Chapter 14 - Cardiac Output, Blood Flow & Pressure Flashcards

1
Q

What is the formula for determining cardiac output?

A

Cardiac output (ml/min) = Stroke volume (ml/beat) X Cardiac rate (beats/min)

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2
Q

The basic heart rate is set by the pacemaker cells. (SA node). What two divisions of the nervous system can influence this rate? What does each do to the rate? How do they do that?

A

A. Sympathetic Nervous System: increased rate of diastolic depolarization; increased cardiac rate; increased conduction rate; increased strength of contraction. Done by release of norepinephrine and epinephrine, which produces cAMP through beta-adrenergic receptors and opens HCN channels.
B. Parasympathetic Nervous System: decreased rate of diastolic depolarization; decreased cardiac rate; decreased conduction rate. Done by release of ACh, which binds to muscarinic ACh receptors, and causes the opening of K+ cannels. The diffusion of K+ produces a slower rate of diastolic depolarization.

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3
Q

Where are the cardiac control centers located?

A

The medulla oblongata.

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4
Q

What factors regulate “stroke volume”? Describe each. Be able to understand the formula I put on the board showing the relationship between SV, TPR, MAP, and Contractility.

A

A. The end-diastolic volume (EDV), which is the volume of blood in the ventricles at the end of diastole; the total peripheral resistance (TPR), which is the frictional resistance, or impedance to blood flow, in the arteries; and the contractility, or strength, of ventricular contraction.
B. Stroke Volume is directly proportional to the preload/end-diastolic volume and contractility, but inversely proportional to total peripheral resistance.

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5
Q

What does “preload” and “afterload” mean? Name factors that are each of these.

A

Preload: the load on a muscle before it contracts. In the ventricles of the heart, the preload relates to the tension on the ventricular walls produces by their filling with the end-diastolic volume of blood.
Afterload: related to the total peripheral resistance and arterial pressure, the afterload presents an impedance to the ejection of blood from the ventricles at systole.

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6
Q

Describe the “Frank-Starling Law of the Heart” (An intrinsic factor).

A

The relationship between EDV, contraction strength, and stroke volume is thus a built-in, or intrinsic, property of heart muscles, and is known as the Frank-Starling Law of the Heart.

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7
Q

Extrinsic control of the heart rate occurs by:

A

Epinephrine

Autonomic nervous system

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8
Q

Epinephrine has what two major actions on the heart?

A
  1. Causes action potentials to be produced more rapidly, resulting in a faster cardiac rate.
  2. Opens the HCN channels of the pacemaker cells, inducing a faster rate of diastolic depolarization.
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9
Q

Stroke Volume is directly proportional to the preload/end-diastolic volume and contractility.

A

But inversely proportional to total peripheral resistance.

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10
Q

What are the compliance, elastic and resistance vessels?

A

A. Compliance: a measure of the ease with which a structure such as the lung expands under pressure; a measure of the change in volume as a function of pressure changes.
B. Capacitance/elastic vessels: veins because of their ability to stretch and hold a great volume of blood.
C. Resistance vessels: muscular and arterioles expand less under pressure (less compliant).

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11
Q

What 3 factors influence the rate of “venous return”?

A

Sympathetic nerve activity; the skeletal muscle pump; the pressure difference between the thoracic and abdominal cavities (venoconstriction).

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12
Q

At any given moment, in what vessels is most of the blood?

A

Veins

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13
Q

Be able to describe the forces involved in fluid exchange between the capillary and interstitial space.

A
  1. Net filtration pressure: equal to the hydrostatic pressure of the blood in the capillaries minus the hydrostatic pressure of tissue fluid outside the capillaries, which opposes filtration.
  2. Colloid osmotic pressure of plasma: the osmotic pressure exerted by plasma proteins is much greater than the colloid osmotic pressure of interstitial fluid
  3. Oncotic pressure: the difference between the osmotic pressure of plasma and interstitial fluid; essentially equal to the colloid osmotic pressure of the plasma (25 mmHG). This pressure favors the movement of water into the capillaries.
  4. Starling forces: opposing forces that affect the distribution of fluid across the capillary. Through the action of these forces, plasma and interstitial fluid are continuously interchanged.
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14
Q

Know and understand the 7 things that can lead to “edema”.

