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Cardio All My Notes > Physiology > Flashcards

Physiology Flashcards

1
Q

Q: What is the approximate weight of the heart?

A

A: The heart weighs approximately 200-300 grams.

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2
Q

Q: Where is the base of the heart located?

A

A: The base of the heart is located on the superior surface, pointing towards the right shoulder.

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3
Q

Q: Where is the apex of the heart located?

A

A: The apex of the heart is located on the inferior surface, pointing to the left hip.

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4
Q

Q: In which part of the thoracic cavity is the heart located?

A

A: The heart is located in the middle mediastinum, covered by a pericardial covering.

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5
Q

Q: What structures are anterior to the heart?

A

A: The sternum and costal cartilage are anterior to the heart.

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6
Q

Q: What structures are posterior to the heart? 4

A

A:
1. The vertebral column from (T5-T8),
2. esophagus, and
3. carina of trachea and
4. primary bronchi are posterior to the heart.

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7
Q

Q: Which tissues make up the endocardium?

A

A: The endocardium is composed of simple squamous epithelial tissue with areolar connective tissue.

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8
Q

Q: What is the function of the endocardium? 3

A

A:
1. The endocardium keeps blood in the heart,
2. prevents clotting, releases PGI2 and Nitric oxide to inhibit platelet activation and aggregation, and
3. acts as a barrier between blood and tissue.

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9
Q

Q: Which layer of the heart contains contractile cardiac muscle?

A

A: The myocardium contains contractile cardiac muscle.

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10
Q

Q: What is the role of non-contractile cardiac muscle in the heart?

A

A: Non-contractile cardiac muscle generates and conducts action potentials.

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11
Q

Q: What is the visceral layer of serous pericardium also known as?

A

A: The visceral layer of serous pericardium is also called epicardium.

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12
Q

Q: What is the function of the pericardial cavity?

A

A: The pericardial cavity contains serous fluid, which lubricates the tissue layers and prevents friction between the two serous layers.

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13
Q

Q: Where else is the endothelium of the endocardium found?

A

A: The endothelium of the endocardium continues as the endothelium in blood vessels.

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14
Q

Q: What lines the outer layer of the valves in the heart?

A

A: The endocardium lines the outer layer of the valves in the heart.

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15
Q

Q: Name the components of the non-contractile cardiac muscle.

A

A: The non-contractile cardiac muscle includes the
*

  • SA node,
  • AV node,
  • bundle of His,
  • bundle branches (right and left), and
  • Purkinje fibers.
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16
Q

Q: What substances are secreted by the contractile cardiac muscle when stretched, and what is their effect?

A

A: When stretched, contractile cardiac muscle secretes
1. atrial natriuretic peptide (ANP) and
2. brain natriuretic peptide (BNP).

  • These peptides increase sodium and water excretion,
  • dilate blood vessels,
  • decrease blood volume, and
  • decrease stretch of the myocardium.
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17
Q

Q: What does the visceral layer of serous pericardium secrete, and what is the purpose of this secretion?

A

A: The visceral layer of serous pericardium secretes pericardial serous fluid into the cavity. This fluid lubricates the tissue layers, reducing friction between them.

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18
Q

Q: Under normal physiologic conditions, is there blood in the pericardial cavity?

A

A: Under normal physiologic conditions, there is usually no blood in the pericardial cavity.

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19
Q

Q: What condition can occur when there is less fluid in the pericardial cavity, and what are the associated symptoms?

A

A: When there is less fluid in the pericardial cavity, pericarditis can occur.
Symptoms may include severe stabbing pain due to increased friction between the serous layers.

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20
Q

Q: What is the composition and function of the parietal layer of serous pericardium?

A

A:
The parietal layer of serous pericardium is continuous with the epicardium and consists of
1. mesothelium (simple squamous epithelium) with loose areolar connective tissue.
2. It secretes pericardial serous fluid into the cavity to lubricate the tissue layers.

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21
Q

Q: Describe the composition and function of the fibrous pericardium.

A

A:
* The fibrous pericardium is made of dense fibrous irregular connective tissue.
* Its functions include
1. anchoring the heart to surrounding structures,
2. preventing the heart from overfilling with blood due to its non-distensible nature, and
3. protecting the heart due to its tough tissue.

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22
Q

Q: What vessels deliver deoxygenated blood to the right atrium? 3

A

A:
1. The superior vena cava brings blood from structures above the diaphragm (e.g., head, neck, and arms),
2. the inferior vena cava brings blood from structures below the diaphragm (e.g., abdomen and liver), and
3. the coronary sinus brings blood from the coronary circulation.

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23
Q

Q: What is the role of the fossa ovalis in the right atrium?

A

A:
* The fossa ovalis is a scar tissue remnant of the foramen ovale, a hole between the RA and LA in the embryo.

  • It closes up at birth to prevent blood from moving from the RA to the RV and into the pulmonary circulation.
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24
Q

Q: Where does the left atrium receive oxygenated blood from?

A

A:

  • The left atrium receives oxygenated blood from the four pulmonary veins:
  • two from the left lung and two from the right lung.
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25
Q

Q: What purpose do the auricles serve in the atrial chambers?

A

A: The auricles (atrial appendages) increase the space and volume of the atria.

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26
Q

Q: What purpose do the auricles serve in the atrial chambers?

A

A: The auricles (atrial appendages) increase the space and volume of the atria.

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27
Q

Q: What is the clinical relevance of thrombi formation in the left and right auricles during atrial fibrillation?

A

A:
* Thrombi (blood clots) commonly form in the left atrial appendage during atrial fibrillation, while

  • thrombi formation is less common in the right atrial appendage.
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28
Q

Q: What is the clinical correlate of a ventricular septal defect?

A

A: A ventricular septal defect is the most common type of heart defect and causes mixing of blood between the RV and LV.

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29
Q

Q: Describe the structure of the heart valves.

A

A:

  • The valves have four annulus rings of fibrous tissue from which leaflets hang.
  • The leaflets consist of an endothelial layer, zona spongiosa, zona fibrosa, and zona ventricularis/atrialis.
  • Chordae tendineae anchor the leaflets to papillary muscles, preventing them from ballooning back into the atrium and causing blood backflow.
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30
Q

Q: What is the function of the heart valves? 2

A

A:
1. The heart valves ensure a one-way flow of blood and prevent backflow.
2. They are also anchored to the cardiac skeleton and act as electrical insulators between the atria and ventricles, ensuring all electrical signals go through the atrioventricular (AV) node.

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31
Q

Q: How many leaflets does the tricuspid valve have?

A

A: The tricuspid valve contains three leaflets.

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32
Q

Q: How many leaflets does the bicuspid/mitral valve have?

A

A: The bicuspid/mitral valve contains two leaflets.

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33
Q

Q: What are the two coronary arteries and where do they originate from?

A

A:

  • The two coronary arteries are the left coronary artery (LCA) and the right coronary artery (RCA).
  • They arise from the aorta just beyond the semilunar valves.
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34
Q

Q: What is the function of the coronary arteries?

A

A:
The coronary arteries supply oxygenated blood to the myocardium (musculature of the heart) during diastole when the increased aortic pressure above the semilunar valves forces blood into the coronary arteries.

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35
Q

Q: What is the function of non-contractile myocardial cells in the heart?

A

A:

  • Non-contractile myocardial cells, such as the SA node, AV node, bundle of His, bundle branches, and Purkinje fibers,
  • are responsible for generating and conducting action potentials.
  • They stimulate contractile myocardial cells, causing them to contract.
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36
Q

: What are the “funny” Na+ channels (If channels) and their role?

A

A:

  • The “funny” Na+ channels (If channels) are open when the cell is at rest.
  • They allow a slow movement of Na+ into the cell, making the inside of the cell more positive.
  • This gradual increase in positive charge moves the resting membrane potential from -60mV to -55mV, which stimulates further depolarization.
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37
Q

Q: What are T-type calcium channels and their role in depolarization?

A

A:

  • T-type calcium channels open at -55mV.
  • They allow calcium to move into the cell, further increasing the positive charge inside the cell.
  • This moves the voltage from -55mV to -40mV, which is the threshold voltage to stimulate L-type calcium channels.
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38
Q

Q: What are L-type calcium channels and their role in depolarization?

A

A:

  • L-type calcium channels open at -40mV.
  • They allow an explosive influx of calcium ions into the cell, significantly increasing the positive charge.
  • This moves the voltage from -40mV to +40mV, leading to depolarization of the nodal cell.
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39
Q

: How does depolarization spread from nodal cells to adjacent contractile myocardial cells?

A

A:
through intercalated discs.

  • These discs contain gap junctions, which are channel proteins (connexin proteins) allowing ions, including calcium, to move from the depolarized nodal cell into the adjacent contractile myocardial cell.
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40
Q

Q: What happens when voltage-gated Na+ channels open in contractile myocardial cells?

A

A:

  • When voltage-gated Na+ channels open in contractile myocardial cells at the threshold voltage of -70mV,
  • Na+ rushes into the cells, causing the inside of the cell to become highly positive.
  • The voltage inside the cell goes from -70mV to +10mV.
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41
Q

Q: How does calcium contribute to muscle contraction in contractile myocardial cells?

