CHAPTER 11 Systemic Arterial Hypertension
GENERAL CONSIDERATIONS
Over time, marked elevation of arterial blood pressure (BP) can cause serious clinical consequences. Various factors influence values obtained for systolic, diastolic, and mean arterial BP in healthy animals. Breed-related variation and variations related to age, gender, reproductive status, and other factors can occur. An average normal BP across breeds of dog is about 133/75 mm Hg (systolic/diastolic), and an average normal BP in cats is about 124/84 mm Hg, using oscillometric methods. However, breed-related variations should always be taken into account; for example, because Greyhounds have higher systolic BP and Irish Wolfhounds lower systolic BP than other breeds, the recommendations of the Veterinary Blood Pressure Society should be interpreted with caution. Variation in measured BP may be related to technique (direct and various noninvasive methods) as well as to patient anxiety. Systolic BP can exceed 180 mm Hg in some stressed normal animals. The demarcation between acceptable and “abnormally high” arterial BP is not clear-cut. Furthermore, although some dogs and cats clearly have clinical disease caused by hypertension, many with “abnormally high” BP have no evidence of related pathology, although a predisposing disease condition may exist. Repeated BP measurements over time along with careful clinical evaluation are indicated when considering a diagnosis of hypertension.
Guidelines from the Veterinary Blood Pressure Society suggest that repeatable (on at least three occasions) pressure measurements of 150 to 160 mm Hg systolic and 95 to 100 mm Hg diastolic constitute mild hypertension; an additional 20 mm Hg is allowed for specific breed differences (e.g., for some sight hounds). Moderate hypertension is associated with BPs between 160 and 180 mm Hg systolic and 100 and 120 mm Hg diastolic (plus ∼30 mm Hg for specific breed differences). Arterial pressures >180/120 mm Hg (plus −50 mm Hg for specific breeds) indicate severe hypertension.
Mild hypertension generally does not require antihypertensive therapy, although any underlying disease should be addressed. Some animals with moderate hypertension also may not need specific antihypertensive therapy. However, severe hypertension should be treated to prevent or reduce end-organ damage. Some animals require urgent antihypertensive therapy (see p. 190). If antihypertensive therapy is used, close monitoring for efficacy, adverse effects, and deterioration of underlying conditions is warranted.
Etiology
Hypertension is usually associated with other diseases (Box 11-1) rather than being a primary condition (idiopathic or essential hypertension) in dogs and cats. There is a high prevalence of at least mild hypertension in cats with renal disease or hyperthyroidism. Renal disease, especially involving glomerular function, and hyperadrenocorticism are commonly associated with hypertension in dogs; diabetes mellitus, hypothyroidism, and liver disease may also be associated with higher BP. Because of the increased risk for hypertension in patients with such conditions, BP should be measured when diagnosing the disease as well as periodically thereafter. Similarly, hypertension discovered during a routine exam may be an early marker of such underlying disease. Certain drugs, such as glucocorticoids, mineralocorticoids, nonsteroidal antiinflammatory agents, phenylpropanolamine, sodium chloride, and even topical ocular phenylephrine, can increase BP. Obesity is known to increase BP mildly in dogs. Inherited idiopathic (essential) hypertension has been documented in dogs and cats, but it is uncommon. Idiopathic hypertension is considered a diagnosis of exclusion.
Pathophysiology
BP depends on the relationship between cardiac output and peripheral vascular resistance. BP is increased by conditions that raise cardiac output (by increasing heart rate, stroke volume, and/or blood volume) or by those that increase vascular resistance. Arterial BP normally is maintained within narrow bounds by the actions of the autonomic nervous system (e.g., via arterial baroreceptors), various hormonal systems (e.g., the renin-angiotensin system [RAAS], aldosterone, vasopressin/antidiuretic hormone, and natriuretic peptides), blood volume regulation by the kidney, and other factors.
