriate decisions to be made. Systolic blood pressure is the pressure exerted against the blood vessel walls during systole, or ventricular contraction. Diastolic blood pressure is the pressure exerted during diastole, or the relaxation phase of the cardiac cycle. Since the duration of diastole is longer than systole the mean arterial pressure (MAP), or the average pressure exerted during the cardiac cycle, is calculated as follows:
Blood pressure may be measured either directly via an indwelling arterial catheter or indirectly, through a variety of techniques. The direct measurement of blood pressure is considered the gold standard. Direct arterial pressure (DAP) is measured by placing a catheter directly into an artery (often the dorsal pedal artery) and connecting the catheter to an electronic pressure transducer. Direct arterial pressure monitoring allows for continuous blood pressure measurement, and provides easy access to arterial blood samples for blood gas analysis.
Indirect blood pressure measurement can be performed using the Doppler flow, or oscillometric sphygmomanometry. All indirect blood pressure measurement techniques are based on detection of blood flow beneath an inflated cuff. The Doppler flow involves a small ultrasound probe placed on a peripheral artery (generally the dorsal pedal). The ultrasound probe contains a piezoelectric crystal that emits ultrasonic waves. These waves encounter RBC in flowing blood and are reflected back to a receiving crystal in the probe where an amplifier converts the pulse wave into an audible sound.
Doppler blood pressure measurement is performed by shaving the area over the artery and applying a coupling gel. A cuff is placed around the limb or tail proximal to the probe. The width of the cuff should be approximately 40% of the circumference of the limb for the measurements to be accurate. The cuff is inflated until the pulse can no longer be heard, then slowly deflated while a hand held manometer records cuff pressure. The pressure at which the pulse sound becomes audible is the systolic arterial blood pressure. Although some clinicians feel they can estimate diastolic pressure from a change in the pitch of the pulse, diastolic pressure cannot be reliably determined using this method in all patients.
Oscillometric sphygmomanometry is based on detection of changes in oscillations produced by changes in artery wall diameter. As a cuff placed over an artery is deflated, oscillation amplitude increases at systolic pressure, reaches a maximum at MAP, and decreases at the diastolic pressure. Measurements of systolic, diastolic and MAP and heart rate are displayed digitally. Proper cuff size (40% of limb circumference) is important to the accuracy of this technique.
If hypotension is identified, the first step is to remove the underlying cause if one can be identified (reversal of anesthetic agents). Volume support using crystalloids, colloids or blood products are necessary if unless the hypotension is of cardiogenic origin. If hypotension persists despite adequate intravascular volume, vasopressors or positive inotropes may be considered. (eg. dopamine or dobutamine). Untreated, hypotension will result in death. Hypertension has been defined as a MAP > 145 mm Hg. Hypertension may be triggered by hyperthyroidism, renal disease, and neoplasia, or can occur from the "white coat" effect. Treatment of hypertension involves removal of the underlying cause if possible. Long-term sequelae of untreated hypertension may include retinal detachment, left ventricular hypertrophy, kidney failure and cerebral vascular accidents.
Central venous pressure
Central venous pressure, which is reflective of right atrial pressure, can be used as an indirect indicator of intravascular volume. Although CVP is frequently used to guide fluid therapy in critically ill dogs and cats, it is important to remember that as an indicator of right atrial pressure, it is not a perfect indicator of what is happening in the left side of the heart. A low CVP may be indicative of low CO due to the effects of hypovolemia while a high CVP and low CO suggests heart failure. In addition, CVP measurements provide early evidence of the patient at risk of volume overload, recurrent pericardial effusion or right-sided heart failure.
Central venous pressure may be estimated or directly measured. Estimates of CVP can made through direct visualization of the jugular vein with jugular venous distension or pulsation visible in patients with volume overload, pericardial effusion or other cause of right-sided heart failure. It is important to remember that peripheral venous distension has no correlation to systemic arterial blood pressure and that animals laying in lateral recumbency will have jugular veins that will appear distended.
Direct measurements of CVP require the placement of a central venous catheter. In order to measure CVP, a catheter must be placed in a central vein with the tip of the catheter located in the cranial venal cava near the right atrium. In cats, a long catheter threaded into the femoral vein to the caudal vena cava has been found to be adequate in measuring CVP. A water manometer or a pressure transducer can then be used to measure CVP. Supplies needed include a central venous catheter, a water manometer, extension tubing, a 3-way stopcock, and a syringe filled with 20-30ml of heparinized saline. The patient should be placed in sternal or ideally, in lateral recumbency. The position chosen should be recorded in the patient's medical record. A reference point that correlates with the right atrium should be determined. The right atrium for the patient in lateral recumbency is approximately at the level of the manubrium, and the scapulohumeral joint is the recommended reference point for the patient in sternal recumbency. This "zero" point should be recorded. Clinically, the manometer is often taped to the cage to simplify repeated measurement over time with the patient in the same position. The manometer is connected to the patient, filled with saline, and then allowed to equilibrate. The level of the fluid (at the level of the meniscus) on the manometer correlates to the CVP of the patient. The value should be recorded, and measurements should be repeated periodically to follow trends.