A

A:

  • L-type Ca++ channels on contractile myocardial cells are activated by the voltage-gated Na+ channels, causing calcium to rush into the cell.
  • This calcium activates proteins on the sarcoplasmic reticulum, leading to the release of more calcium into the cytoplasm of the muscle cell.
  • The rise in intracellular calcium triggers muscle contraction by interacting with troponin C and tropomyosin.
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42
Q

Q: What is the mechanism of repolarization in nodal cells?

A

A:

  • After nodal depolarization and the entry of calcium into nearby myocardial cells via intercalated discs,
  • voltage-gated K+ channels in nodal cells open at +40mV.
  • This allows K+ to leave the cell, making the inside of the cell increasingly negative and preparing the nodal cell for the next stimulation.
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43
Q

Q: How does repolarization occur in contractile myocardial cells?

A

A:

  • At +10mV, voltage-gated K+ channels in contractile myocardial cells open, allowing K+ to move out of the cell, which makes the inside of the cell negative.
  • However, L-type Ca++ channels are still open, and calcium is entering the cell while K+ is leaving.
  • This maintains the voltage at 0mV for a short period, knownas the plateau phase.
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44
Q

Q: What happens during the plateau phase of repolarization in contractile myocardial cells?

A

A:

  • During the plateau phase at 0mV, the movement of K+ out of the cell is balanced by the entry of calcium, keeping the voltage plateaued.
  • This phase is sustained for a brief period, contributing to the extended duration of muscle contraction.
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45
Q

Q: How is the voltage restored to the resting membrane potential in contractile myocardial cells?

A

A:

  • After contraction, the L-type Ca++ channels close, and K+ continues to leave the cell while no further calcium enters.
  • This causes the voltage to drop from 0mV to -90mV, which is the resting membrane potential of the contractile myocardial cell.
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46
Q

Q: How is calcium removed from the cytoplasm of contractile myocardial cells after contraction?

A

A:

  • Calcium in the cell is shunted back into the sarcoplasmic reticulum (SR) or out of the cell to prevent prolonged contraction.
  • This is accomplished through ATP-dependent Ca++/H+ exchange mechanisms and
  • the Na+/Ca++ exchanger via secondary active transport.
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47
Q

Which nodal cell ensures synchronized contraction of the ventricular myocardium?

A

Answer: Purkinje fibers

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48
Q

What is the function of Purkinje fibers?

A

Answer: Purkinje fibers receive impulses from the bundle branches and
ensure synchronized contraction of the ventricular myocardium.

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49
Q

Where are the bundle branches located?

A

Answer: The bundle branches span along the length of the interventricular septum until the apex of the heart.

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50
Q

Which nodal cell reduces high-frequency impulses from traveling into the ventricles from the atria?

A

Answer: The Bundle of His reduces high-frequency impulses from traveling into the ventricles from the atria.

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51
Q

What is the function of the AV node?

A

Answer: The AV node receives impulses from the SA node and conducts them slowly, creating a delay to allow for sequential atrial and ventricular contraction.

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52
Q

What is the location of the SA node?

A

Answer: The SA node is located near the entrance of the superior vena cava (SVC) into the right atrium.

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53
Q

What is the function of the parasympathetic nervous system (PSNS) on the heart?

A

Answer: The PSNS decreases heart rate (chronotropy) and conduction (dromotropy), but has no direct effect on contractility.

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54
Q

How does the PSNS exert its effect on heart rate and conduction?

A

Answer: PSNS fibers
1. release acetylcholine (Ach), which binds to muscarinic type 2 receptors.
2. This activates inhibitory proteins, leading to hyperpolarization of cells,
3. decreased action potentials, and a
4. decrease in heart rate and conduction.

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55
Q

What is the intracellular mechanism of action of the PSNS on nodal cells?

A

Answer:
1. PSNS activation leads to increased K+ efflux through binding to K+ channels, hyperpolarization of cells, and decreased phosphorylation of L-type Ca++ channels.
2. This results in reduced calcium influx, decreased action potentials, and a decrease in heart rate.

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56
Q

What is the function of the sympathetic nervous system (SNS) on the heart?

A

Answer: T
he SNS increases

  • heart rate (chronotropy),
  • conduction (dromotropy), and
  • contractility (inotropy).
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57
Q

How does the SNS exert its effect on heart rate and conduction?

A

Answer:

  • The SNS releases norepinephrine (NE), which binds to beta one -adrenergic receptors.
  • This increases cAMP levels, leading to enhanced phosphorylation of L-type Ca++ channels and
  • increased calcium influx.
  • This results in increased action potentials, heart rate, and conduction.
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58
Q

What are the effects of the SNS and PSNS on heart rate?

A

Answer: The PSNS decreases heart rate, while the SNS increases heart rate.

A heart rate below 60 bpm is called bradycardia, while a heart rate above 100 bpm is called tachycardia.

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59
Q

What is the intracellular mechanism of action of the sympathetic nervous system (SNS) on nodal cells?

A

Answer:

  • SNS fibers release norepinephrine (NE) and epinephrine, which activate beta-1 adrenergic receptors.
  • This leads to increased cAMP levels, phosphorylation of L-type Ca++ channels,
  • increased calcium influx, depolarization rate, action potentials, heart rate, conduction, and contractility.
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60
Q

What is the intracellular mechanism of action of the sympathetic nervous system (SNS) on contractile cells?

A

Answer:
1. SNS fibers release NE and epinephrine, which activate beta-1 adrenergic receptors.
2. This increases cAMP levels, phosphorylation of phospholamban, enhanced influx of Ca++ back into the sarcoplasmic reticulum, increased speed of relaxation,
3. phosphorylation of L-type Ca++ channels, increased calcium influx in contractile cells, increased Ryr-2 activity,
4. increased Ca++ in the sarcoplasm,
5. increased interactions with troponin,
6. increased cross-bridge formation,
7. increased contraction rate and speed, increased heart pumping,
8. increased stroke volume (SV), and
9. increased cardiac output (CO).

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61
Q

What is the refractory period in cardiac action potentials?

A

Answer:

  • The refractory period occurs during phases 3 and 4 (repolarization and resting membrane potential) of the cardiac action potential.
  • It consists of an absolute refractory period and a relative refractory period, during which the heart is in a resting state and less responsive to stimuli.
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62
Q

What is the duration of the relative refractory period?

A

Answer: The relative refractory period lasts about 250 ms.

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63
Q

Which type of channels are phosphorylated by stimulation of the sympathetic nervous system (SNS)?

A

Answer: L-type Ca++ channels are phosphorylated by SNS stimulation.

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64
Q

Can the parasympathetic nervous system (PSNS) affect the contractility of the heart?

A

Answer: False. T
he PSNS has no direct effect on contractility; it primarily influences heart rate and conduction.

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65
Q

Does the sympathetic nervous system (SNS) have a positive chronotropic action?

A

Answer: True. The SNS increases heart rate (chronotropy).

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66
Q

Can action potentials be triggered during the relative refractory period?

A

Answer: True.

  • Action potentials can be triggered during the relative refractory period,
  • although a stronger stimulus is required compared to the absolute refractory period.
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67
Q

What is the duration of the average cardiac cycle?

A

Answer: The average cardiac cycle takes approximately 0.8 seconds.

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68
Q

What are the four phases of the cardiac cycle?

A

Answer: The four phases of the cardiac cycle are
ventricular filling,
isovolumetric contraction,
ventricular ejection, and
isovolumetric relaxation.

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69
Q

During which phase does ventricular filling occur?

A

Answer: Ventricular filling occurs during the mid to late ventricular diastole (relaxation) phase.

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70
Q

How does blood passively flow from the atria into the ventricles during ventricular filling?

A

Answer: Without contraction, 70-80% of the blood passively flows down from the atria into the ventricles due to gravity.

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71
Q

What happens during the reduced filling phase of ventricular diastole?

A

Answer: During the reduced filling phase,

  • the SA node fires, depolarizes the atria, and
  • the atria contract to actively push the remaining blood down into the ventricles.
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72
Q

What occurs during the isovolumetric contraction phase?

A

Answer: The isovolumetric contraction phase is

  • when the ventricles start to depolarize and contract,
  • increasing ventricular pressure.
  • No blood enters or leaves the ventricles during this phase.
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73
Q

What is the end diastolic volume?

A

Answer:
The end diastolic volume refers to the blood accumulated in the left ventricle before it contracts.

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74
Q

What causes the closure of the AV valves during isovolumetric contraction?

A

Answer:
The rise in ventricular pressure above atrial pressure causes the AV valves to shut close, producing the first heart sound (S1).

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75
Q

What happens during the mid to late ventricular systole phase?

A

Answer: Blood leaves the ventricles, and ventricular pressure continues to rise as the ventricles depolarize and contract more intensely.

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76
Q

When do the semilunar valves open during the cardiac cycle?

A

Answer: The semilunar valves open during the mid to late ventricular systole phase when the ventricular pressure becomes greater than the pressure in the arteries.

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77
Q

What occurs during the isovolumetric relaxation phase?

