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
2
Q
What are the three tissues to form the heart wall ?
A
Epicardium
Myocardium
Endocardium
3
Q
Describe the pericardium
A
Fibrous layer
Serous layer
Visceral layer
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
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
6
Q
Describe the spread of excitation through the heart
A
- SA node
- AV node
- Atrioventricular bundle of his
- Right and left bundle branches
- Purkinje fibres
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
8
Q
Describe pacemaker cells
A
Auto-rhythmic fibres
- driving auto-rhythmic contractility activity of heart
- form specialised conducting system allow coordinated excitation of different regions of the heart
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
10
Q
Describe the refractory period
A
Time when the muscle cell cannot fire a second action potential
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
12
Q
Describe the AV node delay
A
Delay allows for atria to contract, result of time taken for calcium ions to enter sarcoplasm
13
Q
Describe delayed depolarisation
A
Repetitive myocyte activity not driven by potentials arising from other cells intracellular calcium concentrations increasing beyond normal
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
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
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
17
Q
Describe ventricular fibrillation
A
Irregular trace seen in acute heart attacks ventricles no longer pumps blood and death occurs
18
Q
Describe the cardiac output
A
- cardiac action potential propagates from SA node through atria and to AV node - P wave on ECG
- 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
- Action potential propagates through bundle of his 0.2 seconds after P wave, depolarisation occurs producing QRS complex, partial repolarisation
- Contraction of ventricles after QRS and continues in ST segment
- Depolarisation of ventricular contractile fibres
- Ventricles relax and ventricular repolarisation is complete, both atria and ventricles and relaxed and cycle repeats
19
Q
Describe 8 stages of heart cardiac cycle
A
- atrial contraction begins
- Atria eject blood into ventricles
- atrial systole ends, AV valve closes
- Isovolumetric ventricular contraction occurs
- Ventricular ejection occurs
- Semilunar valve closes
- Isovolumetric relaxation occurs
- AV valves open and passive ventricular filling occurs
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
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
22
Q
Describe tropomyosin
A
Rod shaped molecule binds via troponin molecule to the groove of actin helix where it masks myosin binding site
23
Q
Describe troponin
A
A complex of 3 polypeptides troponin TIC.
T binds to actin
I binds to tropomyosin
C binds to calcium
24
Q
Describe arterioles
A
Influence peripheral resistance and modify blood flow from arteries into capillaries - resistance vessels
25
Describe the metarteriole
- 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
26
What is vasomotion?
Intermittent blood flow due to alternating contraction and relaxation of smooth muscle cells of metarterioles
27
Describe capillaries
Microcirculatory system - connect arterioles to venules
| - allow exchange fo fluid and metabolites between blood circulatory system and tissues
28
Describe venules
- 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
29
Describe veins
Thin walls large lumen, contain valves
| Takes blood to the heart, low pressure capacitance vessels
30
How much of the body's blood os held in the different blood vessels?
```
Veins - 64%
Systematic capillaries - 7%
Arteries - 13%
Pulmonary capillaries - 9%
Heart - 7%
```
31
What are veins and venules known as?
Blood reservoirs
32
Describe transcytosis
Small quantities of material transported across capillary walls by being encapsulated within invaginations of the serial endothelial membrane released by exocytosis
33
Describe bulk flow
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
34
What is the equation for net filtration pressure?
(Blood hydrostatic pressure + interstitial fluid osmotic pressure) - (Blood colloid osmotic pressure + interstitial fluid hydrostatic pressure)
35
Describe blood hydrostatic pressure
BHP = hydrostatic pressure generated by blood pumping action of the heart and interstitial fluid osmotic pressure (IFOP)
- Promotes filtration
36
Describe blood colloid osmotic pressure (BCOP)
Promotes reabsorption
37
Describe oedema
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
What is End diastolic volume?
Amount of blood in each ventricle at the end of ventricular diastole
39
What sis end systolic volume ?
Amount of blood in each ventricle at the end of ventricular systole
40
What is stroke volume?
Amount of blood pumping out of each ventricle during single heart beat
41
Describe blood pressure
```
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
At what blood pressure does a person become unconscious if it drops below this level?