Modulation of these systems by various disease conditions can lead to chronic elevation of arterial BP. For example, hypertension can result from increased sympathetic nervous activity or responsiveness (e.g., hyperthyroidism, hyper-adrenocorticism), increased catecholamine production (e.g., pheochromocytoma), or volume expansion caused by increased sodium retention (e.g., decreased glomerular filtration and reduced sodium excretion in renal failure, hyperaldosteronism, hyperadrenocorticism, acromegaly). RAAS activation, with subsequent salt and water retention and vasoconstriction, may result from intrarenal diseases (e.g., glomerulonephritis, chronic interstitial nephritis), enhanced production of angiotensinogen (e.g., hyperadrenocorticism), and extrarenal diseases that increase sympathetic nervous activity or interfere with renal perfusion (e.g., hyperthyroidism, renal artery obstruction). Impaired production of vasodilator substances (e.g., prostaglandins, kallikreins) and effects related to secondary hyperparathyroidism may be involved in chronic renal failure.
High perfusion pressure can damage capillary beds. In most tissues capillary pressure is regulated by vasoconstriction of arterioles that feed the capillaries, although this control may be inadequate because of underlying organ disease. The continued arteriolar constriction secondary to chronic hypertension leads to hypertrophy and other vascular remodeling changes that can further increase vascular resistance. These structural changes and vascular spasm can cause capillary hypoxia, tissue damage, hemorrhage, and infarction, which can lead to organ dysfunction (Box 11-2).
Organs that are particularly vulnerable to damage resulting from chronic hypertension are the eye, kidney, heart, and brain. These structures are often referred to as target-organs or end-organs. In the eye hypertension often causes focal perivascular edema, hemorrhage, and ischemia, especially in the retina and choroid layers. Bullous or total retinal detachment is common. Hyphema, vitreal hemorrhage, and optic neuropathy can also occur. Renal glomerular hypertension occurs when afferent arteriolar autoregulation is disrupted. The resulting glomerular hyperfiltration can lead to glomerulosclerosis, renal tubular degeneration, and fibrosis. These changes contribute to renal function deterioration and increasing vascular resistance; thus chronic hypertension tends to perpetuate itself. Proteinuria is an important manifestation of renal damage and has been associated experimentally with severity of hypertension in cats and dogs. Blood pressure is not directly correlated with serum creatinine concentrations, and hypertension can develop prior to azotemia. Increased systemic arterial pressure and vascular resistance increase the afterload stress on the heart and stimulate left ventricular hypertrophy. Increased cerebral vascular pressure can promote edema formation, raise intracranial pressure, and cause hemorrhage.
Clinical Features
Clinically recognized arterial hypertension usually occurs in middle-aged to older dogs and cats, presumably because of the associated disease conditions. Cats with severe end-organ disease secondary to hypertension tend to be geriatric. Signs of hypertension relate either to underlying disease or to end-organ damage caused by the hypertension itself.
Ocular signs are the most common presenting issue, especially sudden blindness, which usually results from acute retinal hemorrhage or detachment. Although the retina may reattach, sight often does not return. Ocular fundic changes associated with hypertension include bullous to complete effusive retinal detachment, intraretinal edema, and hemorrhage. Vascular tortuosity, hyperreflective scars, retinal atrophy, papilledema, and perivasculitis are other signs. Hemorrhage in the anterior or posterior chamber, closed-angle glaucoma, and cornal ulceration may also occur.
Another common complaint is polyuria and polydipsia, which can be associated with renal disease, hyperadrenocorticism (in dogs), or hyperthyroidism (in cats). Furthermore, hypertension itself causes a so-called pressure diuresis. Epistaxis can result from vascular rupture in the nasal mucosa. Hypertensive encephalopathy resulting from edema and vascular lesions can cause lethargy, seizures, abnormal mentation, collapse, or other neurologic or nonspecific signs. Paresis and other focal defects can occur as a result of cerebrovascular accident (stroke) caused by hypertensive arteriolar spasm or hemorrhage.
A soft, systolic cardiac murmur is commonly heard on auscultation in animals with hypertension. A gallop sound may also be present, especially in cats. Clinical heart failure is uncommon.