A

Answer:

  • In the isovolumetric relaxation phase, no blood enters or leaves the ventricles as they relax.
  • The ventricular pressure decreases, but it is still greater than the atrial pressure, keeping the semilunar valves closed.
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78
Q

What causes the closure of the semilunar valves during isovolumetric relaxation?

A

Answer:

  • The arterial pressures are higher than the ventricular pressures,
  • causing the semilunar valves to shut close and producing the second heart sound (S2).
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79
Q

What is the end-systolic volume?

A

Answer:
The end-systolic volume refers to the amount of blood left in the left ventricle after it contracts.

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80
Q

What happens to the atrial pressure compared to the ventricular pressure during isovolumetric relaxation?

A

Answer: The atrial pressure is lower than the ventricular pressure during isovolumetric relaxation, causing the AV valves to remain closed.

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81
Q

What is the significance of the T wave on the ECG during phase 4?

A

Answer:
The T wave on the ECG represents ventricular repolarization, indicating that the ventricles are relaxed and repolarized.

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82
Q

What is the formula for cardiac output?

A

Answer: Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)

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83
Q

What factors increase heart rate?

A

Answer:
Factors that increase heart rate include
1. sympathetic nervous system activation,
2. hormones such as thyroid hormone,
3. exercise, increased body temperature,
4. certain drugs (e.g., epinephrine, atropine), and
5. imbalances in ions such as calcium and potassium.

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84
Q

How does the sympathetic nervous system increase heart rate?

A

Answer:
The sympathetic nervous system increases heart rate through the release of norepinephrine and epinephrine,

  • which stimulate beta-1 adrenergic receptors,
  • leading to increased calcium influx and depolarization rate in nodal cells.
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85
Q

What factors decrease heart rate?

A

Answer:
1. parasympathetic nervous system activation, the release of acetylcholine,
2. certain drugs (e.g., beta blockers, calcium channel blockers),
3. imbalances in ions such as calcium and potassium, and
4. decreased levels of thyroid hormone.

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86
Q

What is the role of the Frank-Starling mechanism in cardiac output?

A

Answer:
increase in ventricular preload (end-diastolic volume) leads to a more forceful contraction and increased stroke volume, thereby increasing cardiac output.

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87
Q

How does the parasympathetic nervous system decrease heart rate?

A

Answer:

  • The parasympathetic nervous system decreases heart rate by releasing acetylcholine,
  • which stimulates M2 receptors on nodal cells,
  • leading to increased potassium efflux,
    decreased cAMP levels, hyperpolarization, and
  • a decreased rate of action potentials.
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88
Q

How do imbalances in calcium and potassium affect heart rate?

A

Answer:

  • Hypercalcemia (increased calcium levels) and
    hypokalemia (decreased potassium levels) can increase heart rate,
  • while hypocalcemia (decreased calcium levels) and
  • hyperkalemia (increased potassium levels) can decrease heart rate.
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89
Q

How does age and gender influence heart rate?

A

Answer: In general,

  • fetuses/infants have a higher heart rate (120-140 bpm), while
  • adults have a normal heart rate range of 60-100 bpm.
  • Females tend to have slightly higher heart rates than males.
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90
Q

What is the definition of bradycardia?

A

Answer: heart rate (HR) below 60 beats per minute (bpm).

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91
Q

What are some causes of bradycardia?

A

Answer:
1. parasympathetic nervous system activation (PSNS),
2. certain drugs, and
3. endurance activities that increase preload and contractility, leading to an increased stroke volume and compensatory decrease in heart rate.

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92
Q

What is the definition of tachycardia?

A

Answer: Tachycardia is defined as a heart rate (HR) above 100 beats per minute (bpm).

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93
Q

What are some causes of tachycardia?

A

Answer:
1. sympathetic nervous system activation (SNS),
2. increased levels of thyroid hormones (T3 and T4),
3. certain drugs, and
4. anxiety.

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94
Q

What is stroke volume (SV)?

A

Answer: the total volume of blood (in milliliters) pumped out of the ventricle in one heartbeat.

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95
Q

What factors regulate stroke volume?

A

Answer: Factors that regulate stroke volume include

  • end-diastolic volume (EDV),
  • end-systolic volume (ESV), and
  • ejection fraction (EF).
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96
Q

How does end-diastolic volume (EDV) affect stroke volume?

A

Answer:
An increase in end-diastolic volume (EDV), which is the pre-pumping volume in the ventricles, leads to an increase in stroke volume assuming normal contractility.

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97
Q

How does end-systolic volume (ESV) affect stroke volume?

A

Answer:
End-systolic volume (ESV), which is the post-pumping volume in the ventricles, is based on contractility and afterload.

  • Good contractility with a constant afterload leads to a decrease in ESV and an increase in stroke volume,
  • while bad contractility with increased afterload leads to an increase in ESV and a decrease in stroke volume.
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98
Q

What is ejection fraction (EF)?

A

Answer:

  • Ejection fraction (EF) is the percentage of blood ejected out of the ventricles per beat.
  • It is calculated by dividing stroke volume (SV) by end-diastolic volume (EDV) and multiplying by 100.
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99
Q

How does a decreased left ventricular ejection fraction (EF) occur?

A

Answer:
A decreased left ventricular ejection fraction can occur in conditions such as

  • systolic heart failure, where there is a decrease in blood leaving the heart, resulting in more blood remaining after contraction,
  • an increase in ESV, a decrease in stroke volume, and a decrease in EF.
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100
Q

What is the definition of preload?

A

Answer: the degree of stretch of the ventricular myocardium.

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101
Q

How does an increase in preload affect stroke volume?

A

Answer:
According to Frank Starling’s Law of the Heart,

  • an increase in preload leads to an increase in cross-bridge formation and force of contraction, resulting in an increase in stroke volume (SV).
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102
Q

How does an increase in venous return to the heart affect preload?

A

Answer:

  • An increase in venous return to the heart, which can be achieved through factors such as
    1. increased blood volume,
    2. muscular milking activity,
    3. respiratory pump, and
    4. venomotor tone or venoconstriction,
  • leads to an increase in preload.
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103
Q

How does lying supine affect preload?

A

Answer: Lying supine prevents blood from being pulled down into the lower extremities by gravity, resulting in increased preload.

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104
Q

How does a slower heart rate (bradycardia) affect preload?

A

Answer: A slower heart rate allows for increased diastolic time, which leads to increased ventricular filling and, subsequently, increased preload.

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105
Q

How does muscle compliance affect preload?

A

Answer:

  • A “stretchy” myocardium with normal compliance allows for normal stretch and preload,
  • while a dilated or flabby myocardium with increased stretch leads to increased preload.
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106
Q

How do heart valve abnormalities, such as stenosis or regurgitation, affect preload?

A

Answer:

  • Stenosis, which reduces blood leaving the ventricles, and
  • regurgitation, which increases blood backflow into the ventricles,

both lead to increased preload.

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107
Q

What factors decrease preload?

A

Answer: Factors that decrease preload include
1. decreased venous return to the heart due to decreased blood volume (hemorrhage, dehydration),
2. decreased sympathetic nervous system (SNS) activity,
3. increased vasodilation of veins,
4. expiration (removal of vacuum pressure during respiration),
5. decreased skeletal muscle contractions in the legs (immobility),
6. standing upright for long periods (gravity pulling blood into lower extremities),
7. decreased muscle compliance (damaged or hypertrophied myocardium), and
8. decreased filling time due to a faster heart rate (tachycardia).

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108
Q

How do mitral and tricuspid valve abnormalities, such as stenosis, affect preload?

A

Answer:
Mitral and tricuspid valve stenosis reduce the flow of blood into the ventricles from the atria, leading to decreased preload.

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109
Q

What is the definition of contractility?

A

Answer: Contractility refers to the strength or force of ventricular contraction.

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110
Q

How does an increase in contractility affect stroke volume?

A

Answer: An increase in contractility leads to an increase in stroke volume.

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111
Q

What are some factors that increase contractility?

A

Answer: Factors that increase contractility include
1. sympathetic nervous system activation (norepinephrine and epinephrine),
2. hormones (thyroid hormone and glucagon),
3. positive inotropic drugs (digitalis, dopamine, atropine, dobutamine, milrinone, norepinephrine, epinephrine), and
4. an increase in intracellular calcium.

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112
Q

What are some factors that decrease contractility?

A

Answer: Factors that decrease contractility include
1. beta blockers,
2. calcium channel blockers,
3. negative inotropic drugs,
4. decreased calcium levels (hypocalcemia),
5. increased potassium levels (hyperkalemia),
6. increased sodium levels (hypernatremia),
7. acidosis, and
8. . hypoxia.

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113
Q

What is the definition of afterload?

A

Answer:
the amount of resistance that the ventricles must overcome to eject blood into the aorta or pulmonary trunk.

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114
Q

How does an increase in afterload affect stroke volume?

A

Answer: An increase in afterload leads to a decrease in stroke volume.

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115
Q

What are some factors that increase afterload?

A

Answer:
Factors that
1. increase afterload include increased vascular resistance in systemic circulation (diastolic hypertension,
2. atherosclerosis, vasoconstrictive drugs) and
3. increased vascular resistance in pulmonary circulation (pulmonary hypertension, pulmonary valve stenosis).

