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Phase 1 > CVR 1: Cardiovascular > Flashcards

CVR 1: Cardiovascular Flashcards

1
Q

What are the four main functions of blood?

A

Transport of nutrients, waste products, and hormones around the body.
Regulation of temp, pH, water balance.
Immunity (white blood cells & antibodies).
Clotting.

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2
Q

What is the base of the heart?

A

Superior surface of the heart, formed mainly of the left atrium.

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3
Q

When do the coronary arteries fill with blood?

A

During diastole.

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4
Q

What is the mediastinum?

A

The thoracic cavity excluding the lungs (but includes the trachea).

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5
Q

In what compartment of the mediastinum would you find the aortic arch?

A

Superior compartment of the mediastinum.

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6
Q

Which compartment of the mediastinum contains the thymus?

A

Trick question! Thymus is across two compartments: the superior and the anterior inferior compartment.

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7
Q

What would you find inside the middle inferior compartment of the mediastinum?

A

Th heart inside the pericardial sac, the pulmonary trunk, and the ascending aorta.

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8
Q

What blood vessel do the coronary arteries originate from?

A

Ascending aorta.

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9
Q

What blood vessels does the brachiocephalic trunk of the aortic arch bifurcate into?

A

Right common carotid (right side of the head & neck).
Right subclavian (right upper limb).

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10
Q

One branch of the aortic arch is the brachiocephalic trunk. Name the other branches.

A

Left common carotid (left side of the head & neck).
Left subclavian (left upper limb).

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11
Q

Why are the aortic bodies important?

A

They contain chemoreceptors monitoring arterial O2 and CO2, visceral sensory information sent to CNS via vagus nerve -> reflex responses which regulate ventilation.

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12
Q

Where does the descending aorta lead to?

A

The thoracic and then abdominal aorta, supplying blood to lower body.

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13
Q

What connects the pulmonary trunk to the aortic arch?

A

Ligamentum arteriosum (fibrous, cord-like connection), remnant of ductus arteriosus.

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14
Q

What veins converge to form the superior vena cava?

A

left & right internal jugular and subclavian veins join to form left & right brachiocephalic veins. These two veins converge to become the superior vena cava.

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15
Q

Where does the trachea originate and terminate?

A

From the larynx in the midline of the neck to the sternal angle, where it bifurcates into left and right main bronchi (the carina).

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16
Q

Where is the trachea palpable?

A

Superior to the suprasternal notch.

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17
Q

Where does the oesophagus originate and terminate?

A

Originates from the pharynx and terminates at the stomach.

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18
Q

Is the oesophagus anterior or posterior to the trachea?

A

Posterior.

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19
Q

How do the phrenic nerves enter the thorax?

A

Descend through the neck and enter via the superior thoracic aperture.

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20
Q

Why are the phrenic nerves important for respiration?

A

Innervate the diaphragm and pericardium.

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21
Q

From what spinal nerves do the phrenic nerves originate from?

A

C3, C4, C5 (“keep the diaphragm alive”).

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22
Q

Where do the vagus nerves originate?

A

Brainstem.

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23
Q

Describe the structure of the pericardium.

A

Two layers:
Tough outer fibrous layer attached superiorly to the great vessels, and inferiorly to the diaphragm. Innervated by phrenic nerves.
Thin inner serous layer; parietal and visceral layers which are continuous with each other, pericardial fluid between them in the pericardial cavity.

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24
Q

What is another name for the inferior surface of the heart?

A

The diaphragmatic surface.

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25
Q

What part of the heart forms the apex and where is the apex palpable?

A

The left ventricle forms the apex.
The apex beat is palpable at the left 5th intercostal space, in the midclavicular line.

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26
Q

What are the ear-like appendages/outpouchings of the walls of the atria called?

A

Auricles.

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27
Q

What causes pericardial effusion?

A

Fluid in pericardial space from e.g. pericarditis or trauma.

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28
Q

Why can severe and rapid pericardial effusion cause cardiac tamponade?

A

Fibrous layer of the pericardium cannot stretch, so heart is compressed and unable to fill properly.

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29
Q

What nerves do the recurrent laryngeal nerves originate from?

A

Vagus nerves - recurrent laryngeal nerves ascend back up the neck to the larynx.

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30
Q

Why might lung cancer cause a hoarse voice?

A

Cancer at apex of lung may involve the recurrent laryngeal nerves, leading to paralysis of the ipsilateral intrinsic laryngeal muscles, so cannot fully adduct vocal cords.

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31
Q

You examine a patient and note they have pitting oedema of their ankles. Blood tests show that their blood albumin level is low. Describe the relationship between albumin and oedema.

A

A low albumin causes a decrease in oncotic pressure and water diffuses from the blood into the interstitial fluid

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32
Q

A healthy student drinks 2 litres of water in 5 mins. Describe the physiological response.

A

The excess fluid causes a decrease in blood osmolality (osmolarity) which in turn causes a reduction / stopping of Anti Diuretic Hormone release. The kidneys therefore excrete more water leading to increased urine volume.

