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Physiology 2 > March 5 - Blood Pressure > Flashcards

March 5 - Blood Pressure Flashcards

1
Q

What are three factors that are important for the regulation of the mean arterial pressure?

A

Cardiac output
Total peripheral resistance
Blood volume

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2
Q

Why is MAP important?

A

MAP maintains the driving force for propelling blood to the tissues. If MAP is too high, extra work is created for the heart and it may also cause vascular damage

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3
Q

What is MAP, mathematically?

A

MAP = CO x TPR

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4
Q

Total peripheral resistance is a function of what?

A

The radius of arterioles

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5
Q

What determines the radius of arterioles?

A

Radius (r) is largely determined by sympathetic stimulation to the arterioles and local metabolic/chemical controls. It is also controlled by hormonal influence

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6
Q

What influences blood volume returning to the heart?

A

Effective circulating blood volume influences the blood volume returning to the heart, and depends on capillary function (bulk-flow fluid shifts)

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7
Q

What controls MAP?

A

Mean arterial pressure is controlled by long-term and short-term measures

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8
Q

What influences cardiac output?

A

Heart rate

Stroke volume

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9
Q

What influences heart rate?

A

Parasympathetic activity

Sympathetic activity and epinephrine

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10
Q

What influences stroke volume?

A

Sympathetic activity and epinephrine

Venous return

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11
Q

What influences venous return?

A 
Sympathetic activity and epinephrine
Blood volume
Respiratory activity
Skeletal muscle activity
Cardiac suction effect
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12
Q

What influences blood volume?

A

Passive bulk-flow fluid shifts between vascular and interstitial-fluid compartments
Salt and water balance (influenced by vasopressin and the RAAS)

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13
Q

What influences total peripheral resistance?

A

Arteriolar radius

Blood viscosity

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14
Q

What influences the blood viscosity

A

The number of red blood cells

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15
Q

What influences arteriolar radius?

A

Local metabolic control

Extrinsic vasoconstrictor control

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16
Q

What influences local metabolic control?

A

Skeletal muscle activity

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17
Q

What influences extrinsic vasoconstrictor control?

A

Sympathetic activity and epinephrine

Vasopressin and angiotensin II

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18
Q

What is the baroreceptor reflex?

A

The baroreceptor reflex is a short-term mechanism for regulating blood pressure. These mechanical stretch sensors are found int he carotid lumen and aortic arch. It involves afferent and efferent pathways. The afferent pathways bring stretch info to the CV control centre (CCC-integrates) in the brain’s medulla

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19
Q

What are baroreceptors sensitive to?

A

These receptors are sensitive to fluctuations in arterial pressure and pulse pressure.

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20
Q

What does the CCC do?

A

The CCC alters the ratio of sympathetic and parasympathetic activity to the heart and blood vessels

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21
Q

What are the effector organs?

A

The heart and blood vessels are the effector organs that respond to control blood pressure

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22
Q

Describe the baroreceptor reflex mechanism

A

Baroreceptors (BRs) generate a stream of action potential spikes to the afferents. The rate of firing changes according to the degree of mechanical stretch

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23
Q

How does the BR reflex respond to an increase of blood pressure to above normal levels?

A

If there’s an increase in blood pressure, the carotid-sinus and arotic-arch receptor potential increases, which increases the rate of firing in afferent nerves. This is transmitted to the cardiovascular centre, which results in a decrease in sympathetic cardiac-nerve activity and sympathetic vasoconstrictor-nerve activity, as well as an increase in parasympathetic nerve activity. The heart rate slows down, stroke volume decreases and there is vasodilation of the arterioles and veins. Cardiac output and total peripheral resistance decreases and blood pressure decreases towards normal

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24
Q

How does the BR reflex respond to a decrease in blood pressure to below normal levels?

A

If there’a an decrease in blood pressure, the carotid-sinus and aortic-arch receptor potential decreases, which decreases the rate of firing of the afferent nerves. This is transmitted to the cardiovascular centre, which results in an increase in sympathetic cardiac-nerve activity and sympathetic vasoconstrictor-activity, as well as a decrease in parasympathetic nerve activity. The heart rate speeds up, the stroke volume increases and there is vasoconstriction of the arterioles and veins. Cardiac output and total peripheral resistance increase, and blood pressure increases towards normal

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25
Q

What are other reflexes that influence blood pressure?