An electronic pressure transducer system may also be used to monitor CVP. Supplies needed for this system include the central venous catheter, a non-distensible extension set, the pressure transducer, and the electronic measuring system. The pressure transducer is placed a set point equivalent to right atrial pressure (as with the water manometer system) and calibrated. The extension set is connected to the central venous catheter and to the transducer. The electronic display correlates to the CVP. This technique allows for CVP waveforms may be observed and recorded.
The reference range for CVP in dogs and cats is 0-5 cm H20. A CVP below 0 cmH20 is indicative of hypovolemia while a CVP greater than 12 cmH20 suggests volume overload. Trends in the CVP may also provide vital information in an individual patient. For example, a gradual rise in CVP to 12 cmH20 in a cat receiving intravenous fluids for vomiting and anorexia may be a warning sign of impending volume overload. CVP will be lowest during inspiration and higher during expiration. In animals receiving positive pressure ventilation, the CVP will be the highest during the inspiratory phase, and lowest at the end of expiration.
Parameters used to identify changes in volume status include the physical examination (skin turgor, mucous membranes, etc), central venous pressure (see above), and urine production. Serial body weights can also helpful in identifying changes in volume in hospitalized animals. Examination of the jugular veins can provide clues relative to intravascular volume, with jugular distension indicating absolute or relative volume overload. The inability to raise a jugular vein with digital pressure in the jugular furrow is suggestive of hypovolemia. Urine specific gravity can be helpful, as most animals receiving intravenous fluids will have a urine specific gravity approximating 1.020. In an animal with challenging volume issues, a urine specific gravity of 1.030 or higher may be useful in determining that additional fluids are required. Finally, visualization of cardiac chambers using ultrasound can be helpful in determining volume status. Parameters that are correlate poorly with volume status include blood pressure, heart rate (often used to raise index of suspicion of a problem), and peripheral pulse quality.
Both the respiratory rate and effort are helpful in monitoring the patient with oxygenation failure. Untreated shortness of breath may result in respiratory failure from hypoxia, or from respiratory fatigue (exhaustion). The respiratory rate may be monitored every few hours, or as frequently as every hour depending on the degree of dypsnea. If oxygenation values (PaO2) or pulse oximetry are within acceptable ranges but there is excessive respiratory effort required to maintain those values, then supplemental oxygenation or mechanical ventilation if necessary, must be instituted to prevent respiratory fatigue.
Arterial blood gas
Serial evaluation of the PaO2 is helpful in monitoring the patient with respiratory disease. It is important to always interpret the PaO2 in light of the PaCO2. For example if the PaO2 is normal but the PaCO2 is very low in the dyspneic dog, then oxygen therapy is warranted because the dog is clearly working very hard (breathing heavily, panting) to maintain adequate oxygenation. Oxygen supplementation should be initiated if the PaO2 falls below 80mmHg.
Pulse oximetry is a simple and non invasive method to monitor oxygenation status. The pulse oximeter detects the saturation of hemoglobin with oxygen, and can be used to approximate the PaO2 using the oxygen dissociation curve. Normal values for pulse oximetry readings are values greater than 97%. In general, a pulse oximeter reading of 90% correlates to a PaO2 of 60mmHg. Arterial blood gas measurement and oxygen supplementation should be considered with a pulse oximeter reading below 92%.
Capnography measures carbon dioxide concentration continuously and non-invasively. The end tidal CO2 (the ETCO2) corresponds to the carbon dioxide left in the alveolus at the end of a normal breath. In general, the ETCO2 is approximately equal to the arterial value under most circumstances, and is very useful in identifying hyper and hypoventilation. In the event of a ventilation-perfusion-mismatch, a shunt, or increased dead-space-ventilation (a panting dog), this correlation may be lost. A normal CO2 tracing is outlined below.
Based on the information above, which letter corresponds to the End Tidal CO2 measurement?
The most important aspect of patient assessment is re-assessment. Your interpretation of hemodynamic stability and volume status may lead to an action step, such as bolus administration of intravenous fluids. Or you might attribute tachycardia to pain in a dog with multiple pelvic fractures from trauma and administer a dose of hydromorphone. In both cases, frequent re-assessment is imperative in order to identify changes before a crisis occurs.
Normal hemodynamic variables in dogs and cats