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33
Q

Renin is a proteolytic enzyme.
What is the principal site of renin production?

A

Juxtaglomerular cells

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34
Q

Anti-diuretic hormone (ADH) acts on the kidneys to promote water retention.
What is the site of synthesis of ADH (antidiuretic hormone)?

A

Synthesised by the supraoptic and paraventricular nuclei of the hypothalamus.

However it is then stored in the posterior pituitary gland.

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35
Q

Renin is a proteolytic enzyme
What is the key action of renin in the renin-angiotensin-aldosterone system (RAAS)?

A

Renin is a proteolytic enzyme which activates angiotensinogen to produce angiotensin I.

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36
Q

Aldosterone promotes sodium reabsorption in the kidneys.

Where is aldosterone synthesised, what is it, and what is its main function in the renin-angiotensin-aldosterone system?

A

Steroid hormone released from the adrenal cortex in response to stimulation by angiotensin II.

It promotes sodium reabsorption and potassium secretion in the distal tubules of the kidneys.

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37
Q

Explain the difference between sensible and insensible fluid loss.

A

Insensible fluid loss is loss that is not easily measured e.g. sweating, water lost from respiration, evaporation during abdominal surgery.

Sensible fluid loss is that which is easily measured e.g. urine output, vomit, fluid in surgical drains.

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38
Q

Where do the coronary arteries originate from and what are they called?

A

The aortic root. Right coronary artery and left main stem.

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39
Q

How many pairs of ribs are there and which vertebra do they attach to?

A

12 pairs, each pair attaching to a thoracic vertebra (of which there are 12!).

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40
Q

Where is the xiphisternum?

A

Inferior end of sternum

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41
Q

What are the three sets of intercostal muscles and which are for inspiration/expiration?

A

External = for inspiration.
Internal & innermost = for expiration.

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42
Q

Where is the mitral valve and how many leaflets/cusps does it have?

A

In between the left atrium and left ventricle. Two cusps/leaflets.

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43
Q

Where does the phrenic nerve originate from?

A

C3, C4, C5

“C3, 4, 5 keep the diaphragm alive”
Innervates diaphragm and pericardium.

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44
Q

Where does the vagus nerve originate from?

A

Cranial nerve X (10th cranial nerve).

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45
Q

How many lobes does each lung have?

A

Right lung = 3 lobes.
Left lung = 2 lobes.

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46
Q

True or false: Each lobe of the lung has its own air, blood, and nerve supply.

A

True!

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47
Q

Which pleura is closer to the lung tissue, parietal or visceral?

A

Visceral pleura.
(Think visceral feeling!)

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48
Q

What is the buffy coat?

A

When blood is put in a centrifuge, the buffy coat is the very small layer in between the haematocrit and the plasma, containing platelets and neutrophils.

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49
Q

What component of the blood causes oncotic pressure?

A

Albumin (a protein).

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50
Q

What is the difference between osmotic and oncotic pressure?

A

Osmotic pressure is the force driving water from low concentration of solutes to high concentration.
Oncotic pressure is specifically the osmotic pressure generated by large molecules in the blood (mainly albumin), also known as colloid osmotic pressure.

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51
Q

What are Starling forces?

A

The forces involved in the movement of water between capillaries and interstitial fluid.
Hydrostatic, osmotic, and oncotic pressure.

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52
Q

What is the function of plasma in relation to temperature?

A

Plasma acts as a heat sink to stabilise overall body temperature. Moves excess heat from “hot” organs e.g. liver and muscle, and circulates to extremities.

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53
Q

How do proteins buffer hydrogen ions in the plasma?

A

Amino acid side chains bond to H+ in acidic conditions, acting as a base, to attempt to return to neutral pH.
In alkaline conditions, amino acid acts as an acid and releases H+.

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54
Q

What is complement?

A

A specialised series of proteins that contribute towards the inflammatory response, main goal is to kill pathogens and deal with rogue proteins. Also called the complement system or the complement cascade.

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55
Q

What are the three pathways in the complement system?

A

Classical pathway.
Alternative pathway.
Lectin pathway (initiated by specific sugars on the surface of microbes)

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56
Q

Why does the alternative pathway in complement cascade occur faster than the classical pathway?

A

It takes time for WBCs to create antibodies, which the classical pathway requires for activation. Where as the alternative pathway is activated directly by pathogens or damaged cells.

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57
Q

What is the term for when complement coats pathogens to enhance their recognition and ingestion by phagocytes?

A

Opsonisation.

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58
Q

What are the main four functions of complement?

A

Opsonisation.
Lysis.
Inflammation (attracting immune cells to site).
Clearance of immune complexes.

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59
Q

What part of complement forms the membrane attack complex?

A

MAC, C5b to 9

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60
Q

Where are plasma proteins such as albumin, complement, and clotting factors produced?

A

In the liver.

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61
Q

What is haemostasis?

A

A normal physiological response to bleeding, involves activation of the coagulation cascade and formation of the platelet plug.

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62
Q

What are the three pathways of the coagulation cascade?

