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Cardiovascular Response to Stressor

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Cardiovascular Response to Stressors (Chapter 26)

 

Objectives

  • Describe the response to postural change: Postural Hypotension
  • Describe the effect of increased intrathoracic pressure - The Valsalva Maneuver
  • Explain the effects of blood loss (hemorrhage) including compensatory and decompensatory mechanisms
  • Describe the cause of fainting (vasovagal syncope)
  • Illustrate the sequence of cardiovascular events during exercise

 

On a daily basis the cardiovascular system must respond to a number of external influences and internal changes that include gravity, exercise, hemorrhage, and others. The objective is to maintain adequate perfusion of tissues. The mechanisms used to achieve this objective are those described previously.

 

  • Response to Postural Change: Postural Hypotension

 

    • Gravity effects on Cardiovascular Parameters

A change in body position from lying to standing imposes a gravity effect on the body. The heart, previously located at the same height as the rest of the body, is suddenly elevated about 120 cm above the feet and about 40 cm below the top of the head. About 500-700 ml of blood settle quickly to the lower extremities resulting in a decrease in venous return (~ 20%), stroke volume (~40%), and cardiac output (15-20%). Remarkably, aortic mean pressure remains almost unchanged because heart rate and total peripheral resistance rise.

 

The cardiovascular system, especially the capillaries and veins, is highly compliant. The added weight of the column of blood from the heart to the veins in the feet adds nearly 90 mmHg of pressure to the veins of the feet because of gravity. Nevertheless, the driving pressure moving blood back toward the heart is unaffected by gravity because the increases in pressure on the arterial and venous sides are the same.

 

The resulting increase in transmural pressure increases filtration of fluid from the capillaries and passively dilates the veins. In a normal person the effect of gravity can produce a further loss of 500 to 700 ml of fluid from the vascular system.

 

If uncompensated, standing may result in hypotension. This phenomenon is commonly referred to as orthostatic hypotension; if the effect is transitory, the term postural hypotension is preferred.

 

 

    • Compensatory mechanisms that minimize postural hypotension

Postural hypotension is an occasional occurrence in normal people. It accounts for the brief, dizzy feeling occasionally felt on standing too suddenly. However, a number of anatomical and reflex mechanisms minimize the gravity effects on blood flow.

 

Venous valves interrupt the column of blood in the veins, limiting the gravity effect to the height of the blood between valves and reducing the intravascular pressure in veins and capillaries.

 

Skeletal muscle contractions usually accompany the postural changes, especially in the lower extremities. The rhythmic cycles of reflex contraction and relaxation muscle pump action propels blood toward the heart. During contraction blood is squeezed out of the veins in an upward direction, and during relaxation veins refill from below. The muscle pump also increases the flow of lymph out of the tissue and back to the venous system (Fig. 1).

 

Circulating blood volume is usually adequate. Pooling, or loss, of small amounts of blood does not seriously compromise venous return.

The baroreceptor reflex initiates a chain of events that compensate for gravity. An initial reduction of venous return, cardiac output, and arterial pressure triggers a baroreceptor mediated decrease in parasympathetic activity and an increase in sympathetic output. Increased sympathetic output has a number of effects including:

      • increased heart rate.
      • general arteriolar constriction - reducing capillary pressure and favoring capillary reabsorption.
      • general venous constriction - reducing venous compliance and limiting the gravity induce stretch of veins - also favoring venous return.
      • reduced blood flow to splanchnic, renal, and skeletal muscle beds producing autotransfusion of blood into the circulation.
      • stimulation of the adrenal medulla with resulting release of epinephrine and norephrine into the circulation further mimicking sympathetic stimulation.
      • stimulation of release of angiotensin II, aldosterone, and antidiuretic hormone that have the effect on the kidney to retain salt and water in the body. This effect, which requires hours to days to be effective, increases the vascular volume.

 

A Cerebral Ischemic Response produces peripheral vasoconstriction and fainting if CNS blood flow is inadequate to maintain nervous system function.

 

    • Pre-existing conditions that exacerbate orthostatic hypotension
      • α-adrenergic blockade or generalized sympathetic blockade
      • Varicose veins
      • Lack of skeletal muscle activity due to paralysis or forced inactivity
      • Reduced circulating blood volume, secondary to hemorrhage, blood donation, prolonged weightlessness, prolonged bed rest, vomiting, diarrhea, etc.
      • Heat - the mechanisms that compensate for high body temperature, increased blood flow to the skin and sweating, both involve increasing, rather than decreasing flow to the legs and arms, in opposition to the mechanisms compensating for orthostatic hypotension

 

  • Increased Intrathoracic Pressure - The Valsalva Maneuver

The Valsalva maneuver is produced by a sudden increase in intrathoracic pressure. It is carried out by forcibly attempting to exhale against a closed airway. This is done daily at stool.

 

The cardiovascular responses to the Valsalva maneuver are shown in the diagram below. The responses are primarily due to the elevated intrathoracic pressure and the effect that has on elevating central venous pressure and reducing venous return to the right heart.

