History and physical examination

The history will begin with the signalment (age, sex, breed). Breed‐associated cardiac disease (such as cardiomyopathy observed with the Doberman Pinscher or Boxer, sick sinus syndrome in Schnauzers) should be considered when managing blood pressure abnormalities in the ICU patient. There is a reported effect of the sex on ABP in dogs, with males having higher and intact females lower values. The difference, however, is less than 10 mmHg [5]. The history continues with the progression of current clinical signs, past medical history (including kidney disease, hyperthyroidism, cardiac disease) and exposure to medications (human and veterinary) and toxins. A list of common drugs and toxins that can affect blood pressure is provided in Table 3.1.

The owners might report clinical signs of weakness, lethargy, and mental depression with either hypo‐ or hypertension. Clinical signs associated with target organ damage from hypertension can be vague (such as lethargy, hiding). Acute blindness or sudden onset of abnormal mentation might be a consequence of severe hypertension. Any history of significant fluid loss such as vomiting or diarrhea requires further investigation for hypotension from hypovolemia. Polyuria can result from kidney disease and hypertension.

The physical examination begins with the temperature, pulse rate and intensity, oral mucous membrane color, and capillary refill time. These physical findings provide a reasonable assessment of peripheral tissue perfusion and as a group can be called the physical peripheral perfusion parameters.

The various stages of shock can be initially detected through the physical peripheral perfusion parameters. Animals with hypotension (early decompensatory and late decompensatory stages of shock) typically manifest one or more of the following characteristics: tachycardia (dogs) or bradycardia (dogs in late stages and cats), pale mucous membrane color, prolonged capillary refill time, abnormal peripheral pulse palpation (weak, thready or absent), dull mentation, and low body temperature (cats). In the early stages of sepsis or severe hyperthermia, the mucous membranes may appear bright red due to peripheral vasodilation. The presence of hypotension should be confirmed and quantified with ABP measurement in each situation.

Palpation of the femoral pulse has been cited to provide an estimate of ABP; however, the strength of the palpated pulse (pulse pressure) provides a more accurate method of feeling the difference between SAP and DAP. A patient with a normal pulse pressure could have an abnormal SAP or DAP reading, making the actual measurement of ABP the more accurate method of assessment.

Complete physical and neurological examinations are then performed. The finding of jugular vein distension or a jugular pulse can indicate an increase in intrathoracic or pericardial pressure, each a potential cause of inadequate venous return and hypotension. Skin turgor, mucous membrane and corneal moisture and eye position within the orbit are used to estimate the hydration status of the patient; patients with severe dehydration may exhibit concurrent hypovolemia (see Chapter 2). The ophthalmic examination might reveal retinal vascular engorgement or hemorrhage, blindness, hyphema or choroidopathy, each a possible consequence of severe hypertension. Evidence of trauma, third body fluid spacing, vomiting, diarrhea or polyuria could be associated with hypovolemia and hypotension. Auscultation of the heart for a murmur or arrhythmias (pulse deficits, tachy‐ or bradyarrhythmias) could direct further testing for cardiac disease as a contributor to hyper‐ or hypotension. Careful palpation for a “thyroid slip” in the cat might demonstrate enlarged thyroid glands with hyperthyroidism and hypertension possible.

Further patient evaluation requires the collection of additional data. Cage‐side or POC testing, clinicopathological testing, diagnostic imaging, and equipment‐based monitoring can provide valuable information to detect alterations in blood pressure, identify the cause, and reveal any potential consequences.

Point of care testing

A minimum database is provided through POC in‐hospital testing and should include the packed cell volume (PCV), total protein (TP), blood glucose, blood urea nitrogen (BUN) electrolyte panel, blood lactate, acid–base status, coagulation profile, and urinalysis. Blood viscosity is directly related to vascular resistance. As the PCV or hematocrit increases, blood viscosity and vascular resistance also increase. The opposite effects are observed with a low hematocrit. Hypoglycemia can affect SVR, with insufficient energy substrate available resulting in poor contraction of vascular smooth muscle and poor vascular tone. An elevated BUN and isosthenuria on urinalysis might direct further investigation for kidney disease, a frequent cause of hypertension in the dog and cat. Electrolyte disorders affecting sodium (Na⁺), potassium (K⁺), magnesium (Mg⁺⁺), ionized calcium (iCa⁺⁺) or chloride (Cl⁻) and severe acidemia or alkalemia could impair cardiac contractility or vascular tone.

A high blood lactate suggests anaerobic metabolism, poor tissue oxygenation, and impaired perfusion. Blood lactate should be assessed during resuscitation and a declining trend documented as evidence of return of blood flow. An elevated blood lactate found with a normal ABP warrants investigation for ischemia localized to an organ or isolated tissue bed as a cause.