A

Intrinsic, extrinsic, and common.

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63
Q

What is the coagulation cascade?

A

Series of proteolytic enzymatic reactions that lead to the formation of a blood clot by converting soluble fibrinogen into insoluble fibrin.

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64
Q

How is the intrinsic pathway of the coagulation cascade triggered?

A

Damage to the vascular endothelium exposes collagen, which activates factor XII, starting cascade.
XII -> XIIa -> XI -> XIa -> IX
IX and VIIIa then both activate factor X in common pathway.

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65
Q

How is the extrinsic pathway of the coagulation cascade triggered?

A

External trauma causing blood to escape from vessel, Tissue Factor (TF) released from damaged tissue. TF combines with Factor VIIa, activating Factor X in common pathway.

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66
Q

Which coagulation cascade pathway is faster, intrinsic or extrinsic?

A

Extrinsic pathway is faster.

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67
Q

What is the convergent point for both intrinsic and extrinsic pathways in the coagulation cascade?

A

Factor X - the start of the common pathway.

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68
Q

What are the key steps of the common pathway of the coagulation cascade?

A
  1. Activated factor X + factor Va converts prothrombin (factor II) to thrombin (factor IIa).
  2. Thrombin converts fibrinogen (factor I) to fibrin.
  3. Fibrin forms a mesh that strengthens platelet plug.
  4. Thrombin also activates factor XIII which cross-links fibrin to form a stable clot.
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69
Q

What regulates the coagulation cascade?

A

Antithrombin III
Protein C and Protein S
Tissue Factor Pathway Inhibitor (TFPI).

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70
Q

How does antithrombin III affect the coagulation cascade?

A

Inhibits thrombin and Factors IXa, Xa, XIa, and XIIa.

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71
Q

What inactivates Factors Va and VIIIa to slow down coagulation cascade?

A

Protein C and Protein S

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72
Q

Does Tissue Factor Pathway Inhibitor (TFPI) inhibit the extrinsic or intrinsic pathways of the coagulation cascade?

A

Extrinsic - blocks Tissue Factor VIIa complex.

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73
Q

What is fibrinolysis?

A

Breakdown of fibrin by a cascade of proteolytic enzymes.

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74
Q

What are the key components in fibrinolysis?

A

Plasminogen, tissue plasminogen activator, plasmin (a fibrinolytic protease).

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75
Q

What is another term for platelets?

A

Thrombocytes.

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76
Q

How are platelets derived?

A

From megakaryocytes in the bone marrow, which produce multiple platelets from one megakaryocyte. Platelets are small, anucleate cell fragments.

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77
Q

How long to platelets live for?

A

7-10 days.

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78
Q

What are the key functions of platelets?

A
  1. Form platelet plug to stop bleeding.
  2. Release chemicals to attract other platelets and clotting factors.
  3. Clot stabilisation - work with fibrin.
  4. Release growth factors for wound healing.
  5. Trigger inflammation - recruit and activate leucocytes, release pro-inflammatory mediators.
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79
Q

How are platelets activated?

A

Damage to blood vessel endothelium exposes collagen.
Platelets stick to exposed collagen and release chemical signals (e.g. ADP, thromboxane) that activate more platelets.

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80
Q

How do platelets form a plug (platelet aggregation)?

A

When platelets are activated e.g. by collagen, they change shape from smooth discoid to spiky stellate. Stick to each other like velcro, and bond together chemically.

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81
Q

Which protein in plasma is essential for blood clotting?

A

Fibrinogen.

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82
Q

Which component in plasma is most responsible for maintaining oncotic pressure?

A

Albumin

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83
Q

What is the primary role of complement proteins in plasma?

A

Coating pathogens to enhance phagocytosis.

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84
Q

What triggers the intrinsic pathway of the coagulation cascade?

A

Damage to the blood vessel’s endothelium, exposing collagen.

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85
Q

What percentage of blood volume is erythrocytes (haematocrit)?

A

45%

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86
Q

Why to erythrocytes have a biconcave shape?

A

To increase the surface area for gaseous exchange.

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87
Q

What is the diameter of an erythrocyte?

A

10 mircometres

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88
Q

Why do erythrocytes have a finite life?

A

No nucleus (to make more space for haemoglobin) so can’t repair itself.

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89
Q

Where are erythrocytes produced?

A

In the bone marrow.

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90
Q

What is the Bohr shift?

A

On the oxygen affinity curve, shift to the right meaning reduced affinity for O2 of haemoglobin, means more O2 is passed onto tissues and occurs in conditions when there is higher demand for O2 e.g. raised temperature.

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91
Q

How is 2,3-DPG produced?

A

Produced by erythrocytes during glycolysis, in the Lubering-Rapoport Pathway.

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92
Q

How is 2,3-diphosphoglycerate different to 2,3-biphosphoglycerate?

A

They’re the same thing!
2,3-DPG and 2,3-BPG are the same thing.

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93
Q

When is production of 2,3-DPG increased and why is this important?

