Cardiovascular Physiology III Flashcards

1
Q

What is the primary function of the cardiovascular system?

A

The primary function is to deliver materials throughout the body to maintain metabolic needs.

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2
Q

Why is it important for physical therapists to understand blood?

A

Understanding blood is crucial for assessing and managing conditions related to circulation, hemorrhage, and overall patient health.

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3
Q

What materials are exchanged between the vasculature and tissues?

A

Gases, solutes, and fluids.

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4
Q

How is total body water divided?

A

Into three compartments: intracellular fluid, interstitial fluid, and plasma.

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5
Q

What is the role of the cell membrane in fluid compartments?

A

It separates intracellular fluid from extracellular fluid.

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6
Q

What are the two compartments of extracellular fluid?

A

Interstitial fluid (in tissues) and plasma (in blood).

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7
Q

What is the typical percentage of total body weight that total body water represents?

A

About 50% to 70%.

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8
Q

How does the ion composition differ between intracellular and extracellular fluid?

A

Intracellular fluid has high potassium and low sodium; extracellular fluid has high sodium and low potassium.

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9
Q

What is the significance of ion composition in fluid compartments?

A

It is important for maintaining resting membrane potentials and action potentials in tissues.

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10
Q

What determines the rate of fluid exchange in the microcirculation?

A

The permeability of the capillary wall and the pressure gradient between the capillary and interstitium.

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11
Q

What are Starling forces?

A

Forces that describe the pressure gradients (hydrostatic and oncotic) affecting fluid movement across capillary walls.

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12
Q

What is hydrostatic pressure in the context of capillaries?

A

The mechanical pressure of fluid against the capillary wall, driving fluid out.

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13
Q

What is oncotic pressure?

A

The osmotic pressure generated by proteins in the plasma that tends to pull fluid into the capillary.

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14
Q

How does fluid movement occur at the arterial end of a capillary?

A

There is a net filtration of fluid out due to higher hydrostatic pressure compared to oncotic pressure.

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15
Q

What happens at the venous end of a capillary regarding fluid exchange?

A

There is a net absorption of fluid into the capillary due to higher oncotic pressure compared to hydrostatic pressure.

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16
Q

What happens to the fluid not reabsorbed at the venous end of the capillary?

A

It is picked up by the lymphatic system to prevent tissue swelling.

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17
Q

How much fluid is typically filtered out of a capillary at the arterial end, and how much is reabsorbed at the venous end?

A

About 3 milliliters filtered out and 2.7 milliliters reabsorbed.

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18
Q

What is the role of the lymphatic system in fluid exchange?

A

It collects excess fluid not reabsorbed and returns it to the vascular system.

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19
Q

What is edema?

A

Edema is the accumulation of fluid in the tissues due to an imbalance between the filtration of fluid out of the vasculature and the reabsorption of fluid back into it.

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20
Q

What are the main mechanisms that can lead to the formation of edema?

A
  1. Disruption of the lymphatic system
  2. Changes in Starling forces (increased hydrostatic pressure or decreased oncotic pressure)
  3. Acute changes in capillary permeability
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21
Q

What is lymphedema?

A

Lymphedema is edema resulting from the disruption of the lymphatic system, leading to fluid accumulation in tissues.

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22
Q

What is the difference between primary and secondary lymphedema?

A

Primary lymphedema is due to congenital abnormalities in the lymphatic system, while secondary lymphedema is more common and often occurs after surgeries, such as lymph node resection due to cancer.

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23
Q

How can increased hydrostatic pressure lead to edema?

A

Increased hydrostatic pressure in capillaries can occur due to venous blockages (like DVT), leading to more fluid being filtered out into the tissues.

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24
Q

What role does oncotic pressure play in fluid exchange?

A

Oncotic pressure, primarily due to plasma proteins like albumin, pulls fluid into the vasculature. A decrease in oncotic pressure (e.g., due to hypoalbuminemia) results in less fluid reabsorption and contributes to edema.

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25
Q

What are some causes of hypoalbuminemia?

A

Hypoalbuminemia can be caused by liver disease, kidney disease, burns, and protein-calorie malnutrition.

26
Q

How does inflammation affect capillary permeability and lead to edema?

A

Inflammation causes the retraction of endothelial cells in capillaries, widening the pores and allowing fluid, proteins, and white blood cells to leak into the tissue, leading to edema.

27
Q

What is the difference between transudate and exudate in edema?

A

Transudate occurs in non-inflammatory edema with low protein content, while exudate occurs in inflammatory edema with high protein content.

28
Q

What is the clinical presentation of non-inflammatory edema?

A

Non-inflammatory edema often leads to pitting edema, where pressing the swollen tissue leaves an indentation for a few seconds, and usually occurs in dependent regions of the body.

29
Q

How does inflammatory edema differ from non-inflammatory edema?

A

Inflammatory edema does not pit when pressed, is firmer, and is associated with other signs of inflammation like redness, heat, and pain.

30
Q

What are the two main components of blood?

A

Blood consists of approximately 45% solid components and 55% plasma.

31
Q

What is the largest component of plasma?

A

The largest component of plasma is water, followed by dissolved proteins (like albumin) and dissolved gases and ions.

32
Q

What are platelets, and what is their function?