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116
Q

What are some factors that decrease afterload?

A

Answer: Factors that decrease afterload include

  • decreased vascular resistance and
    2.
  • drugs that vasodilate vessels (
  1. ACE inhibitors, angiotensin II receptor blockers,
  2. hydralazine,
  3. isosorbide dinitrate,
  4. phosphodiesterase inhibitors).
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117
Q

What is the relationship between stroke volume and cardiac output?

A

Answer:

  • Stroke volume is one of the factors determining cardiac output, which is the product of stroke volume and heart rate.
  • An increase in stroke volume leads to an increase in cardiac output.
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118
Q

Question: Which factors increase contractility and their effects on stroke volume and cardiac output?

A

Answer: Factors that increase contractility, such as positive inotropic agents, lead to an increase in stroke volume and cardiac output.

119
Q

Question: Hyperkalemia is not a positive chronotropic agent?

A

Answer: yes is not a positive chronotropic agent.

120
Q

Question: What is the role of thyroid hormone in cardiac function?

A

Answer: Thyroid hormone acts as a positive chronotropic agent, increasing heart rate.

121
Q

Question: Define end-diastolic volume (EDV).

A

Answer: End-diastolic volume (EDV) is the volume of blood in the ventricles at the end of diastole, just before contraction.

122
Q

Question: Which of the following factors does not increase preload?

A

Answer: Decreased return to the heart does not increase preload.

123
Q

Question: Which drug is a negative inotropic agent?

A

Answer: Metoprolol is a negative inotropic agent.

124
Q

Question: What is the definition of afterload?

A

Answer: Afterload is the amount of resistance that the ventricles must overcome to eject blood into the aorta/pulmonary trunk.

125
Q

Question: What is the arterial course of blood vessel circulation?

A

Answer: The arterial course of blood vessel circulation is from the heart to elastic arteries, then to muscular arteries, arterioles, and finally to capillaries.

126
Q

Question: What is the venous course of blood vessel circulation?

A

Answer:
from capillaries to venules, then to veins, and back to the heart.

127
Q

Question: Name two types of vessels based on their function.

A

Answer: Two types of vessels based on function are

  • elastic conducting arteries and
  • muscular distributing arteries.
128
Q

Question: What is the difference in blood flow direction between arteries and veins?

A

Answer: Arteries carry blood away from the heart, while veins carry blood back to the heart.

129
Q

Question: What is the difference in pressure between arteries and veins?

A

Answer: Arteries have higher pressure compared to veins.

130
Q

Question: What is the difference in oxygen content between arteries and veins?

A

Answer: Arteries generally have high oxygen content, while veins have low oxygen content, except for the pulmonary veins.

131
Q

Question: Name two characteristics of muscular arteries.

A

Answer: Muscular arteries are smaller to medium-sized vessels and have a thicker tunica media.

132
Q

Question: What is the function of arterioles?

A

Answer: Arterioles regulate blood flow to target organs through vasoconstriction and vasodilation. They also develop the most resistance to blood flow.

133
Q

Question: What is the main significance of true capillaries?

A

Answer: True capillaries have a diameter of 8-10 μm and are designed for the exchange of substances such as gases, nutrients, hormones, and wastes.

134
Q

Question: What is the structure of tunica intima in capillaries?

A

Answer: The tunica intima in capillaries consists of simple squamous epithelial cells and a basement membrane or basal lamina.

135
Q

uestion: What is the role of pre-capillary sphincters?

A

Answer:

  • Pre-capillary sphincters are smooth muscle layers wrapped around arterioles or the capillary bed.
  • They can constrict or relax under the control of the sympathetic nervous system, regulating blood flow into the capillaries.
136
Q

Question: What is the main function of veins?

A

Answer:
to serve as capacitance or reservoir vessels, occupying a large volume of blood and acting as a low-pressure system.

137
Q

Question: How do veins overcome gravity and push blood back up towards the heart?

A

Answer:
* Veins develop adaptations to overcome gravity, including

  • the presence of valves in the tunica interna,
  • muscular milking through contraction of nearby muscles, the
  • respiratory pump facilitated by breathing, and
  • sympathetic tone.
138
Q

Question: What is the role of valves in veins?

A

Answer:

  • Valves in veins prevent the backflow of blood by folding inward and closing when blood circulation tries to push it back down.
  • They help prevent pooling of blood and the development of varicose veins.
139
Q

Question: How does muscular milking contribute to blood flow in veins?

A

Answer:
Muscular milking refers to the slow process of muscular contraction near veins, which squeezes the blood vessels and pushes the blood upward, aiding in venous return.

140
Q

Question: How does the respiratory pump assist in venous blood flow?

A

Answer:
1. Breathing increases the volume of the thoracic cavity, which pushes on some lower vessels and helps the blood move upward.
2. It increases blood flow from the lungs and back to the heart and also assists in pushing blood flow from the lower systemic veins back up to the heart.

141
Q

Question: What is the effect of sympathetic tone on veins?

A

Answer: Sympathetic tone in veins helps maintain venous tone and assists in venous return by promoting vasoconstriction and preventing blood from pooling.

142
Q

Question: What are varicose veins?

A

Answer:
Varicose veins are tortuous, dilated, twisted, and/or enlarged blood vessels that occur when the valves in veins become incompetent and leaky.

143
Q

Question: Where are varicose veins commonly found?

A

Answer:
Varicose veins are commonly found in the

  1. calves, testes (varicoceles), and
  2. anus (hemorrhoids).
144
Q

Question: What are some potential causes of varicose veins?

A

Answer: Varicose veins can be caused by factors such as

  • prolonged standing,
  • increased pressure in the testes due to backflow of blood, and
  • accumulated pressure in the anal area due to various scenarios like high-pressure straining or prolonged sitting.
145
Q

Question: What are the layers of an artery and vein?

A

Answer: :

  • tunica interna/intima,
  • internal elastic lamina,
  • tunica media,
  • external elastic lamina, and
  • tunica externa/adventitia.
146
Q

Question: What is the main function of the tunica interna/intima?

A

Answer:
The tunica interna/intima is the innermost layer of blood vessels and includes

  • the endothelial layer, which acts as a barrier between blood and tissue, prevents clotting, controls blood vessel growth, and can form valves in veins to prevent backflow.
  • It also has a subendothelial layer made of loose areolar connective tissue.
147
Q

Question: What is the function of the internal elastic lamina?

A

Answer:
The internal elastic lamina, composed of

  • elastic connective tissue, allows blood vessels to stretch and recoil when blood is rushing through them.
  • Its absence or abnormalities can increase the risk of aortic dissection or aneurysms in conditions like Marfan syndrome or Ehlers-Danlos syndrome.
148
Q

Question: What is the role of the tunica media?

A

Answer:

  • The tunica media is the middle layer of blood vessels and is primarily composed of smooth muscle cells.
  • It regulates the lumen diameter by controlling vasoconstriction and vasodilation.
  • It is under sympathetic innervation and has vasomotor tone.
149
Q

Question: What is the function of the external elastic lamina?

A

Answer:
* The external elastic lamina, made of elastic connective tissue, allows blood vessels to stretch and recoil when blood is rushing through them.

  • Its presence is essential to prevent rigidity, hardening, and thickening of vessels.
150
Q

Question: What is the tunica externa/adventitia responsible for?

A

Answer:

  • The tunica externa/adventitia is the outermost layer of blood vessels and consists of dense fibrous irregular connective tissue.
  • Its main functions are to anchor vessels to surrounding structures and provide its own blood supply through vasa vasorum.
151
Q

uestion: What are the differences between arteries and veins in terms of the tunic layers?

A

Answer:

  • Arteries have thicker tunica media compared to veins. Arteries possess internal and external elastic lamina,
  • while veins may have little to no internal/external elastic lamina.
  • Additionally, veins have valves in the tunica intima, unlike arteries.
152
Q

Question: Why do veins have thinner tunica media and less elastic lamina compared to arteries?

A

Answer:

  • Veins have thinner tunica media because they function as capacitance or reservoir vessels, holding a larger volume of blood.
  • They also have less elastic lamina because they are low-pressure systems and do not require as much distensibility or stretching as arteries.
153
Q

Question: What is the histological characteristic of veins?

A

Answer: Histologically, veins may have a collapsed lumen due to their capacitance nature and lack of high pressure.

154
Q

Question: What are the three types of capillaries?

A

Answer: The three types of capillaries are

  • sinusoidal capillaries,
  • continuous capillaries, and
  • fenestrated capillaries.
155
Q

Question: What are the distinguishing features of sinusoidal capillaries?

A

Answer:

  • large intercellular clefts, making them highly permeable.
  • They allow the movement of large proteins and cells through the gaps between endothelial cells.
  • Sinusoidal capillaries are commonly found in the spleen, red bone marrow, and liver.
156
Q

Question: What are the distinguishing features of continuous capillaries?

A

Answer:

  • Continuous capillaries are the least permeable type of capillaries.
  • They have small intracellular clefts, except for those forming the blood-brain barrier, which have tight junctions between endothelial cells.
  • Continuous capillaries contain pericytes, control endothelial cell growth, and can undergo transcellular transport.
  • They are found in the skin, blood-brain barrier, muscles, and lungs.
157
Q

Question: What are the distinguishing features of fenestrated capillaries?