A

Increased by factors associated with increased tissue O2 demand e.g. hypoxia, anaemia, low pH.
Important because 2,3-DPG reduces the affinity of haemoglobin for O2, so promotes release from RBCs into tissues.

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94
Q

What has a higher affinity for O2, myoglobin (Mb) or foetal haemoglobin (HbF)?

A

Myoglobin in muscle has the highest affinity for O2!
Both HbF and Mb have higher affinity for O2 than adult haemoglobin (HbA), so can “steal” O2 from HbA.

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95
Q

What is carbaminohaemoglobin?

A

When CO2 binds to haemoglobin for transport to the lungs.

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96
Q

How does the chloride (Hamburger) shift relate to transport of CO2?

A

CO2 isn’t soluble in blood, so moves into RBCs and is converted to HCO3- by carbonic anhydrase. HCO3- leaves RBC in 1:1 ratio with Cl- to maintain neutral charge. This is the chloride shift. CO2 transported as HCO3- to the lungs, where it then re-enters RBCs again in exchange for Cl- as reverse chloride shift, and is converted back into CO2, which is diffused into alveoli and exhaled.

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97
Q

How is CO2 transported in the blood?

A

As carbaminohaemoglobin (CO2 bound to haemoglobin)
As HCO3- (converted in RBC then moved into blood by chloride shift)
As CO2, directly dissolved in plasma (10%).

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98
Q

How long does it take for bone marrow to produce RBC and what is this process called?

A

3 weeks. Erythropoiesis.

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99
Q

Where is erythropoietin produced?

A

In the kidney (peritubular fibroblasts).

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100
Q

How are old RBCs removed and what is this process called?

A

Surface changes e.g. damage recognised by macrophages and RBC is digested by them in the spleen and liver. Erythrophagocytosis.

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4
5
Perfectly
101
Q

What is the most common leucocyte and what is their function?

A

Neutrophils, involved in initial response and engulf/destroy pathogens.

102
Q

What are B cells, T cells, and Natural Killer (NK) cells?

A

All are types of lymphocytes.
B & T cells = adaptive immunity.
B cells produce immunoglobulins (antibodies).
T cells release cytokines and cytotoxic molecules.
Natural Killer cells = innate immunity. They destroy virus-infected cells and tumour cells.

103
Q

Which cells present antigens?

A

Macrophages and dendritic cells.

104
Q

Which leucocytes are involved in innate immunity?

A

Basophils, eosinophils, neutrophils, mast cells, natural killer cells.

105
Q

How do neutrophils destroy pathogens?

A

Neutrophils are phagocytes - they engulf bacteria and fungi and break them down. First responders to sites of infection or injury.

106
Q

What is the lifespan of neutrophils?

A

5-90 hours.

107
Q

What do B cells differentiate into when activated by an antigen?

A

Plasma cells that produce antibodies.
Memory cells which retain immunity.

108
Q

What are immunoglobulins?

A

Glycoprotein molecules produced by B cells (and plasma cells) in response to an antigen. E.g. IgG, IgM.

109
Q

How long does it take to produce IgM/IgG response?

A

Around 4 days.

110
Q

Why is IgM important?

A

It’s the first antibody produced in response to an infection and is effective at activating complement.

111
Q

Where might you find IgA and what is its role?

A

In mucosal areas e.g. digestive and respiratory tracts. Protects mucous membranes.

112
Q

Why is IgG important?

A

It’s the most abundant antibody in extracellular fluid, provides long-term immunity.

113
Q

What immunoglobulin is involved in allergic responses and defence against parasitic infections?

A

IgE.

114
Q

What is the key role of IgD?

A

Functions mainly as receptor on immature B cells, helping initiate immune response.

115
Q

What are the 5 key roles of immunoglobulins?

A
  1. Neutralisation (bind to pathogens to prevent them entering cells).
  2. Opsonisation (tag pathogens for destruction by phagocytes).
  3. Complement activation (IgG & IgM).
  4. Agglutination (clump pathogens together so immune cells can find them easily)
  5. Antibody-Dependent Cellular Cytotoxicity (bind to infected cells to signal NK cells to destroy).
116
Q

Where are T cells produced?

A

In the bone marrow, but mature in the thymus.

117
Q

What are CD4+?

A

Helper T cells, assist other immune cells e.g. B cells

118
Q

What are CD8+

A

Cytotoxic T cells, directly kill infected or abnormal cells.

119
Q

What is the key function of regulatory T cells (Tregs)?

A

Help suppress inappropriate immune responses and maintain immune tolerance.

120
Q

How do natural killer cells destroy virus-infected and cancer cells?

A

Release perforin and granzymes to induce apoptosis.

121
Q

Which is the largest leucocyte?

A

Monocytes.

122
Q

What do monocytes differentiate into?

A

Macrophages and dendritic cells.

123
Q

What is the main function of monocytes?

A

Phagocytose (eat) dead cells, pathogens, and debris.
Also play a role in chronic inflammation.

124
Q

What leucocyte is useful in killing parasites and how does it do this? What else is this neutrophil involved in?

