Physiology Seminar (F1 17/11) Flashcards

1
Q

The first priority of blood pressure homeostasis is to maintain adequate profusion to what two organs?

A

The brain and the heart.

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2
Q

List the components of blood vessel walls and, in order from inner lining to outer covering, describe the importance of each component.

A
  1. Tunica intima: the thinnest layer in all blood vessels. It has a single layer of endothelial cells and is supported by a subendothelial layer of connective tissue and supportive cells. The tunica intima is surrounded by a thin membrane comprised of elastic fibers running parallel to the vessel.
  2. Tunica media: comprised of smooth muscle cells and elastic and connective tissues.
  3. Tunica externa: composed entirely of connective fibers and surrounded by an external elastic lamina which functions to anchor vessels with surrounding tissues.
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3
Q

Blood flow to individual tissues is regulated by selective vasoconstriction and dilation of which vessels?

A

arterioles

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4
Q

Aortic pressure reaches a typical high value of ______________ (give units) during ______________, or contraction of the heart. As the heart relaxes during the event called ______________ ,aortic pressure declines to a typical low value of ______________. This blood pressure reading would be written as______________/______________.

A
  • Aortic pressure reaches a typical high value of _120 hg (mercury)__ (give units) during __systole___, or contraction of the heart.
  • As the heart relaxes during the event called _diastole__ , aortic pressure declines to a typical low value of ______80 hg________.
  • This blood pressure reading would be written as______120________/_______80_______.
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5
Q

The rapid pressure increase that occurs when the ventricles push blood into the aorta can be felt as a pressure wave, or ____________. What is the equation used to calculate the strength of this pressure wave?

A
  • pulse/ pressure wave
  • pulse pressure = systolic pressure - diastolic pressure
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6
Q

List the factors that aid venous return to the heart.

A
  • one way valves in the veins
  • low pressure in the thorax during breathing?
  • Muscle contraction: skeletal muscle pump
  • Decreased venous compliance?
  • Respiratory activity: low pressure in the thorax during breathing?

Vena cava compression?

Gravity?

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7
Q

What is hypertension, and why is it a threat to persons well-being?

A

Chronic, elevated blood pressure can cause a weakened blood vessel to rupture and bleed. Can cause atheroscolorosis, MI, stroke.

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8
Q

What causes Korotkoff sounds, and when are you likely to hear them?

NEED MORE WORK ON THIS

A
  • The sounds heard during measurement of blood pressure are not the same as the heart sounds ‘lub’ and ‘dub’ that are due to vibrations inside the ventricles that are associated with the snapping shut of the valves. If a stethoscope is placed over the brachial artery in the antecubital fossa in a healthy person (without arterial disease), no sound should be audible. As the heart beats, these pulses are transmitted smoothly via laminar (non-turbulent) blood flow throughout the arteries, and no sound is produced.
  • Korotokoff sounds occur when cuff pressure is less than systolic pressure but higher than diastolic pressure.
  • If the cuff of a sphygmomanometer is placed around a patient’s upper arm and inflated to a pressure above the patient’s systolic blood pressure, there will be no sound audible. This is because the pressure in the cuff is high enough such that it completely occludes the bloodflow.
  • If the pressure is dropped to a level equal to that of the patient’s systolic blood pressure, the first Korotkoff sound will be heard. As the pressure in the cuff is the same as the pressure produced by the heart, some blood will be able to pass through the upper arm when the pressure in the artery rises during systole. This blood flows in spurts as the pressure in the artery rises above the pressure in the cuff and then drops back down beyond the cuffed region, resulting in turbulence that produces an audible sound.
  • As the pressure in the cuff is allowed to fall further, thumping sounds continue to be heard as long as the pressure in the cuff is between the systolic and diastolic pressures, as the arterial pressure keeps on rising above and dropping back below the pressure in the cuff.
  • Eventually, as the pressure in the cuff drops further, the sounds change in quality, then become muted, and finally disappear altogether. This occurs because, as the pressure in the cuff drops below the diastolic blood pressure, the cuff no longer provides any restriction to blood flow allowing the blood flow to become smooth again with no turbulence and thus produce no further audible sound.
  • There are five Korotkoff sounds:[4]

Phase I—The first appearance of faint, repetitive, clear tapping sounds which gradually increase in intensity for at least two consecutive beats is the systolic blood pressure.

