Pressures Flashcards by Dr. Joseph Masciana

Central Venous Pressure Measurement by Water Manometer
Central venous pressure (CVP) is a luminal pressure measurement taken from the intrathoracic portions of the cranial vena cava. The accepted normal range for CVP is 0 to 10 cm H2O.
Supplies Needed for Central Venous Pressure Measurement

A catheter with the tip properly placed in the intrathoracic vena cava is required. The materials needed include a sterile bag of fluids with an attached fluid administration set, an IV fluid extension set, a three-way stopcock, and a water manometer.
Procedure

The dog or cat should be positioned in lateral or sternal recumbency. A water manometer is placed in the fluid line via a three-way stopcock and the extension set

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The fluid administration set and the extension set are primed with sterile fluids from the fluid bag while the stopcock is in the “Off” position to the water manometer. There must be no air bubbles in the fluid lines. The primed extension set is attached to the patient’s catheter. The stopcock at the bottom of the manometer should rest on the table or cage floor. The administration set is opened, again with the stopcock in the “Off” position to the manometer, to allow fluid to flow into the patient’s catheter, thus ensuring that the catheter is patent. If fluid does not flow freely into the patient’s catheter, a valid CVP measurement will not be obtained. Next, the stopcock is turned so that the “Off” position is now to the patient. The fluid will now fill the manometer, which is allowed to fill about three-quarters full. The stopcock then is turned “Off” to the fluids, allowing a pathway only from the fluid-filled manometer and the patient’s catheter.

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The level of fluid in the manometer falls until the hydrostatic pressure of the column of fluid reaches equilibrium with the hydrostatic pressure of the blood at the end of the catheter. Therefore it is essential to know where the catheter tip lies in relation to the manometer fluid column. When the animal is in lateral recumbency, the cranial vena cava lies near the midline, and the manubrium is a good reference point. When the animal is in sternal recumbency, the cranial vena cava is about at the level of the point of the shoulder or the scapulohumeral joint. With the stopcock resting on the tabletop or cage floor, a zero reference point is determined by a horizontal line drawn between the manometer and the appropriate external anatomic landmark (manubrium or scapulohumeral joint). The centimeter mark where the horizontal line intersects the manometer is the zero reference point. A carpenter’s level fastened to a taut string is an excellent guide for the horizontal line from the anatomic landmark to the manometer. The difference between the equilibrium point reading and the zero reference point is the CVP measurement. For example, if the initial reading is 15 cm H2O (where the fluid level stopped falling) and the zero reference point is 10 cm H2O (horizontal line drawn between the external anatomic landmark and the manometer), the CVP is 5 cm H2O. The presence of a well-placed, unobstructed catheter can be verified by the fluid column in the manometer, which will slightly oscillate up and down as the animal’s heart beats or as the animal breathes. Readings are taken between ventilatory excursions. Trends in central venous pressure are more informative than single values. Each time a CVP measurement is obtained, the patient should be in the same recumbent position. The goal is to be consistent in taking the readings and to monitor the trends.

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Evaluation of Hemostasis

Examination of a dog or cat suspected of having a bleeding disorder includes assessment of vascular response and platelet function with formation of the platelet plug (primary hemostasis) and of the coagulation cascade leading to formation of fibrin and stabilization of the plug (secondary hemostasis). Persistent hemorrhage from superficial cutaneous injuries and mucosal surfaces (nasal, gingival, gastrointestinal, genitourinary) and formation of petechiae or ecchymoses are characteristic indicators of abnormalities in primary hemostasis. Primary hemostasis can be evaluated through quantitative measures (platelet estimate from blood smear, platelet count, mean platelet volume) and qualitative measures (von Willebrand factor [vWF] concentration and in vitro platelet function tests, such as optical aggregometry, aperture closure time, and flow cytometry). The buccal mucosal bleeding time (BMBT) is an in vivo, easily performed screening test for evaluation of primary hemostasis in dogs and cats.

Evaluation of Hemostasis

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The traditional coagulation pathway has been updated so that it more accurately reflects the in vivo mechanisms of secondary hemostasis (modern coagulation cascade). Abnormalities in secondary hemostasis can cause hematomas, hemarthrosis, and bleeding into the pleural and peritoneal cavities. These abnormalities are identified by coagulation screening tests (prothrombin time, activated partial thromboplastin time, activated coagulation time, fibrinogen), proteins induced by vitamin K absence or antagonism (PIVKA), and individual coagulation factor assays.

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Published reference ranges for the BMBT are 1.4 to 3.5 minutes in dogs and 1.5 to 2.5 minutes in cats. For clinical purposes in dogs, a BMBT of less than 4 minutes is considered normal.

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BMBT measurement is not indicated in animals with thrombocytopenia (less than 70,000/µL), because an abnormal result would be expected. Other causes of a prolonged BMBT are von Willebrand disease (vWD), thrombocytopathies, and vascular disorders. Impaired platelet adhesion and aggregation are present in vWD, a hereditary deficiency of vWF that is reported in various dog breeds but is rare in cats. In a dog with a normal plasma vWF concentration and absence of thrombocytopenia, a prolonged BMBT suggests a defect in platelet function that can be congenital or acquired. Inherited thrombocytopathies (intrinsic platelet function defects) are rare. They include disorders of platelet membranes (e.g., Glanzmann’s thrombasthenia in Otterhounds and Great Pyrenees dogs) and disorders of platelet secretion (e.g., Spitz and Basset Hound thrombopathy and platelet granule storage pool deficiency in American Cocker Spaniels and feline Chédiak-Higashi syndrome). These defects have been associated with a prolonged BMBT. However, not all conditions or agents that cause a platelet dysfunction are reported to result in an abnormal BMBT.