60 mmHg
43
What is vascular resistance?
Dependent on lumen diameter, viscosity of blood and blood vessel length
44
Describe blood viscosity
Dehydration and polycythaneia increase viscosity and resistance
45
What are peripheral and systematic resistance/
Force that opposes blood flow in vascular system, dependent on the smaller vessels, arterioles being the most important
46
Describe mean blood pressure with cardiac output and peripheral resistance
Decreased MBP = decreased CO x PR
Increased MBP = CO x increased PR
MPB= increased PR x decreased CO
Overall CO = MBP/PR
47
Describe venous return
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
Describe skeletal muscle pump
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
Describe the respiratory pump
Movement of the diaphragm causing pressure changes
50
Describe the cardiovascular centre control
- 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
Describe cardiac reflexes
- 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
Describe long term regulation of blood pressure
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
What three hormones increase heart rate by effect on SA node?
Epinepherine/ adrenaline, noradrenaline/epinephrine and thyroid hormone
54
What is preload?
Degree of stretching in ventricle muscle cells during ventricular diastole. Proportional to EDV - greater the preload = greater EDV
55
What is after load ?
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
What is preload influenced by?
1. Venous return
| 2. Filing time - duration of ventricular diastole
57
Describe contractibility of ventricles
- Amount of force produced during contraction at a given preload, regulated by autonomic innervation and hormones
58
What are factors that increase ventricle contractility?
- Positive inotropic agents
- Neurotransmitter and hormones of sympathetic nervous system
- Beta adrenogergic agonists
59
What are factors that decrease ventricle contractility?
- Negative inotropic agents
- parasympathetic neurotransmitters, Ca2+ channel blockers
- Muscarinic agonists
- sympathetic antagonists
- Increase in K+ concentrations
- Anoxia + acidosis
60
Describe the cardioacceleratory centre and cardioinhibitory centre
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
Describe the autonomic regulation of the heart
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
Describe the atrial reflex
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
What nerves are involved in propagating impulses from baro and chemoreceptors ?
Afferent neurones in glossopharyngeal nerve from carotid sinus and vagus nerve from aortic arch
64
What is tissue perfusion influenced by?
1. cardiac output
2. blood pressure
3. peripheral resistance
65
What are the tissue perfusion mechanisms/
1. Autoregulation in tissues
2. Neural mechanisms
3. Endocrine response
66
What are 6 local vasodilators?
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
What are two vasoconstrictors?
1. Thromboxanes - released by platelets in wound sites
| 2. Endothelins - damaged endothelial cells
68
Describe the vasomotive centre
Two populations of cells located in the medulla oblongata, large group associated with wide spread vasoconstriction and smaller group associated with vasodilation
69
Describe the control of vasoconstriction
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
Describe control of vasodilation
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
Describe the baroreceptor reflex
located in carotid sinus , aortic sinus and wall of right atrium
Aortic monitors degree of aortic stretch
72
Describe the atrial reflex
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
Describe chemoreceptor reflex
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
Describe control of increasing blood pressure with ADH
- 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
Describe control of increasing blood pressure with angiotensin 2
- 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
Describe control of increasing blood pressure with erythropoietin
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
Describe control of decreasing blood pressure with natriuretic peptides
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
Describe cardiovascular response to haemorrhaging short term response
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
Describe long term response to haemorrhaging
- 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
What are 4 causes of circulatory shock?
1. Drop in blood pressure due to haemorrhage
2. Damage to the heart
3. External pressure on the heart
4. Extensive peripheral vasodilation
81
What are the symptoms of circulatory shock?
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
Describe the coronary veins
Coronary capillaries, veins, coronary sinus then to greater and middle cardiac vein
83
Where do the greater and middle cardiac veins drain?
Greater - anterior region of the heart
| Middle - Posterior region of the heart
84
Describe ischaemia
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
Describe angina pectoralis
- Severe pain associated with myocardial ischaemia
- Pain often referred to neck, chin or down the left arm
- Tight sensation in the chest
86
Describe an MI
- 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
Describe coronary artery disease
Atherosclerosis in coronary arteries - decreases blood flow in the myocardium
88
Describe process of atherosclerotic plaque formation
- 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