Four distinct phases can be seen in the blood pressure response to the increased intrathoracic pressure (Fig. 2 upper). Phase I begins with the onset of elevated intrathoracic pressure. An increase in arterial pressure is noted because although the venous return to the right heart is reduced, the increased intrathoracic pressure briefly favors return of blood from the lungs to the left heart with a brief increase in left heart output as the result.

 

In Phase II arterial pressure falls. Intrathoracic pressure has limited return to the right heart and subsequently reduced right cardiac output and left venous return.

 

Phase III represents the release of intrathoracic pressure and the return to normal. Initially arterial pressure remains low because blood returns to the left heart remains suppressed although return to the right heart has increased above normal.

 

However, releasing intrathoracic pressure allows the blood pooled in the peripheral veins to return to the right heart in greater than normal volumes. Eventually, this excess venous return is pumped by the right heart through the lungs to the left heart. During Phase IV left heart venous return is elevated and expelled as increased cardiac output. The arterial pressure increases, both pulsatile pressure and mean pressure, until the excess venous return has been pumped through the system.

 

Fig. 2 (lower) depicts the heart rate changes that occur throughout the Valsalva maneuver. The changes in heart rate largely reflect the baroreceptor response to the arterial pressure changes directly induced by the intrathoracic pressure changes.

 

Altered responses to the Valsalva maneuver in various circumstances

      • If the sympathetic nervous system is blocked, the heart rate changes resulting from the Valsalva maneuver will not be seen.
      • In people with congestive heart failure the Valsalva maneuver may demonstrate reduced or absent results. Congestive heart failure is associated with large increases in circulating blood volume and high venous pressures. High intrathoracic pressure may not be adequate to prevent venous return under these circumstances.

 

  • Hemorrhage

The circulatory responses to hemorrhage are instructive in that the same reflexes and responses that may have compensatory effects under some circumstances may have negative effects under others. The body has a limited range of responses, not all of which may helpful in every situation.

 

Hemorrhage occurs when blood is lost from the vascular system by any means. The cardiovascular effects are similar regardless, whether blood lost from the circulation by say: knife or bullet wounds, trauma, internal abdominal bleeding caused by trauma or ulcer, subcutaneous bleeding secondary to radiation exposure, and other causes. The primary effect on the vascular system is the reduction of blood volume and resulting decrease in venous return and cardiac output. Tissue perfusion may ultimately suffer.

 

The impact of hemorrhage on the vascular system depends on the extent of blood loss. A loss of 5 to 10% of blood volume (250-500 ml) will usually produce no change in arterial pressure and result in spontaneous recovery. A loss of 15 to 20% of blood volume may reduce arterial pressure to the range of 80-90 mmHg. More substantial loss (20 to 30%) may reduce arterial pressure to 60-80 mmHg, with signs of early cardiovascular shock - usually reversible. Larger losses (30 to 40%) reduce arterial pressure to 50-70 mmHg and frequently result in irreversible shock if not corrected promptly.

 

The involvement of compensatory mechanisms is similarly dependent on the extent of hemorrhage. With any significant blood loss, the reduction of venous return limits cardiac output and reduces arterial pressure. The baroreceptor reflex is activated and increases sympathetic output, especially increasing arterial resistance in the splanchnic bed. The shift of blood flow allows maintenance of arterial pressure and adequate blood flow to other tissues.

 

More severe reduction of venous return – through the baroreceptor reflex and sympathetic stimulation – results in increased heart rate and contractility along with further increases in peripheral vascular constriction of both resistance and capacitance vessels to maintain blood pressure. The elevated sympathetic output has additional effects. Capillary hydrostatic pressure, already reduced by the hemorrhage, will be reduced even further by the arteriolar constriction. These changes favor reabsorption of fluid from the interstitium into the blood stream. Constriction of skin blood vessels leads to a cool, pale skin. Reduction of renal blood pressure will increase circulating levels of angiotensin II, aldosterone, and antidiuretic hormone, promoting retention of salt and water in the body. Reduced atrial pressure will also increase the level of antidiuretic hormone via the cardiopulmonary receptors. Stimulation of thirst will also promote restoration of circulating blood volume.

With more severe blood loss these compensatory mechanisms may become harmful. The attempt to maintain arterial pressure by the baroreceptor reflex may reduce tissue perfusion below critical levels. The splanchnic bed may become severely ischemic, even necrotic. Blood flow to skeletal muscle and kidney may be severely reduced. The kidney may fail due to lack of blood flow. Under these circumstances the cardiovascular system may fail to compensate, even if the original blood volume is restored. Fig. 3 illustrates the onset of cardiovascular shock.

 

In this experiment, blood was withdrawn for nearly two hours. The expected reductions in blood pressure and cardiac output were seen along with a compensatory increase in heart rate. After about 2.5 hours the blood volume was restored, resulting in improvement in blood pressure and cardiac output. Yet over time, with no further intervention, blood pressure and cardiac output again fall, leading to irreversible shock and death.

