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Concern about dangers associated with systemic hypertension in veterinary patients is now widely realized by the veterinary profession. Hypertension is a potentially life-threatening medical problem, often caused by a another (primary) disease. Devastating cardiovascular (heart and circulatory system) , renal (kidney), opthalmic (eye-related) and neurological (brain-central nervous system) manifestation of hypertension are likely if untreated. Most animals with primary diseases resulting in hypertension can be concurrently treated for this secondary complication, provided it is recognized early. This page will focus upon aspects of this problem that are of importance to you, the conscientious pet owner, and to your dog or cat. This information is now available for your perusal .

Information will be added as new data emerge...and as my time allows) until its logical conclusion. The following topics are covered:

  1. General

  2. Specific

  1. Heart

  2. Circulatory System

  3. Eyes

  4. Central Nervous System...Brain

  5. Kidney

 

What Is Systemic Hypertension?

The term hypertension refers to the abnormal elevation of the pressure exerted by blood...specifically arterial blood... against the vasculature (blood vessels)- and organs they supply. Blood pressue is determined by the blood and extracellular fluid volumes, the capacity and expansile capacity of the blood vessel (vascular) system....which will be explained in a later section, the forces exerted upon the vascular system during the contraction (known as "systole") and relaxation (known as "diasole") phases of the heart muscle activity, during the pumping of blood. Those properties affecting the capacity of the vasculature to adapt to blood volume fluctuations and oscillating pressure gradients generated against vessel walls during systole and diastole are major determinants of the term "Total Peripheral Resistance...(TPR)". As TPR rises, so goes blood pressure. In addition to TPR, blood pressure is also affected by the average pressure generated by the force and frequency of each systole-diastole cycle of the heart ( the heart beat); this is a function of both 1) the force (strength) of heart muscle contraction and subsequent volume of blood ejected from the heart chambers into the general circulation and 2) the frequency (heart beats per unit of time...usually "beats per minute")...i.e.the "heart rate". Together, these latter two parameters define heart functionality, measured as the total "Cardiac Output... (CO)".

In the simplest terms, then, Blood Pressure ~ CO x TPR; this is usually expressed in millimeters of mercury (mm Hg). Normal values for Systolic/Diastolic and Mean Arterial Pressure (MAP,... is approximately the diastolic pressure + 1/3 the systolic pressure) in dogs and cats vary somewhat, depending on the method of measurement (to be discussed later). The following are approximate systolic and diastolic normals:

 

What Causes Hypertension ?

Essential or Primary Hypertension occurs without a clear underlying cause in some humans. This form of hypertension is rare in veterinary medicine, and will not be considered here. In dogs and cats, hypertension is most often a consequence of another primary disease. In cats, Renal (Kidney) Failure and Hyperthyroidism are the most frequent causes of systemic hypertension. In dogs, Hyperadrenocorticism (Cushing's Disease), and Renal Failure are the most likely primary etiologies. However, other medical conditions..albeit sometimes rare conditions..may also predispose to this problem. Example include aberrations in adrenal gland function (hyperadrenocorticism OR pheochromocytoma),acromegaly, certain central nervous system diseases, and some primary cardiomyopathies (heart muscle diseases).

You may wonder: "How do these varied and different medical conditions and illnesses, each manifest as unique in its own right, medically separate fom the others...yet somehow shares with the others the same end point: systemic hypertension?" Rest assured, you are not alone in your wondering. However there are reasonable hypotheses which probably reflect common physiological realities. All wondering can be satisfied if one thinks about the causes of hypertension only in terms of those basic parameters which define its essence: the concepts of Total Peripheral Resistance (TPR) and Cardiac Output (CO)---introduced in a previous section. Each of the medical conditions which lead to hypertension, alluded to above, in its own unique fashion adversely alters TPR and/or CO. In yet another attempt to make this information as simple as possible, these concepts will be presented once more, though this time in a slightly different manner.

TPR

 

Below is a crude and simplistic representation of the circulatory system (pardon my drawing, please)

 

 

 

Movement of Blood: Deoxygenated blood is pumped to the lungs and becomes oxygenated; this blood returns to the heart and is pumped to the general circulation; oxygen is consumed, deoxygenated blood returns to the heart and the cycle repeats

 

 

 

The Salient Features are:

  1. where K1 = "fudge factor" representing inherent average strength, integrity and elasticity of vessel walls and surrounding tissue-organs, and other applicable mathematical "pressure constant(s)".
  2. this relationship states that peripheral resistance (TPR) increases if the blood volume increases or the capacity of the circulatory system decreases.
  3. you can liken this to blowing up a balloon; with the first few breaths, inflation is relatively easy. However, as air fills the balloon, (here used analogously to the circulatory system), pressure increases and your face gets redder with succeeding breaths. With a larger balloon, there is room for more air (and more breaths before you turn red or faint.