Clinicopathological testing

A complete blood count and serum biochemical profile with thyroid panel will provide data pertaining to possible contributions of the internal organs to abnormalities of the blood pressure. An elevation in serum creatinine and BUN directs further investigation for kidney disease and possible renal hypertension. Problems such as liver disease, pancreatitis or hypoadrenocorticism might be found as a cause of hypovolemia from vomiting and diarrhea; this should be interpreted along with a urinalysis. Fecal examination for parasites might find a cause for diarrhea and hypovolemia. Additional testing is often required and could include serology for inciting pathogens (cause of systemic inflammatory response syndrome (SIRS)‐related hypotension), fluid analysis with culture and susceptibility, adrenal function testing (for hypoadrenocorticism, hyperadrenocorticism or pheochromocytoma) and diagnostic imaging. Rarely, further clinicopathological testing may be useful in the diagnosis of pheochromocytoma.

Diagnostic imaging

Survey thoracic and abdominal radiographs provide the initial diagnostic imaging data once the patient has been stabilized. Thoracic radiographs can demonstrate the heart size and shape, evidence of heartworm disease or other pulmonary vascular changes, lung parenchymal fluid or masses, pleural fluid or air, and rib or vertebral changes. The size of the caudal vena cava can represent central venous volume and preload to the heart (when no evidence of pleural air or pericardial fluid). Abdominal radiographs could show evidence of peritoneal fluid or air and provide an initial assessment of abdominal organ size, shape, and position.

Abdominal and thoracic ultrasound provides a more in‐depth assessment of organ structure and can identify fluid pockets not seen on plain radiographs. Diagnostic and therapeutic centesis can be performed as indicated. Evaluation of the size and structure of the adrenal glands might identify adrenal hypertrophy or a mass, potentially contributing to blood pressure abnormalities. Documentation of primary cardiac disease often requires a combination of thoracic radiography, electrocardiography (ECG), and echocardiography. Echocardiographic findings associated with sepsis‐related myocardial dysfunction include biventricular dilation with reduced ejection fraction and reduced fractional shortening [6]. Advanced imaging with computed tomography or nuclear magnetic resonance imaging may be warranted to better define an organ structure or evaluate the tissues of the central nervous system.

Equipment‐based monitoring methods

Indications for monitoring ABP are numerous and include any animal with a history of hypo‐ or hypertension, an underlying physiological derangement that could predispose an animal to a blood pressure disorder or the need for heavy sedation or general anesthesia.

Direct and indirect methods are available to monitor ABP in the dog and cat. Traditional techniques include direct arterial catheterization, Doppler ultrasonography, and oscillometric sphygmomanometry. Alternate techniques include high‐definition oscillometry and photoplethysmography.

Direct ABP monitoring

Direct ABP (dABP) monitoring is considered to be the “gold standard” for ABP measurement but requires placement and maintenance of an indwelling arterial catheter. Arterial pressure within the catheterized vessel is detected and converted to an electrical signal by a pressure transducer and amplified and continuously displayed as a waveform (Figure 3.1) and numeric values. Advantages of dABP monitoring include real‐time data display, ability for continuous monitoring, reliability, accuracy of measurement, and accessibility for arterial blood gas sampling.

The vast amount of information gleaned from dABP monitoring often balances the time and invasiveness of arterial catheterization. Critically ill animals that might warrant dABP monitoring include severe hypotension related to cardiogenic or vasodilatory shock, severe hypertension requiring pharmacological intervention, and patients requiring general anesthesia that are assessed to have a high physical status classification score (see Table 22.1).

Arterial catheter placement is typically achieved in the dorsal metatarsal, radial, coccygeal or femoral artery of the dog and cat. Catheterization of the femoral artery may carry a greater risk for catheter dislodgment, bleeding or thrombosis compared to the other arterial locations. The materials required for arterial catheterization as well as the steps for the procedure are listed in Box 3.2a. The steps for setting up direct blood pressure monitoring are provided in Box 3.2b with the set‐up pictured in Figure 3.2 [7] and steps to perform direct arterial measurement in Box 3.3. Complications associated with dABP monitoring include catheter site hemorrhage, infection, thrombosis, and accidental intraarterial drug administration. Contraindications to dABP are relative to the need for invasive monitoring but may include coagulopathy, thrombocytopenia or thrombocytopathia, local skin necrosis or infection, or animals receiving anticoagulant or thrombolytic agents.

An arterial pressure waveform is produced by dABP monitoring which visually demonstrates varying arterial pressures obtained throughout the cardiac cycle. The components of this waveform are illustrated in Figure 3.1. The upstroke of the waveform (anacrotic rise) is closely related to cardiac inotropy and the rate of blood acceleration during contraction. The SAP is measured at the top of this upstroke. During the downward slope, the aortic valve closes at the onset of diastole, with the elastic recoil causing the dicrotic notch. Blood continues to run distally until baseline is reached where the DAP is measured.

Alterations in waveform morphology are most commonly observed with cardiac arrhythmias (sloped anacrotic rise with a lower peak pressure), hypotension (decreased anacrotic rise; rate, slope, and amplitude, lower peak pressure and disappearance of the dicrotic notch), and hypertension (rapid anacrotic rise, higher peak and baseline pressure, enlarged waveform phases) [3].

