The cardiovascular system - Physiology Flashcards
1
Q
What is the 2 main role of the cardiovascular system?
A
- Rapid transport of nutrients (metabolic substrates) to tissues
- Rapid removal of metabolic waste products from tissues
2
Q
Describe two challenges facing the coronary circulation?
A
Coronary blood flow occurs in diastole - 2/3 of the coronary arterial tree is intramural. These vessels get compressed during systole - therefore most (80%) of coronary blood flow occurs during diastole
The coronary arteries are function end arteries - they do not have effective anastomoses and therefor functional END arteries. This means a blockage has much more serious effects
3
Q
The heart has a very high oxygen requirement even at rest. During extortion the oxygen requirements are even higher. Therefore, to meet these needs the coronary circulation has developed structural and functional adaptation.
a) Name 2 structural adaptations
b) Name 2 functional adaptations
A
a)
1. Myocardial capillary density is very high
2. Distance that oxygen and nutrient need to travel from blood to the myocyte is shorter
b)
1. Metabolic hyperaemia (release of cardiac metabolites e.g., adenosine) increases blood flow during exercise
2. Autoregulation - coronary circulation can maintain constant blood flow despite changes to blood pressure
4
Q
a) Define cardiac output (CO)
b) Define stroke volume (SV)
c) What is the equation relating CO and SV
A
a) The volume of blood ejected by 1 ventricle in 1 minute
b) The volume of blood ejected from the ventricle in systole (1 heartbeat/contraction)
c) CO = SV x HR
5
Q
Cardiac output is not evenly distributed between tissues. Myocardium does not receive much oxygen compared to other organs e.g., muscles, liver and GIT. What is the medical significance of this?
A
Coronary blood has little spare and so reserve oxygen
Cardiac pain due to oxygen lack (angina) can be triggered, by a relatively modest fall in coronary blood flow
6
Q
What is heart rate controlled by?
A
Sympathetic and parasympathetic nerves which innervate the sinoatrial (SA) and atrioventricular (AV) nodes
7
Q
What factors control stroke volume?
A
Preload - filling pressure (Starling’s law)
Contractility - sympathetic nerves, circulating factors
Afterload - pressure opposing ejection
8
Q
a) What is preload?
b) Preload cannot be measured directly, therefore an indirect indices of preload is used?
A
a) The stretch of the ventricular fibres just before contraction (at end diastole)
b) End Diastolic Volume or End Diastolic Pressure
9
Q
Describe the Frank-Starling mechanism
A
The greater the preload, the greater the force of contraction and so the greater the stroke volume
10
Q
Describe the relationship between an increase venous return and cardiac output
A
Increase venous return –> increase end diastolic volume/pressure –> increase preload –> increase contraction –> increase cardiac output
11
Q
Describe the relationship of central venous pressure (CVP) to the right ventricular preload
A
- CVP is the pressure in the vena cava at the entrance to the right atrium (so filling of blood in right atrium)
- During diastole the right atrial pressure is the same as the right ventricle pressure
- Therefore, CVP can be used as an estimate of the right ventricular end diastolic pressure/preload
- CVP determines right ventricular preload
12
Q
What factors influence central venous pressure?
A
- Volume of blood in circulation
- Distribution of blood between central and peripheral veins
13
Q
Describe 5 factors that influence the distribution of blood between central and peripheral veins (venous return - return of blood from the periphery back to the right atrium hence CVP and hence preload)
A
- Gravity - blood pools as we stand reducing CVP. Opposite effects occurs when we are supine
- Skeletal muscle pump - operate when we walk squeezing blood into the central circulation
- Sympathetic nerves- sympathetic nerves cause vasoconstriction of the peripheral veins, squeezing blood into the central veins back into heart
- Respiratory pump - when we breathe in the pressure inside our chest becomes mores negative, this encourages venous return to the right atrium and increases RV stroke volume
- Pumping ability of the heart - when the heart is beating faster it transfers blood more quickly from the central veins to the arteries
14
Q
Why is fainting common among guards?
A
- This is due to venous pooling, lack of calf muscle pump activity and heat induced vasodilation
- This causes decreased CVP and therefore reduced filling of right side heart –> reduced filling of left side of heart –> reduced SV and CO
- This leads to cerebral hyoperfusion and fainting
15
Q
Why is the most important role of Starling’s law?
A
To balance the outputs of the right ventricle and left ventricle
16
Q
What is contractility?
