Cardiovascular Flashcards

1
Q

What are the three artery branches from the aortic arch?

A
  • Braceocephalic - Right subclavian + right common carotid
  • left common carotid
  • Left subclavian
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2
Q

What are the three tissues to form the heart wall ?

A

Epicardium
Myocardium
Endocardium

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3
Q

Describe the pericardium

A

Fibrous layer
Serous layer
Visceral layer

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4
Q

Describe the left and right coronary arteries and their branches

A

Left - Circumflex to coronary sulcus
anterior interventricular sulus
Right - Posterior interventricular
right marginal branch

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5
Q

Describe the coronary capillaries

A

capillaries to coronary veins to coronary sinus and then right atrium
coronary sinus from greater and middle cardiac veins

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6
Q

Describe the spread of excitation through the heart

A
  1. SA node
  2. AV node
  3. Atrioventricular bundle of his
  4. Right and left bundle branches
  5. Purkinje fibres
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7
Q

Describe the SA node

A

SA node sets the excitation of the heart, doesn’t have resting membrane at a stable level, depolarises to threshold spontaneously
- membrane has a leakage current in of sodium and efflux of potassium and funny current

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8
Q

Describe pacemaker cells

A

Auto-rhythmic fibres

  1. driving auto-rhythmic contractility activity of heart
  2. form specialised conducting system allow coordinated excitation of different regions of the heart
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9
Q

Describe the contractile fibres action potentials

A
  • Cardiac myocytes have a resting potential of -90mv and rapidly depolarise to +20mv when voltage gated sodium channels open then inactivated for a short time
  • Plateau - sodium current triggers opening of slow membrane bound ca2+ ion channels allowing small Ca2+ influx, triggers release of Ca2+ from sarcoplasmic reticulum and 250ms decreased k+ permeability
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10
Q

Describe the refractory period

A

Time when the muscle cell cannot fire a second action potential

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11
Q

Describe the three waves and intervals of ECG

A

P - depolarisation of atria
QRS - depolarisation of ventricles
T - depolarisation of ventricles
P-Q - conduction time between SA node and ventricles depolarise
S-T - period ventricular cells depolarised in plateau phase
Q-T - Ventricular depolarisation to depolarisation
0.6 seconds

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12
Q

Describe the AV node delay

A

Delay allows for atria to contract, result of time taken for calcium ions to enter sarcoplasm

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13
Q

Describe delayed depolarisation

A

Repetitive myocyte activity not driven by potentials arising from other cells intracellular calcium concentrations increasing beyond normal

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14
Q

Describe re entry as a disturbance of cardiac rhythm

A

Cardiac action potential dies out at the ventricles

  • unusual anatomical variations can form a network of cells that form a conductive ring
  • Re-enrty can occur because of slow conducting pathways following myocardial damage
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15
Q

Describe abnormal pacemaker activity

A
  • Pacemaker activity or ectopic pacemakers can develop elsewhere in the heart
  • Ectopic pacemaker can be induced by excessive sympathetic stimulation - caffeine, nicotine and hypoxia
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16
Q

Describe a heart block

A

Arises because the AV node becoming electrically isolated

  • partial into which to every 2/3 atrial contractions the ventricles will contract or in total where atria and ventricles contract independently
  • sporadic total AV node block can also occur results in periods of unconsciousness
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17
Q

Describe ventricular fibrillation

A

Irregular trace seen in acute heart attacks ventricles no longer pumps blood and death occurs

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18
Q

Describe the cardiac output

A
  1. cardiac action potential propagates from SA node through atria and to AV node - P wave on ECG
  2. After P wave begins atria contract, conduction of action potential slows at AV node as fibres have smaller diameters and fewer gap junctions, AV delay allowing atria to contract, ventricular systole begins
  3. Action potential propagates through bundle of his 0.2 seconds after P wave, depolarisation occurs producing QRS complex, partial repolarisation
  4. Contraction of ventricles after QRS and continues in ST segment
  5. Depolarisation of ventricular contractile fibres
  6. Ventricles relax and ventricular repolarisation is complete, both atria and ventricles and relaxed and cycle repeats
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19
Q