A

Eosinophils - release toxic granules.
Also involved in inflammatory responses e.g. in asthma.

125
Q

Which is the least common leucocyte and what is its functions?

A

Basophils. Involved in allergic reactions, inflammation - release histamine and heparin. Also help defend against parasites.

126
Q

Name three antigen presenting cells.

A

B cells, macrophages, dendritic cells.

127
Q

Which neutrophils are granulocytes?

A

Basophils, eosinophils, neutrophils.

128
Q

Which neutrophils are agranulocytes?

A

Lymphocytes and monocytes.

129
Q

What cell do all granulocytes differentiate from?

A

Myeloblasts.

130
Q

Where is the sternal angle?

A

Between the manubrium and the sternal body, at level between 4th & 5th thoracic vertebra.

131
Q

How does the sternal angle divide the mediastinum?

A

Above sternal angle = superior mediastinum.
Below sternal angle = inferior mediastinum.

132
Q

What is the mediastinum?

A

Everything in the thoracic cavity between the lungs. Lungs are not included in the mediastinum!

133
Q

What would you find in the middle mediastinum?

A

The heart!

134
Q

What would you find in the posterior mediastinum?

A

Oesophagus, thoracic duct, phrenic nerve etc.

135
Q

What is the fossa ovalis?

A

Depressed structure in between right and left atriums, remnant of foramen ovale.

136
Q

What are the smooth and rough portions of the atria called?

A

Smooth = sinus venarum
Rough = trabeculated

137
Q

What is the crista terminalis?

A

Ridge of myocardium in the right atrium, vertical, separates sinus venarum and trabeculated portions of atrium.

138
Q

Does the left atrium have a crista terminalis?

A

No, only the right atrium has a crista terminalis.

139
Q

In the fibrous skeleton of the heart, which valves are connected, and what is this connection called?

A

Mitral and aortic valves.
The aorto-mitral continuity.

140
Q

Where does the coronary sinus drain into?

A

The right atrium.

141
Q

Where do the coronary arteries lie in the heart?

A

In grooves in between the chambers of the heart, under pericardium embedded in fat.

142
Q

What arteries does the left mainstem split into?

A

Left anterior descending, which splits into septal and diagonal arteries.
Circumflex, which becomes obtuse marginal artery.

143
Q

What is coronary arterial dominance?

A

Determined by the vessel which gives rise to the posterior descending artery (PDA).
80-85% of people are right dominant, meaning the PDA is supplied by the right coronary artery from the acute marginal.

144
Q

What makes up the right heart border?

A

Superior vena cava and the right atrium.

145
Q

What makes up the left heart border?

A

Aortic knuckle, left pulmonary artery, left atrial appendage, and left ventricle.

146
Q

What divides the anterior, middle, and posterior mediastinum?

A

The pericardium.

147
Q

Are the mitral and tricuspid valves an intrinsic part of the atria or ventricles?

A

Ventricles.

148
Q

How are the atrioventricular valves prevented from everting into the atria during systole?

A

Papillary muscles (part of the ventricle) are attached to the valves via chordae tendinae.

149
Q

Are the semilunar valves (aortic and pulmonary) an intrinsic part of the ventricles or the great arteries?

A

The great arteries.

150
Q

How many pulmonary valves are there?

A

Four.

151
Q

Which coronary artery runs in the anterior inter-ventricular groove?

A

Left Anterior Descending.

152
Q

What part of the heart does the diagonal coronary artery branch supply?

A

Left ventricle.

153
Q

Which groove does the circumflex artery run in?

A

Left atrioventricular groove.

154
Q

What part of the heart does the obtuse marginal branches supply?

A

Posterolateral left ventricular wall

155
Q

Which groove does the right coronary artery run in?

A

The right atrioventricular groove.

156
Q

Which groove does the posterior descending artery run in and where does it supply?

A

Posterior interventrciular groove.
Supplies inferior septum and left ventricle.

157
Q

What percentage of people are left dominant (circumflex supplies posterior descending artery)?

A

10%

158
Q

What does it mean if someone is co-dominant in relation to their coronary arteries, and what percentage of people are co-dominant?

A

Right coronary artery and circumflex both help supply the posterior descending artery.
20% of people are co-dominant.

159
Q

Why is the oxygen affinity curve non-linear?

A

Because of co-operative binding. When O2 binds to haemoglobin, it changes shape which increases affinity to bind more O2.

160
Q

How does 2,3 DPG reduce affinity of Hb for O2?

A

2,3 DPG reduces the co-operative binding effect by stabilising the low O2 binding state of Hb, not allowing bound O2 to change the shape of Hb to increase affinity.

161
Q

In the Luberin-Rapoport pathway, what enzyme is important to catalyse the reaction of 1,3 Biphosphoglycerate into 2,3 Biphosphoglycerate?
What happens to this enzyme in conditions where tissues have high O2 demand?

A

Biphosphoglycerate mutase.
Preferentially active in conditions where tissues have high O2 demand to increase 2,3 DPG production.

162
Q

What different actions does MHC Class II presentation vs MHC Class I presentation have?