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Acquired thrombocytopathies are seen in uremic animals, in whom the prolonged BMBT is primarily due to defective platelet adhesion. Platelet aggregation is not consistently altered in uremic animals. Uremic toxins are thought to play a role in the pathogenesis of this condition. A prolonged BMBT compared with pretreatment measurements was noted after intravenous infusion of dextran 70 in dogs. Nonsteroidal antiinflammatory agents interfere with platelet function through inhibition of cyclooxygenase 1 (COX-1), leading to decreased synthesis of thromboxane A2, a platelet-aggregating and vasoconstricting factor. Aspirin was found to prolong the canine BMBT. Carprofen and meloxicam both have COX-1–sparing properties and did not prolong the BMBT in dogs, although platelet aggregation in response to adenosine diphosphate (measured by use of an aggregometer) was decreased after treatment with carprofen, meloxicam, and aspirin in dogs with osteoarthritis. Administration of etodolac, firocoxib, or indomethacin also did not affect the BMBT in healthy dogs. Reports on ketoprofen have been conflicting. Acquired thrombocytopathies associated with dysproteinemias and with disseminated intravascular coagulation are thought to result from platelet coating by paraproteins and fibrin degradation products. Other causes of a prolonged BMBT include infectious diseases (e.g., feline retrovirus-induced thrombocytopathy, canine leishmaniasis, infections with Ehrlichia canis or Anaplasma platys), myeloproliferative diseases, and vasculopathies (e.g., vasculitis and inherited vascular defects). Coagulation factor deficiencies do not produce an abnormal BMBT because functional primary hemostasis leads to the formation of an unstable platelet plug; however, rebleeding can occur.

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The BMBT is a quick, useful cage-side test for evaluation of primary hemostasis. It requires minimal preparation and few materials, and it is fairly noninvasive, safe, cost-effective, and easy to perform. Results are available immediately, which allows efficient presurgical screening and repeated evaluation to assess response to treatment. The test can be used as a complement to in vitro function tests, which may not fully reflect platelet function in vivo. However, the BMBT procedure is affected by iatrogenic variables that could normalize the result. Reports on sensitivity and specificity for the detection of primary hemostatic disorders vary, and some studies question the sensitivity of the BMBT measurement. A normal result does not eliminate a diagnosis of vWD or a platelet function defect, especially if the degree of dysfunction is mild. No correlation was found between the BMBT and plasma vWF concentration in dogs. The BMBT test is not standardized (e.g., degree of venostasis) and not reproducible. For any two readings in the same dog, the BMBT may vary by up to 2 minutes with one observer or between two observers.

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Doppler ultrasonic flow detection through the use of a piezoelectric crystal allows detection of flow in a peripheral artery. Hair is clipped just proximal to the palmar metacarpal pad at the level of the superficial palmar arterial arch for forelimb measurement; over the dorsal pedal artery for hindlimb measurement; or on the ventral aspect of the tail for tail measurement. An occluding cuff (sized as outlined for oscillometric techniques) is placed proximal to the point of flow detection (midradius in the forelimb, proximal to the hock in the hindlimb, or proximal to transducer placement on the tail), and measurements are obtained with the cuff at the level of the heart. Ultrasonic coupling gel is placed on the concave surface of the Doppler transducer, and the transducer is held in position during measurements (Figure 104-4) or fixed in position using adhesive tape.

An audible pulse signal is obtained, and the cuff is inflated with a bulb attached to a pressure gauge. The cuff is inflated to a pressure no less than 40 mm Hg above the audible cutoff point of the signal. The cuff is then slowly deflated, and the pressure at which the Doppler signal is again audible is recorded as the systolic pressure. The cuff is deflated further, and the pressure at which the audible signal abruptly changes in pitch or becomes muffled is recorded as the diastolic pressure.

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The Doppler flow detection system of BP measurement is considered the most accurate and repeatable of studied noninvasive BP measurement techniques in conscious cats. It is frequently used in dogs but may provide spurious high readings in some individuals. When abnormal readings are obtained by this method from dogs, care should be taken to make sure the abnormal readings are repeatable over multiple measurement periods. The advantages of this technique include flexibility with regard to motion, low pressure, small vessels, or the presence of arrhythmias, as well as speed of measurement. The rapidity of the measurement techniques allows for prompt assessment of changing BP, but meticulous attention must be paid to obtaining strong, audible signals in order to obtain the most accurate BP readings. This technique is also the most operator dependent of the techniques discussed. Accurate identification of diastolic pressures improves with operator practice, and BP measurement using Doppler ultrasonic flow detection techniques is most accurate if a few well-trained individuals in a practice are responsible for this diagnostic test and perform the test frequently.