A
Contractility is the force of myocardial contraction that is caused by neurohumeral factors (autonomic + blood borne factors or drugs which is independent of initial fibre length) (i.e., not dependent on the Frank Starling mechanism)
17
Q
What is the key difference between filling pressure (Starling’s law) and contractility
A
Filling pressure (Starling’s law) - acts by stretch, not altering intracellular Ca2+ level
Contractility - acts by altering intracellular Ca2+ level, no stretch
18
Q
Name 5 factors that cause an increase in contractility
A
- Raised extracellular calcium
- Increased preload
- Sympathetic stimulation
- Drugs e.g., inotropes, digoxin
- Hormones e.g., catecholamine, thyroxine, growth hormone, glucagon
19
Q
Name 5 factors that cause a decrease in contractility
A
- Decreased extracellular calcium
- Decreased preload
- Parasympathetic stimulation
- Drugs e.g., beta-blockers, aesthetics, antiarrhythmics
- Hypoxia
- Hypercapnia (Increases CO2)
- Acidosis
20
Q
What is after load?
A
Refers to the amount of resistance that the heart overcomes to eject blood/degree of heart muscle stretching during systole
21
Q
What is the relationship between after load and stroke volume
A
it is inversely related to stroke volume
22
Q
Name 4 factors that increase afterload
A
- Raised aortic pressure
- Aortic stenosis
- Increased systemic vascular resistance such as hypovolemic shock
- Ventricular dilatation
23
Q
Name 2 factors that decreas after load
A
- Vasodilator drugs e.g., nitrates calcium channel blockers
- Vasodilator metabolise in sepetic shock
24
Q
What factors increase cardiac output during exercise
A
Increase stroke volume
- Increase pre load -> skeletal muscle pump and peripheral vasoconstriction
- Contractility –> increased sympathetic activity
Increase heart rate
- Decrease parasympathetic activity
- Increase sympathetic activity
25
Why does blood flow to active muscles increase during exercise?
Active muscles release metabolites that causes vasodilatation in the muscles thereby increasing the blood flow
26
a) There is a threat of hypotension during exercise. Explain why this is the case?
b) How is this avoided?
a)
- Vasodilatation occurs during exercise to increase blood flow to muscles. however, this vasodilation has the potential to cause problems because the systemic resistance reduces significantly
- BP = CO X SVR (systemic vascular resistance)
b) This is avoided by compensatory vasoconstriction in inactive tissue which prevents fall in SVR e.g., splanchnic, kidneys, inactive muscle
27
Vasodilatation occurs during exercise. This diverts blood away from the heart, so the preload is reduced but the heart maintains the cardiac output by increasing the heart rate.
During exercise in hot weather even more blood is diverted away from the heart and the cardiac output can’t be maintained despite the increased heart rate.
a) How is this prevented?
b) What is the disadvantage of this?
a)
- There are baroreceptors in the heart that detect the reduced cardiac output and activate the sympathetic nervous system
- This results in vasoconstriction of the skin blood vessels. While this means
b) While this means that more blood can now return to the heart it does so at the expense of rising core temperature and can lead to heat stroke
28
Explain the difference in how cardiac output is increased during upright and supine exercises
An increase in cardiac output during upright exercise is brought about partly by an increase in stroke volume and partly by an increase in heart rate.
During supine exercise (e.g., swimming), stroke volume is high even at rest, because central venous pressure and so pre-load and so stroke volume is high. Therefore there is less scope for stroke volume to increase during exercise. So, tachycardia is the main factor raising the cardiac output during supine exercise
29
The transplanted heart is enervated (there are no cardiac autonomic nerves). How do heart transplant patients increase cardiac output with exercise?
Heart transplant patients have circulating catecholamines that increase heart rate and the skeletal muscle pump acting via the Frank-Starling increases pre-load
30
Explain the difference in stroke volume and resting heart rate in the athletic heart vs non-athletic heart
The athletic heart is stronger and hypertophied. This leads to an increase in stroke volume and decrease in resting heart rate.
31
Name the 7 phases of the cardiac cycle
1. Atrial systole
2. Isovolumetric contraction
3. Rapid ejection
4. reduced ejection
5. Isovolumetric relaxation
6. Rapid ventricular filling
7. Diastasis
32
Describe the 7 phases of the cardiac cycle including what part of the ECG the phases correspond to and any heart sound that occur
Atrial systole
- Causes rise in atrial pressure causing blood to move from the atria to the ventricles
- AV valves (mitral and tricuspid) are open
- P wave on ECG
- 4th heart sound generated = atrial gallop (extra heart sound during late diastole)
(Ventricular systole) Isovolumetric contraction
- Ventricles contract without any change in volume
- All valves are closed
- Initiated by ventricular depolarisation which corresponds to QRS complex on ECG
- 1st heart sound generated - due to closure of AV valves (mitral and tricuspid) from previous
Rapid ejection
- Ventricles pump out blood from the left ventricle to aorta and from right ventricle to pulmonary artery
- Pressure goes up until reaches peak
- AV valves remain closed preventing reflux of blood into atria
- Aortic and pulmonary valves open
- ST segment on ECG (Start of repolarisation which is then followed by relaxation)
Reduced ejection
- Soon will hear 2nd heart sound
Isovolumetric relaxation
- End of systole
- Ventricles relax without a change in volume
- Atria starts to fill with blood
- All valves closed
- Initiated by repolarisation which corresponds to T wave on ECG
- 2nd heart sound produced from semilunar (aortic and pulmonary closing)
- If 3rd heart sound is produced at this stage = can reflect of heart failure
Rapid ventricular filling
- AV valves open as ventricular pressure drops below atrial pressure
- Aortic and pulmonary vales remain closed
- Most blood flows passively from atria to ventricles
- 3rd heart sound produced
Diastasis
- Atria and ventricles filling
- Ventricles filling 70-80% passively during diastesis, rest 25% actively filling during atrial systole
33
a) What does the S1 heart sound reflect? and what does it sound like?