 

CO

 

  1. volume of blood returned to the heart during diastole
  2. the volume capacity of the heart
  3. the integrity of the heart muscle (and valves) to relax during diastole and to contract during systole.

So...... getting back to how these other diseases are involved in the development of hypertension, the answer is that they affect, in various, sometimes complicated ways, the TPR (often via altering vascular tone and/or blood volume) and CO (increasing the rate and/or force of contraction). The details, for example of how kidney failure, hyperadrenocorticism or hyperthyroidism each uniquely effects these changes., .will be addressed in the "episode" on Treatment for Hypertension". Hopefully, you will marvel with interest in these concepts ....

 

 

So...What Are the Physiological Consequences of Systemic Hypertension?.......Here is a simplified list...

Physiological Consequences of Systemic Hypertension

I. General:

The most commonly noted tissues affected by systemic hypertension are the cardiovascular, kidney ("renal"), eyes ("ocular"), and central nervous system...particularly the brain.

II. Specific:

 

  1. Heart:

    • Secondary to poor perfusion (with oxygenated blood) there is localized loss of muscle cell viability; the outcome can result in:

      • Arrhythmia

      • Reduced Contractility (decreased strength of contraction): results in inadequate CO

      • Congestive Heart Failure

    • Increased Workload Due to Excess Pressure AND Increased Blood Volume (see "Kidney" for explanation):

      • Enlargement and/or Thickening of Heart Muscle-->

        1. potentially reduction in chamber size (and thus, reduction in volume of ejected blood)

        2. malalignment of valve component parts (and thus, decreased efficency of ejected blood volume, further damage to heart muscle, "murmurs", electrical conduction abnormalities ("arrythmias")).

  2. Circulatory System:

  • Structural alterations in arteriolar linings and walls, localized swellings of vessels ...that negatively affect vessel integrity, localized tissue perfusion (with oxygen and nurtient-enriched blood), and viablity of smaller ("downstream") vessels.

  • Aberrations in functionality...including leakage, hemorrhage and inappropriate responses of vascular muscle to local and systemic neurotransmitter signals

  • Increased potential for the development of intravascular thrombus (a blood "clot") as a consequence of altered vascular lining (making the vessel walls "stickier"). The potential for total vessel obstruction is possible and, depending where a clot forms, immediate death is possible.

3. Eyes:

  • Increased pressure within the vessels supplying blood to the eyes

  • Intraocular ("inside the eyeball") swelling

  • Intraocular hemorrhage

  • Retina detachment

  • Glaucoma

4. Central Nervous System:

  • Cerebral hemorrhage

  • reduction in blood to portion of brain

  • localized damage to integrity of brain

 

  • Increased intracranial pressure...within the brain-compartment of the skull

  • pressure/swelling transferred to brain tissue...localized damage to integrity of brain

5. Kidney:

  • Damage to and loss of kidney filtration units ("nephron")

  • loss of functionality..poorer ability to eliminate toxic metabolic wastes; many clinical effects (to be described later....)

  • inopportune loss of proteins, including coagulation factors; can result in hemorrhage, fluid losses to lungs, & body cavities

  • Degeneration of kidney tubules and surrounding (interstitial) tissues

  • adversely affects fluid and electrolyte elimination/conservation: potential for arrythmias, and other multi-system effects

  • adversely affects the regulation of systemic "acid-base" balance (to be discussed sometime in 1998)

  • Kidney disease/failure also can contribute to hypertension by:

  • triggering biochemical pathways that result in increased sodium and fluid retension (..resulting in increased blood volume, increased heart and circulatory workload)

  • triggering related biochemical pathways leading to enhanced vasoconstriction (smaller average diameter [or "radius", if you prefer] of blood vessels; Remember, smaller diameter means higher blood pressure!)***

 

 

*** In essence, the kidney appears to be commiting.....suicide!!! "Why?", you ask. An attempt to make sense of this will be forthcoming on another page to be published here in the (relatively) near future.

 

 

 

So...What are The Clinical Signs of Systemic Hypertension? They can be Quite Variable!...............................

 

What are the Clinical Signs of Systemic Hypertension?

