Hypotension

Chapter 6 Hypotension



Jeffery P. Simmons, DVM, MS, DACVECC, James S. Wohl, DVM, MPA, DACVIM, DACVECC



Key Points



• Blood pressure is a combination of the effects of various elements. These include heart rate, stroke volume, and systemic vascular resistance.

• Hypotension occurs when at least one of the controls of blood pressure is overcome or neutralized.

• Treatment of hypotension involves treating the underlying cause and targeting the patient’s normal control mechanisms.


INTRODUCTION


Hypotension, or low arterial blood pressure, is not a disease. Instead, hypotension is a clinical manifestation of many different diseases. Although a wide variety of diseases can cause hypotension, it results from a failure of common regulatory mechanisms. Understanding these mechanisms helps to guide the diagnosis and treatment of hypotensive disorders.



COMPONENTS OF BLOOD PRESSURE



Physiology of Blood Pressure


Blood pressure is the force that the flow of blood puts on the walls of the vessels. The three measurements of arterial blood pressure are systolic arterial pressure (SAP), diastolic arterial pressure (DAP), and mean arterial pressure (MAP). SAP and DAP measurements correspond to the respective phase of the cardiac cycle. MAP equates to overall pressure throughout the cardiac cycle. Because most of the cardiac cycle is spent in diastole, so too most of the mean blood pressure is affected by the diastolic blood pressure. This can be demonstrated by one of the formulas used to calculate MAP: MAP = ([SAP − DAP] ÷ 3) + DAP. When considering the perfusion pressure of organs, the MAP is more important than either SAP or DAP.1,2 However, coronary perfusion occurs during diastole.


The cardiovascular determinants of blood pressure are cardiac output and systemic vascular resistance (SVR). Therefore blood pressure can be represented by the following formula:



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where BP is blood pressure, CO is cardiac output, and SVR is systemic vascular resistance. Cardiac output is the product of the heart rate and the stroke volume (CO = HR × SV). Stroke volume is the amount of blood ejected with each heartbeat and is affected by the preload, contractility, and afterload.1Vascular resistance refers to the effects of vascular tone and blood viscosity on flow through a blood vessel. Resistance to blood flow through a vessel increases as the blood becomes more viscous and as the vessel becomes more constricted. Thus hypotension is typically the result of a decrease in the heart rate, stroke volume, the systolic vascular resistance of the entire arterial vasculature, or, more commonly, a combination.2



Pathophysiology of Blood Pressure


Within physiologic limits, neural, hormonal, and local metabolites regulate the control of systemic blood pressure. All blood vessels containing smooth muscle are innervated by fibers of the sympathetic arm of the autonomic nervous system. Sympathetic fibers innervating resistance vessels are noradrenergic and vasoconstricting in function, except in the skeletal muscle, where sympathetic fibers are cholinergic and vasodilatory. Noradrenergic fibers course through the adventitia of arterioles and release the neurotransmitter norepinephrine in a persistent or tonic fashion. Intracellular events following receptor binding of norepinephrine result in contraction of the smooth muscle. Constriction of resistance vessels is mediated by an increase in the frequency of sympathetic noradrenergic release of norepinephrine. In contrast, vasodilation results from a decrease in the rate of tonic sympathetic discharge of norepinephrine.1-3


Sympathetic noradrenergic innervation of cardiac muscle mediates increases in heart rate (chronotropic effect) and force of contraction (inotropic effect). Cholinergic fibers carried in the vagus nerve mediate a decrease in heart rate and oppose the chronotropic effects of sympathetic discharge. Both sympathetic and vagal fibers discharge in a tonic fashion, although vagal tonic discharge predominates at rest.1,2


The rate of tonic sympathetic discharge is controlled by a group of neurons in the medulla oblongata called the vasomotor center. Vasomotor center neurons activate sympathetic preganglionic neurons on the intermediolateral gray matter of the spinal cord. These fibers leave the spinal cord and converge at sympathetic ganglia. Postganglionic nerves arise from the sympathetic ganglia and terminate in the adventitia of blood vessels. Stimulation of vasomotor center neurons occurs directly during hypoxia and hypercapnia. The resultant increase in sympathetic tonic discharge leads to a rise in systemic blood pressure.


The vasomotor center receives afferent fibers from arterial and venous baroreceptors and from carotid and aortic chemoreceptors. Baroreceptors are stretch receptors located in the left atrium, aortic arch, and carotid sinus. Upon distention or increased pressure in these structures, baroreceptor discharges are increased, leading to inhibition of the sympathetic nervous system and activation of the parasympathetic nervous system. This results in vasodilation, bradycardia, and a decrease in contractility in an attempt to decrease MAP. Conversely, when hypotension is present, the rate of baroreceptor discharge decreases, and this minimizes the inhibitory (vasodilatory) influence on the vasomotor center results in activation of the sympathetic nervous system and inhibition of the parasympathetic nervous system. This feedback system controls arterial blood pressure within physiologic limits of approximately 50 mm Hg and 150 mm Hg.3 Beyond these limits, the rate of baroreceptor discharge has been maximized or minimized, respectively, and cannot cause a further change in blood pressure.