Diagnosis
Blood pressure measurements are indicated not only when signs compatible with hypertension are found but also when a disease associated with hypertension is diagnosed. A diagnosis of arterial hypertension should be confirmed by measuring BP multiple times and on different days. A routine laboratory database (complete blood count [CBC]; serum biochemical profile; and urinalysis, with or without a urine protein : creatinine ratio [UPC]) is indicated in all hypertensive patients. However, not all hypertensive patients with underlying chronic renal disease are azotemic. Other tests are done as needed to rule out possible underlying diseases or complications. These might include various endocrine tests, thoracic and abdominal radiographs, ultrasonography (including echocardiography), electrocardiography, ocular examination, and serologic tests.
Thoracic radiographs often reveal some degree of cardiomegaly in patients with chronic hypertension. Cats especially may have a prominent aortic arch and an undulating (wavy) appearance to the thoracic aorta, although these findings may not be exclusive to hypertension. Electrocardiographic (ECG) findings may suggest left atrial (LA) or left ventricular (LV) enlargement. Arrhythmias do not appear to be common.
Mild to moderate LV hypertrophy is seen on echocardiography in some cases, although often measurements are within normal reference range. LV wall and septal hypertrophy may be symmetric or asymmetric. Other echocardiographic findings may include mild LA enlargement and sometimes mitral or mild aortic regurgitation. Proximal aortic dilation is another echocardiographic finding in some animals with systemic hypertension. Nelson et al. (2002) found that almost all hypertensive cats, but not healthy older cats, had a ratio of proximal ascending aortic diameter : aortic valve annulus diameter of ≥1.25.
BLOOD PRESSURE MEASUREMENT
Several methods can be used to measure systemic arterial BP in the clinic. Calculating the average of several measurements (generally between three and five) in succession is recommended to increase accuracy. When readings differ widely, the highest and lowest are discarded and an average value from at least three readings is used. High pressures should be confirmed by repeated measurement sessions before a diagnosis of hypertension is made. Anxiety related to the clinical setting may falsely increase blood pressure in some animals (i.e., the “white-coat effect”). Using the least restraint possible in a quiet environment and allowing time (e.g., 5 to 15 minutes) for acclimatization is best for awake animals. Use of a consistent technique and cuff size is important.
Direct Blood Pressure Measurement
Arterial pressure is measured directly by a needle or catheter placed into an artery and connected to a pressure transducer. Direct arterial pressure measurement is considered the gold standard, but it requires greater technical skill; moreover, in awake animals the physical restraint and discomfort associated with arterial puncture may falsely increase BP. Direct arterial pressure measurement is more accurate than indirect methods in hypotensive animals.
For arterial pressure monitoring over a period of time, an indwelling arterial line is often the best approach. The dorsal metatarsal artery is commonly used for this technique. An electronic pressure monitor provides continuous measure ment of systolic and diastolic pressures and calculated mean pressure. With fluid-filled systems, the pressure transducer must be placed at the level of the patient’s right atrium to prevent a false increase or decrease of the measured pressure related to the effects of gravity on the fluid within the connecting tubing. The use of wireless, telemetric blood pressure monitors for dogs is currently under investigation.
When occasional BP measurement is needed, a small-gauge needle attached directly to a pressure transducer may be used to puncture the dorsal metatarsal or femoral artery. To prevent hematoma formation, direct pressure should be applied to the arterial puncture site for several minutes after removing the catheter or needle used for BP measurement.
Indirect Blood Pressure Measurement
Several noninvasive methods are available to indirectly measure BP. These techniques involve the use of an inflatable cuff that is placed around a limb, usually the radial artery (most dogs) or brachial artery (small dogs and cats) or the median caudal artery of the tail to occlude blood flow. Controlled release of cuff pressure is monitored to detect the return of flow. Doppler ultrasonic flow detection and oscillometric methods are used most often. Both techniques produce measurements that correlate fairly well with direct BP measurement but are not exactly predictive of it. Indirect methods are most reliable in normotensive and hypertensive animals. The Doppler method has shown greater correlation with direct BP measurement in conscious cats compared with the oscillometric method. Other methods, such as auscultation and arterial palpation, are not recommended for estimating BP. The auscultatory method (used to detect Korotkoff sounds in people) is technically impractical because of the limb conformation of dogs and cats. Direct arterial palpation is not reliable for estimating BP because pulse strength depends on the pulse pressure (systolic minus diastolic arterial pressure), not the absolute level of systolic or mean pressure. Pulse strength is also influenced by body conformation and other factors.