A

Platelets, or thrombocytes, are cell fragments that play a crucial role in blood clotting to minimize blood loss during injury.

33
Q

What are the normal ranges of blood cells per microliter of blood?

A

Red blood cells (erythrocytes): 4-6 million
White blood cells (leukocytes): 5,000-10,000
Platelets (thrombocytes): 140,000-400,000

34
Q

What is hematopoiesis, and where does it occur?

A

Hematopoiesis is the process of blood cell formation, occurring in the bone marrow.

35
Q

What types of blood cells do myeloid and lymphoid progenitors differentiate into?

A

Myeloid progenitors: Megakaryocytes (thrombocytes), erythrocytes, mast cells, and several types of leukocytes (neutrophils, basophils, eosinophils, monocytes).
Lymphoid progenitors: Natural killer cells, T lymphocytes, and B lymphocytes.

36
Q

What are the two main categories of disorders related to red blood cells?

A

Anemia (too few red blood cells) and polycythemia (too many red blood cells).

37
Q

What can cause anemia?

A

Anemia can result from blood loss (acute or chronic), accelerated destruction of red blood cells (hemolysis), or decreased production (e.g., iron deficiency).

38
Q

What are the major symptoms of anemia?

A

Major symptoms include poor endurance, fatigue, and elevated heart rate.

39
Q

What is polycythemia and its potential health concerns?

A

Polycythemia is an excess of red blood cells, which can lead to increased blood viscosity and higher risks of cardiovascular issues like stroke or heart attack.

40
Q

What do leukopenia and leukocytosis refer to?

A

Leukopenia refers to too few white blood cells, while leukocytosis refers to too many white blood cells.

41
Q

What are the major concerns with leukopenia?

A

Individuals with leukopenia have increased susceptibility to infections due to insufficient white blood cells.

42
Q

What can cause leukocytosis?

A

Common causes include infections, inflammation, trauma, and certain medications or malignancies.

43
Q

What do thrombocytopenia and thrombocytosis mean?

A

Thrombocytopenia means too few platelets, while thrombocytosis means too many platelets.

44
Q

What are potential causes of thrombocytopenia?

A

Causes include platelet consumption (e.g., hemorrhage), destruction due to autoimmune conditions, decreased production from bone marrow issues, or sequestration in the spleen.

45
Q

What are the risks associated with excessive thrombocytes?

A

Excessive thrombocytes can lead to clot formation, which may block blood flow and result in stroke or myocardial infarction.

46
Q

What are bleeding disorders and some examples?

A

Bleeding disorders impair the ability to clot blood, leading to excessive bleeding; examples include Von Willebrand disease and hemophilia.

47
Q

What are clotting disorders and their possible origins?

A

Clotting disorders involve excessive clotting, which can be genetic (e.g., Factor V Leiden) or acquired (e.g., venous thromboembolism).

48
Q

What is Virchow’s triangle?

A

Virchow’s triangle outlines the three factors that increase the risk of thromboembolism: stasis of blood, hypercoagulable state, and vessel injury.

49
Q

What is the body’s initial response to acute blood loss?

A

The initial response is the baroreceptor reflex, triggered by a decrease in arterial blood pressure.

50
Q

How do baroreceptors contribute to heart function during blood loss?

A

They decrease parasympathetic activity, increasing heart rate, and increase sympathetic activity, enhancing heart rate and contractility.

51
Q

What effect does sympathetic activity have on blood vessels during blood loss?

A

It causes constriction of arterioles and veins, increasing peripheral resistance and venous return, which helps restore blood pressure.

52
Q

What is the renin-angiotensin-aldosterone system’s role in response to blood loss?

A

It increases blood pressure by promoting sodium and water reabsorption, increasing fluid volume, and causing vasoconstriction.

53
Q

What happens when blood pressure decreases in the capillaries?

A

There is a decrease in capillary hydrostatic pressure, leading to increased fluid reabsorption and preservation of blood volume.

54
Q

What is circulatory shock?

A

Circulatory shock results from hypoperfusion or diminished blood flow to tissues, leading to decreased oxygen delivery and cellular hypoxia.

55
Q

What are the metabolic consequences of cellular hypoxia during shock?

A

Cells rely on anaerobic metabolism, producing lactate and contributing to metabolic acidosis.

56
Q

What are common signs of shock?

A

Weak, rapid pulse; hypotension; low urine output; altered mental status (anxiety, confusion, loss of consciousness).

57
Q

What are the four stages of shock?

A
  1. Initial Response: Cellular hypoxia.
  2. Compensatory Phase: Activation of mechanisms to stabilize blood pressure.
  3. Progressive Stage: Failure of compensatory mechanisms and increased metabolic acidosis.
  4. Refractory Period: Irreversible damage, organ failure, and death.
58
Q

What happens during the compensatory phase of shock?

A

The body activates mechanisms like hyperventilation and increases in heart rate and blood pressure due to the baroreceptor reflex and renin-angiotensin system.

59
Q

What occurs if compensatory mechanisms fail during shock?

A

There is greater metabolic acidosis, general vasodilation, decreased peripheral resistance, and massive edema, leading to further blood pressure decline.

60
Q

What is the final outcome of the refractory period in shock?

A

Irreversible damage to cells, organ failure, and ultimately death occur in the refractory period of shock.