Phase II—A brief period may follow during which the sounds soften and acquire a swishing quality.

Phase III—The return of sharper sounds, which become crisper to regain, or even exceed, the intensity of phase I sounds.

Phase IV—The distinct abrupt muffling of sounds, which become soft and blowing in quality.

Phase V—The point at which all sounds finally disappear completely is the diastolic pressure.

The second and third Korotkoff sounds have no known clinical significance.[5]

In some patients, sounds may disappear altogether for a short time between Phase II and III which is referred to as auscultatory gap.

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9
Q

List at least three paracrines that cause vasodilation. What is the source of each one? In addition to paracrines, there are two other ways to control smooth muscle contraction in arterioles what are they?

A

Vasodilator paracrines released from the vascular endothelium and from tissues include nitric oxide, H+, K+, CO2, prostaglandins, adenosine, and histamine. Low dissolved oxygen levels also cause vasodilation. Endothelins are powerful vasoconstrictors??

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10
Q

What is hyperaemia? How does active hyperaemia differ from reactive hyperaemia?

A

A region of increased blood flow

Active hyperemia is a process in which increased blood flow accompanies increased metabolic activity

Reactive hyperaemia is an increase in tissue blood flow following a period of low perfusion

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11
Q

Most systemic arterioles are innovated by the ____________ branch of the nervous system.

A

Sympathetic innervation causes vasoconstriction

The exception are arterioles in the brain.

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12
Q

Vasoconstriction of intestinal arterioles Vasodilation of coronary arterioles Increased heart rate Decreased heart rate Vasoconstriction of coronary arterioles

Match the events above with all appropriate neurotransmitter(s) and receptor(s) from the list below.

Norepinephrin Epinephrine Acetylcholine β1 receptor Α receptor β 2 receptor Nicotinic receptor Muscarinic receptor

A

Vasoconstriction of intestinal arterioles:

α receptor

Norepinephrin

Epinephrine

Vasodilation of coronary arterioles:

β 2 receptor

Norepinephrin

Epinephrine

Increased heart rate:

β1 receptor

Norepinephrin

Epinephrine

Decreased heart rate

Muscarinic receptor

Acetylcholine

Vasoconstriction of coronary arterioles

α receptor

Norepinephrin

Epinephrine

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13
Q

Which organs receive over two-thirds of the cardiac output at rest? Which opens at the highest flow of blood, on a per-unit weight basis?

A
  • Kidneys have the highest flow on a per unit weight basis???
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14
Q

By looking at the density of capillaries in tissue, you can make assumptions about what property of the tissue? Which tissues have the lowest and highest capillary densities?

A

The capillary density surrounding an organ is proportional to the tissue’s metabolic rate.

Cartilage- lowest metabolic rate.

Muscles and glands- highest metabolic rate.

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15
Q

Name the type of transport across the capillary endothelium for each substance listed?

  • Oxygen
  • Proteins
  • Glucose
  • Water
A
  • Oxygen: diffusion
  • Proteins: transcytosis??
  • Glucose: active transport
  • Water: osmosis
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16
Q

With which three physiological systems to the vessels of the lymphatic system interact?

A

immune, cardiovascular, and digestive systems??????

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17
Q

Define oedema. List some ways in which it can arise.

A

Oedema is excess fluid in interstitial space.

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18
Q

Define the following terms and explain the significance to cardiovascular physiology. a. Perfusion b. Colloid osmotic pressure c. Vasoconstriction d. Angiogenesis e. Pericytes

A

a- blood flow through a tissue

b- the contribution of plasma proteins to the osmotic pressure of the plasma

c- a decrease in blood vessel diameter

d- growth of new blood vessels, especially capillaries, into a tisse

e- cells that from a meshlike outer layer between the capillary endothelium and interstitial fluid

19
Q

The two major like protein carriers of cholesterol are ____________ and ____________. Which type is bad in elevated amounts?