Cuff size and placement.
Human pediatric- and infant-size cuffs can be used for indirect BP measurement in dogs and cats. The cuff must be the correct size for the patient. The width of the inflatable balloon (bladder) within the cuff should be about 30% (especially for cats) to 40% (especially for dogs) of the circumference of the extremity it surrounds. The length of the balloon should cover at least 60% of this circumference. Some of the cuff inflation pressure goes toward tissue compression. Cuffs that are too narrow are more affected by this phenomenon and produce falsely increased pressure readings; cuffs that are too wide may underestimate BP. The cuff bladder should be centered over the target artery. Common cuff locations are midway between the elbow and carpus or in the tibial region; skeletal prominences are avoided. The cuff should encircle the limb snugly without being excessively tight. Tape (not just Velcro on the cuff) is used to secure the cuff in position.
Oscillometric method.
The indirect oscillometric method uses an automated system for detecting and processing cuff pressure oscillation signals. Veterinary models are available (e.g., Cardell Veterinary Blood Pressure Monitor, Sharn, Inc; Memoprint, S&B medVET). With these systems the flow occlusion cuff is inflated to a pressure above the systolic pressure and then slowly deflated in small pressure decrements. The microprocessor measures and averages the resulting pressure oscillations that are characteristic of systolic, diastolic, and/or mean pressures (depending on the system). Accurate results with oscillometric methods depend on careful adherence to the directions for use and an immobile subject. Because muscle contraction can produce oscillations, the limb used should not be bearing weight. At least five readings should be obtained; the lowest and highest are discarded, and the remaining measurements are averaged. The oscillometric method may be difficult to use effectively in small dogs and cats; underestimation of systolic BP is common.
Doppler ultrasonic method.
This method employs the frequency change between emitted ultrasound and returning echoes (from moving blood cells or vessel wall) to detect blood flow in a superficial artery. This frequency change, the so-called Doppler shift, is converted to an audible signal. One system commonly used in animals is designed to determine systolic pressure by detecting blood cell flow (Ultrasonic Doppler Flow Detector, Model 811, Parks Medical Electronics, Inc).
Effective locations for pressure measurement include the dorsal metatarsal, palmar common digital (forelimb), and median caudal (tail) arteries. The probe is placed distal to the occluding cuff. A small area of hair is clipped over the artery for probe placement. Ultrasonic coupling gel is applied to the flat Doppler flow probe to obtain air-free contact with the skin. The probe is positioned so that a clear flow signal is heard; it must not be held so tightly that it occludes flow. The probe must remain still to minimize noise; it can be taped in place. A low volume setting on the Doppler unit or a headset is used to minimize patient anxiety caused by the loud audio signals.
The flow-occluding cuff is attached to a sphygmomanometer and inflated to about 20 to 30 mm Hg above the point at which arterial flow ceases and no audible signals are heard. The cuff is slowly deflated (by a few mm Hg per second). During deflation, characteristic pulsatile flow signals from blood cell (or arterial wall) motion return during systole. The systolic pressure is the pressure at which blood flow first recurs (indicated by brief swishing sounds). Sometimes a change in the flow sound from short and pulsatile to a longer, more continuous swishing can be detected as cuff pressure diminishes; the pressure at which this change occurs is an approximation of diastolic pressure. Doppler estimation of diastolic BP is less accurate because of its subjective nature. The change in flow sound is not always detectable, especially with small or stiff vessels. As with the oscillometric method, it may be difficult to obtain measurements in small or hypotensive animals with the Doppler method. Patient movement also interferes with measurement.
Treatment and Prognosis
Antihypertensive therapy is indicated for animals with severe hypertension and those with clinical signs presumed to be caused by hypertension. Measured BP in such animals is generally over 180/120 mm Hg. Although some cases constitute hypertensive emergencies that require immediate therapy and intensive monitoring (discussed in more detail later), most hypertensive animals can be managed more conservatively (Box 11-3). Gradual reduction in BP may be safer in patients with long-standing hypertension. Chronically high BP leads to vascular adaptations in the cerebral autoregulatory process; if BP is suddenly reduced, cerebral perfusion may be adversely affected. It is unclear whether all dogs and cats with moderate hypertension (e.g., repeatable systolic pressures of 160 to 180 mm Hg) benefit from specific antihypertensive treatment. Nevertheless, patients with high BP that persists after treatment for the primary disease, as well as those with evidence of end-organ damage, should be treated. The goal of therapy is to reduce the BP to below 150/95 mm Hg. The expense and time commitment required for long-term antihypertensive therapy and monitoring as well as the potential for adverse medication effects are considerations.
