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:
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:
- Dogs: Systolic/Diastolic = 147/83 mm Hg
- Cats: .Systolic/Diastolic = 160/100 mm Hg
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:
- During sytole, blood leaves the heart via a few great vessels and with distance from these, on average vessel size decreases (but vessel number increases)
- To a first approximation, TPR ~= {Blood Volume/ Volume [i.e.--Capacity] of Circulatory System} x K1
- 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)".
- this relationship states that peripheral resistance (TPR) increases if the blood volume increases or the capacity of the circulatory system decreases.
- 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.
- The artery/arterolar vessel walls are surrounded by tiny muscles and function to maintain "vascular tone". Vascular tone is, to some extent, amenable to fine control by circulating and local neurotransmitter molecules. Contraction or relaxation of vessel musculature as a result of changing neurotransmitter input decreases or increases vascular tone and thus the diameter (and thus the volume-capacity) of vessels, respectively. Owing to the large number of tiny vessels, fine tuning of "average" vessel tone (and volume) is possible. To further appreciate how incremental variations in vessel diameter and tone can significantly alter TPR, you are encouraged to view a more detailed discussion, on this web site. ....Otherwise, let's move to CO...
CO
- As mentioned earlier, CO is a function of both the strength of contraction and volume of blood ejected during systole.
- The volume of blood ejected during systole depends upon the:
- volume of blood returned to the heart during diastole
- the volume capacity of the heart
- the integrity of the heart muscle (and valves) to relax during diastole and to contract during systole.
- Keep in mind that TPR also affects CO (and the reverse can be true, as well)
As TPR increases, the force of contraction must be sufficient to overcome backpressure (sometimes referred to as "afterload")..kind of like the extra force and work needed to blow into a full balloon
More about this under "Physiological Consequences...." section...in a future "episode".
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 ....
Physiological Consequences of Systemic Hypertension The most commonly noted tissues affected by systemic hypertension are the cardiovascular, kidney ("renal"), eyes ("ocular"), and central nervous system...particularly the brain.
Hypertension causes primary damage to organs and blood vessels
Damage to vessels can result in hemorrhage and other adverse effects impacting perfusion of blood to tissues and, secondarily, via decreases flow of oxygen and nutrients (and increases accumulation of toxic was products in tissues) damage integrity and functionality of essential organs
Elevated blood pressure markedly alters circulatory hemodynamics; there is increased workload placed upon the heart muscle with concommitant alterations in chamber size, valvular integrity and electrical conduction and consequential loss of pumping capability, arrhythmias, and exacerbation of hypertensive parameters due to increased fluid accumulation..blood volume.
Central Nervous System..especially the Intracranial (Brain) portion ... and the related (eye.["ocular"]) structures are subject to hemmorhage and increased pressure on sensitive tissues, swelling and, consequently , irreversible loss in functionality. Any of the various clinical manifestations of central nervous and ocular diseases is possible.
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-->
potentially reduction in chamber size (and thus, reduction in volume of ejected blood)
malalignment of valve component parts (and thus, decreased efficency of ejected blood volume, further damage to heart muscle, "murmurs", electrical conduction abnormalities ("arrythmias")).
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.
Increased pressure within the vessels supplying blood to the eyes
Intraocular ("inside the eyeball") swelling
Intraocular hemorrhage
Retina detachment
Glaucoma
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
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)
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.
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:
Pupils may remain dilated and non-responsive to a bright light source or other visual stimuli.
The animal bumps into objects or exhibits reluctance to navigate normally in the home or outdoors
Using a Opthalmascope, your veterinarian may notice intraocular (within the eyeball..or within the "globe") abnormalities such as altered vessel morpholgy, swelling and inflammation, retina-detachment and/or hemorrhage.
Increased pressure within the globe (as measured with an instrument named a "tonometer"), if present, indicates that glaucoma is present.
Cardiovascular: Damage to heart muscle is exacerbated by damage to the vessels supplying the heart with blood. The result can be quite variable, from catastrophic to insidious:
Arrythmias
Murmurs
Sudden collapse and death
Sluggish, inappetant, respiratory distress /cough, non-specific gastroenteritis, pale mucus membranes, poor pulse, weak
Thromboembolic/Vascular "Accident"
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)
Animals may present acutely and near death as a clot forms in and obstructs the major vessels of the lung or heart, respectively.
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.