A

Answer:

  • Fenestrated capillaries have medium-sized intracellular clefts and fenestration pores running through endothelial cells.
  • They have moderate permeability, allowing the passage of small proteins and solutes through fenestrations while preventing blood cells from passing.
  • Fenestrated capillaries can also undergo pinocytosis.
  • They are commonly found in the kidneys and endocrine/exocrine glands, such as the small intestine.
158
Q

Question: What is the function of pericytes in continuous capillaries?

A

Answer:

  • Pericytes in continuous capillaries control endothelial cell growth, cause vasoconstriction, and act as phagocytes for substances leaking out of the cell.
  • They play a role in maintaining the stability and integrity of continuous capillaries.
159
Q

Question: Where are sinusoidal capillaries commonly found?

A

Answer: Sinusoidal capillaries are commonly found in the spleen, red bone marrow, and liver.

160
Q

Question: Which type of capillaries form the blood-brain barrier?

A

Answer:

  • Continuous capillaries form the blood-brain barrier.
  • In this barrier, there are tight junctions between endothelial cells instead of intracellular clefts.
161
Q

Question: What is the main characteristic of fenestrated capillaries?

A

Answer:

  • the presence of fenestration pores running through endothelial cells,
  • which allow the passage of small proteins and solutes while restricting the movement of blood cells.
162
Q

Question: What are endocrine and exocrine glands, and where are fenestrated capillaries commonly found?

A

Answer:

  • Endocrine glands are ductless glands that use hormones for signaling,
  • while exocrine glands are glands that have ducts.

Fenestrated capillaries are commonly found in endocrine and exocrine glands, including the kidneys and small intestine.

163
Q

Question: What are the components of the microcirculation pathway?

A

Answer:
1. terminal arteriole,
1. metarteriole,
1. true capillaries,
1. precapillary sphincter,
1. thoroughfare channel,
1. vascular shunt, and
1. post-capillary venule.

164
Q

Question: What is the function of the precapillary sphincter?

A

Answer:

  • The precapillary sphincter is a ring of smooth muscle tissue located around the true capillaries.
  • It controls the blood flow into the true capillaries by constricting or dilating.
  • Constriction of the sphincter prevents blood flow into the capillaries, while dilation allows blood to flow into the capillaries.
165
Q

Question: What is the pathway when the precapillary sphincters are closed?

A

Answer

  1. When the precapillary sphincters are closed, the blood flow follows this pathway: terminal arteriole → metarteriole → thoroughfare channel → postcapillary venule.
  • it doesn’t go through true capillary
  1. Additionally, blood can flow through the vascular shunt from the metarteriole to the thoroughfare channel.
166
Q

Question: What is the pathway when the precapillary sphincters are open?

A

Answer:
When the precapillary sphincters are open, the blood flow follows this pathway:

  • terminal arteriole → metarteriole → true capillaries → thoroughfare channel → postcapillary venule.
167
Q

Question: What is net filtration pressure (NFP)?

A

Answer:
* is the pressure difference that determines the movement of fluid across the capillary walls.

  • It is calculated by subtracting the forces pushing or pulling fluid into the vessel from the forces pushing or pulling fluid out of the vessel.
168
Q

Question: What does a positive net filtration pressure indicate?

A

Answer:
* that fluid is moving out of the vessel into the interstitial space.

169
Q

Question: What does a negative net filtration pressure indicate?

A

Answer:
* that fluid is moving into the vessel from the interstitial space.

170
Q

Question: What are the forces pushing or pulling fluid out of the vessel (capillary bed) and into the interstitial space?

A

Answer:
* capillary hydrostatic pressure (HPC) and

  • interstitial osmotic pressure (OPI).
171
Q

Question: What are the forces pushing or pulling fluid into the vessel from the interstitial space?

A

Answer:

  • capillary osmotic pressure (OPC) and
  • interstitial hydrostatic pressure (IHP).
172
Q

Question: What is the average value of capillary hydrostatic pressure on the arterial and venous sides of the capillary?

A

Answer: 35 mmHg, and on the venous side, it is 17 mmHg.

173
Q

Question: What is the average value of interstitial hydrostatic pressure?

A

Answer: The average value of interstitial hydrostatic pressure is 0 mmHg, assuming normal lymphatic function.

174
Q

Question: What are some diseases or conditions that can cause protein loss in the urine and lead to edema?

A

Answer:
Glomerulonephritis,
nephrotic syndrome,
hypoalbuminemia, and
hypoproteinemia

  • can cause protein loss in the urine, leading to edema.
175
Q

Question: How can cancer-related occlusion in lymphatic vessels lead to edema?

A

Answer:

  • When cancer causes occlusion within a lymphatic vessel,
  • it can result in backflow of lymph fluid,
  • leading to swelling and edema.
176
Q

Question: What is the purpose of anastomoses in the circulatory system?

A

Answer:

  • Anastomoses are alternative or collateral channels that provide alternative blood flow if one vessel is blocked.
  • They allow blood to move through collateral or fusion connections and still supply the tissue or maintain blood flow.
177
Q

Question: What are the three types of anastomoses?

A

Answer:

  • arterial anastomoses,
  • venous anastomoses, and
  • arterio-venous anastomoses.
178
Q

Question: What is an example of an arterial anastomosis?

A

Answer: the Circle of Willis in the brain.

179
Q

Question: What is an example of a venous anastomosis?

A

Answer:

  • the median antecubital vein,
  • which is a fusion of the basilic and axillary veins and is commonly used for blood draws.
180
Q

Question: What is an example of an arterio-venous anastomosis?

A

Answer:

  • the vascular shunt at the capillary bed,
  • where a metarteriole connects directly to a venule.
181
Q

Question: What is an AV malformation and what can it lead to?

A

Answer:

  • AV malformation is a condition where true capillaries are absent,
  • leading to high pressure from the artery straight to the vein.
  • This can cause vessels to coil up and rupture, and it is commonly found in the brain.
  • Treatment for AV malformation involves embolization.(from ebmoi prevent blood flow to these areas)
182
Q

Question: How does blood flow change in skeletal muscles during exercise?

A

Answer:

  • During exercise, skeletal muscles produce CO2, H+, and decrease in O2 and K+.
  • These chemicals cause vasodilation and increase blood flow to the muscles to meet increased demand.
183
Q

Question: How does mean arterial pressure (MAP) affect cerebral vessels?

A

Answer:

  • Increased MAP leads to stretching of cerebral vessels, triggering a myogenic mechanism that causes vasoconstriction.
  • Conversely, low MAP does not stretch cerebral vessels, resulting in vasodilation.
184
Q

Question: How does decreased oxygen in the alveoli affect pulmonary arterioles?

A

Answer:
Decreased oxygen in the alveoli, which may be due to obstruction or mucus buildup, causes pulmonary arterioles to constrict.

185
Q

Question: What happens in the gastrointestinal tract and skin during a fight or flight response?

A

Answer: In a fight or flight situation, the sympathetic nervous system (SNS) is activated, leading to vasoconstriction in the gastrointestinal tract and skin as blood is redirected to more critical areas.

186
Q

Question: What are the five types of blood vessels?

A

Answer:
terminal arterioles,
metarterioles,
true capillaries,
thoroughfare channels, and
post-capillary venules.

187
Q

Question: What is the function of precapillary sphincters?

A

Answer

  • regulate regional blood flow to the capillary bed in a few tissues by controlling the blood flow of the true capillaries.
  • They can constrict to reduce blood flow or dilate to allow blood to flow into the capillary bed.
188
Q

Question: How does fluid movement across the capillary wall occur?

A

Answer:

  • The movement of gases and solutes follows Fick’s Law of Diffusion,
  • while lipid-soluble substances pass through endothelial cells, and water-soluble substances pass through water-filled pores.
189
Q

Question: What is net filtration pressure (NFP)?

A

Answer:
Net filtration pressure (NFP) is the difference between the forces pushing fluid out of the capillary (capillary hydrostatic pressure and interstitial fluid osmotic pressure) and

the forces pushing fluid into the capillary (capillary osmotic pressure and interstitial fluid hydrostatic pressure).

190
Q

Question: What is capillary hydrostatic pressure (HPc)?

A

Answer:

  • is the pressure exerted by blood in the capillaries against the capillary wall.
  • It forces fluid out of the capillary and depends directly on systolic blood pressure.
191
Q

Question: What is capillary osmotic pressure (OPc)?

A

Answer:
* is the pressure exerted by proteins, mainly albumin, in the blood within the capillaries. ]

  • It pulls fluid into the blood and opposes filtration.
192
Q

Question: What is interstitial fluid hydrostatic pressure (IHP)?

A

Answer:

  • is the pressure of the fluid in the interstitium.
  • It forces fluid back into the capillary and opposes filtration.
193
Q

Question: What is interstitial fluid osmotic pressure (OPi)?

A

Answer:

  • is the pressure exerted by proteins in the interstitium.
  • It pulls fluid out of the capillary and favors filtration.
194
Q

Question: How does filtration and reabsorption occur across the capillary bed?