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Arterial Puncture or Arterial Cannulation (“Invasive” or “Direct” Technique)

Direct BP measurement involves advancing a needle attached to a pressure transducer directly into an artery to measure BP. This procedure may be performed acutely to obtain instantaneous BP readings, or BP can be measured over time through the use of an indwelling arterial catheter instead of a needle. Invasive BP measurements are typically used during anesthetic procedures, in critical care patients when ongoing BP information is desired, or to document or exclude hypertension acutely as a clinical diagnosis in dogs. Acute arterial puncture is seldom used for clinical diagnosis of hypertension in cats.
Direct BP measurement is usually performed by means of puncture of the femoral artery in dogs. Use of local anesthesia is strongly recommended for this procedure and when used, the procedure is well tolerated by most dogs. The patient is gently restrained in lateral recumbency. Approximately 5 minutes prior to arterial puncture, 1 to 2 mL of 2% lidocaine hydrochloride is injected subcutaneously over the area in which the femoral pulse is palpated. A 22-gauge, 1-inch needle is attached to a transducer and flushed with heparinized saline, ensuring that no bubbles remain in the transducer. The transducer is zeroed at the level of the sternum in the laterally recumbent dog. The femoral pulse is palpated in the femoral triangle, and the needle is carefully advanced into the femoral artery (Figure 104-1) until a satisfactory pressure waveform is recorded on the monitor screen.

Arterial Puncture or Arterial Cannulation (“Invasive” or “Direct” Technique)

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A sample of the tracing is recorded, and the needle is withdrawn. Firm pressure is applied to the area of arterial puncture for a minimum of 5 minutes after measurement. The patient should be monitored closely for at least 1 hour after the procedure for any complications related to hematoma formation. Systolic, diastolic, and mean BP values from five consecutive cardiac cycles during normal sinus rhythm are averaged to obtain a representative value for the patient. When use of an arterial catheter is preferred, the catheter is usually inserted into the dorsal pedal artery. A local anesthetic may be used as described previously.

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Oscillometric Technique

Oscillometric BP measurement involves the use of an automated detection system and a cuff that is wrapped around a limb or tail over an artery. The cuff is inflated automatically to a pressure that causes occlusion of the artery and then slowly deflated. The machine detects oscillations in the vessel wall as the occlusion is eased, and the pressure at which oscillations are maximal is recorded as the mean arterial pressure. Systolic and diastolic pressures are then calculated by the monitor using algorithms specific to the technique. This technique uses data from many cardiac cycles to render a single reading and is therefore unsuitable for use in animals with rapidly changing BP.
Oscillometric BP measurement methods are more accurate in dogs than in cats. This measurement method may return inaccurate results if the patient is not motionless (e.g., trembling), has a weak or irregular pulse, or has a small artery (i.e., most cats). Use of a cuff of appropriate size is extremely important to ensure accurate measurements. Cuff width should be approximately 40% of the circumference of the limb or tail in dogs and approximately 30% of the appendage circumference in cats. When used on the tail, the cuff is wrapped snugly high on the tail head with the dog in sternal or lateral recumbency. Although tail cuffs can be used in standing animals, animal movement often interferes with accurate measurement. Limb cuffs are wrapped around the forelimb distal to the elbow or around the midmetatarsus at the level of the superficial plantar arterial arch.
To maximize accuracy, the cuff should be at the level of the heart during readings; therefore lateral or sternal recumbency is preferred, and use in standing patients is not recommended. In cats, tail cuffs return more repeatable measurements than limb cuffs. Typically, the cat rests in sternal recumbency during readings

Oscillometric Technique

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In all cases, best results are obtained when the patient is minimally restrained and soothed during the procedure. A short acclimation period prior to measurement is recommended to allow the cat to become more calm. A series of at least five readings are obtained at approximately 1-minute intervals. Any readings that are clearly erroneous are discarded. The multiple readings are then averaged to obtain a representative result.
Oscillometric techniques are valuable in anesthetized dogs and cats to monitor trends in BP. Because the animal is immobilized and BP shows less variability over time, repeatable and accurate readings can be obtained over time in both dogs and cats.

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Effect of body position on indirect measurement of systolic arterial blood pressure in dogs

A diagnostic test evaluation to determine whether a difference existed in Doppler ultrasonographic measurements of systolic arterial blood pressure (SAP) in sitting versus laterally recumbent dogs and to determine the degree of variability in measurements made in each position.
In a crossover design, SAP was measured in 51 healthy or sick adult dogs, without recent sedation or anesthesia and with an SAP ≤ 300 mm Hg via Doppler ultrasonography when dogs were sitting (on hind limbs with nonmeasured forelimb bearing weight) and laterally recumbent, with the cuff position at the level of the right atrium for both positions. Seven measurements were obtained per position for each dog.
Mean ± SD SAP was significantly higher in the sitting (172.1 ± 33.3 mm Hg) versus recumbent (147.0 ± 24.6 mm Hg) position, and this difference was evident for 44 of 51 (86%) dogs. The mean difference in measured SAP between the 2 positions was 25.1 ± 28.5 mm Hg. Blood pressure measurements had a significantly higher repeatability in the recumbent position than in the sitting position.
Blood pressure measurements in dogs were significantly affected by body position, and they were higher for most dogs when sitting rather than laterally recumbent. Blood pressure measurements in the laterally recumbent body position were less variable than in the sitting position.