Central Nervous System:....The Brain: Signs of brain dysfunction secondary to hypertension relate to increased intracranial pressue, hemorrhage and "vascular accidents" within the small, boney structure in the head...the cranium..where the brain normally rests.
Loss of Normal Motor Function:
lameness, altered gait or posture, loss of prehension, mastication and swallowing,capabilities decreased blinking,
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.
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.
Direct:
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.
Indirect:
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:
Medications which Slow Heart Rate
Beta-blockers: The heart rate is determined, in part, by the action of neurotransmitter molecules such as norepinephrine, epinephrine ('Adrenalin") and others which act on the heart at sites known as beta-adrenergic receptor molecules> the interaction of these neurotransmitters with these receptor trigger a sequence of of electromechanical events...the end result of which is a more rapid heart rate.
A beta-blocker is a drug that can physically block or in some other way interfere with the binding and subsequent activation of muscle cell activity by neurotansmitters at beta-receptor sites.
Examples: Propanolol (Inderal® ), Atenolol (Tenormin® ), others
Calcium Channel blockers: The rate and force of contraction by heart muscle is determined in a number of ways by electromechanical events, namely the movement of charged particles ("ions", such as Ca+2 , Na+ and K+....calcium, sodium and potassium ions, respectivley) across nerve and muscle cell membranes.
Organized movements of charges through designated membrane "channels stimulates "firing" of nerve cell impulse that
cause release of neurotransmitter at nerve-muscle junctions that then acts to stimulate muscle electromechanical activity in a similar fashion.
Among the effects of muscle- membrano-electropotential stimulation are 1) more rapid firing at "pace-maker" sites (these are named the SA and AV Nodes)....producing an increase in the heart rate , and 2) the concurrent calcium ion uptake and also movement and release of calcium ion stores from certain compartments within the muscle cells . This intracellular calcium ion store is required for contractile activity of the specialized muscle contractile proteins. Its availability to contractile muscle proteins results in more forceful muscle contracts.
Calcium Channel blockers slow the movement of calcium ions through membrane calcium ion channels:
Thus drugs which block the movement of calcium through membrane calcium channels will reduce both the heart rate and the force of contraction...diminshing cardiac output (that is our goal...right?)
Examples: Diltiazem (Cardizem® ), Captopril (Capoten® )
ACE-Inhibitors : The "ACE..." in ACE Inhibitor stand for Angiotensinogen Converting Enzyme . This enzyme is normally responsible for the conversion of presursor molecules to a substance known as Angiotensin II. This latter substance has many, many physiological effect (too many to discuss here). Within the context of this subject, suffice it to state that Angiotensin II has profound effects on the neurotransmitter(s) that stimulate the heart. Logically, then, it follows that ACE Inhibitors would result in reduced cardiac stimulation, with resultant lowering of CO.
Examples: Enalapril, (Enacard® , Vasotec® ), Linisopril,Benazepril (Lotensin® )
*Another, newer class of drugs that block the action (rather than the synthesis) of angiotensin II may become useful in veterinary medicine soon
Medications which Reduce Blood Volume (thus amount of blood ejected from the heart [.....and also decrease TPR])
ACE inhibitors: Yes, the one and the same as above. Remember, I said the Angiotensin II has many functions. Oneof which is to promote the retension of sodium and water by the kidneys (thus increasing blood volume)
Diuretics: These drugs specifically direct the net flow of fluid from the body, usually by promoting enhancement of fluid losses though the kidney.
Reduce TPR
Reduce Blood Volume
ACE inhibitors
Diuretics
Vasodilators (Enlarge vessels' diameter/radius; see here for rationale)
Vasospecific Calcium Channle Blocker: There are calcium channel blockers that act on vascular smooth muscle...rather than heart muscle...in a manner similar to that described above. The drugs block calcium ion movement across membranes associate with muscle that surround vessels (with minimal activity on cardiac muscle Ca+2 flux.). The effect of calcium movement blockade on vascular musculature is vessel dilation (increase in vessel diameter/ radius). As discussed in detail on this web site, even a small magnitude increase in vessel diameter can have a profound decrease in peripheral resistance.
Example: Amlodipine (Norvasc® ),
Non-Vasospecific Agents:
ACE Inbibitors: Back again! Probably work by reduction in availability of vascular smooth muscle- stimulating-neurotransmitters...net effect is vessel relaxation (increase in diameter/ radius)
Miscellaneous: Many different drugs...nitroglycerin, other classes of mediciation with vasodilatory effects
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