A

Both are antigen-presenting molecules.
MHC class II presentation activates helper T cells (CD4+), causing them to release cytokines.
MHC class I presentation activates cytotoxic T cells (CD8+), which directly kill infected cells via apoptosis.

163
Q

What processes does cytokine release trigger?

A

Activates B cells to produce antibodies to neutralise and opsonise pathogens, and activate complement.
Enhances macrophage activity to destroy pathogens.
Activates cytotoxic T cells to kill infected cells.

164
Q

What percentage of blood flow (cardiac output) goes to the brain?

A

14%

165
Q

What organ receives the largest proportion of cardiac output?

A

The liver, 27%

166
Q

What percentage of cardiac output is received by the kidneys?

A

22%

167
Q

Which receives a higher percentage of cardiac output, the brain or the muscles?

A

The muscles, 15% (the brain receives 14%).

168
Q

What percentage of blood volume is held in the small veins and venules, and what term describes these vessels?

A

43%
Capacitance vessels (they hold the majority of blood in the body, can accommodate change in blood volume)

169
Q

What holds a larger percentage of blood volume, large systemic veins or systemic arteries?

A

Systemic veins; 20%
(systemic arteries = 10%)

170
Q

What would happen to MAP if the aortic valve failed?

A

Diastolic pressure would be lost, therefore MAP would decrease.

171
Q

Which vessels provide the principal site of resistance to vascular flow?

A

The arterioles.

172
Q

What is the relationship between radius and flow in Total Arteriolar Resistance (TPR)?

A

Vascular smooth muscle contracts (vasoconstriction) -> decreased radius -> increases resistance -> decreases flow.

173
Q

What does myogenic tone mean?

A

Vascular smooth muscle is never completely relaxed, resting level of contractility.

174
Q

How does the body control Total Arteriolar Resistance?

A

Local signalling/factors, autonomic nervous system, and hormonal control.

175
Q

How does the respiratory pump aid venous return?

A

Inspiration:
1. Diaphragm descends which increases intra-abdominal pressure, increasing pressure in abdominal veins.
2. Pressure in thorax decreased (because of diaphragm descending), decreasing pressure in right atrium and intrathoracic veins.
3. Increases pressure difference between peripheral veins and heart, increasing venous return.
4. Reverse does not occur during expiration because of valves.

176
Q

What is the equation for cardiac output?

A

CO = HR x SV

(cardiac output = heart rate x stroke volume)

177
Q

What is cardiac output?

A

Quantity of blood in L being pumped around the body.

178
Q

What is stroke volume?

A

The amount of blood leaving the left ventricle and entering the aorta.

179
Q

What is the equation for mean arterial pressure (MAP)?

A

MAP = diastolic + 1/3 PP

PP (pulse pressure) = systolic - diastolic.

180
Q

What is the equation for blood pressure and what other equation does this relate to?

A

BP = CO x TPR

(blood pressure = cardiac output x total peripheral resistance)

Ohm’s law: V=IR
(voltage (or pressure) = current (or flow) x resistance)

181
Q

What is important to remember about Poiseuille’s equation?

A

It is to do with how flow is mainly governed by vessel diameter - the equation uses radius and it is to the power of 4, so exponential curve.

182
Q

Explain how the Frank-Starling Mechanism relates to cardiac muscle.

A

Stroke volume increases as end-diastolic volume (EDV) increases due to the length-tension relationship of muscle.
If EDV is low, sarcomeres aren’t stretched enough to contract forcefully.
If EDV is too high (e.g. in heart failure), sarcomeres are overstretched and can’t contract efficiently -> therefore lower stroke volume.

183
Q

What is myogenic autoregulation?

A

How arterioles maintain constant pressure (also seen in other vessels).
When vascular smooth muscle is under increased pressure it is stretched, increasing the diameter, and then lowering the pressure, it responds by constricting until diameter is back to normal or slightly reduced.

184
Q

Which organs have excellent intrinsic ability of myogenic autoregulation?

A

Kidney, Brain, Heart.

185
Q

Does the skin have good myogenic autoregulation?

A

No. It has poor myogenic autoregulation.

186
Q

Does skeletal muscle use extrinsic or intrinsic control to regulate blood pressure in vessels?

A

Both.
Extrinsic at rest, during exercise intrinsic mechanisms dominate.

187
Q

Is EDRF (Endothelium Derived Relaxing Factor) the same as NO (Nitric Oxide)?

A

NO is a type of EDRF.

188
Q

What effect does NO (Nitric Oxide) have on vascular endothelium and where is it produced?

A

NO is produced in the endothelium, acts on smooth muscle cells of vessel wall to cause vasodilation.

189
Q

What is endothelin?

A

A peptide produced in vascular endothelium that causes smooth muscle contraction in blood vessels, causing vasoconstriction.

190
Q

Name some triggers for endothelin production.

A

Angiotensin II.
Vasopressin (ADH).
Cytokines.
Thrombin.
Oxygen free radicals.
Shearing forces.

191
Q

Name some inhibitors of endothelin production.