A
  1. Atrial volume and hypothalamic osmoreceptors are important for water and salt balance (plasma; long-term)
  2. Carotid and aortic arch chemoreceptors are sensitive to low oxgyen and high [H+] in the blood. Increases respiratory activity to reverse these trends (increased AP burst into CCC)
  3. Emotions: emotive input from the cerebral cortex/hypothalamus (high level CNS function) influence CV responses (e.g., fight or flight, blushing, etc.)
  4. Exercise centres (discrete) in the brain. Causes increased cardiac output, flow to muscles, fall in TPR, increased MAP, reinforced by afferents from the chemoreceptors
  5. Hypothalamic control over arterioles in the skin to eliminate excess heat
  6. Endothelial release of vasoactive substances (nitric oxide)
  7. Vasoactive neurotransmitters
26
Q

What are chronic problems associated with the regulation of blood pressure?

A

Primary and secondary hypertension

Prehypertension

27
Q

What is primary hypertension?

A

90% of all hypertension is primary hypertension. What is referred to as primary hypertension may actually be a group of multi-gene diseases. It is also referred to as idiopathic hypertension

28
Q

What is secondary hypertension?

A

Hypertension that is secondary to other primary problems, such as cardiovascular, renal, endocrine, and neurogenic secondary hypertension

29
Q

What causes cardiovascular secondary hypertension?

A

Elevated TRP caused by CAD aka narrowing of the artieres

30
Q

What causes renal secondary hypertension?

A

Occlusion of renals leads to elevated release of angiotensin and retention of salt and water with vasoconstriction

31
Q

What causes endocrine secondary hypertension?

A

Phaechromocytoma - adrenal medullary tumour as well as Conn’s syndrome wherein the adrenal cortex produces too much aldosterone which leads to salt and water retention

32
Q

What causes neurogenic secondary hypertension?

A

Lesions in the CCC or baroreceptors or in response to a chronic decrease in the blood flow to the brain

33
Q

What is prehypertension?

A

Blood pressure between normal and overtly hypertensive - 120/80 and 139/89. It is managed without medication

34
Q

What causes primary hypertension?

A

It may be due to: salt mismanagement, defective plasmalemmal Na/K pumps, inappropriate stimulation of the CCC, abnormal expression of components of the renin-angiotensin axis, altered regulation of NO, endogenous digitalis-like substances, abnormal vasopressin production

35
Q

Primary hypertension contributes to what?

A

It contributes to atherosclerosis, congestive heart failure with cardiac hypertrophy, stroke, and multiple organ failure due to small vessel damage.

36
Q

What don’t baroreceptors lower the blood pressure in hypertension?

A

Baroreceptors don’t help correct blood pressure in chronic hypertension, because they reset themselves to read high blood pressure as the norm. They then effectively maintain blood pressure at a higher level

37
Q

Describe low blood pressure or hypotension?

A

Abnormally low blood pressure occurs with disproportionate vascular capacity or reduced cardiac output

38
Q

What is orthostatic hypotension?

A

Orthostatic hypotension (“head rush”) results from transient inadequate sympathetic activity as one stands up after extended periods of watching TV on the couch

39
Q

How do emotions affect hypotension?

A

Emotional stress may cause a decrease in sympathetic output to the vasculature. Squirrels, gophers “play dead”: may be adaptive response

40
Q

What is circulatory shock?

A

Blood pressure is so low that inadequate blood flow results in tissues

41
Q

What are the four main types of circulatory shock?