A

hdl and ldl,

ldl is harmful in elevated amounts

20
Q

Describe arterioles

A

Main site of variable resistance

Diameter can be altered by nervous input

Walls are both stiff and elastic

21
Q

Describe arteries

A
  • Store pressure generated by the heart
  • Have walls that are both stiff and elastic
22
Q

Describe capillaries

A
  • have thin walls of exchange epithelium
  • blood flow slowest through these vessels
23
Q

Describe veins

A
  • carry low oxygen blood
  • act as volume reservoir (a blood reservoir is an organ or vessel that holds large proportions of blood. Veins hold the largest amount of blood, which is about 50 to 60 percent of the entire body’s blood volume. They have thin walls and much wider lumens compared to the arteries, thereby enabling them to contain much more blood than any other human vessel).
  • have lowest blood pressure (these blood reservoirs have a very low pressure and are only able to move blood back and forth through expansion and contraction of their walls aided with the help of valves). Capillaries have higher pressure than the veins because they are very thin, and hydrostatic pressure pushes fluid out.
24
Q

Describe venules?

A
  • capillary turns into venule, turns into vein.
  • carry low oxygen blood
25
Q

What are the main types of hypertension?

A
  • Primary/essential hypertension: most people with high blood pressure are diagnosed with primary hypertension, meaning there is no single obvious cause.
  • Secondary hypertension: there is an identifiable cause. The most common causes are pregnancy and kidney disease. If you can treat the underlying condition the hypertension will be reversed.
  • Malignant/ accelerated hypertension: a hypertensive emergency. Refer the person to specialist care the same day if they have: BP more than 180/110 mm Hg, with signs of papilloedema (optic disc swelling caused by increased intracranial pressure) or retinal haemorrhage.
26
Q

Possible causes of secondary hypertension?

A

KIDNEY PROBLEMS

CANCER ON ADRENAL GLANDS- CATECHOMINES, TOO MUCH NORADRENALINE

27
Q

What are the risk factors associated with the development of hypertension?

A
  • age – the risk of developing high blood pressure increases as you get older
  • a family history of high blood pressure
  • being of African or Caribbean origin: defects in nitric oxide synthesis or defects in baroreceptor set point
  • a high amount of salt in your food: salt in sytemic circulation, not filtered in kidneys yet, water moves from intracellular compartment into blood.
  • a lack of exercise
  • being overweight or obese
  • regularly drinking large amounts of alcohol: Effect on TPR? Apparently, ‘the mechanism through which alcohol raises blood pressure remains elusive.’
  • smoking: activation of they sympathetic nervous system = vasoconstriction and/or decreased sensitivity of baroreceptors
  • long-term sleep deprivation
  • stress: Dysregulation of stress hormones cortisol and epinephrine.
28
Q

Learning outcomes:

  • Describe how hypertension is defined and its relationship to cardiovascular risk
  • List the main types of hypertension and distinguish between essential and accelerated hypertension
A

Learning outcomes:

  • Describe how hypertension is defined and its relationship to cardiovascular risk
  • List the main types of hypertension and distinguish between essential and accelerated hypertension
29
Q

What is hypertension and how it is diagnosed?

A
  • Low blood pressure: readings lower than 90/ 60 mm Hg
  • Hypertension is persistently elevated blood pressure: above 120/80mmHg
30
Q

What is stage one hypertension defined as?

A
  • Stage 1 hypertension: Blood pressure is 140/90 mmHg or higher
  • Subsequent ambulatory blood pressure monitoring or home blood pressure monitoring average is 135/85 mmHg or higher
31
Q

What is stage two hypertension defined as?

A

Clinic blood pressure is 160/100 mmHg or higher

Subsequent ABPM or HBPM average is 150/95 mmHg or higher.

32
Q

What is severe hypertension defined as?