BOX 11-3 Approach to the Patient with Hypertension
ACEI, Angiotensin-converting enzyme inhibitor; BP, arterial blood pressure; CBC, complete blood count; ECG, electrocardiogram.
Suspect Hypertension or Disease Associated with Hypertension (see Box 11-2, text)
Several drugs are used as antihypertensive agents in dogs and cats (Table 11-1). Usually one drug is administered at a time, with initially low doses, and the animal is monitored to assess efficacy. It may take 2 or more weeks for a significant decrease in BP to be observed. The drugs used most often are angiotensin-converting enzyme inhibitors (ACEIs), the Ca++-blocker amlodipine, and β-adrenergic blockers. Therapy with a single agent is effective in some cases, whereas combination therapy may be needed for adequate BP control in others. An ACEI is recommended as the initial antihypertensive drug in dogs, and amlodipine in cats, unless hyperthyroidism is the underlying cause. For hyperthyroid-induced hypertension, atenolol or another β-blocker is used first.
TABLE 11-1 Drugs Used to Treat Hypertension
| DRUG | DOG | CAT |
|---|---|---|
| ACEIs (see Chapter 3) | ||
| Enalapril | 0.5 mg/kg PO q24(−12)hr | 0.25-0.5 mg/kg PO q24hr |
| Benazepril | 0.25-0.5 mg/kg PO q24(−12)hr | same |
| Ramipril | 0.125-0.25 mg/kg PO q24hr | — |
| Captopril | 0.5-2.0 mg/kg PO q8-12hr | 0.5-1.25 mg/kg PO q12-24hr |
| Calcium Channel Blocker | ||
| Amlodipine | 0.1-0.3 (−0.5) mg/kg PO q24(−12)hr | 0.625 mg/cat (or 0.1-0.2 mg/kg) PO q24(−12)hr |
| β-Adrenergic Blockers (see Chapter 4) | ||
| Atenolol | 0.2-1.0 mg/kg PO q12-24hr (start low) | 6.25-12.5 mg/cat PO q(12-)24hr |
| Propranolol | 0.1-1.0 mg/kg PO q8hr (start low) | 2.5-10 mg/cat PO q8-12hr |
| α1-Adrenergic Blockers | ||
| Phenoxybenzamine | 0.2-1.5 mg/kg PO q(8-)12hr | 0.2-0.5 mg/kg PO q12hr |
| Prazosin | 0.05-0.2 mg/kg PO q8-12hr | — |
| Diuretics (see Chapter 3) | ||
| Furosemide | 0.5-3 mg/kg PO q8-24hr | 0.5-2 mg/kg PO q12-24hr |
| Hydrochlorothiazide | 1-4 mg/kg PO q12-24hr | 1-2 mg/kg PO q12-24hr |
| Drugs for Hypertensive Crisis | ||
| Hydralazine (see Chapter 3) | 0.5-2.0 mg/kg PO q12h (titrate up to effect); or 0.2 mg/kg IV or IM, repeat q2h as needed | same |
| Nitroprusside (see Chapter 3) | 0.5-1 μg/kg/min CRI (initial) to 5-15 μg/kg/min CRI | same |
| Enalaprilat | 0.2 mg/kg IV, repeat q1-2h as needed | same |
| Esmolol | 50-75 μg/kg/min CRI | same |
| Propranolol | 0.02 mg/kg (initial) to 0.1 mg/kg slow IV | same |
| Labetolol | 0.25 mg/kg IV over 2 min, repeat up to total dose of 3.75 mg/kg, followed by CRI of 25 μg/kg/min | same |
| Acepromazine | 0.05-0.1 mg/kg (up to 3 mg total) IV | same |
| Phentolamine | 0.02-0.1 mg/kg IV bolus, followed by CRI to effect | same |
ACEI, Angiotensin-converting enzyme inhibitor; PO, by mouth; IV, intravenous; CRI, constant rate infusion.