Effect of body position on indirect measurement of systolic arterial blood pressure in dogs

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A pulse oximeter is a device designed to measure the percent saturation of arterial hemoglobin with oxygen. The value calculated is usually referred to as SpO2 to differentiate it from a value obtained by direct measurement from arterial blood (SaO2). To understand the likelihood of this device producing an accurate result it is important to understand how it works.

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Principles of pulse oximetry:

The basis for this technology is that oxygenated hemoglobin and deoxygenated hemoglobin have different light absorption characteristics and hence different colors. Light absorption is usually measured as an extinction coefficient (ε), which was originally defined as the thickness of the material that was required to decrease the intensity of light passing though it to one tenth of the incident light.1 This is depicted in Figure 105-1 showing ε for hemoglobin (Hb), oxyhemoglobin (HbO2), methemoglobin (MetHb), and carboxyhemoglobin (HbCO) over a spectrum of light wavelengths from orange (600 nm) through to infrared (>700 nm).

Principles of pulse oximetry:

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Pulse oximeters are a standard of care in human anesthesia and critical care. There is some controversy over the true benefit of this requirement but it would be difficult to get an estimate of its impact since it would now be almost impossible to eliminate access to this technology.13-16 Most veterinary practices have at least one pulse oximeter, but it appears that understanding the information provided by the device is deficient.17 It is important to recognize that pulse oximeters do not measure the amount of Hb present or the quantity of blood flow. It is quite possible for saturation to be normal but oxygen delivery inadequate if Hb concentration and/or cardiac output are low.

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Pulse oximetry in anesthetized animals would appear to be good for monitoring desaturation. However, when one examines the oxyhemoglobin dissociation curve (Figure 105-4), it is clear that Hb becomes almost fully saturated at a PaO2 of about 100 mm Hg, which is achievable when breathing room air.

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When an animal is breathing a high concentration of oxygen and has a PaO2 of 500 mm Hg, the pulse oximeter should read 99% to 100%, and if something significant happens to the animal (e.g., pneumothorax, pulmonary edema, atelectasis) that decreases the PaO2 to ~250 mm Hg, the pulse oximeter will likely continue to read 99% to 100%, and it will not get to an SpO2 of 95% until PaO2 gets to about 90 mm Hg.20 This makes the tool a crude monitor for healthy animals breathing >90% O2, and the problem is compounded by the lack of reliability of the technology. It is common to see pulse oximeters giving SpO2 values of

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Measurement of Blood Pressure

Since the pulse oximeter can display a pulse signal, it can be placed on a distal extremity and a cuff placed above this site to occlude blood flow. The cuff can be inflated to a point above systolic arterial blood pressure and then deflated while watching the plethysmographic trace on the pulse oximeter. Systolic pressure should be the pressure in the cuff where the trace returns. In one study, in cats, the pressure measured by this method had a greater correlation to mean pressure than to systolic pressure.21 In dogs using the tongue as the measurement site the technique was neither accurate nor precise.22

Measurement of Blood Pressure

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Systemic hypertension (HT) refers to the persistent elevation of systemic blood pressure (BP). Systemic hypertension is an increasingly recognized source of morbidity and, in some cases, mortality in human and veterinary patients.1-7 Overt and sometimes devastating damage caused by HT is typically noted in the eyes,5,8 central nervous system,9,10 heart,7,11-13 and kidneys.2,6,14 Injury related to HT in these organ systems is often collectively termed target organ damage (TOD). TOD is often clinically obvious, especially in the ocular or nervous systems. In some cases, however, TOD can be insidious, resulting in undetected progressive deterioration of damaged organs (e.g., accelerated deterioration of renal function6,9).

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Systemic HT is typically subclassified as primary (“essential”) HT or secondary HT. Some veterinarians have attempted to distinguish essential, or primary, HT from idiopathic HT (i.e., systemic HT in the absence of overt, clinically apparent causal disease). Use of the term idiopathic acknowledges that there may be a causal disease (e.g., renal disease) that is responsible for HT but that the causal disease is in a preclinical phase.15 In cases where the underlying disease is rare (e.g., pheochromocytoma), discovery of the cause of the HT is dependent on thorough diagnostic testing. In most dogs and cats, HT is a complication of a systemic disease rather than being primary.

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The pathophysiologic mechanisms involved in the development and sustenance of human and veterinary HT remain unclear and may, at least in part, vary by causative disease. Mean arterial pressure is affected by both cardiac output and systemic vascular resistance. Both of the latter parameters are in turn affected by other physiologic factors (Figure 151-1).

Abnormalities in any of the contributing factors may alter mean arterial pressure. In the presence of normal renal function, increased BP leads to natriuresis and lowering of systemic BP. Regardless of the mechanism for the initial increase (e.g., catecholamine excess, alterations in renin-angiotensin-aldosterone axis activity), some abnormality in renal sodium handling that prevents appropriate response to HT is implicated in patients with HT.