Clinical signs of systemic hypertension may range from subtle, even imperceptable to acute death. Noticable effects are frequently (but not exclusively) related to the organs with rich blood supplies: the eyes, heart, kidney and brain. However, all major systems are affected by hypertension and clinical signs can be referable to any of them. In addition, clinical signs may be overshadowed by symptom of the primary disease (i.e. initial clinical abnormality which caused secondary hypertension...e.g. adrenal dysfunction, kidney,heart and specific endocrine disorders). In many instances the presence of secondary hypertension, whether or not specific clinical signs of hypertension are obvious, must be presumed. Signs most frequently observed that are reflective of systemic hypertension include:

  • Arrythmias

  • Murmurs

  • Sudden collapse and death

  • Sluggish, inappetant, respiratory distress /cough, non-specific gastroenteritis, pale mucus membranes, poor pulse, weak

  • Thromboembolic/Vascular "Accident"

  1. Either the primary (underlying) disease (e.g. adrenal, renal/kidney, cardiac, thyroid) or damage to vessels from secondary hypertension itself predispose to the formation of clots (thrombi, thromboemboli) within affected vessels (euphemistically labeled Vascular Accidents)

  2. Animals may present acutely and near death as a clot forms in and obstructs the major vessels of the lung or heart, respectively.

  3. A clot may develop in the heart, expecially in cats, and migrate a part of the aorta (the greatest of the "great vessels of the body") that, by virtue of its position, obstructs blood flow to one or both rear legs. The affected animal is usually unable to use the limb, which is cold and EXTREMELY painful. Howling, (due to pain) is a common finding.

 

  • Loss of Normal Motor Function:

  1. lameness, altered gait or posture, loss of prehension, mastication and swallowing,capabilities decreased blinking,

  2. Incontinence

  • Signs of blindness NOT referable to the globe itself

  • Seizures

  • Vascular accidents can occur and affect one or more specific portions of the brain resulting in subtle, assymetric (affecting only one side of the head or body) neurological abnormalities.

  • Disorientation/Dementia may also be apparent.

 

 

Diagnosis of Systemic Hypertension

As mentioned earlier. clinical signs can be subtle!. Thus, the clinician should have a strong index of suspicion, based upon the presence of diseases frequently associated with secondary hypertension, the results of the physical exam, and the history. Also, as animals approach geriatic years, routine measurments for the potential of hidden (occult) hypertension should be considered, as well.

There are actually quite a few ways to measure blood pressure in animals and in people. The most useful in the average clinic setting will be mentioned here. Others may be added in upcoming weeks; rest assured that there are hosts of high-tech variations on the same themes and principles, but these will NOT be examined.

Basically measuring of blood pressure is either via DIRECT or INDIRECT means.

This entails inserting a catheter into an artery and passing a transducer which directly measures pressure. In general, in veterinary medicine such an undertaking requires sedation...more likely anesthesia and for routine screenings, is impractical. However, It may be useful as a means of continuous and accurate assessment of systemic blood pressure during surgery.

Auscultatory Technique: in humans, a stethoscope is used to auscult (listen to/for) the return of blood flow to an artery in an arm in which flow was completely blocked by a tight cuff applied to the upper arm. The pressure applied to the cuff around the arm is deliberately reduced in small increments. The initial return of pulse occurs when pressure in the cuff is at or just below the pressure in the systolic blood pressure. As cuff pressure is further reduced, more blood flows and the sound of a discrete pulse disappears. The pressure in the cuff corresponding to this occurence represents the diastolic pressure.

This auscultatory technique is not generally useful in veterinary medicine, as the amplitude/ frequency of the sounds associated with blood flow to a limb are difficult to ascertain with just a stethoscope.

 

Doppler Flow Meter: in this procedure, a cuff is again applied to the limb, but instead of using the stethoscope, a transducer is applied below the cuff and the presence of blood flow is determined via measurement of the change in frequency of sound reflected back to the transducer, in comparison to the frequency of the sound initally emitted by the transducer; such a change occurs when red blood cells are moving (blood is flowing).

This technique is readily performed in the veterinary clinical setting, though anxious or nervous animals normally require several measurements and then an average value is determined from these. Another point: ....for the most part only the systolic pressure can be determined confidently via this technique; however in veterinary medicine, this value alone is significant and can be used to diagnose hypertension

Miscellaneous: other non-invasive methods that may become useful in the average veterinary clinic setting include Oscillometric Sphygmomanometry, and Photoplethysmography. For veterinarians interested in a technical discussion of these techniques, please read a recent issue of Veterinary Medicine 93: 48-59, 1998.

 

 

Treatment of Systemic Hypertension: Principles

The preceding discussion has emphasized the concept of hypertension: namely, that it is a function of both Cardiac Output (CO) and Total Peripheral Resistance (TPR). When either of these parameters exceeds its normal value (AND...there is inadequate compensatory adjustment by the other) then systemic hypertension inevitably results.

It therefore follows that treatment goals for hypertensive patients are to reduce CO and/or TPR. Sometimes simple dietary therapy may suffice (e.g. decreases salt---> decreased water retension and blood volume--->decreased TPR AND decreased CO (reduced volume per systolic contraction) Other , more aggressive medical modalities may be required in addtion to dietary modification in the vast majority of symptomatic hypertensive animals.


Reduce CO:

Reduce TPR

Example: Amlodipine (Norvasc® ),

 

 

 

 

 

 

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