Describe 8 stages of heart cardiac cycle

A
  1. atrial contraction begins
  2. Atria eject blood into ventricles
  3. atrial systole ends, AV valve closes
  4. Isovolumetric ventricular contraction occurs
  5. Ventricular ejection occurs
  6. Semilunar valve closes
  7. Isovolumetric relaxation occurs
  8. AV valves open and passive ventricular filling occurs
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20
Q

Describe myosin

A

Two identical heavy chains bound to a pair of light chains

  • Amino terminal of heavy chain forms a motor head domain while carboxyl ended section of the heavy chain forms elongated tail
  • Tail forms alpha helix with second heavy myosin chain to form a dimmer
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21
Q

Describe Actin

A

Chain of globular actin molecules joined to form a helix
Each actin molecule has a binding site doe myosin head, the actin helix is coupled at every 7th. molecule to two other proteins tropomyosin and troponin

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22
Q

Describe tropomyosin

A

Rod shaped molecule binds via troponin molecule to the groove of actin helix where it masks myosin binding site

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23
Q

Describe troponin

A

A complex of 3 polypeptides troponin TIC.
T binds to actin
I binds to tropomyosin
C binds to calcium

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24
Q

Describe arterioles

A

Influence peripheral resistance and modify blood flow from arteries into capillaries - resistance vessels

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25
Q

Describe the metarteriole

A
  • terminal end of arteriole - supplies between 10-100 capillaries
  • Capillary junction the distal most muscle cells form precapillary sphincter and monitor blood flow into the capillary
  • distal end of the vessel has no smooth muscle and resembles capillary - thoroughfare channel
  • thoroughfare channel provides direct rout for blood from an arteriole to venule bypassing capillaries
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26
Q

What is vasomotion?

A

Intermittent blood flow due to alternating contraction and relaxation of smooth muscle cells of metarterioles

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27
Q

Describe capillaries

A

Microcirculatory system - connect arterioles to venules

- allow exchange fo fluid and metabolites between blood circulatory system and tissues

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28
Q

Describe venules

A
  • Collect blood from capillaries
  • Walls are ports and function as significant sites for exchanges of nutrients/ waste and white blood cell migration
    Venules merge to form larger vessels which the merge to form veins
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29
Q

Describe veins

A

Thin walls large lumen, contain valves

Takes blood to the heart, low pressure capacitance vessels

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30
Q

How much of the body’s blood os held in the different blood vessels?

A
Veins - 64%
Systematic capillaries - 7%
Arteries - 13%
Pulmonary capillaries - 9%
Heart - 7%
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31
Q

What are veins and venules known as?

A

Blood reservoirs

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32
Q

Describe transcytosis

A

Small quantities of material transported across capillary walls by being encapsulated within invaginations of the serial endothelial membrane released by exocytosis

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33
Q

Describe bulk flow

A

Fluid flows from blood to tissues via filtration dependent on blood hydrostatic pressure and interstitial fluid osmotic pressure
- reabsorption is pressure driven from interstitial fluid into blood capillaries

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34
Q

What is the equation for net filtration pressure?

A

(Blood hydrostatic pressure + interstitial fluid osmotic pressure) - (Blood colloid osmotic pressure + interstitial fluid hydrostatic pressure)

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35
Q

Describe blood hydrostatic pressure

A

BHP = hydrostatic pressure generated by blood pumping action of the heart and interstitial fluid osmotic pressure (IFOP)
- Promotes filtration

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36
Q

Describe blood colloid osmotic pressure (BCOP)

A

Promotes reabsorption

37
Q

Describe oedema

A

Increase in interstitial fluid volume
Filtration > Reabsorption
Normally only noticeable after a 30 % increase
- Increased capillary blood pressure increases capillary wall permeability to solutes
- caused by decrease in concentration of plasma proteins and kidney disease

38
Q

What is End diastolic volume?