Local hypoxia or hypercarbia (acidosis) resulting from arterial hypotension stimulates chemoreceptors in the carotid sinus and aortic bodies. Afferent fibers from the chemoreceptors stimulate the vasomotor center and result in vasopressor and tachycardic responses. The chemoreceptor feedback system is less important than the baroreceptor reflex for acute changes in blood pressure.4,5


Stretch receptors in the atria and pulmonary artery respond to distention of the venous system. Stimulation of these stretch receptors results in inhibition of the vasomotor center, vasodilation, and a decrease in blood pressure. Similar to what occurs with the baroreceptors of the arterial system, the absence of venous distention and increased atrial filling pressure removes this inhibitory influence on the vasomotor center.


Circulating hormones released during inflammation have vasodilating properties on resistance vessels.5,6 Adrenal medullary norepinephrine and epinephrine, vasopressin, and angiotensin II are examples of circulating hormones that have vasoconstricting properties on vascular smooth muscle. Metabolites derived from endothelial cells, inflammatory cells, and platelets exert a paracrine effect on vasomotor tone and can influence systemic blood pressure. Prostacyclin is a metabolite of arachidonic acid produced by endothelial cells. Prostacyclin inhibits platelet aggregation and causes vasodilation. Nitric oxide (NO) is a gaseous molecule derived from arginine within endothelial cells. There is a tonic production and release of NO in the presence of the calmodulin-dependent enzyme NO synthase in the cell membrane. This constitutive synthesis by NO synthase is in contrast to inducible production of NO by inducible NO synthase located in the cytosol. Inducible nitric oxide production occurs in response to inflammatory stimulation. Both forms of NO cause vascular smooth muscle relaxation by activating guanylyl cyclase. Various cytokines (interleukin [IL]-1B, IL-2, IL-6, tumor necrosis factor, and interferon-γ) and lipopolysaccharide derived from the cell membrane of gram-negative bacteria are also potent inducers of cytosolic NO synthase.6,7


Thromboxane A2 and endothelins are metabolites that cause vasoconstriction of vascular smooth muscle. Thromboxane A2 is synthesized from arachidonic acid in the presence of phospholipid A2 by platelets. In addition to facilitating platelet aggregation, thromboxane A2 is a vasoconstricting agent. Endothelins are a group of vasoconstricting polypeptides produced by endothelial cells. When administered intravascularly in experimental animals, endothelins produce an initial fall in blood pressure followed by a prolonged pressor response. Endothelins also have positive inotropic and chronotropic properties.


The baroreceptor-mediated increase in sympathetic output is the initial and most important physiologic response to hypotension. Although adrenal medullary secretion of catecholamines is increased, it is the local release of norepinephrine by postganglionic nerve fibers at the arteriolar level that is responsible for the generalized vasoconstrictor response. Vasoconstriction is greatest in the skin, kidneys, and viscera, shunting blood to the systemic circulation. The brain and heart experience vasodilation in an attempt to maximize blood flow to these vital organs. Increased circulating levels of angiotensin II, aldosterone, and vasopressin also assist the pressor response by direct vasoconstriction or expansion of intravascular volume (see Chapter 177, Vasopressin).


In refractory shock, hypotension persists despite physiologic compensation and an adequate intravascular fluid volume. Vascular spasm or extreme vasodilation of precapillary arterioles, blunting of vasomotor function due to prolonged cerebral ischemia, increased capillary permeability and fluid loss, and myocardial dysfunction result from persistent tissue hypoxia. Distributive (or vasogenic) shock, a common result of diseases such as sepsis or anaphylaxis, is associated with extreme vasodilation of some vascular beds and vasoconstriction in other tissues. Vasoplegia is the lack of responsiveness of blood vessels to physiologic regulatory mechanisms. Overproduction of NO, depletion of endogenous vasopressin, downregulation of catecholamine receptors, and disruption of vascular smooth muscle calcium metabolism are thought to be responsible for vasoplegia and refractory shock.


Cardiogenic causes for hypotension may also occur. This can occur with either primary or secondary cardiac diseases.1,3 Primary cardiac diseases occur when the pathologic process originates within the heart, as seen in dilated cardiomyopathy or third-degree atrioventricular block. Secondary cardiac diseases occur when pathology originates outside the heart, but either suppresses normal heart function or causes secondary sites of pathology in the heart. Diseases that induce systemic inflammatory response syndrome, for instance, may cause the release of cardiac suppressing factors or decrease the heart’s response to sympathetic nervous system stimulation.4

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Hypotension

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