Although damage to vascular beds causes widely varied clinical findings based on the system affected, TOD appears to be mediated by similar processes in the eye,8 kidney,3 and brain.10 In dogs and cats, early cardiac changes induced by HT appear to be adaptive rather than pathologic, although this not the case in people with chronic HT. Arterial blood flow is maintained at relatively constant levels in the brain, kidneys, and eyes through a process of vascular autoregulation. When systemic BP increases, small resistance vessels constrict, restricting flow in the vascular bed. When systemic BP falls, vessels dilate to maintain flow. Hypertensive damage in these organs occurs when these autoregulatory mechanisms fail. When resistance vessel constriction is inadequate, small vessels overdistend, breaking down endothelial tight junctions and allowing protein and plasma leakage into interstitial tissue. This leakage, augmented when high pressure is transmitted to the capillary bed, leads to tissue edema. If vascular resistance vessel constriction is excessive, ischemia of local tissues may result. Depending on the organ involved, focal hemorrhage and necrosis may also occur. Lastly, arteriolar hyalinosis and arteriosclerosis may develop, decreasing vascular distensibility (Figure 151-2).

Ophthalmologic Changes Ophthalmologic changes secondary to HT are better described in cats than dogs and include intraocular hemorrhage (i.e., hyphema) and fundic changes. Three manifestations of fundic changes are possible and are termed hypertensive retinopathy, hypertensive choroidopathy, and hypertensive optic neuropathy,5,8 respectively.

Neurologic Changes Similar to the eye, the autoregulatory system in the central nervous system maintains blood flow to the brain at optimal levels despite variability in relatively normal systemic BPs. When BP is far outside of the regulatory range, however, the autoregulatory system is less successful, and failure of adaptive vasoconstriction may result in cerebral edema, vascular hyalinosis, vascular sclerosis, or focal hemorrhage.10 Inadequate vasodilation may result in areas of ischemia.

Renal Changes In the kidneys, HT can lead to leakage of plasma proteins due to failure of autoregulation. Glomerular HT results in absolute protein loss through glomerular capillaries (i.e., proteinuria) as well as glomerulosclerosis. Proteinuria has been implicated as a cause of progressive renal tubulointerstitial damage and fibrosis. Proteinuria may contribute to progression of renal disease independent of BP.16,17 The interaction of glomerular HT and subsequent proteinuria worsens renal function and provides a feedback loop for worsening HT. In addition to proteinuria, glomerular ischemia occurring though autoregulatory malfunction contributes to interstitial inflammation, fibrosis, and progression of renal damage.

Cardiovascular Changes Left ventricular hypertrophy develops in patients with chronic HT as result of myocardial adaptation to increased afterload. Reductions in diastolic function may occur prior to overt cardiac hypertrophy in dogs.18 Once hypertrophy occurs, the myocardium is more sensitive to adrenergic stimulation, has decreased coronary reserve, and is more susceptible to ischemic injury. In cats, LV diastolic functional changes were similar to those seen with hypertrophic cardiomyopathy.19 Morphologic cardiac changes in hypertensive cats are heterogeneous and usually involve thickening of the left ventricular free wall, interventricular septum, or both. Additionally, some hypertensive cats exhibit left ventricular dilation, left atrial dilation, or abnormalities in systolic function indices.11,13 Congestive heart failure secondary to hypertensive cardiac changes appears to occur rarely in dogs and cats, but they may exhibit increased sensitivity to fluid administration.

Previous high-end reference BP values for dogs varied between 160 and 180 mm Hg and between 160 and 200 mm Hg in cats. However, progression of renal damage in dogs is already enhanced with systolic BP values in this range and clinical studies have documented end-organ damage at systolic BP values as low as 170 mm Hg.5,14 Accordingly, current recommendations consider a systolic BP greater than or equal to 160 mm Hg (as measured by oscillometric or Doppler ultrasonographic methods) worthy of further diagnostic concern in both dogs and cats,20,38 although the use of antihypertensive medications may not be warranted if BP elevations are mild and causative situations can be remedied. The prevalence and importance of diastolic HT in dogs and cats are not well defined; therefore, most recommendations for BP assessment relate to systolic BP measurement.

HT detection goals in cats and dogs are to alleviate clinical signs, prevent future clinical signs, and prevent or delay subclinical deterioration of organ function. Clinical signs of “early” or mild HT in dogs and cats may appear to the owner or veterinarian as evidence of aging. Because the first overt clinical sign of HT in dogs and cats may be catastrophic (e.g., retinal detachment), detection of BP elevations below the level likely to produce clinical signs is preferable. Except for pets with overt clinical signs, detection of HT is a preventive measure.

BP assessment is a diagnostic test indicated in dogs and cats likely to have HT and as part of preventive medical care in those “at risk.” Although acceptable BP ranges and measurement indications may change as data accumulate, persistent elevation of BP is a clinical finding that leads to further clinical investigation and may lead to consideration of therapy based on the presence of clinical signs and presence of causative disease.

Hypertension in pets is a commonly recognized complication of a variety of diseases such as renal disease, hyperthyroidism, and hyperadrenocorticism. In older cats hypertension may also occur without a disease being present known to cause hypertension, best termed idiopathic hypertension. Once a definitive diagnosis of hypertension is made, treatment may be indicated in the hope of minimizing target organ damage (TOD) to eyes, kidneys, the heart and central nervous system. In some cases, successfully treating the initiating disease may resolve the elevation in high blood pressure; however, in many cases this is not adequate and antihypertensives are needed.