Ancillary strategies may be helpful in patients with hypertension, although alone they are unlikely to markedly reduce BP. Moderate dietary salt reduction (e.g., ≤0.22% to 0.25% sodium on a dry matter basis) is advised for all cases. Although not expected to normalize BP by itself, it may enhance antihypertensive drug effectiveness. A high-salt diet may contribute to development of hypertension in some cats, although salt intake does not generally affect BP in normal cats. Conversely, neurohormonal activation and potassium excretion may be increased in cats with renal dysfunction that are fed a low-sodium diet. Weight reduction is usually advised for obese animals. It is prudent to avoid prescribing drugs that can potentiate vasoconstriction (e.g., phenylpropanolamine and other α1-adrenergic agonists). Glucocorticoids and progesterone derivatives should also be avoided when possible because steroid hormones can increase BP. A diuretic (thiazide or furosemide; see Chapter 3) may help by reducing blood volume in patients with volume expansion, but a diuretic alone is rarely effective. Diuretics are avoided or used only with caution in animals with renal disease because they can lead to dehydration and exacerbate azotemia. Serum potassium concentration should be monitored, especially in cats with chronic renal disease.
The ability to monitor BP is important when antihypertensive drugs are prescribed. Serial measurements are needed to assess treatment efficacy and prevent hypotension. Adverse effects of antihypertensive therapy usually relate to hypotension, manifested by lethargy or ataxia, and reduced appetite. Attaining initial BP control may take several weeks. Monitoring may be done every 1 to 2 weeks to assess the efficacy of antihypertensive treatment in non-urgent cases. Once satisfactory regulation is achieved, BP should be measured at least every 2 or 3 months. Some animals become refractory to therapy that was initially effective. Increased antihyper tensive dosage, adjunctive therapy, or a change of antihypertensive drug can be tried. Continued attention to the underlying disease process is important. Routine CBC, serum biochemistry profile, and urinalysis (with or without a UPC) are also recommended every 6 months. Decreasing the magnitude of proteinuria associated with hypertension is a desired treatment outcome.
The long-term prognosis for animals with hypertension is usually guarded because underlying disease processes tend to be severe and progressive. Therapy for some primary diseases can exacerbate hypertension or complicate its control. Fluid therapy, corticosteroids, and erythropoietin are examples. The degree of proteinuria appears to be a negative prognostic factor in cats with chronic renal disease.
ANTIHYPERTENSIVE DRUGS
The ACEIs (e.g., enalapril, benazepril) reduce angiotensin II production, thereby reducing vascular resistance and volume retention (see p. 63). These agents have been more effective in dogs, although their efficacy depends on the degree of RAAS activation underlying the hypertension. Cats with chronic kidney disease and hypertension often are not responsive to ACEIs. However, an ACEI may help protect against hypertensive renal damage by preferentially reducing efferent arteriolar constriction and reducing glomerular hypertension.
Amlodipine besylate is a long-acting dihydropyridine Ca++-blocker that causes vasodilation without appreciable cardiac effects. It can be effective as a primary antihypertensive agent in cats and has a duration of effect of at least 24 hours. Amlodipine generally does not alter serum creatinine concentration or body weight in cats with chronic kidney disease. Mild hypokalemia should respond to oral potassium supplementation. The drug is usually dosed once daily and may be given with or without food. Administration q12h may be used in large cats or in those that do not respond sufficiently to the lower dose. Alternatively, a β-blocker or ACEI may be added for cats that do not respond adequately to amlodipine alone. Amlodipine tablets are difficult to split evenly but they can be compounded using lactose as a diluent.
Amlodipine also is effective in some dogs. A lower dose is tried initially and titrated upward as necessary over a period of days. Amlodipine’s half-life is about 30 hours in dogs; maximal effects occur 4 to 7 days after initiating therapy. Oral bioavailability is high, and peak plasma concentrations are reached 3 to 8 hours after administration; plasma concentrations increase with chronic therapy. The drug undergoes hepatic metabolism, but there is not extensive first-pass elimination; caution is warranted when liver function is poor. The drug is excreted through the urine and feces. A Ca++-channel blocker used as adjunctive therapy with an ACEI in dogs may control BP while yielding a balanced effect on glomerular pressure and glomerular filtration rate (GFR) through equal dilation of afferent and efferent arterioles.