A

Answer:

Filtration of fluid out of the capillary usually occurs on the arterial side of the capillary bed, driven by increased capillary hydrostatic pressure and decreased capillary osmotic pressure.

Reabsorption of fluid into the capillary occurs on the venous side of the capillary bed,
driven by decreased capillary hydrostatic pressure and increased capillary osmotic pressure.

195
Q

Question: How is excess fluid returned to the circulation?

A

Answer:
is returned to the circulation via the lymphatics as lymph.

196
Q

Q: How does the pulmonary capillary hydrostatic pressure (Pc) compare to capillary osmotic pressure in the pulmonary capillaries?

A

A: Pulmonary capillary hydrostatic pressure is low compared to capillary osmotic pressure, favoring absorption of fluid (Pc is low).

197
Q

Q: How is the accumulation of interstitial fluid prevented under normal circumstances?

A

A: Lymphatic drainage removes any filtered fluid, preventing the accumulation of interstitial fluid.

198
Q

Q: What happens during Glomerulonephritis, Nephrotic syndrome, hypoalbuminemia, and hypoproteinemia?

A

A:

  • These conditions involve the loss of protein, particularly albumin, in the urine.
  • This loss of protein leads to a decrease in capillary osmotic pressure (OPC), resulting in increased filtration of fluid into the interstitium and the development of edema.
199
Q

Q: How does cancer contribute to the development of edema?

A

A: Cancer can cause edema by occluding lymphatic vessels, leading to backflow of fluid and subsequent swelling.

200
Q

Q: What are anastomoses?

A

A:

  • Anastomoses are alternative or collateral channels that allow blood to flow through alternative pathways if needed.
  • They involve the fusion of blood vessels to provide alternative routes for blood circulation.
201
Q

Q: What is the definition of edema?

A

A: Edema refers to the accumulation of fluid in the interstitial space.

202
Q

Q: What are the causes of edema related to raised capillary hydrostatic pressure (high Pc)?

A

A: Causes include arteriolar dilation, followed by raised venous pressure.

Examples of conditions leading to raised capillary hydrostatic pressure are left ventricular failure (pulmonary edema), right ventricular failure (peripheral edema), and prolonged standing (swollen ankles).

203
Q

Q: What is pulmonary edema?

A

A:

  • Pulmonary edema is the accumulation of fluid in the interstitial and intraalveolar lung spaces.
  • It is characterized by varying degrees of shortness of breath, crepitations in lung auscultation, and haziness in the perihilar region on a chest X-ray.
  • It is commonly associated with left ventricular failure.
204
Q

Q: What happens in heart failure (HF) that contributes to edema formation?

A

A:

  • Heart failure is a clinical syndrome characterized by reduced cardiac output and/or elevated intracardiac pressures.
  • The upregulation of the Renin-Angiotensin-Aldosterone System (RAAS) in HF leads to fluid retention, contributing to the development of edema.
205
Q

Q: What are the causes of reduced plasma osmotic pressure leading to edema?

A

A: Causes include

  • malnutrition,
  • protein malabsorption,
  • excessive renal excretion of protein, and
  • hepatic failure.
206
Q

Q: What are some examples of conditions that can cause lymphatic insufficiency?

A

A:

  • Lymph node damage,
  • filariasis (elephantiasis), and
  • cancer can result in lymphatic insufficiency.
207
Q

Q: What are some factors that contribute to changes in capillary permeability?

A

A:

  • Inflammation and histamine can increase the leakage of protein,
  • leading to changes in capillary permeability.
208
Q

Q: Which pressure does not have the same average pressure value for the arterial and venous side?

A

A: Capillary Hydrostatic Pressure does not have the same average pressure value for the arterial and venous side.

209
Q

Q: Which pressure does not have the same average pressure value for the arterial and venous side?

A

A: Capillary Hydrostatic Pressure does not have the same average pressure value for the arterial and venous side.

210
Q

Q: Which pressure is directly dependent on systolic blood pressure?

A

A: Capillary Hydrostatic Pressure is directly dependent on systolic blood pressure.

211
Q

Q: What is the role of the pulmonary circulation in meeting the metabolic needs of the airways?

A

A: The metabolic needs of the airways are met by the systemic bronchial circulation, not the pulmonary circulation.

212
Q

Q: How does the resistance of the pulmonary circulation compare to that of the systemic circulation?

A

A: The resistance of the pulmonary circulation is only about 10% of that of the systemic circulation.

213
Q

Q: What are some special adaptations of the pulmonary circulation?

A

A:

  • include low pulmonary capillary pressure compared to systemic capillary pressure,
  • absorptive forces exceeding filtration forces to protect against pulmonary edema, and
  • vasoconstriction of pulmonary arterioles in response to hypoxia.
214
Q

Q: How do high levels of lactate and CO2 cause vasodilation in skeletal muscle?

A

A:

  • High levels of lactate can activate certain receptors on blood vessels, such as the adenosine receptor, leading to vasodilation.
  • High levels of CO2 directly act as a potent vasodilator on smooth muscle cells in blood vessels, regulating blood flow.
215
Q

Q: What happens when venous valves in the lower limb become incompetent?

A

A: If venous valves become incompetent, blood can pool in the lower limb veins, leading to the development of varicose veins.

216
Q

Q: Do varicose veins lead to a reduction in CO2 levels?

A

A:

  • No, varicose veins do not typically lead to a reduction in CO2 levels.
  • There is a chronic compensatory increase in blood volume that helps maintain appropriate CO2 levels.
217
Q

Q: What is the function of the tunica intima?

A

A:

  • The tunica intima is composed of a single layer of squamous epithelial cells (endothelium) supported by a basal lamina and a thin layer of connective tissue.
  • Its function is to provide a smooth surface for blood flow and facilitate the exchange of substances between the blood and surrounding tissues.
218
Q

Q: What characterizes muscular arteries?

A

A:

  • Muscular arteries distribute blood to specific parts of the body and account for most of the named arteries.
  • They have less elastin but more smooth muscle compared to elastic arteries, allowing them to regulate blood flow to specific areas.
219
Q

Q: What is the structure of arterioles?

A

A:

  • Arterioles have one or two layers of smooth muscle in the tunica media and almost no adventitia.
  • They play a crucial role in regulating blood flow and determining peripheral resistance.
220
Q

Q: How do veins differ from arteries in terms of structure?

A

A:
Veins have the same three layers as arteries but

  • contain less smooth muscle and connective tissue, resulting in a thinner structure.
  • Veins also often have valves to prevent backflow of blood.
221
Q

Q: What is the structure of capillaries?

A

A:

  • Capillaries are small blood vessels with thin walls, usually composed of a single layer of endothelial cells.
  • This thin structure enables easy diffusion of molecules between capillaries and body tissues.
222
Q

What is autoregulation in the context of blood vessels?

A

Autoregulation is a mechanism that allows vascular resistance to be adjusted to maintain a constant blood flow in an organ across a pre-determined range of arterial pressures.

223
Q

Which organs demonstrate autoregulation?

A

The kidneys and brain demonstrate autoregulation to ensure constant perfusion.

224
Q

What is reactive hyperemia?

A

Reactive hyperemia refers to the automatic increase in blood flow that occurs following a temporary interruption of blood supply to a tissue or organ.

225
Q

What is functional (active) hyperemia?

A

Functional hyperemia is the mechanism that automatically increases blood flow in response to increased metabolic demand in tissues, such as during exercise.

226
Q

What is the role of endothelin in blood vessels?

A
  • Endothelin is the most potent and long-lasting endogenous vasoconstrictor.
  • Its production is stimulated by angiotensin II and vasopressin.
227
Q

What is the role of nitric oxide in blood vessels?

A

Nitric oxide is a vasodilator that helps to relax and widen blood vessels, promoting increased blood flow.

228
Q

Which type of blood vessels demonstrate autoregulation?

A

Arterioles, also known as resistance vessels, demonstrate autoregulation.

229
Q

What is the purpose of autoregulation in the kidneys and brain?

A

Autoregulation ensures that these organs receive constant perfusion despite fluctuations in systemic blood pressure.

230
Q

What is the purpose of reactive hyperemia?

A

Reactive hyperemia compensates for a period of reduced blood flow by automatically increasing blood flow once the obstruction is removed.

231
Q

How does functional hyperemia support increased metabolic demand?

A

Functional hyperemia automatically increases blood flow to tissues in response to increased metabolic demand, ensuring an adequate supply of oxygen and nutrients.

232
Q

Question: What is the equation for calculating blood pressure?

A

Answer: Blood Pressure = Cardiac Output (CO) * Total Peripheral Resistance (TPR)

233
Q

Question: How does blood volume affect blood pressure?

A

Answer:

Blood volume is directly proportional to blood pressure.

234
Q

Question: Name three conditions that can cause an increase in blood volume and subsequently increase blood pressure.

A

Answer:
Congestive heart failure,
liver failure, and
kidney failure

  • can all cause an increase in blood volume and subsequently increase blood pressure.
235
Q

Question: Name three conditions that can cause a decrease in blood volume and subsequently decrease blood pressure.