Hypertension can have a variety of deleterious consequences.1 The risk of TOD increases with increasing blood pressure (Table 152-1).2 Elevations in blood pressure can result in autoregulatory vasoconstriction in those vascular beds that have this capability. If this is sustained for a period of time, medial hypertrophy, ischemia, infarcts, and hemorrhage can occur. Organs that are commonly damaged in this manner include the eye (retinal detachments) and brain. In most instances hypertension is caused by an increase in systemic vascular resistance. This means that the heart has to pump blood into these narrower spaces. This translates into increased afterload, which can lead to cardiac compensatory changes such as left ventricular hypertrophy. Generally the healthy kidney is not susceptible to damage by increased blood pressure in small animal patients; however, the ability to autoregulate against elevated blood pressures is lost with renal insufficiency. With the loss of autoregulation systemic pressure is transmitted to the glomerulus leading to renal injury. Loss of autoregulation has been demonstrated in dogs with reduced renal mass.3 Loss of autoregulation also means that lower blood pressures are more poorly tolerated and can lead to loss of renal function and potentially acute renal failure.

Unfortunately, there is no cookbook approach to the treatment of hypertension as many factors need to be considered before treatment is initiated. Each patient’s unique clinical situation will also influence which medications are preferred if treatment is initiated. When medical treatment is started, the treatment plan needs to take into consideration how fast blood pressure needs to be decreased and what the target blood pressure is. As an example, with suspected hypertensive encephalopathy or choroidopathy/retinopathy, more rapid reduction in blood pressure is needed than in a patient where TOD is not evident. Concurrent diseases may also significantly influence which medications are chosen. For example, an ACE inhibitor would be an ideal agent to use in an animal with hypertension and concurrent proteinuria or cardiac disease. If any medications are being used that could elevate blood pressure (e.g., corticosteroids, phenylpropanolamine), these should be discontinued or the dose reduced to the lowest possible.

It is uncertain if blood pressure control improves survival in pets as it does in humans. In a study of 141 cats, blood pressure control was not associated with survival. In these cats, proteinuria was the only variable that influenced outcome.4 This study did not, however, assess diastolic blood pressure or pulse pressures, factors that influence outcome in humans. In addition, the overall treatment goal was to lower blood pressure below 160 mm Hg. In humans, however, it has been shown that more aggressive blood pressure control is associated with improved outcomes in patients with chronic renal disease, especially if proteinuria is present.5 Although the current veterinary literature does not provide information on ideal therapies, there is little doubt that successfully treating hypertension will prevent or minimize TOD. Table 152-2 lists medications that have been suggested for the treatment of hypertension. Given the paucity of veterinary literature, some treatment recommendations have to be extrapolated from literature on human hypertensives.

Enalapril Benazapril Ramipril Amlodipine Atenolol Acepromazine Hydralazine Phenoxybenzamine Prazosin

Blood pressure is measured as systolic, diastolic, and mean arterial pressures. Systolic and diastolic pressure correspond to the phases of the cardiac cycle. Mean arterial pressure (MAP) is calculated from the equation and is the most important value when considering perfusion of the organs and tissues. Hypotension is defined as a systolic arterial blood pressure of less than 80 mm Hg and/or a mean pressure of less than 60 mm Hg in either dogs or cats.

Causes of hypotension include decreased preload to the heart, decreased vascular tone, and cardiac dysfunction. Untreated hypotension can lead to shock from inadequate tissue perfusion and oxygen delivery to the tissues. Treatment of hypotension should consist of identifying and correcting the underlying problem. Recognition and treatment of hypotension are essential to prevent the development of refractory shock, organ failure, and death (Figure 153-1)

Blood pressure provides a measurement of tissue perfusion. The two are not equivalent, but blood pressure monitoring is the simplest means of obtaining an objective parameter. Subjective measures of tissue perfusion are obtained by physical examination; they include pulse quality, mucous membrane color, capillary refill time, and heart rate and rhythm. Combined with blood pressure monitoring, these parameters provide the basis for a more accurate assessment of tissue perfusion. A normal blood pressure does not necessarily mean that the tissues are adequately perfused, as blood pressure may be maintained with severe peripheral vasoconstriction and/or increased cardiac output.

The clinical signs associated with hypotension depend on the severity and cause of the condition. In dogs, hypotension is usually associated with tachycardia, bounding to weak pulses, pale mucous membranes, slow capillary refill time, mental dullness, and weakness. If the underlying cause is sepsis, the mucous membranes may be injected or red with a rapid capillary refill time. Cardiac causes of hypotension can alter the clinical picture, with arrhythmias, weak, irregular pulses, and even severe bradycardia possible. Hypotensive cats also usually have tachycardia, poor pulse quality, pale mucous membranes, slow capillary refill time, mental dullness, and weakness. However, unlike dogs, cats with sepsis or systemic inflammatory response syndrome (SIRS) often have bradycardia rather than tachycardia and rarely have injected mucous membranes. In both species, hypotension is often associated with decreased urine output, hyperventilation, hypothermia, and cold extremities.