A

NO (Nitric Oxide).
Prostacyclin.
ANP (Atrial Natriuretic Peptide).

192
Q

What affect does prostacyclin (PGI2) have on blood vessels and where/how is it produced?

A

Prostacyclin is a vasodilator.

In vascular endothelium, from breakdown of membrane phospholipids into arachiodonic acid (AA), COX enzyme converts AA into prostacyclin.

193
Q

Does adrenaline cause vasoconstriction or vasodilation?

A

Vasoconstriction in the skin, but causes vasodilation in vital organs to increase flow to these important areas.

194
Q

Where are the primary baroreceptors?

A

In the carotid sinus and aortic arch.

195
Q

Where are the secondary baroreceptors?

A

Veins, myocardium, and pulmonary vessels.

196
Q

In the baroreceptors, which nerve is afferent (going to the brain) and which are efferent (going to vessels to effect change)?

A

Afferent = glossopharyngeal (cranial nerve IX)
Efferent = sympathetic and vagus (cranial nerve X)

197
Q

What happens to baroreceptors when there is long-term change e.g. in hypertension?

A

They adapt/reset to a new baseline.

198
Q

Which part of the brain controls BP and how?

A

The medulla.
Receives information from baroreceptors, chemoreceptors (O2/CO2/pH), hypothalamus, cerebral cortex, skin.
Stimulates either parasympathetic or sympathetic nervous systems.

199
Q

Which part of the hypothalamus increases BP and HR?

A

Posterolateral.

200
Q

Explain what happens when baroreceptors sense increased BP?

A

↑BP ⇒ ↑Firing of baroreceptors ⇒ ↑PNS and↓SNS ⇒ ↓CO (by ↑HR) and TPR (by vasoconstriction) = ↓BP

201
Q

What are the short-term and long-term controls of BP?

A

Short-term: baroreceptors.
Long-term: blood volume (controlled by kidneys, RASS)

202
Q

What is the primary role of arterioles in the vascular system?

A

Arterioles are the main site of resistance to vascular flow, impacting total peripheral resistance and distributing blood flow.

203
Q

Describe the function of baroreceptors in blood pressure regulation.

A

They sense arterial pressure changes and adjust autonomic output to stabilise blood pressure.

204
Q

What does it mean that the heart is a functional syncytium?

A

All the cells in the heart are linked, so can function and contract as one. Atria and ventricles form two different syncytiums so they don’t contract at the same time!

205
Q

How are myocytes linked together?

A

At intercalated discs, physically slot together, and linked by desmosomes (joining the intermediate filaments of different cells) and gap junctions for electrical impulses to move across.

206
Q

What does the myocyte membrane pump do?

A

K+ pumped IN to cells.
Na+ and Ca2+ pumped OUT of cells.
Being pumped against electrical and concentration gradients, so requires active transport (ATP).

207
Q

What does the nernst equation calculate?

A

Resting membrane potential.

208
Q

What channels/pumps are active in myocyte membrane during resting potential and why?

A

Na/K ATPase - using active transport to pump K+ into cell and Na+ out against concentration gradient, creating a voltage.

Na/K leak channels - passive diffusion, not much allowed through.

209
Q

When do voltage gated sodium channels open in myocyte cell membranes, and what happens?

A

Depolarisation, once certain action potential reached.
Large number of Na+ ions enter cell down their concentration gradient, causing charge inside the cell to increase rapidly.

210
Q

What happens in the small dip at the end of depolarisation in the cardiac action potential graph?

A

Transient outward potassium channel triggered to open by depolarisation, small number of K+ ions allowed to leave cell causing a small repolarisation (the dip).

211
Q

Why does the cardiac action potential graph plateau after depolarisation, instead of rapid repolarisation?

A

Slow calcium channels have a delayed opening following depolarisation, maintain the depolarisation by allowing Ca+ ions into the cell. Transient outward potassium channel is still open so some K+ leaving the cell, causing slight downwards slope towards repolarisation.

212
Q

When do delayed rectifier channels open during the cardiac action potential cycle?

A

During repolarisation to make charge inside the cell more negative again, cause large quantity of potassium to leave the cell by passive diffusion.
At the same time, slow calcium channels close so no further Ca+ ions can enter the cell.
Repolarisation occurs, bringing back to resting potential.

213
Q

How does the action potential spread along a muscle fibre and through the myocardium syncytium?

A
  1. Local depolarisation activates nearby Na+ channels, Na+ ions rush into cell.
  2. This causes adjacent Na+ channels to open.
  3. At gap junctions, Na+ ions allowed to travel directly across from one cell cytoplasm to next.
214
Q

How does intracellular calcium concentration become amplified during repolarisation?

A

Slow calcium channels allow calcium to diffuse into the cell.

SR (sarcoplasmic reticulum) triggered by RyR calcium receptors to release stored calcium in SR when intracellular calcium levels high.

215
Q

How does calcium cause contraction in the troponin-tropomyosin-actin complex?