A
  1. High arterial blood pressure, which increases capillary pressure and causes excessive filtration;
  2. Venous obstruction – as in phlebitis or mechanical compression of veins – which produces a congestive increase in capillary pressure;
  3. Leakage of plasma proteins into interstitial fluid, which causes reduced osmotic flow of water into the capillaries;
  4. Myxedema – the excessive production of particular glycoproteins (mucin) in the extracellular matrix caused by hypothyroidism;
  5. Decreased plasma protein concentration, as a result of liver disease or kidney disease where plasma proteins are excreted in the urine;
  6. Obstruction of the lymphatic drainage.
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15
Q

The volume of blood is regulated in part by the kidneys. The textbook describes 4 such mechanisms. What are they

A

Regulation by Antidiuretic Hormone (ADH)
Regulation by Aldosterone
Renin-Angiotensin-Aldosterone System
Atrial Natriuretic Peptide

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16
Q

Blood Regulation by Antidiuretic Hormone (ADH)

A
Antidiuretic hormone (produced by hypothalamus, secreted by posterior pituitary gl.) stimulates reabsorption of water from the kidney filtrate, and thus acts to maintain the blood volume.
Dilution of the blood by water temporarily increases the blood volume, decreases the plasma osmolality, and inhibits the release of ADH.
17
Q

Regulation by Aldosterone

A

Aldosterone, secreted by the adrenal cortex, acts on the kidneys to promote the retention of salt and water. “Salt-retaining hormone.”
Retention of salt indirectly promotes retention of water. Stimulated by salt deprivation.

18
Q

Renin-Angiotensin-Aldosterone System

A

A decrease in blood flow through the kidneys activates the renin-angiotension-aldosterone system. Angiotension II stimulates vasoconstriction and the secretion of aldosterone by the adrenal cortex.
The relationship between the kidneys, angiotensin II, and aldosterone is described by this system. As a result of thirst and the activation of this system, we drink more, retain more NaCl, and urinate less (increasing blood volume).

19
Q

Atrial Natriuretic Peptide

A

ANP increases the urinary excretion of salt and water, thereby lowering the blood volume. ANP stimulates natriuresis, which is an increased excretion of Na+ in the urine.

20
Q

Describe what “Renin” and “Angiotensin II” are and what they do.

A

Renin: an enzyme secreted by the juxtaglomerular apparatus in the kidneys, which cleaves a 10-amino-acid polypeptide called angiotensin I from a larger plasma protein.
Angiotensin II: formed when angiotensin I passes through the capillaries of the lungs and angiotensin-converting enzyme (ACE) removes two amino acids
It stimulates contraction of the smooth muscle layers of the small arteries and arterioles
Also promotes a rise in blood volume (increasing blood pressure) by stimulating the thirst center in the hypothalamus, and the adrenal cortex to secrete aldosterone.

21
Q

What is “Atrial Natriuretic Factor (Peptide)”? What does it do and what causes it to be released?

A

A. ANP is produced by the atria of the heart. It is stimulated when there is an increase in blood volume or by the stretching of the atria.
B. It causes natriuresis to occur, which leads to an increase in the excretion of Na+ in the urine and lowers blood volume.

22
Q

What is the basic equation relating blood flow to blood pressure and resistance?

A

??

23
Q

What is a “Mean Arterial Pressure”? How is it determined?

A

An adjusted average of the systolic and diastolic blood pressures. It averages about 100 mmHg in the systemic circulation and 10 mmHg in the pulmonary circulation.
Result of the pressure difference between the beginning of the tube (the aorta) and the end of the tube (the junction of the venae cavae with the right atrium).

24
Q

If you double the diameter of a blood vessel, what do you do to its resistance and blood flow?

A

You increase the blood flow and decrease the resistance.

25
Q

The flow of blood in a vessel is directly proportional to the pressure difference between the two ends of the tube, and

A

inversely proportional to the frictional resistance to blood flow through the vessels.

26
Q

What are the 2 extrinsic regulators of vessel diameter? What does each do? How?

A
  1. Autonomic nervous system: stimulates vasoconstriction of arterioles in the viscera and skin
  2. Endocrine system through the release of hormones such as ADH (vasoconstriction).
27
Q

What are the 2 intrinsic regulators of vessel diameter?

A
  1. Myogenic regulation occurs when vessels constrict or dilate as a direct response to a rise or fall in blood pressure.
  2. Metabolic regulation occurs when vessels dilates in response to the local chemical environment within the organ.
28
Q

If you narrow the diameter of a vessel at one place, what happens to the pressure in the vessel distally?

A

The pressure in the vessel distally decreases.

29
Q

Where are the “Baroreceptors” located and what do they do?

A

Baroreceptors are pressure sensors for arterial blood pressure, located in the carotid sinuses and the arch of the aorta. They are constantly active, producing a baseline frequency of action potentials in their sensory neurons.

30
Q

Where are the “Atrial Stretch Receptors” (volume receptors)? What do they do?

A

Located in the atria of the heart, these receptors are activated by increased venous return to the heart and in response (1) stimulate reflex tachycardia, as a result of increased sympathetic nerve activity; and (2) inhibit ADH release, resulting in the excretion of larger volumes of urine and a lowering of blood volume; and (3) promote increased secretion of atrial natriuretic peptide.