A

Amount of blood in each ventricle at the end of ventricular diastole

39
Q

What sis end systolic volume ?

A

Amount of blood in each ventricle at the end of ventricular systole

40
Q

What is stroke volume?

A

Amount of blood pumping out of each ventricle during single heart beat

41
Q

Describe blood pressure

A
Blood flows from high to low pressure 
Flow is directly proportional to pressure and inversely proportional to resistance 
- Provides driving force 
- effective tissue perfusion 
- keep vessels open
42
Q

At what blood pressure does a person become unconscious if it drops below this level?

A

60 mmHg

43
Q

What is vascular resistance?

A

Dependent on lumen diameter, viscosity of blood and blood vessel length

44
Q

Describe blood viscosity

A

Dehydration and polycythaneia increase viscosity and resistance

45
Q

What are peripheral and systematic resistance/

A

Force that opposes blood flow in vascular system, dependent on the smaller vessels, arterioles being the most important

46
Q

Describe mean blood pressure with cardiac output and peripheral resistance

A

Decreased MBP = decreased CO x PR
Increased MBP = CO x increased PR
MPB= increased PR x decreased CO
Overall CO = MBP/PR

47
Q

Describe venous return

A

Volume of blood flowing back to the heart through systematic veins occurring due to left ventricle pressure
- If pressure increases in right atrium/ventricle venous return decreases
can be caused by a leaky tricuspid valve causes a build up of blood on venous side

48
Q

Describe skeletal muscle pump

A

While standing venous valves = open and blood flows up towards the heart, contraction of muscles compresses veins pushing blood through valve proximally

  • distal valve closes to prevent back flow
  • Muscle relaxation, pressure falls in compressed section and proximal valves close and distal opens
49
Q

Describe the respiratory pump

A

Movement of the diaphragm causing pressure changes

50
Q

Describe the cardiovascular centre control

A
  • Receives afferent information from sensory receptors and high brain centres ( limbic system and cerebral cortex)
  • Acted on by increase or decrease in firing rate by sympathetic/ parasympathetic neurones from autonomic nervous system
  • Heart receives sympathetic inputs via cardiac accelerator nerves that extend thoracic region of spinal cord
    Cardiac accelerator nerve and vagus nerve
51
Q

Describe cardiac reflexes

A
  • Status pf cardiovascular system arrives over visceral sensory fibres accompanying the vagus nerve and sympathetic nerves of cardiac plexus
  • Cardiac centres monitor baro and chemoreceptors innervated by glossopharyngeal and vagus nerve
  • Parasympathetic stimulus releases ACh to extend Repolarisation
  • Sympathetic stimulus releases noradrenaline to shorten repolarisation
52
Q

Describe long term regulation of blood pressure

A

Angiotensin- aldosterone system

  • When BP is low renin secreted by kidneys, transforms angiotensinogen to angiotensin 1 which is converted to angiotensin 2 by angiotensin converting enzyme (ACE)
  • Angiotensin 2 vasoconstricts arterioles and increases peripheral resistance increasing aldosterone secretion from adrenal gland and ADH secretion from the posterior pituitary to increase fluid retention and Nacl uptake
53
Q

What three hormones increase heart rate by effect on SA node?

A

Epinepherine/ adrenaline, noradrenaline/epinephrine and thyroid hormone

54
Q

What is preload?

A

Degree of stretching in ventricle muscle cells during ventricular diastole. Proportional to EDV - greater the preload = greater EDV

55
Q

What is after load ?

A

the amount of tension that the contracting ventricles must produce to force open the semilunar valves and eject blood - proportional to arterial BP + pulmonary BP

56
Q

What is preload influenced by?

A
  1. Venous return

2. Filing time - duration of ventricular diastole

57
Q

Describe contractibility of ventricles

A
  • Amount of force produced during contraction at a given preload, regulated by autonomic innervation and hormones
58
Q

What are factors that increase ventricle contractility?

