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PHARM 213 Cardiovascular System > 2. Anatomy & Physiology of the Cardiovascular System > Flashcards

2. Anatomy & Physiology of the Cardiovascular System Flashcards

1
Q

Myocardial structure - macro-anatomy

A
  • Left ventricle is thicker to pump blood at a higher pressure around the body
  • Valves prevent backflow to increase efficiency of blood pumping through the heart
  • Spinal arrangement of heart muscle squeezes blood up the apex
  • In a healthy heart 60% of the volume of the heart chamber is squeezed out in each heartbeat – ejection fraction
  • Cardiac muscle cells contract ~20% due to shortening & bulging of the muscle cells
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2
Q

Intercalated discs contain

A
  • Gap junctions for cell-to-cell ion movement (rapid spread of electrical signals)
  • Desmosomes transfer force from cell-to-cell (end to end)
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3
Q

Cardiomyocyte sarcomere components

A
  • Myosin – thick filaments
  • Actin – thin filaments
  • Titin – spring which relaxes the muscle after contraction
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4
Q

Cardiomyocyte length-tension relationship

A
  • Frank-Starling Law states that the stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing a more forceful systolic contraction
  • Force development proportional to myofilament (actin & myosin) overlap
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5
Q

Cardiomyocyte ultrastructure

A
  • ~30% of the energy is used for regulation of contraction

- Depolarisation triggers calcium induced calcium release from the sarcoplasmic reticulum

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6
Q

Cardiac excitation-contraction coupling

A
  1. Ca enters cell during action potential plateau
  2. Triggers release of more Ca from sarcoplasmic reticulum
  3. Ca binds to myofilaments (troponin-C)
  4. Activates cross-bridge cycling
  5. Cell shortens
  6. Most Ca pumped back in SR
  7. Some Ca exits cell by Na-Ca exchanger & sarcolemmal Ca pump
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7
Q

Myofilament Ca2+ sensitivity & movement

A
  1. Ca2+ binds to Troponin-C (TnC)
  2. TnC changes conformation
  3. Tnl moves away from actin-myosin binding site
  4. Actin binds to myosin & contraction occurs
  5. As [Ca2+]I falls, Ca2+ dissociates from TnC
  6. Tnl again blocks actin-myosin binding site
  7. Relaxation occurs

Phosphorylation of Tnl (i.e. by beta-adrenergic signalling) promotes dissociation of Ca2+ from TnC & myocyte relaxation

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8
Q

Cardiac cycle - left vs right

A
  • Pressure is greater in the left side vs right side due to pumping blood further away from the heart
  • Ventricular volume is the same in both sides
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9
Q

Measuring cardiac function - echocardiography

A
  • Systolic function can be assessed by looking at a cross-sectional view of the heart (parasternal short axis)
  • Diastolic function can be assessed by looking at a longitudinal view of the heart (apical 4 chamber view)
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10
Q

Diastolic function - doppler flow (mitral inflow)

A

Measures blood flow velocity through mitral valve:

  • E wave – blood flowing into the ventricle by passive filling (due to pressure gradient)
  • A wave – blood flowing from atrium into the ventricle by active filling (due to atrial contraction)

Normal: E/A > 1
Impaired relaxation E/A < 1

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11
Q

Diastolic function - tissue doppler (mitral valve movement)

A

Measures velocity of tissue movement at mitral valve

  • E’ wave – passive LV filling
  • A’ wave – filling due to atrial contraction
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12
Q

Diastolic function – E/e’

A

E/e’ ratio increases with the severity of heart failure, correlates well with heart failure biomarkers (e.g. NT pro BNP values), & declines when heart failure improves

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13
Q

Electrical activation of the myocardium

A
  1. Depolarise atria
  2. Depolarise septum (left to right)
  3. Depolarise ventricular walls towards apex & up towards base
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14
Q

Biomarkers of heart damage

A
  • During onset of myocardial infarction plasma membranes of necrotic myocytes becomes leaky
  • Molecules e.g. CK-MB, myoglobin, troponin I leak out of the cell into circulation
  • These molecules can be used as biomarkers for diagnosis of myocardial infarction
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15
Q

Vascular tree

A
  • Arterial side is thicker than the venous side due to pressure difference
  • Valves are present in the venous side to help blood return to the heart
  • Movement such as walking/running helps blood flow back to the heart
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16
Q

Cardiac output distribution

A
  • Vascular ‘tree’ perfused in series
  • Organ ‘beds’ perfused in parallel
  • At rest, highest flow to gut & kidney ‘reconditioning’ organs
  • Flow through each ‘bed’ controlled at arterioles by local & central signals
17
Q

Capillary exchange

A

Comprised of hydrostatic fluid & osmotic pressure that drive interstitial fluid out of capillary (net filtration) & into capillary (net absorption)

18
Q

Capillary exchange & lymph formation

A
  • Network of blind-ending lymph capillaries lying near blood capillaries – permeable to protein & fluid
  • The lymphatic vessels contain excess interstitial fluid, white blood cells (immune cells), also transports fats from gut
  • Lymph flow is slow – aided by smooth muscle contractions around the lymph vessels – also used valves to aid flow
  • Lymph is directed through lymph nodes before returning to blood

Enters blood via:

  • Lymphatic duct (right side)
  • Thoracic duct (left side)

Both ducts empty into subclavian veins

Lymph nodes are important in the adaptive immune response
- Macrophages phagocytose microbes at the site of infection, then travel to the lymph nodes to trigger the immune response (via lymphocyte activation)

19
Q

Oedema

A

Accumulation of interstitial fluid

Increase in venous pressure:
- E.g. Congestive heart failure leads to venous pooling which results in fluid accumulation in the lungs

Increase in interstitial pressure

  • E.g. Lymph vessel blockage due to a parasitic infection results in gross oedema of the limbs (i.e. elephantiasis)
  • Note – caused by poor lymph drainage rather than capillary dysfunction
20
Q

Blood pressure

A
  • The driving force to push blood through the circulation
  • Pressure is related to resistance of the vessels
  • Resistance (systemic)&raquo_space; Resistance (pulmonary)
  • Biggest pressure drop in arterioles
  • Largest overall resistance in arterioles
21
Q

Mean arterial pressure (MAP)

A 
MAP = DP + 1/3 PP
PP = SP-DP
22
Q

Regulation of blood flow

A
  • Vasoconstriction – smooth muscle cells contract & increase the resistance of the vessels
  • Vasodilation – smooth muscle cells relax & decrease the resistance of the vessel
  • Blood flow decreases with increased resistance & increases with increased pressure gradient
CO = HR x SV
BP = CO X TPR
23
Q

Determinants of arteriolar blood flow

A

Systemic pressure maintenance:

  • Neural: Sympathetic tone autonomic nervous system (Adrenaline & Noradrenaline)
  • Circulating hormones (constrict): Angiotensin II, endothelin, adrenaline

Tissue flow protection:

  • Locally produced mediators (dilate): Nitric oxide (‘EDRF’), bradykinin, prostaglandins, histamine
  • Locally produced metabolites (dilate): CO2, adenosine, H+ (decrease pH), K+, temp, osmolarity, low O2
24
Q

Determinants of vessel blood flow – sympathetic NS activation

A
  • Noradrenaline constricts blood vessels
  • Adrenaline dilates blood vessels

Both act on smooth muscle cells

25
Q

Baroreflex regulation of blood pressure

A

Act on baroreceptors which are located in the carotid sinus & aortic arch

PHARM 213 Cardiovascular System (10 decks)

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