β-adrenergic blockers may reduce BP by decreasing heart rate, cardiac output, and renal renin release. Atenolol and propranolol have been used most often (see p. 89). A β-blocker is recommended for cats with hyperthyroid-induced hypertension. However, β-blockers are often ineffective when used as the sole antihypertensive agent in cats with renal disease.
α1-adrenergic antagonists oppose the vasoconstrictive effects of these α-receptors. Their main use is for hypertension caused by pheochromocytoma. Phenoxybenzamine is a noncompetitive α1- and α2-blocker used most often for pheochromocytoma-induced hypertension. Treatment is initiated with a low dose that is titrated upward as necessary. The α1-blocker prazosin is another option for large dogs. After α-blocker dosing is begun, adjunctive therapy with a β-blocker can help control reflex tachycardia or arrhythmias.
Hypotension is a potential adverse effect of antihypertensive drugs and is usually manifested as periods of lethargy or ataxia. Reduced appetite may be another adverse effect. Rebound hypertension can occur if antihypertensive therapy is suddenly discontinued. This is especially of concern when using β- or α2-blockers. If therapy with such agents is to be terminated, the dosage should be gradually tapered down.
HYPERTENSIVE EMERGENCY
Urgent antihypertensive therapy is indicated when new or progressive signs of severe hypertension are identified. Examples include acute retinal detachment and hemorrhage, encephalopathy, or other evidence of intracranial hemorrhage, acute renal failure, aortic aneurysm, and acute heart failure.
Direct-acting vasodilator agents generally produce faster reduction in BP (e.g., nitroprusside, hydralazine). Nitroprusside can be dosed to effect by constant intravenous (IV) infusion, but arterial pressure should be closely monitored to prevent hypotension (see Table 11-1). Hydralazine given intravenously or orally is an alternative, especially for dogs. Oral amlodipine can be effective in quickly reducing blood pressure in cats and has less risk of inducing hypotension. An IV β-blocker (propranolol, esmolol, or labetolol), ACEI (enalaprilat), or acepromazine (see Table 11-1) also can be used. One of these agents can be added to oral hydralazine therapy if that has not adequately reduced BP within 12 hours.
When hypertensive crisis is related to pheochromocytoma or other cause of catecholamine excess, the α-blocker phentolamine is used IV (see Table 11-1) and titrated to effect. Addition of a β-blocker can help mitigate pheochromocytoma-induced tachyarrhythmias, but it should not be administered alone or before an α-blocker is given. Use of a β-blocker as the sole agent in this setting leaves α1-receptors unopposed and is likely to exacerbate hypertension. Antihypertensive treatment is recommended for 2 to 3 weeks before surgery for pheochromocytoma excision, if possible. For inoperable pheochromocytoma, therapy is continued orally to prevent hypertensive emergencies.
Acierno MJ, Labato MA. Hypertension in dogs and cats. Compend Cont Educ Pract Vet. 2004;26:336.
Arnold RM. Pharm profile: amlodipine. Compend Contin Educ. 2001;23:558.
Belew AM, Barlett T, Brown SA. Evaluation of the white coat effect in cats. J Vet Intern Med. 1999;13:134.
Bodey AR, Rampling MW. Comparison of haemorrheological parameters and blood pressure in various breeds of dog. J Small Anim Pract. 1999;40:3.
Bright JM, Dentino M. Indirect arterial blood pressure measurement in nonsedated Irish Wolfhounds: reference values for the breed. J Am Anim Hosp Assoc. 2002;38:521.
Brown S, et al. Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats. ACVIM Consensus Statement. J Vet Intern Med. 2007;21:542.
Brown S. The kidney as target organ. In: Egner B, Carr A, Brown S, editors. Essential facts of blood pressure in dogs and cats. Babenhausen, Germany: BE Vet Verlag; 2003:121-128.
