Approach to hypotensive patients (Proceedings)

In order to understand and approach hypotensive patients, one must first understand blood pressure. Although not a true measure of perfusion, blood pressure is one of the most non-invasive means the veterinary field has of measuring whether or not the tissues are getting enough blood and ultimately enough oxygen. Blood pressure is defined by the following equation:

Blood Pressure (BP) = Cardiac Output (CO) x Systemic Vascular Resistance (SVR)

Cardiac output is the amount of blood pumped by the heart per minute. Systemic vascular resistance is the amount of tone of the peripheral blood vessels. Cardiac output is not easily measured and is defined as stroke volume multiplied times heart rate. Heart rate is easily measured, but stroke volume is not easily measured in the clinical setting which is why cardiac output is not generally measured. Sympathetic and parasympathetic tone regulate heart rate. Four factors effect stroke volume: preload, myocardial relaxation, myocardial contractility, and afterload. Systemic vascular resistance is effected by the adrenergic receptors, dopamine, and vasopressin receptors in the vasculature, which cause alterations in resistance of the blood vessels. Many neurohormonal responses to hypotension also play a role in maintaining blood pressure, including the renin-angiotensin-aldosterone system, antidiuretic hormone, atrial natriuretic peptide, stretch receptors, and baroreceptors. The body's response to hypotension is very complex and therefore, a general understanding of the factors involved in blood pressure regulation is necessary in order to properly approach the hypotensive patient.

Indirect blood pressure monitoring

In general, the mean pressure should be kept above 60 mmHg and the systolic pressure above 80 mmHg to ensure adequate organ perfusion in the anesthetized patient. In the awake patient, mean pressure should be kept above 80 mmHg and the systolic pressure above 100 mmHg. Doppler blood pressure monitors and oscillometric blood pressure machines have been validated in small animals and give tremendous insight into the blood pressure status of an animal. There is controversy over whether the Doppler pressure reading in anesthetized cats is closer to systolic or mean blood pressure. Traditionally, oscillometric blood pressure monitors have been unreliable in the cat. However, the recent validation of the Cardell® oscillometric blood pressure monitor in cats has proven to be extremely useful.

Appropriate cuff size is necessary in order to get a proper blood pressure reading. Too large of a cuff or a too loosely placed cuff will frequently give falsely low readings and too small of a cuff or a too tightly placed cuff will frequently give falsely high readings. Many oscillometric blood pressure monitors display a heart rate reading in addition to the blood pressure display. Ensuring that the heart rate on the monitor matches the actual heart rate is a good way to determine if the results displayed are believable. Poor perfusion and hypotension are two common causes of aberrant blood pressure readings.

Direct blood pressure monitoring

The critically ill patient frequently needs to have beat to beat monitoring of the blood pressure due to the dynamic nature of patient. This is achieved by placing an arterial catheter and connecting it to a transducer for beat to beat blood pressure readings. Invasive blood pressure monitoring is useful for arterial blood gas sampling, continuous real-time monitoring, intentional pharmacological or mechanical cardiovascular manipulation, and in cases of failure of indirect blood pressure monitoring. Analysis of the arterial waveform can also give insight into the nature of the blood pressure problem. A rapid decline in the downstroke of the waveform frequently indicates decreased systemic vascular resistance (SVR). A slow decline in the downstroke may indicate increased SVR. A low end-diastolic pressure typically indicates hypovolemia.

Kinking of the arterial catheter or severe spasm of the artery can both lead to dampening of the arterial waveform. During arterial waveform dampening, the mean arterial pressure is frequently still reliable even though the systolic and diastolic blood pressures cannot be relied upon. Care needs to be taken never to inject anything except heparinized or nonheparinized saline through the arterial line. Air bubbles can lead to air embolism, so extra caution is necessary to avoid injecting air bubbles into the arterial catheter.