A
  • Clinic blood pressure is 180/ 110 mmHg or higher.
33
Q

How do you diagnose hypertension?

A
  • Do BP on both arms in the clinic. If BP is different by >20 mmHg between arms, repeat measurements. If the difference remains >20 mmHg measure subsequent BPs in the arm with the higher reading.
  • Then, if BP is 140/90 mmHg or higher, take a second measurement during the consultation. If the second measurement is substantially different from the first, take a third measurement. Record the lower of the last two measurements as the clinic BP.
  • Offer ABPM to confirm the diagnosis of hypertension.
34
Q

What is the relationship between hypertension and organ damage?

A
  • Increased blood volume and pressure increase shear factors which lead to endothelial damage, atherosclorosis, clots, ischeamic cell death.
  • Hypertension is the most important risk factor for premature cardiovascular diseases: stroke, coronary artery disease, heart failure, atrial fibrillation, and peripheral vascular disease.
  • Hypertension accounts for an estimated 54 percent of all strokes and 47 percent of all ischemic heart disease events globally.
  • Epidemiological studies show the risk for both coronary disease and stroke increases progressively with incremental increases in blood pressure above 115/75 mmHg.
  • The best evidence for a causal role of increasing blood pressure in cardiovascular complications is an improvement in outcome with antihypertensive therapy.
  • Organ function can be impacted due to damage to their microcirculation.
  • In the kidney hypertension can cause proteinuria and reduced GFR
  • In the eye it can cause hypertensive retinopathy
  • In the brain it can cause vascular dementia
35
Q

What are the symptoms of hypertension (not the cause)?

A
  • headaches
  • shortness of breath
  • dizziness
  • chest pain
  • heart palpitations
  • nose bleeds
  • stomach pain
  • fever
  • blurred vision
36
Q

Left ventricular failure may be accompanied by oedema, shortness of breath and increased venous pressure. Explain how these symptoms develop due to left ventricular failure,

A
  • The left side of the heart is responsible for receiving oxygen-rich blood from the lungs and pumping it forward to the systemic circulation (the rest of the body). Failure of the left side of the heart causes blood to back up into the lungs, as the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs. This is oedema.
  • Shortness of breath devolps in left sided heart failure, because the left ventricle can’t eject the blood effectively, so blood backs up in the lungs. There is increased presure in the vessels surrounding the lung, this causes fluid to move into the pulmonary interstitum (the area between the capillary and alveolar membrane). This causes increased airway resistance, harder for the gas exchange to happen. Also hypoxemia (low oxygen in tissues) causes increased ventilatory drive.
  • Increased venous pressure: there is a transient compensatory rise in SV via the Frank Starling mechanism. Persistently impaired contractility, end-diastolic volume remains high.
37
Q

Sylvia fell on the ice and spread her knee, requiring three days of bed rest. When she got up on the third day, she experienced dizziness and loss of balance and had to sit on the side of the bed for a few minutes to avoid falling down. Why did she become dizzy?

A
  • Sylvia may have orthostatic hypotension, due to dehydration or heart problems.
  • Orthostatic hypotension: a decrease in systolic blood pressure of 20 mm Hg or a decrease in diastolic blood pressure of 10 mm Hg within three minutes of standing when compared with blood pressure from the sitting or supine position
  • She recovers soon because the decrease in blood pressure when she stands triggers the baroreceptor reflex. The carotid and aortic baroreceptors respond to the drop in arterial blood pressure by decreasing their firing rate. Diminished sensory input in to the cardiovascular control center increases the sympathetic activity. As a result of autonomic changes, heart rate and force of contraction increase, while arterioles and veins constrict. The combination of increased cardiac output and increased peripheral resistance raises mean arterial pressure and restore it to normal usually within two heart beats. The skeletal muscle pump also contributes to the recovery by enhancing venous return when abdominal and leg muscles contract to maintain an upright position.
  • BTW: the baroreceptor reflex is not always effective, however. For example, during extended bed rest blood from the lower extremities is redistributed more evenly throughout the body. This redistribution raises arterial pressure, triggering the kidneys to excrete what they perceive to be excess fluid. Over the course of three or so days, excretion leads to a 12% decrease in blood volume. When the person finally gets out of bed gravity again causes blood to pool in the legs. Orthostatic hypotension occurs, and the baroreceptors attempt to compensate. But in this instance, the cardiovascular system is unable to restore normal pressure because of the loss of blood volume. As a result the subject may become dizzy or even faint from reduced delivery of oxygen to the brain.
38
Q

What is the first step in treatment for hypertension?