 

The subject of cardiovascular shock is multifactorial and will be discussed near the end of this course. Yet the underlying difficulty relates to the fact that the cardiovascular system has limited control mechanisms, e.g. baroreceptor reflex, at its disposal. The reduction of blood pressure initiates the only possible response, elevated sympathetic output. This response may successfully maintain arterial pressure, but in severe situations blood pressure maintenance is accomplished at the expense of tissue perfusion. The resulting tissue damage may lead to irreversible shock.

 

  • Fainting (syncope)

Fainting is the loss of consciousness consequent to cerebral ischemia from either “organic” or “functional” causes. Organic causes include cerebral arterial sclerosis, orthostatic hypotension, supraventricular tachycardia, α adrenergic blockade and others.

 

Ordinary fainting (vasovagal syncope) is caused by massive sympathetic inhibition from the hypothalamic cardio-inhibitor center. Onset may be sudden with a marked slowing of the heart (bradycardia), decrease in mean arterial pressure and a decrease in pulse pressure. These effects may occur within seconds and cause unconsciousness (Fig. 4). Often fainting is triggered by an emotional shock. Predisposing factors include: blood withdrawal, prolonged bed rest, diarrhea or prolonged standing in a hot atmosphere.

(Reprinted from circulatory Physiology-the essentials 2nd ed.,(1984) by J.J.Smith & J.P. Kampine, Figure13.1, page 262, Lippincott, Williams & Wilkins.)

 

Exercise

    • The circulatory response to exercise includes the following:

 

      • Increased sympathetically-mediated chronotropic and inotropic stimulation of the heart. At moderate work-rates, cardiac output increases because of an increase in heart rate and stroke volume. At higher work-rates, heart rate increases to the point that ventricular filling time is compromised. Inadequate ventricular filling reduces stroke volume. As a result cardiac output increases no further, and may actually decrease.
      • Increased sympathetic stimulation of the vascular smooth muscle promotes vasoconstriction and venoconstriction throughout much of the body. Major exceptions are:
        • brain and heart – whose blood supplies are scarcely influenced by alpha adrenergic stimulation;
        • muscle – α-1 adrenergic stimulation promotes arteriolar constriction in all muscle. However, in working (active) muscle, the vasoconstriction is overcome by the local release of metabolites (CO2, H+, K+, adenosine) that elicit vasodilatation;
        • skin – during exercise, provided body temperature remains unelevated, α-1 adrenergic stimulation decreases blood flow to the skin. As core body temperature rises, hypothalamic stimulation initiates sweating and increased blood flow to the skin surface.
      • Increased vasoconstriction in the viscera, the skin, and non-active muscle decreases net filtration pressure in these tissues. As a result, reabsorption of interstitial fluid occurs in these tissues, making additional blood volume available for perfusion of active muscles.
      • Increased venoconstriction shifts venous blood into the heart and arteries, making it available for increased perfusion of the active tissues.

      • The increased β-1 stimulation of the heart and α-1 stimulation of the vasculature cause mean arterial pressure to be maintained (perhaps increase slightly) in spite of a large decrease in total peripheral resistance caused by dilation of the vascular beds of working muscles.

 

    • Circulatory variables during exercise as a function of work load

 

Systolic pressure increases during exercise because cardiac output (SV x HR) increases more than the fall in total peripheral resistance (Fig. 5).

 

Locally produced metabolites produce dilation of arterioles in working muscles. This opens (recruits) many previously closed capillaries, lowering resistance to flow. The combination of an elevated systolic and a relatively constant diastolic pressure produces an increased pulse pressure.

 

The absence of an increase in end-diastolic volume during exercise indicates that the “Frank-Starling” mechanism is not an important factor for increasing the force of ventricular contraction during exercise. First, the decreased filling time prevents the end diastolic volume from enlarging greatly. Secondly, the increased contractility causes a large proportion of the end-diastolic volume to be ejected during systole.

 

    • Factors that limit exercise performance:

The inability to deliver additional O2 to the working muscle limits power (work per unit time) and duration of exercise. Factors contributing to this limitation include:

 

      • Lactic acidosis develops consequent to anaerobic metabolism and decreases the cardiac response to sympathetic agonists. The sensation of fatigue is also correlated with the degree of acidosis.
      • If blood pressure starts to fall during strenuous exercise (because of inadequate cardiac pumping), the vasomotor center initiates additional vasoconstriction throughout the body - even in the working muscle. This slightly decreases delivery of O2 to the working muscle limiting muscle performance.

 

    • Changes that occur with physical training and conditioning:

 

      • Training increases the amount of O2 that can be delivered to working muscle, primarily by improving pulmonary and cardiac function.
      • Training increases both the resting and exercising stroke volume (ejection fraction), due to a small hypertrophy of the ventricles as well greater force of contraction. Resting heart rate decreases keeping cardiac output constant. The maximum achievable heart rate does not increase with training. However, because potential stroke volume is increased, the maximum achievable cardiac output is increased.
      • Because in trained muscles capillary recruitment is increased, diffusion distance from capillary to cell is reduced and O2 is more easily and thoroughly extracted from the blood.
      • In cardiac muscle, the number of mitochondria, the activity of oxidative enzymes, and myosin ATPase increase in response to training.
      • The left ventricle hypertrophies more in response to strength-training than to endurance-training.

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