The direct arterial blood pressure waveform

     • The width of the waveform correlates with stroke volume

     • A rapid or steep decline in the waveform indicates decreased systemic vascular resistance (SVR)

     • A slow decline in the waveform indicates increased SVR

     • A low end-diastolic pressure frequently indicates hypovolemia

Reasons for direct arterial bp monitoring

     1. Arterial blood gas sampling

     2. Continuous real-time monitoring

     3. Intentional pharmacological or mechanical cardiovascular manipulation

     4. Failure of indirect BP monitoring

     5. Supplementary diagnostic clues

Approach to the hypotensive patient

An animal that is hypotensive is frequently in decompensatory shock. An animal in compensatory shock frequently has normal to high normal blood pressure due to having a proper response to norepinephrine/epinephrine release. However, if compensatory shock goes unrecognized and the problem progresses, then the animal will likely go into decompensatory shock and become hypotensive. An animal that is hypotensive usually has the following physical and laboratory parameters:

     1. Weak/non-palpable pulses (exception: animals with inappropriate vasomotor tone as the cause of hypotension will frequently have bounding pulses)

     2. Tachycardia (exception: severe bradycardia can rarely cause hypotension, especially in neonates where the sympathetic nervous system is poorly developed)

     3. Pale/while mucous membranes (exception: animals with inappropriate vasomotor tone as the cause of hypotension will have bright red mucous membranes)

     4. Low urine output (<0.5 ml/kg/hr)

     5. Low diastolic pressure (frequently indicates hypovolemia or low systemic vascular resistance)

     6. Low central venous pressure (indicates a preload problem)

     7. Increased lactate (note: a normal lactate does not indicate that perfusion is adequate)

Once an animal is confirmed to be hypotensive, then the cause of hypotension must be determined. The most common causes of hypotension are preload issues (hypovolemic shock) or inappropriate vasodilation (distributive shock). These will be discussed last. Less common causes of hypotension will addressed first.

Extreme tachycardia rarely causes hypotension, but it can if the rate is extraordinarily high by preventing filling. Depending on the arrhythmia, these need to be treated with the appropriate anti-arrhythmic agent. For severe or unstable ventricular tachycardia, lidocaine or amiodarone is indicated. For severe sinus tachycardia, beta blockers are usually the first drug of choice.

Severe bradycardia is also a rare cause of hypotension, but can be an issue due to excessively high vagal tone or 3rd degree AV block. Hyperkalemia also needs to be ruled out. High vagal tone should be treated with anticholinergics and complete AV block usually needs cardiac pacing. Hyperkalemia should be treated directly to combat the bradycardia. It should be noted that neonates have an under-developed sympathetic nervous system and are much more heart rate dependent to maintain their blood pressure than adults are. Therefore, hypotension due to bradycardia is more common in neonates and should be addressed earlier in this age group.

Decreased myocardial contractility issues are usually due to underlying cardiac disease, such as dilitative cardiomyopathy (DCM). However, the systemic inflammatory response syndrome and sepsis have been shown to decrease myocardial contractility as well. These syndromes will have signs of distributive shock as well and can be easily differentiated from syndromes where myocardial contractility issues are the sole cause of the hypotension. Animals with DCM and hypotension need inotropic support with beta agonists, such as dobutamine. The B1 effects will help with contractility and the B2 effects will cause vasodilation allowing the afterload to be decreased and improving forward flow. Although blood pressure may not increase per se due to the vasodilatory B2 effects, perfusion is usually improved and can be monitored with lactate or oxygen extraction. An echocardiogram is usually necessary to confirm this diagnosis, although the physical examination, ECG, and radiographs are helpful in making the diagnosis. Many DCM patients are simultaneously in atrial fibrillation which will also decrease forward flow and may need to be treated with anti-arrhythmics such as Diltiazem, which is counterintuitive since calcium channel blockers can further decrease myocardial contractility.