A
  1. Calcium binds to troponin.
  2. Conformational change in tropomyosin reveals myosin binding sites.
  3. Myosin head can then cross-link with actin.
  4. Myosin head pivots causing muscle contraction.
216
Q

How does Sino-Atrial Node (SAN) myocytes differ in action potential from normal myocytes?

A

SAN myocyte has gradual increase towards depolarisation constantly, once reaches certain threshold triggers full depolarisation.
While normal myocytes do this too, SAN myocytes trend towards depolarisation more rapidly.

217
Q

What is the funny current and where do you find it?

A

Sodium leak channel in SAN myocyte that is always open, causes the more rapid trend towards depolarisation.

218
Q

How is heart rate increased/decreased in relation to calcium channels in the SAN?

A

Through actions on either number or permeability of calcium ion channels.

219
Q

How does age affect heart rate?

A

Number of calcium channels decreases with age, causing slower depolarisation in SAN.

220
Q

What is a chronotrope?

A

Something which increases the heart rate.

221
Q

What is an inotrope?

A

Something which increases the force of contraction.

222
Q

Does parasympathetic stimulation increase or decrease HR/force of contraction/CO?

A

Decreases.

223
Q

Which hormones control the sympathetic stimulation of the heart?

A

Adrenaline and noradrenaline.

223
Q

What hormone controls parasympathetic stimulation of the heart?

A

Acetylcholine.

224
Q

How does the His-Purkinje system allow rapid conduction of electrical impulse?

A

High permeability at gap junctions and very large fibres.

224
Q

How does the Atrioventricular Node delay the electrical impulse?

A

AVN has fewer gap junctions.

225
Q

What happens to fast Na+ channels during the absolute refractory period in the cardiac cycle, and when is this period?

A

Closed and inactivatable during the refractory period, during plateau phase, so depolarisation cannot occur too early, allowing heart time to refill.

226
Q

What are the Na+/K+ channels doing in the relative refractory period and when is this period?

A

Some Na+ channels are still inactivated.
K+ channels are still open.
During repolarisation, just before resting potential.

227
Q

Is sympathetic stimulation of heart positive or negative inotrope & chronotrope?

A

Positive; increases HR and contractility.

228
Q

How many squares is 1 second on an ECG?

A

25 x small 1mm squares = 5 big squares.
(speed = 25mm/sec)

229
Q

How many squares represent 1mV on an ECG?

A

2 big squares (10x small 1mm squares).

230
Q

How would you calculate the rate on an ECG?

A

Number of QRS segments x6

(1 ECG = 10 seconds)

231
Q

What does a positive deflection mean on an ECG?

A

Net current flow is towards the lead.

232
Q

What part of the ECG represents the SAN firing and atria depolarising?

A

P wave.

233
Q

What is happening during the PR interval?

A

Delay of signal passing through AV node.

234
Q

Why is the QRS complex higher voltage than P wave?

A

Ventricles have thicker walls than atria so have higher voltage in total.

235
Q

Where on the ECG does ventricular repolarisation occur?

A

In the T wave.

236
Q

What is a normal PR interval?

A

120-300 ms = 3-5 small squares.

237
Q

What is a normal QRS complex width?

A

less than 120ms (3 small squares).

238
Q

What is the QT interval and what is a normal QT interval?

A

Measure of time from ventricular depolarisation repolarisation.
Men: 350-440ms
Women: 350-460ms

239
Q

What is a bipolar lead? Give examples.

A

Measures potential difference (voltage) between two electrodes; one electrode designated positive, other negative.
Leads I, II, and III are all bipolar leads.

240
Q

What is a unipolar lead? Give examples.

A

Measures potential difference (voltage) between an electrode (positive) and a combined reference electrode (negative) using data from other electrodes.
aVR, aVL, and aVF are all unipolar. V1-V6 are also unipolar. Reference point in these leads is the middle of the heart.

241
Q

What is left axis deviation?

A

When lead I is positive QRS, lead II is negative.
They are Leaving each other. Left axis deviation.
Normal is both lead I and II have positive QRS.

242
Q

What is right axis deviation?

A

Lead I has negative QRS, lead II positive.
They are Reaching toward each other. Right axis deviation.
Normal is both lead I and II have positive QRS.

243
Q

Which coronary artery is represented by the inferior leads?

A

The right coronary artery.

244
Q

Which coronary artery is represented by the lateral leads?

A

Left circumflex.

245
Q

Which plane of the heart do the limb leads represent?

A

Coronal plane.

246
Q

Which plane of the heart do the chest leads represent?

A

Transverse plane.

247
Q

Which chest leads represent septal part of the heart and which coronary artery does this relate to?

A

V1 & V2
Left anterior descending/right coronary artery.

248
Q

Which chest leads represent the anterior part of the heart and which coronary artery does this relate to?

A

V3 & V4
Left anterior descending.

249
Q

Which chest leads represent the lateral part of the heart and which coronary artery does this relate to?

A

V5 & V6
Circumflex.

250
Q

ECG as a graph, what is the X axis and what is the Y axis?

A

X = time
Y = voltage

Phase 1 (11 decks)

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