A
  • Positive inotropic agents
  • Neurotransmitter and hormones of sympathetic nervous system
  • Beta adrenogergic agonists
59
Q

What are factors that decrease ventricle contractility?

A
  • Negative inotropic agents
  • parasympathetic neurotransmitters, Ca2+ channel blockers
  • Muscarinic agonists
  • sympathetic antagonists
  • Increase in K+ concentrations
  • Anoxia + acidosis
60
Q

Describe the cardioacceleratory centre and cardioinhibitory centre

A

Acceleratory - accelerates heart rate via sympathetic innervation of SA node and AV node
Inhibitory - Slows the heart rate
Both monitor changes in blood pressure via baroreceptors and pH via chemoreceptors

61
Q

Describe the autonomic regulation of the heart

A

Controlled by cardiovascular centre

  • receives afferent information from sensory receptors and higher brain centres (limbic system +cerebral cortex)
  • acts by increasing or decreasing firing rate of sympathetic inputs via cardiac acceleratory nerves extending from thoracic region of spine
  • ACh released by parasympathetic neurones opens chemically gated K+ channels in plasma membrane, slows rate of spontaneous depolarisation by increasing K+ - decreasing heart rate
62
Q

Describe the atrial reflex

A

Adjustments in heart rate in response to increase venous return.
when venous return increases and stretch receptors in right atrium walls - increase sympathetic activity - increasing heart rate and then cardiac output

63
Q

What nerves are involved in propagating impulses from baro and chemoreceptors ?

A

Afferent neurones in glossopharyngeal nerve from carotid sinus and vagus nerve from aortic arch

64
Q

What is tissue perfusion influenced by?

A
  1. cardiac output
  2. blood pressure
  3. peripheral resistance
65
Q

What are the tissue perfusion mechanisms/

A
  1. Autoregulation in tissues
  2. Neural mechanisms
  3. Endocrine response
66
Q

What are 6 local vasodilators?

A
  1. Decrease O2 and increase CO2
  2. Lactic acid
  3. NO
  4. Decrease pH and increase K+
  5. Histamine + pro inflammatory agents
  6. Elevated local temperature
67
Q

What are two vasoconstrictors?

A
  1. Thromboxanes - released by platelets in wound sites

2. Endothelins - damaged endothelial cells

68
Q

Describe the vasomotive centre

A

Two populations of cells located in the medulla oblongata, large group associated with wide spread vasoconstriction and smaller group associated with vasodilation

69
Q

Describe the control of vasoconstriction

A

Neurones inervating peripheral blood vessels in most tissues are adrenergic.
- they release NA which stimulates alpha adrenoreceptors located In plasma membrane of smooth muscle cells of blood vessels

70
Q

Describe control of vasodilation

A

Neurones innervating blood vessels in skeletal muscle and brain - stimulation of these neurones relaxes smooth muscle cells in arterioles - vasodilation
Most common synapse = cholinergic ACH trigger NO release
other synapses are nitroxidergic - NO release triggers vasodilation in smooth muscle cells

71
Q

Describe the baroreceptor reflex

A

located in carotid sinus , aortic sinus and wall of right atrium
Aortic monitors degree of aortic stretch

72
Q

Describe the atrial reflex

A

Increase blood pressure detected by baroreceptors, initiates regulatory feedback, signals to cardiovascular centre promoting

  • Inhibition of cardio acceleratory centre and stimulation of cardioinhibitory centre
  • inhibition of vasomotor cells associated with vasoconstriction
73
Q

Describe chemoreceptor reflex

A

Mediated by chemoreceptors in carotid bodies, aortic bodies in medulla oblongata
Sensitive to change
vasoconstriction - Decrease O2 and pH, increase cO2
vasodilation - Increase O2