Myocardial relaxation problems are usually due to hypertrophic cardiomyopathy (HCM) or pericardial effusion. HCM is usually in cats and they may or may not be in congestive heart failure. Echocardiography is necessary to make the definitive diagnosis. Calcium channel blockers are the drug of choice to help with myocardial relaxation. Pericardial effusion prevents expansion of the myocardium, thus decreasing stroke volume. Central venous pressure (CVP) will be increased in these patients, due to decreased forward flow. Once the effusion is relieved, the CVP will drop. Treatment for this syndrome is pericardiocentesis.

Afterload issues are an extremely rare cause of hypotension. The most common cause is aortic stenosis. Usually this would be in young animals and a heart murmur would be ausculted on the left side of the chest. A history of syncope may be present. Echocardiography is necessary to make the diagnosis and invasive procedures are usually necessary to correct the stenosis.

Inadequate preload or inappropriate vasodilation are probably the most common cause of hypotension in veterinary medicine. Causes of inadequate preload include intravascular fluid loss or maldistribution of blood (inappropriate vasodilation) which decreases effective circulating volume. Inappropriate vasodilation most commonly occurs in patients that are septic, but can also occur in patients with the systemic inflammatory response syndrome, endocrine disease, and toxins.

The treatment of choice for these patients is IV fluid therapy. The blood volume, and hence the shock dose of fluids, in the dog is 90 mls/kg and in the cat is 45-60 mls/kg. Initially, isotonic, isoelectric replacement crystalloid fluids are used. Generally, ¼ of the shock dose is given to the animal over 10-15 minutes and the animals re-assessed. This translates into 22 mls/kg in the dog and 12-15 mls/kg in the cat. A proper response to fluids is a decrease in heart rate, improved mentation, stronger pulses, and improved mucous membrane color. If the patient remains tachycardic and hypotensive after ¼ of a shock dose, then another ¼ shock dose of crystalloids over 10-15 minutes is administered. If the animal is still in need of fluids after ½ a shock dose, colloids (such as hetastarch) should be administered at 5-10 mls/kg over 10-15 minutes. If approaching a full shock dose of crystalloid and 20 mls/kg of colloid, then other methods of bringing up the blood pressure need to be considered.

A central line and urinary catheter should be placed to determine if intravascular volume has been met and if urine output is >0.5 ml/kg/min. Remember that in the hypotensive patient, urine output <0.5 ml/kg/min js actually appropriate due to stimulation of the renin-angiotensin-aldosterone system. However, if the patient is properly volume resuscitated (i.e. euvolemic), then the urine output should be >0.5 ml/kg/min. To determine if the preload is adequate, a central venous pressure is the best way to determine this. A CVP >3 cmH2O indicates that the intravascular volume is adequate. A fluid challenge can help determine if a patient is volume loaded. If the CVP rises during a fluid bolus, but then drops < 3 cmH2O after the bolus stops, then the patient is likely not volume loaded. In hypotensive patients it is common to push the CVP to 6-8 cmH2O before determining that they are fully volume loaded.

If the CVP is 6-8 cmH2O and the animal remains hypotensive, then one must resort to the fact that the hypotension is also due to either a systemic vascular resistance problem and/or a myocardial contractility issue (both common in sepsis and the systemic inflammatory response syndrome). A direct arterial blood pressure is ideal in this situation, as the blood pressure can be titrated easily with inotropes and pressors with beat to beat monitoring. Combination inotropes/pressors can be utilized such as dopamine, epinephrine, or norepinephrine. Alternatively, one can use inotropes, such as dobutamine, separately from pressors, such as vasopressin, to target each system separately. It is ultimately personal preference, but familiarity with the drug is necessary. My preference is to begin with dopamine in the mid-range (5-10 mcg/kg/min), then switch to dobutamine (5 - 10 mcg/kg/min) and vasopressin (0.2 – 2.0 mU/kg/min) if the dopamine is not working. The following table is a general schematic of various inotropes and pressors, which receptors they act on, and their relative strengths.

Overall, there are many ways to approach hypotension. Knowledge of what comprises blood pressure is necessary to troubleshoot the causes of hypotension and properly treat the patient.