Inability to palpate pulses peripherally can be useful in assessing blood pressure. When metatarsal pulses are palpable, the systolic blood pressure is above 70 to 80 mm Hg. Although measurement of blood pressure confirms the presence of hypotension, the diagnosis can be made on physical examination findings alone.

Systemic blood pressure (BP) is dependent on cardiac output (CO) and systemic vascular resistance (SVR) (Figure 153-2): Cardiac output is determined by heart rate, contractility, preload, and afterload. The three main causes of hypotension are decreased preload, decreased cardiac function, and decreased vascular tone (Box 153-1). These may occur individually or in combination.

Systemic blood pressure is maintained via neural, hormonal, and local mechanisms. Smooth muscle in blood vessel walls is innervated by fibers from the sympathetic nervous system. Activation of this system results in vasoconstriction of vessels in tissue beds with the exception of skeletal muscle, where it causes vasodilation. Sympathetic innervation of cardiac muscle causes increased heart rate and contractility. Sympathetic stimulation occurs when the vasomotor center, located in the medulla oblongata, is activated. Hypovolemia and hypotension can lead to activation of the vasomotor center due to the baroreceptors in the carotid sinuses and aortic body sensing a lack of stretch, and the stretch receptors in the atria and pulmonary artery sensing a lack of distension and atrial filling. The vasomotor center is also activated by local hypoxia or hypercapnia causing stimulation of the chemoreceptors in the carotid sinus and aortic bodies, although this mechanism is less important than the baroreceptor reflex.

Hypotension also causes release of antidiuretic hormone (ADH) and adrenocorticotropic hormone (ACTH) from the pituitary, as well as release of catecholamines (norepinephrine and epinephrine) and cortisol from the adrenal glands. Increased concentrations of these hormones stimulates an increase in heart rate, vasoconstriction, and water retention by the kidneys. Simultaneously, the macula densa in the glomeruli are affected, and the renin-angiotensin-aldosterone system is activated, resulting in sodium retention by the kidneys and further vasoconstriction. These mechanisms serve to increase blood volume by means of sodium and water retention and to preferentially perfuse the brain and heart while decreasing perfusion to the skin, muscles, and abdominal organs, including the kidneys. Recognition and treatment of hypotension are essential to prevent the development of refractory shock and organ failure. Acute renal failure is one of the most common consequences of hypotension, but others include decreased coronary artery perfusion due to the increased heart rate, increased risk of bacterial translocation from the gastrointestinal tract, impaired hepatic function, and activation of the coagulation cascade.

In addition to the mechanisms listed above, there are several other important effectors of blood pressure and vascular tone. Activation of the arachidonic acid cascade leads to production of prostacyclin and thromboxane A2. Prostacyclin causes vasodilation, but thromboxane A2 causes vasoconstriction. Nitric oxide (NO), produced by endothelial cells via nitric oxide synthase, is an important regulator of vascular tone, resulting in vasodilation. There are two types of nitric oxide synthase, the constitutive form and the inducible form. In sepsis and SIRS, there is a tremendous increase in NO production from inducible NO synthase, which is activated by a variety of inflammatory mediators including interleukin-1 (IL-1), IL-2, IL-6, and tumor necrosis factor. This overproduction of NO, coupled with depletion of vasopressin, down-regulation of catecholamine receptors, and disruption of vascular smooth muscle calcium metabolism can result in vasoplegia, severe hypotension, and refractory shock.

Hypovolemia results in decreased cardiac output secondary to decreased venous return to the heart. This, in turn, results in decreased preload. Moderate to severe hypovolemia must be present to affect blood pressure due to the normal compensatory actions that occur, including increased heart rate to maintain cardiac output and increased peripheral vascular resistance secondary to vasoconstriction. The compensatory mechanisms maintain adequate blood pressure until more than 20% to 25% of the intravascular volume has been depleted. Hypovolemia can occur with blood loss or increased fluid losses secondary to vomiting, diarrhea, polyuria, or third spacing of fluid.

Restriction of cardiac filling can also result in decreased preload, decreased cardiac output, and hypotension. Pericardial effusion with tamponade and restrictive pericarditis can result in hypotension by this mechanism. Severe pneumothorax and positive pressure ventilation can also reduce venous return to the heart. Hypertrophic cardiomyopathy in cats reduces left ventricular volume, thereby reducing preload and cardiac output.

Bradyarrhythmias can affect blood pressure by reducing cardiac output, especially when the heart rate is extremely slow. Although pulses may be normal or strong in a dog or cat with bradyarrhythmia, overall cardiac output can be drastically reduced by the infrequency of systole. The resulting low cardiac output may be severe enough to cause syncopal episodes secondary to hypotension and decreased perfusion of the brain. Tachyarrhythmias can result in hypotension by reducing preload to the heart. At extremely rapid heart rates, filling of the heart is limited by the relatively short time for diastole. This can result in reduced cardiac output despite an increased heart rate. Also, coronary perfusion occurs during diastole, so at rapid rates, cardiac perfusion is significantly decreased and can eventually result in decreased contractility and decreased cardiac output.