74
Q

Describe control of increasing blood pressure with ADH

A
  • Decrease blood volume
  • Increase osmotic plasma concentration
  • ADH released at posterior lobe of pituitary gland
  • Increases peripheral constriction, increasing resistance and blood pressure
  • stimulates water conservation by the kidneys
75
Q

Describe control of increasing blood pressure with angiotensin 2

A
  • Decrease in blood pressure in kidneys
  • Juxtaglomerular cells release renin - angiotensin 2
  • Stimulates secretion of adrenal production of aldosterone
  • Stimulates secretion of ADH water reabsorption
  • Stimulates thirst
  • Stimulates CO and increases vasoconstriction of arterioles to increase blood pressure
76
Q

Describe control of increasing blood pressure with erythropoietin

A

Decrease blood pressure and O2 - kidneys release EPO
- causes vasoconstriction in blood vessels and stimulates production of red blood cells, increasing volume and viscosity of blood improving O2 carrying

77
Q

Describe control of decreasing blood pressure with natriuretic peptides

A

Atrial natriuretic peptide released from atrial myocytes in response to excessive stretching increasing atrial blood pressure

  • Increase in urine, decreasing blood vol, blood pressure and thirst
  • Increases peripheral vasodilation
78
Q

Describe cardiovascular response to haemorrhaging short term response

A
  1. Decrease in blood pressure detected by baro receptors in carotid sinus and aortic sinus, promoting visceral vasoconstriction and increase stimulation of cardiac sympathetic inputs
  2. stress and anxiety related response - stimulates sympathetic nervous system via hypothalamus
  3. Sympathetic system causes release of noradrenaline and adrenaline from adrenal medulla - increasing CO and vasoconstriction. ADH release, increase angiotensin 2, increase water retention and peripheral vasoconstriction
79
Q

Describe long term response to haemorrhaging

A
  • Mechanisms focussing on restoration of normal blood volume by activation of renin angiotensin system, ADH system and erythropoietin secretion
  • Can counter blood loss up to 20% of blood volume
80
Q

What are 4 causes of circulatory shock?

A
  1. Drop in blood pressure due to haemorrhage
  2. Damage to the heart
  3. External pressure on the heart
  4. Extensive peripheral vasodilation
81
Q

What are the symptoms of circulatory shock?

A
  1. hypotension
  2. Pale cool clammy skin
  3. Confusion and disorientation
  4. Increased heart rate accompanied by weak pulse
  5. cessation of urination and acidosis due to lactic acid build up
82
Q

Describe the coronary veins

A

Coronary capillaries, veins, coronary sinus then to greater and middle cardiac vein

83
Q

Where do the greater and middle cardiac veins drain?

A

Greater - anterior region of the heart

Middle - Posterior region of the heart

84
Q

Describe ischaemia

A

Partial obstruction of coronary arteries
- Causes hypoxia which decreases ability to produce ATP
- modifies actin/myosin driven muscular contraction
- inhibits K+/Na+ pumps
Inhibits gated K+channels

85
Q

Describe angina pectoralis

A
  • Severe pain associated with myocardial ischaemia
  • Pain often referred to neck, chin or down the left arm
  • Tight sensation in the chest
86
Q

Describe an MI

A
  • Caused by death of myocardial cells induced by blockage of blood supply
  • Myocardium replaced by connective tissue forming scar tissue
  • Scar tissue may affect AV node from atrial muscle and cause death by ventricular fibrillation
87
Q

Describe coronary artery disease

A

Atherosclerosis in coronary arteries - decreases blood flow in the myocardium

88
Q

Describe process of atherosclerotic plaque formation

A
  • Increase LDL lipoproteins removed by circulatory monocytes
  • monocytes for foam cells (macrophages) attach to endothelial cells
  • Foam cells release cytokines, induce replication of smooth muscle cells of tunica intima and attracting more monocytes
  • monocytes, smooth muscle and endothelial cells uptake lipoproteins resulting in plaque formation
  • Gaps form in endothelium and platelets attach to exposed collagen forming a cloth