A

Answer:

  • Severe vomiting or diarrhea,
  • diuretic use leading to increased urine output, and
  • hemorrhage (bleeding externally or internally) can cause a decrease in blood volume and subsequently decrease blood pressure.
236
Q

Question: What is the equation for calculating blood flow?

A

Answer: Blood Flow (F) = Cardiac Output (CO) = Volume of blood being pumped out of the heart within one minute.

237
Q

uestion: How is velocity of blood flow calculated?

A

Answer: Velocity of Blood Flow = Flow (cm3/min) / Cross-sectional area of the blood vessel (cm2).

238
Q

Question: How does cardiac output affect the velocity of blood flow?

A

Answer:

  • Flow (Cardiac Output) is directly proportional to the velocity of blood flow.

An increase in cardiac output leads to an increase in the velocity of blood flow, while a decrease in cardiac output leads to a decrease in velocity.

239
Q

Question: How does the cross-sectional area of blood vessels affect the velocity of blood flow?

A

Answer:
* Cross-sectional area is inversely proportional to the velocity of blood flow.

Smaller cross-sectional areas result in higher velocity, while larger cross-sectional areas result in lower velocity.

240
Q

Question: What is total peripheral resistance (TPR) and how is it calculated?

A

Answer:

  • Total Peripheral Resistance is the resistance to blood flow in the systemic circulation.

It can be calculated using the formula

  • R = ∆p / CO or R = 8ηl / πr^4,
    based on Poiseuille’s equation.
241
Q

Question: What are the three factors that affect total peripheral resistance?

A

Answer: The three factors that affect total

  • peripheral resistance are viscosity of blood (η),
  • length of blood vessels (L), and
  • radius of the vessel (r).
242
Q

Question: How does viscosity of blood affect peripheral vascular resistance?

A

Answer:

  • Viscosity of blood is directly proportional to peripheral vascular resistance.

An increase in viscosity leads to an increase in resistance, while a decrease in viscosity leads to a decrease in resistance.

243
Q

Question: How does length of blood vessels affect peripheral vascular resistance?

A

Answer:

  • Length of blood vessels is directly proportional to peripheral vascular resistance.

An increase in length leads to an increase in resistance, while a decrease in length leads to a decrease in resistance.

244
Q

Question: How does the radius of the blood vessel affect peripheral vascular resistance?

A

Answer:

  • The radius of the blood vessel is the major determinant of peripheral vascular resistance.

A decrease in vessel radius (vasoconstriction) leads to an increase in resistance, while an increase in vessel radius (vasodilation) leads to a decrease in resistance.

245
Q

Question: What are some factors that cause vasoconstriction and increase peripheral vascular resistance?

A

Answer

  • sympathetic nervous system activation (norepinephrine and epinephrine release),
  • angiotensin II,
  • vasopressin (ADH), and
  • endothelin.
246
Q

Question: What are some factors that cause vasodilation and decrease peripheral vascular resistance?

A

Answer:

  • nitric oxide,
  • prostaglandins,
  • atrial natriuretic peptide, and
  • increased cellular activity
    1. such as decreased oxygen,
    2. increased carbon dioxide, and
    3. increased protons).
247
Q

Question: How does resistance to blood flow add up in series and parallel circuits?

A

Answer: In series, resistance adds up linearly, meaning that the total resistance is the sum of individual resistances.

In parallel, the total resistance is the reciprocal of the sum of reciprocals of individual resistances (1/R total = 1/R1 + 1/R2 + 1/R3).

248
Q

Question: How does resistance to blood flow add up in series and parallel circuits?

A

Answer: In series, resistance adds up linearly, meaning that the total resistance is the sum of individual resistances.

In parallel, the total resistance is the reciprocal of the sum of reciprocals of individual resistances (1/R total = 1/R1 + 1/R2 + 1/R3).

249
Q

Question: What is Reynolds number and what factors does it depend on?

A

Answer:

  • Reynolds number (Re) is a dimensionless number that determines the type of blood flow.
  • It depends on the density of blood, the diameter of the vessel, the velocity of blood flow, and the viscosity of blood.
250
Q

Question: How does density, diameter, and velocity of blood flow affect the Reynolds number?

A

Answer:
Density, diameter, and velocity of blood flow are directly proportional to the Reynolds number.

An increase in density, diameter, or velocity leads to an increase in the Reynolds number, while a decrease in these factors leads to a decrease in the Reynolds number.

251
Q

Question: How does viscosity of blood affect the Reynolds number?

A

Answer:

  • Viscosity of blood is inversely proportional to the Reynolds number.
  • An increase in viscosity leads to a decrease in the Reynolds number, while a decrease in viscosity leads to an increase in the Reynolds number.
252
Q

Question: What is laminar flow and how does it occur?

A

Answer:

  • Laminar flow is a smooth, layered flow pattern of blood.
  • It occurs when the highest velocity of blood flows in the center of the blood vessel, while the lowest velocity flows near the walls of the vessel.
253
Q

Question: What is turbulent flow and what are its causes?

A

Answer:

  • Turbulent flow is a chaotic flow pattern of blood.
  • It can be caused by vasoconstriction, high velocities in large vessels, arterial bifurcation points, atherosclerotic plaque/thrombus, aortic stenosis, and anemia.
254
Q

Question: What is perfusion pressure?

A

Answer:

  • Perfusion pressure (∆p) is the pressure difference that drives blood flow.
  • It is the difference between mean arterial pressure (MAP) and central venous pressure (CVP).
255
Q

Question: What is pulse pressure and how is it calculated?

A

Answer: Pulse pressure is the difference between systolic blood pressure and diastolic blood pressure. It is calculated as SBP - DBP.

256
Q

Question: What can cause a wide pulse pressure and what are some examples?
A

A

nswer: A wide pulse pressure (greater than 40 mmHg) can be caused by increased stroke volume (SV).

Examples include anemia, hyperthyroidism, and aortic regurgitation.

257
Q

uestion: What can cause a narrow pulse pressure and what are some examples?

A

Answer: A narrow pulse pressure (less than 40 mmHg) can be caused by decreased stroke volume (SV). Examples include systolic congestive heart failure and cardiac tamponade.

258
Q

Question: What are Korotkoff sounds?

A

Answer: Korotkoff sounds are the sounds heard when measuring blood pressure using the auscultatory method.

259
Q

Question: Describe the process of measuring blood pressure using the auscultatory method.

A

Answer:

  • The process involves wrapping the blood pressure cuff, inflating the cuff to a pressure higher than the systolic blood pressure,
  • gradually deflating the cuff while listening for tapping and swishing sounds (Korotkoff sounds), identifying the first pulse sound as the systolic blood pressure,
  • and continuing to deflate until the sounds disappear, indicating the diastolic blood pressure.
260
Q

Question: What are baroreceptors and where are they located?

A

Answer: Baroreceptors are stretch-sensitive nerve endings located in the aortic arch and the bifurcation of the common carotid artery.

261
Q

Question: Which cranial nerves innervate the baroreceptors in the aortic arch and carotid sinus?

A

Answer:

  • The sensory fibers of the vagus nerve (cranial nerve X) innervate the baroreceptors in the aortic sinus,
  • while the sensory fibers of the glossopharyngeal nerve (cranial nerve IX) innervate the baroreceptors in the carotid sinus.
262
Q

Question: Describe the baroreceptor reflex in response to low blood pressure.

A

Answer:

  • When blood pressure is low, there is decreased stretch on the vessel walls, leading to reduced activation of the baroreceptor nerve endings.
  • This results in decreased action potentials carried down the glossopharyngeal and vagus sensory fibers to the medulla.
  • In the medulla, the signals are relayed to the nucleus tractus solitarius (NTS), which then stimulates the cardiovascular centers.
  • The cardioinhibitory center in the medulla is inhibited, while the cardioacceleratory center and vasomotor center are stimulated.
  • This leads to an increase in sympathetic nervous system activity, release of norepinephrine, increased heart rate (HR), increased cardiac output (CO), and increased blood pressure (BP).
263
Q

Question: What is the role of the cardioinhibitory center and cardioacceleratory center in the baroreceptor reflex?

A

Answer:

  • The cardioinhibitory center, located in the dorsal nucleus of the vagus, is inhibited due to the low blood pressure signal coming through the sensory afferent fibers of cranial nerves X and IX to the NTS.
  • The cardioacceleratory center, connected with the sympathetic nervous system, is stimulated due to the low blood pressure signal, leading to increased sympathetic activity and increased heart rate.
264
Q

Question: How does activation of the sympathetic nervous system affect heart rate and cardiac output?

A

Answer:

  • Activation of the sympathetic nervous system leads to the release of norepinephrine, which stimulates beta-1 receptors on nodal cells.
  • This results in an increased heart rate (HR), increased stroke volume (SV), and increased cardiac output (CO).
265
Q

Question: How does vessel radius affect peripheral vascular resistance?

A

Answer:

  • An increase in vessel radius leads to decreased peripheral vascular resistance, while a decrease in vessel radius leads to increased peripheral vascular resistance.
266
Q

Question: How does activation of the sympathetic nervous system affect contractility in myocardial cells?