Waveform changes will prompt immediate assessment of patient perfusion parameters to determine if a true change in the condition of the animal has occurred. Should patient status appear stable, the monitoring system and set‐up are checked for problems.

Basic system troubleshooting begins with assessing the patient position relative to the transducer, system lines free of air bubbles or kinks, a patent arterial catheter (flushes easily, no kink or thrombus, positioned within the middle of the arterial lumen) and an adequately pressurized saline bag. Additional conditions inherent to the monitoring system itself (known as damping) should then be assessed. Damping is a loss of pulse pressure energy between the catheter tip and the transducer due to frictional resistance and absorption of energy [7]. The effects of overdamping and underdamping are listed in Table 3.2. To determine if the monitoring system has an adequate dynamic response and is optimally damped, a “square wave” test may be performed. This is done by opening the continuous flush valve (from the pressurized flush system) for a few seconds, creating a square wave and then quickly closing the system [7]. A system with appropriate dynamic response characteristics will return to baseline waveforms within one or two oscillations. If this fails, further troubleshooting of the system is required.

Status	Signs	Effect
Overdamping Long or overly compliant tubing, air bubbles, clots or kinks	Less distinct waveform Obscure dicrotic notch	Falsely low SAP, exaggerated DAP
Underdamping Most systems. Due to inadequate frequency response for patient pulsatile signal	Sharp waveform points Display artifacts	Exaggerates SAP, falsely low DAP
Fast flush or square wave test	A square wave form is produced	System with appropriate dynamic response will return to baseline waveform within 1–2 oscillations

DAP, diastolic arterial pressure; SAP, systolic arterial pressure.

The values for SAP, DAP, and MAP can each be evaluated with the waveforms. Minor variations in ABP will naturally occur in concert with the respiratory cycle. During spontaneous breathing, SAP drops during inspiration as intrapleural pressure becomes more negative, causing cardiac and vessel pressures to fall. The SAP then rises during spontaneous expiration. The phenomenon known as pulsus paradoxus, by which abnormally large decreases in SAP (defined as >10 mmHg) are observed during spontaneous inspiration, is often associated with cardiac tamponade or severe respiratory tract disease [8].

When a patient is undergoing mechanical ventilation, the opposite cardiovascular effects are expected during inspiration (increased SAP) and expiration (decreased SAP). Mechanically ventilated animals demonstrate decreased cardiac output and stroke volume as inspiratory‐to‐expiratory ratio and airway pressure increase [9]. In ventilated animals with consistent tidal volumes, the change in SAP associated with inspiration versus expiration (known as systolic pressure variation (SPV)) may be used to predict volume responsiveness. Hypovolemia exacerbates changes in stroke volume, SAP, and subsequently SPV (Figure 3.3). Typical SPV in healthy anesthetized dogs is approximately 5.3  + 1.8 mmHg. Increases in SPV (inspiratory SAP‐expiratory SAP) have been associated with ongoing hemorrhage and hypovolemia [10].

A similar calculation known as pulse pressure variation (PPV) [12] determines volume responsiveness using a continuous arterial waveform (see Figure 3.3). The PPV is a percentage calculated by dividing the maximum and minimum pulse pressures (PP_max–PP_min) over a single breath by the mean of the two values [(PP_max–PP_min)/2]. PPV has been found to be more reliable than SPV when determining preload dependency. It controls for changes in extramural pressure during respiration and focuses on changes related to left ventricular stroke volume [13]. Automatic calculation of PPV and other dynamic parameters by modern‐day monitors has contributed to their popularity and clinical use. These parameters are not without limitations and it is important to remember that PPV is not useful during spontaneous breathing, cardiac arrhythmias, right‐sided heart failure, and large variations in tidal volume [14].

Indirect ABP monitoring

Indirect arterial blood pressure monitoring (also known as noninvasive blood pressure (NIBP) monitoring) is preferred when cardiovascular status is stable and large fluctuations in ABP are unlikely to occur. NIBP measurement allows for rapid determination of ABP without the morbidities associated with intraarterial catheterization. Disadvantages to NIBP measurement are largely due to its indirect nature. These devices estimate ABP through detection of arterial blood flow rather than directly measuring pressure within the artery itself. Accuracy of the device may be affected by dramatic changes in arterial flow or the device’s ability to detect that flow.

Noninvasive blood pressure measurements in animals are easily influenced by various patient factors, such as species, anesthetized or conscious state, degree of illness, cuff placement along a limb with varying circumference, size and anatomical accessibility of the artery being occluded, and patient movement during ABP measurement. The American College of Veterinary Internal Medicine (ACVIM) has created veterinary‐specific recommendations for the validation of NIBP measurement devices (Box 3.4) [15]. When considering use of a specific NIBP monitor in clinical practice, it is advisable to (1) determine which species and conditions the monitor will be used for, and (2) investigate if the monitor has been validated for the expected circumstances according to peer‐reviewed literature or ACVIM recommendations.