A

Step 1 treatment:

  • Offer people aged under 55 years an AC) inhibitor. If an ACE inhibitor is prescribed and is not tolerated, offer a low-cost ARB (angiotensin-II receptor blocker). Do not combine an ACE inhibitor with an ARB to treat hypertension.
  • Offer people aged over 55 years and to black people of African or Caribbean family origin of any age, a calcium-channel blocker (CCB). If a CCB is not suitable, for example because of oedema or intolerance, or if there is evidence of heart failure or a high risk of heart failure, offer a thiazide-like diuretic.
39
Q

What is the second step in treatment for hypertension?

A

If blood pressure is not controlled by step 1 treatment, offer step 2 treatment with a Calcium Channel Blocker in combination with either an ACE inhibitor or an Angiotensin 11 Receptor Blocker. If a CCB is not suitable for step 2 treatment, for example because of oedema or intolerance, or if there is evidence of heart failure or a high risk of heart failure, offer a thiazide-like diuretic. For black people of African or Caribbean family origin, consider an ARB in preference to an ACE inhibitor, in combination with a CCB.

40
Q

What is the third step in treatment for hypertension?

A

If treatment with three drugs is required, the combination of ACE inhibitor or angiotensin II receptor blocker, calcium-channel blocker and thiazide-like diuretic should be used.

41
Q

What is the fourth step in treatment for hypertension?

A

Consider further diuretic therapy with low-dose spironolactone (25 mg once daily) if the blood potassium level is 4.5 mmol/l or lower. Consider higher-dose thiazide-like diuretic treatment if the blood potassium level is higher than 4.5mmol/l. If further diuretic therapy for resistant hypertension at step 4 is not tolerated, or is contraindicated or ineffective, consider an alpha- or beta-blocker.

42
Q

Using the appropriate equation, mathematically explain what happens to blood flow if the diameter of a blood vessel increases from 2 mm to 4 mm.

A
  • Think of it as if the blood vessels were straws and the blood coke, which straw would allow you to suck the coke up fastest. The 4mm straw.
  • Flow equals pressure gradient times radius to the power 4.
  • Resistance equals one over the radius to the power four.
  • So if radius has doubled, resistance has decreased by 16 fold.
43
Q

Calculate the mean arterial pressure (MAP) and pulse pressure for a person with a blood pressure of 115/73 mmHg.

A

P.P = SYTOLIC PRESSURE - DIASTOLIC PRESSURE

Pulse pressure = 115 mmHg -73 mmHg

Pulse pressure = 42 mmHg

MAP=diastolic pressure + 1/3 (systolic pressure-diastolic pressure)

MAP= 73 + 1/3 (115-73)

MAP = 87 mmHg

44
Q

According to the Fick principal:

Oxygen consumption rate of an organ = blood flow through that organ x the amount of oxygen extracted from the blood as it flows through the organ

so

Oxygen consumption rates = blood flow x systemic mLO2 consumed/ min (arterial oxygen content – venous oxygen content)

A person has a total-body oxygen consumption rate of 250 mL oxygen consumed per minute. The oxygen content of the blood in his aorta is 20 mL O2/ 100 mL blood. The oxygen content of pulmonary artery blood is 16mL O2/100mL blood. What is his cardiac output?

A

CO = VO2

Ca-Cv

Cardiac output is measured in L/min so convert the oxygen content of the blood in his aorta to a L 200 mL O2/ 1 L blood. The oxygen content of pulmonary artery blood is 160mL O2/1 L blood.

So 250 mL/ 40 mL= 6.25 L/min