A

Answer:

  • Activation of the sympathetic nervous system leads to the release of norepinephrine, which stimulates beta-1 receptors on contractile cells.
  • This stimulation increases contractility, leading to an increase in stroke volume, cardiac output, and blood pressure.
267
Q

Question: What is the mechanism of the alpha-1 receptor in the vasomotor center?

A

Answer:
* Activation of the sympathetic nervous system leads to the release of norepinephrine, which stimulates alpha-1 receptors on smooth muscle cells in arterioles.

  • This stimulation causes vasoconstriction of arterioles, reducing vessel diameter, increasing resistance, and ultimately increasing blood pressure.
  • Similarly, alpha-1 receptor stimulation on smooth muscle cells in venules causes vasoconstriction, which increases venous return to the heart, preload, stroke volume, cardiac output, and blood pressure.
268
Q

Question: How does the direct renal mechanism regulate blood pressure?

A

Answer:

  • , decreased systemic blood pressure leads to decreased hydrostatic pressure in the glomerulus, resulting in reduced glomerular filtration rate (GFR) and decreased urine output.
  • This decrease in urine output leads to an increase in blood volume, ultimately increasing blood pressure.
269
Q

Question: What are the three ways in which the renin-angiotensin-aldosterone system (RAAS) is stimulated?

A

Answer:

  • decreased systemic blood pressure (sympathetic effect on juxtaglomerular cells),
  • decreased NaCl concentration at the macula densa, and
  • decreased renal perfusion pressure (renal baroreceptors).
270
Q

Question: What are the components and actions of the renin-angiotensin-aldosterone system (RAAS)?

A

Answer:
1, renin,
2.angiotensinogen
3. angiotensin-I,
4. angiotensin-converting enzyme (ACE), and
5. angiotensin-II.

Angiotensin-II acts through two pathways:

  • vasoconstriction (stimulating angiotensin-II receptors on the tunica media of arterioles) and
  • increased blood volume (stimulating aldosterone production, leading to sodium and water reabsorption in the distal convoluted tubules of the kidney).
271
Q

Question: How does the adrenal medulla contribute to an increase in blood pressure?

A

Answer:

  • The adrenal medulla is activated by the sympathetic nervous system, leading to the production of epinephrine (80%) and norepinephrine (20%).
  • These hormones act on beta-1 and alpha-1 receptors, causing an increase in heart rate, contractility, and vasoconstriction, which ultimately leads to an increase in blood pressure.
272
Q

Question: What is the mechanism of action of aldosterone in the kidneys?

A

Answer:

  • Aldosterone acts on the distal convoluted tubules of the kidneys.
  • It binds to intracellular receptors, which activate specific genes.
  • This activation leads to increased production of three proteins: Na+ channels (allowing more Na+ to flow into the cells), K+ channels (causing more K+ to flow out of the cells into the distal convoluted tubules), and Na+/K+/ATPase pump (on the basolateral membrane, facilitating reabsorption of 3 Na+ in exchange for 2 K+).
  • Water follows Na+ back to the circulation, leading to an increase in blood volume.
273
Q

Question: What is the role of ADH (antidiuretic hormone) in increasing blood volume?

A

Answer:
* ADH acts on the collecting duct and distal convoluted tubules of the nephron.

  • It binds to V2 receptors, activating a Gs-protein signaling pathway.
  • This pathway leads to an increase in cAMP, which activates protein kinase A (PKA).
  • PKA phosphorylates vesicles containing aquaporin-2 (AQ-II), increasing their expression on the membrane.
  • This results in increased reabsorption of water in the kidney’s collecting duct, leading to an increase in blood volume.
274
Q

Question: How does angiotensin-II increase blood volume in the kidneys?

A

Answer:

  • Angiotensin-II stimulates Na+, Cl-, and water reabsorption in the proximal convoluted tubules of the kidney.
  • This leads to an increase in blood volume, as more solutes and water are reabsorbed, reducing their excretion in the urine.
275
Q

Question: How do higher brain centers, such as the cerebral cortex and hypothalamus, influence blood pressure?

A

Answer:

  • Although the cerebral cortex and hypothalamus are not directly involved in routine control of blood pressure, they can modify arterial pressure through relays to the medullary centers in the brain stem.
  • For example, the hypothalamus plays a role in the fight-or-flight response and can have profound effects on blood pressure.
  • Higher brain centers can also influence blood pressure in response to stress, emotions, and other factors.
  • The hypothalamus mediates the redistribution of blood flow and other cardiovascular responses during exercise and changes in body temperature.
276
Q

Q: What are the Korotkoff sounds?

A

A: Korotkoff sounds are specific sounds heard during the measurement of arterial blood pressure using a stethoscope and a blood pressure cuff.

277
Q

Q: When is the first Korotkoff sound heard?

A

A: The first Korotkoff sound is heard at the peak systolic pressure when the cuff pressure becomes lower than the systolic pressure, causing turbulent blood flow.

278
Q

Q: What do the second and third Korotkoff sounds represent?

A

A:
The second and third Korotkoff sounds are intermittent sounds heard during the gradual release of cuff pressure.

They occur due to turbulent spurts of blood flow that exceed the cuff pressure.

279
Q

Q: What does the fourth Korotkoff sound indicate?

A

A:
* The fourth Korotkoff sound is heard at the minimum diastolic pressure.

  • It is softer and muffled compared to the previous sounds.
280
Q

Q: What does the fifth Korotkoff sound represent?

A

A:
* The fifth Korotkoff sound corresponds to the point when the sounds completely disappear.

  • It indicates the diastolic pressure.
281
Q

Q: What is the role of the baroreceptor reflex in short-term blood pressure control?

A

A:

  • The baroreceptor reflex is responsible for short-term regulation of MAP.
  • Baroreceptors located in the aortic arch and carotid sinus detect changes in blood pressure and initiate appropriate responses via the autonomic nervous system.
282
Q

Q: How does the body respond to increased blood pressure?

A

A:

  • Increased blood pressure triggers the baroreceptors, leading to a reduction in heart rate and cardiac contractility through parasympathetic stimulation and a decrease in sympathetic constrictor tone.
  • These responses help decrease blood pressure.
283
Q

Q: What is postural or orthostatic hypotension?

A

A:

  • Postural or orthostatic hypotension refers to a condition where a person experiences a sudden drop in blood pressure when transitioning from a seated or lying position to a standing position.
  • It can cause symptoms like dizziness, lightheadedness, and fainting.
  • It can be caused by factors such as dehydration, prolonged bed rest, medication side effects, or certain medical conditions.
284
Q

Q: What is Extracellular Fluid Volume (ECFV)?

A

A: ECFV refers to the volume of fluid outside the cells and is composed of plasma volume and interstitial fluid volume.

285
Q

Q: What are the two factors that can affect ECFV?

A

A: The two factors that can affect ECFV are water excess or deficit and Na+ (sodium) excess or deficit.

286
Q

Q: Name three hormones that regulate ECFV.

A

A:
1. the Renin-Angiotensin-Aldosterone System (RAAS),
2. Natriuretic Peptides (NPs), and
3. Antidiuretic Hormone (ADH).

287
Q

Q: What triggers the release of renin in the Renin-Angiotensin-Aldosterone System (RAAS)?

A

A: Renin is released

  • in response to sympathetic stimulation of renal nerves,
  • decreased blood flow to the kidneys (systemic hypotension), or
  • reduced sodium-chloride delivery to the distal convoluted tubule sensed by the macula densa.
288
Q

Q: What is the role of angiotensin II in the RAAS?

A

A:

  • Angiotensin II is a potent vasoconstrictor that increases systemic vascular resistance (SVR).
  • It also stimulates the release of aldosterone from the adrenal cortex.
289
Q

Q: What is the effect of aldosterone on renal function?

A

A: Aldosterone increases the renal absorption of sodium (and water) in the distal convoluted tubules and collecting ducts, which leads to increased plasma volume.

290
Q

Q: What triggers the release of Natriuretic Peptides (NPs)?

A

A:

  • Natriuretic Peptides (NPs) are released in response to atrial stretch or neurohormonal stimuli.
  • They are released in hypervolemic states.
291
Q

Q: What is the role of NPs in regulating blood pressure?

A

A:

  • NPs cause excretion of salt and water in the kidneys, reducing blood volume and blood pressure.
  • They also decrease renin release and act as vasodilators, decreasing systemic vascular resistance (SVR) and blood pressure.
292
Q

Q: Name two types of Natriuretic Peptides.

A

A: The two types of Natriuretic Peptides are atrial natriuretic peptide (ANP) and brain-type natriuretic peptide (BNP).

293
Q

Q: What is the role of Antidiuretic Hormone (ADH)?

A

A:

  • ADH acts to increase the reabsorption of water in the kidney tubules, concentrating urine and increasing extracellular and plasma volume.
  • It also causes vasoconstriction of blood vessels, increasing SVR and blood pressure.
294
Q

Q: What stimulates the secretion of ADH?

A

A: ADH secretion is stimulated by reduced extracellular fluid volume (ECFV) or increased extracellular fluid osmolarity, which is monitored by osmoreceptors.

Cardio All My Notes (13 decks)

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