Decreased cardiac output can also occur due to primary cardiac disorders. Dilated cardiomyopathy is characterized by reduced stroke volume and reduced cardiac output caused by decreased contractility. Valvular incompetence, resulting in regurgitant flow, can also lead to decreased stroke volume. Other causes of decreased cardiac contractility include myocarditis, myocardial infarction, myocardial depression secondary to sepsis, SIRS, anesthetic drugs, beta blockers and calcium channel blockers, and acid-base and electrolyte abnormalities.

Decreased systemic vascular resistance can also cause hypotension. Common causes of vasodilatation are sepsis/SIRS; anaphylaxis; anesthesia; use of vasodilators, including beta blockers and calcium channel blockers; electrolyte abnormalities; and acid-base disturbances. Many of these mechanisms also affect cardiac contractility, resulting in hypotension mediated by decreased cardiac output and vasodilatation simultaneously.

It is essential that initial treatment of hypotension always be aimed at correction of the underlying physiologic problem: decreased preload, cardiac dysfunction, or peripheral vasodilatation. Differentiation of cardiac and noncardiac causes of hypotension is a critical first step (see Figure 153-1). If the animal is hypovolemic, intravenous fluids and/or blood products should be administered until euvolemia has been attained. If hypovolemia is severe enough to cause hypotension, a shock bolus should be given. The standard doses of isotonic crystalloids are 60 to 90 mL/kg for dogs and 45 to 60 mL/kg for cats. If colloids are indicated in place of crystalloids, approximately one fourth of the crystalloid dose should be given. Hypertonic saline (5% to 7.5%) is a rapid intravascular volume expander and can be used when immediate resuscitation is needed. The dose for hypertonic saline is 5 mL/kg given over 5 to 10 minutes for dogs and 3 to 4 mL/kg given over the same time period for cats. After administration of hypertonic saline, it is essential to follow with one third to one half of a shock bolus of isotonic crystalloids to provide continued intravascular volume expansion and to replenish the interstitial space. If hypovolemia occurs secondary to blood loss, blood products, such as whole blood or packed red blood cells, or a hemoglobin-based oxygen-carrying solution may need to be administered to provide adequate oxygen-carrying capacity.

If the volume status is unknown or if there are concerns about overloading the animal with intravenous fluids, a central venous catheter can be placed for central venous pressure (CVP) monitoring. A low CVP (less than 0 cm H2O) indicates hypovolemia due to fluid loss or vasodilatation secondary to decreased peripheral resistance. A high CVP (greater than 10 cm H2O) indicates volume overload, right-sided heart failure, or increased pulmonary vascular resistance (afterload). If the significance of a low to normal CVP reading is questionable, a small test bolus of fluids can be given. A rapid bolus of 10 to 15 mL/kg of crystalloid or 3 to 5 mL/kg of colloid is used. It is important to remember that the vascular bed is a compliant system, able to accommodate changes in volume with minimal changes in pressure. If the animal has a low CVP due to hypovolemia, the CVP will show either no change or a transient rise toward normal followed by a rapid decrease. The MAP also increases transiently. A bolus given to a dog or cat that is euvolemic usually causes a small increase in the CVP of 2 to 4 cm H2O with a return to baseline within 15 minutes. A large increase (greater than 4 cm H2O) followed by a slow return to baseline (longer than 30 minutes) is seen with hypervolemia or reduced cardiac compliance.

If the animal remains hypotensive once euvolemia has been achieved, the use of pressors should be considered. Commonly used pressors for treating vasodilation include dopamine, epinephrine, norepinephrine, and phenylephrine, administered for their alpha agonist effects, as constant-rate infusions. Only phenylephrine is a pure alpha agonist; the others have varying degrees of beta effects in addition to their alpha effects. Vasopressin can also be used in cases with vasodilatory shock. These drugs need to be titrated to effect, requiring frequent blood pressure monitoring. They should never be used in place of adequate volume expansion, because most patients with hypovolemic shock already have compensatory vasoconstriction.

Cardiac causes of hypotension must be addressed on a case-by-case basis. If tachyarrhythmias are the cause, antiarrhythmic therapy should be administered. Bradyarrhythmias may respond to medical therapy or may require placement of a pacemaker. Obstruction of cardiac filling by pericardial effusion or severe pneumothorax should be addressed by appropriate centesis. Positive inotropes such as dobutamine, a beta agonist, should be administered as a constant rate infusion when decreased cardiac contractility is suspected.

Diagnosis of the underlying cause of the hypotension must often wait until after therapy has been initiated due to the critical nature of hypotension. History and physical examination abnormalities can often help in the determination of a tentative diagnosis, allowing therapy to be started. Initial diagnostics in an unstable hypotensive dog or cat should include packed cell volume, total solids, blood glucose, and an estimate of the blood urea nitrogen level (Azostix, Bayer Corporation, Elkhart, Ind.). Electrolytes, acid-base status, and lactate can also be helpful. Depending on the clinical signs, an electrocardiogram (ECG), abdominal and thoracic radiographs, abdominal ultrasonography, echocardiography, CVP and pulse oximetry determinations, and arterial blood gas analysis can be useful. A complete blood count, serum chemistry profile, and urinalysis should also be performed. If indicated by a suspicion of Addison’s disease, an ACTH stimulation test should be completed. If sepsis is suspected, blood and urine cultures should be done unless the source of sepsis can be directly cultured.

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