Brown SA, et al. Effects of the angiotensin converting enzyme inhibitor benazepril in cats with induced renal insufficiency. Am J Vet Res. 2001;62:375.
Buranakarl C, Mathur S, Brown SA. Effects of dietary sodium chloride intake on renal function and blood pressure in cats with normal and reduced renal function. Am J Vet Res. 2004;65:620.
Chetboul V, et al. Spontaneous feline hypertension: clinical and echocardiographic abnormalities, and survival rate. J Vet Intern Med. 2003;17:89.
Egner B. Blood pressure measurement: basic principles and practical applications. In: Egner B, Carr A, Brown S, editors. Essential facts of blood pressure in dogs and cats. Babenhausen, Germany: BE Vet Verlag; 2003:1-14.
Elliot J, et al. Feline hypertension: clinical findings and response to antihypertensive treatment in 30 cases. J Small Anim Pract. 2001;42:122.
Erhardt W, Henke J, Carr A. Techniques of arterial blood pressure measurement. In: Egner B, Carr A, Brown S, editors. Essential facts of blood pressure in dogs and cats. Babenhausen, Germany: BE Vet Verlag; 2003:34-59.
Finco DR. Association of systemic hypertension with renal injury in dogs with induced renal failure. J Vet Intern Med. 2004;18:289.
Henik RA, Snyder PS, Volk LM. Treatment of systemic hypertension in cats with amlodipine besylate. J Am Anim Hosp Assoc. 1997;33:226.
Jacob F, et al. Association between initial systolic blood pressure and risk of developing a uremic crisis or of dying in dogs with chronic renal failure. J Am Vet Med Assoc. 2003;222:322.
Jensen JL, et al. Plasma renin activity and angiotensin I and aldosterone concentrations in cats with hypertension associated with chronic renal disease. Am J Vet Res. 1997;58:535.
Jepson RE, et al. Effect of control of systolic blood pressure on survival in cats with systemic hypertension. J Vet Intern Med. 2007;21:402.
Kallet AJ, Cowgill LD, Kass PH. Comparison of blood pressure measurements obtained in dogs by use of indirect oscillometry in a veterinary clinic versus at home. J Am Vet Med Assoc. 1997;210:651.
Kraft W, Egner B. Causes and effects of hypertension. In: Egner B, Carr A, Brown S, editors. Essential facts of blood pressure in dogs and cats. Babenhausen, Germany: BE Vet Verlag; 2003:61-86.
Maggio F, et al. Ocular lesions associated with systemic hypertension in cats: 69 cases (1985–1998). J Am Vet Med Assoc. 2000;217:695.
Meurs KM, et al. Arterial blood pressure measurement in a population of healthy geriatric dogs. J Am Anim Hosp Assoc. 2000;36:497.
Nelson OL, et al. Echocardiographic and radiographic changes associated with systemic hypertension in cats. J Vet Intern Med. 2002;16:418.
Sansom J, Rogers K, Wood JLN. Blood pressure assessment in healthy cats and cats with hypertensive retinopathy. Am J Vet Res. 2004;65:245.
Snyder PS, Sadek D, Jones GL. Effect of amlodipine on echocardiographic variables in cats with systemic hypertension. J Vet Intern Med. 2001;15:52.
Sparkes AH, et al. Inter- and intraindividual variation in Doppler ultrasonic indirect blood pressure measurements in healthy cats. J Vet Intern Med. 1999;13:314.
Steele JL, Henik RA, Stepien RL. Effects of angiotensin-converting enzyme inhibition on plasma aldosterone concentration, plasma rennin activity, and blood pressure in spontaneously hypertensive cats with chronic renal disease. Vet Therap. 2002;3:157.
Stepien RL, Rapoport GS. Clinical comparison of three methods to measure blood pressure in non-sedated dogs. J Am Vet Med Assoc. 1999;215:1623.
Stepien RL, et al. Comparative diagnostic test characteristics of oscillometric and Doppler ultrasound methods in the detection of systolic hypertension in dogs. J Vet Intern Med. 2003;17:65.
Tissier R, Perrot S, Enriquez B. Amlodipine: one of the main anti-hypertensive drugs in veterinary therapeutics. J Vet Cardiol. 2005;7:53.