A

Hypovolemic (caused by a fall in blood volume - hemorrhage)
Cardiogenic - due to a weakened heart
Vasogenic - From widespread vasodilation due to a release of vasodilator substances, including: septic (massive infection), anaphylactic (extensive histamine (vasodilation) release due to generalized allergic reaction)
Neurogenic - from widespread vasodilation due to “crashing” decrease of sympathetic tone (extreme pain can cause this)

42
Q

Describe the pathway for compensatory events in response to shock (hemorrhage, which leads to decreased blood volume, cardiac output, and MAP)

A
  1. Reduced firing by the baroreceptors
  2. Integration of the signal in the CCC
  3. CCC modulates increased sympathetic and decreased parasympathetic output to the heart and periphery
43
Q

CCC integration and output yields what?

A

Decreased parasympathetic neuron activity to the heart, increasing the heart rate and the cardiac output
Increased sympathetic output to the heart increases cardiac contractility, stroke volume and cardiac output
Increased sympathetic output to the veins and arterioles leading to arteriolar and venous vasoconstriction, increasing TPR (increases blood pressure) and venous return (increases stroke volume and cardiac output)

44
Q

What are other factors that operate the mediate blood pressure?

A

Decreased capillary blood pressure leads to reduced filtration and increased reabsorption in capillary beds, thus fluid shifts from the interstitium to the plasma volume and increasing cardiac output.
Also reduced blood flow to the kidneys causes conservation of plasma volume. Activation of release of angiotensin and vasopressin causes salt and water retention

45
Q

How do parasympathetics affect the heart?

A

They decrease the heart rate, which decreases cardiac output, which decreases blood pressure

46
Q

How do sympathetics affect the heart?

A

They increase heart rate. They increase contractile strength of the heart, which increases stroke volume. All this increases cardiac output, which increases blood presssure

47
Q

How do sympathetics affect the arterioles?

A

They increase vasoconstriction, which increases total peripheral resistance, which increases blood pressure

48
Q

How do sympathetics affect the veins?

A

They increase vasoconstriction, which increases venous return, which increases stroke volume, which increases cardiac output, which increases blood pressure

49
Q

What supply’s the heart with blood for oxygen and nutrient delivery?

A

The heart receives most of its blood supply through the coronary circulation during the rest phase (diastole)

50
Q

What causes vasodilation of the coronary arteries? What is the result?

A

Adenosine is critical for coronary vessel dilation. Vasodilation of the coronaries leads to increased delivery of blood. Normally the heart removes 65% of the oxygen available in the blood (higher than other tissues)

51
Q

What is CAD?

A

Pathology of coronary artery disease = atherosclerosis and it blocks coronaries leading to ischemia (lack of oxygen)

52
Q

Ischemia occurs by what three mechanisms?

A

Vascular spasm of coronary arteries
Atherosclerotic plaques plug the coronary lumen
Thromboembolism

53
Q

What causes vasospasm?

A

Reduced oxygen leads to release of platelet activating factor (PAF) which causes vascular smooth muscle cell (VSMC) contraction in coronary arteries

54
Q

What causes atherosclerosis?

A

Begins with the development of atheromas = benign tumours of VSMC’s. These cells are motile and migrate to just below the endothelial layer in the vessel wall. They accumulate cholesterol and lipids (and fibroblasts). When calcium also accumulates in these regions, if forms a bone-like plaque

55
Q

What is a thrombus?

A

Enlarged plaques break through the endothelial layer, causing platelets to aggregate and bind to underlying collagen in the vessel wall

56
Q

What is thromboembolism?

A

The term used when the thrombus breaks fress and results in the sudden occlusion of a coronary.

57
Q

What are HDL?

A

Cholesterol protein complex. Has the most protein and the least cholesterol. It moves cholesterol to the liver for elimination (“good” cholesterol)

58
Q

What is LDL?

A

Cholesterol protein complex. Less protein and more cholesterol than HDL. Transported to cells (“bad” cholesterol”)

59
Q

What is VLDL?

A

Cholesterol protein complex. Has the least protein and the most cholesterol (“bad” cholesterol)

60
Q

What causes the uptake of bad cholesterol?

A

Uptake of bad cholesterol by cells occurs via LDL receptors. When non-liver cells require cholesterol. They synthesize LDL receptors, endocytose LDL and lyse the lipoprotein to yield free cholesterol

Physiology 2 (19 decks)

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