b) When is it loud?
c) When is it soft?
d) Where can it be best heard?
a) Reflects closure of mitral valve first and tricuspid valve
b) thin patients, hyper dynamic circulation (e.g., pregnancy), mitral stenosis
c) Obesity, emphysema, pericardial effusion, mitral regurgitation or severe mitral stenosis
d) Apex
34
a) What does the S2 heart sound reflect? and what does it sound like?
b) When is it loud?
c) When is it soft?
a) Reflects closure of the aortic and pulmonary valves
b) Systemic hypertension, hyper dynamic circulation
c) Soft in aortic stenosis
35
a) What does the S3 heart sound reflect?
b) When does it occur?
c) When may it be seen in?
d) Where is it best heard?
a) Reflect rapid ventricular filling when blood strikes a compliant left ventricle
b) Occurs in early diastole, just after S2 when the mitral valve opens
c) May be physiological in young, fit patients or children. In older patients, may be due to heart failure or volume overload
d) Best heard at apex
36
a) What does the S4 heart sound like?
b) When does it occur?
c) When may it be seen?
d) Where is it best heard?
a) Reflects surge of ventricular filling in atrial systole
b) Occurs in late diastole, immediately before S1, when the atria contract to force blood into non-compliant left ventricle
c) Always pathological. May be seen in hypertension, aortic stenosis, acute myocardial infarction
d) Best heard at apex
37
Why is there splitting of the S2 in inspiration?
Inspiration sucks blood into right heart and right heart takes longer to pump out the increased volume
38
a) What is the equation for Ohm's law?
b) What two equations relating to cardiac output is the ohm's law depicted in?
a) Current (Amperes) through a conductor is directly proportional to the voltage (Volts) across the conductor and inversely proportional to its resistance (Ohm’s)
I = V/R
b)
Cardiac Output (CO) = Mean arterial pressure (MAP) / systemic vascular resistance (SVR)
Cardiac power (CPO) = MAP x CO
39
What are the two functional components of the circulatory system?
1. Blood vascular system (circulation of blood)
2. Lymph vascular system (circulation of lymph)
40
What are the 3 layers of blood vessels?
- Tunica interna
- Tunica media
- Tunica externa
41
Describe the components of the 3 layers of blood vessels
Tunica interna (intima)
- endothelial layer that lines the lumen of all vessels
Tunica media
- Smooth muscle and elastic fibre layer
Tunica externa
- Collagen fibres
42
a) What is an endothelium?
b) Describe 3 roles of the endothelium
a) A single layer of squamous epithelium, lining the internal surfaces of all components of the blood and lymphatic systems
b)
1. Acts as a selective permeable, anti-thrombotic barrier
2. Determines when and where white blood cells leave the circulation for the interstitial space of tissue
3. Secretes paracrine factors for vessel dilation, constriction, and growth of adjacent cells
43
Explain the nutrient supply to intermediate and large vessels
Intima and internal region of the media
- Intima and internal regions of the media are closer to the lumen and so receive oxygen and nutrition by diffusion from the blood in the lumen
Tunica externa (adventitia) and outer layers
- further away from the lumen and too thick to be nourished by diffusion from blood in lumen
- Therefore, larger vessels have vasa vasorum "vessels of the vessel" arterioles, capillaries and venues that branch profusely in the adventitia and outer media
- The vasoconstriction vasorum provides metabolites to the adventitia and the media
44
Describe the structure of large elastic (conducting) arteries
t.Intima
- Endothelium
- Subendothelium of connective Aussie
t. Media
- Alternating layers of smooth muscle and elastic fibres
t. Externa/Adventitia thin layer
- Collagen and elastic fibres, fibroblasts
45
Describe the structure of medium muscular (distributing) arteries
t. Intima
- Endothelium
- Internal elastic membrane
t. Media
- Mostly smooth muscle
- Collagen fibres
- Occasional elastic fibres
t. Exerna/Adventita thin layer
- Connective tissue
- +/- external elastic membrane
46
Describe the structure of small arteries and ateriole structure
Tunia intima
- Endothelium and its basement membrane
- Thin sub endothelial connective tissue
- Thin, fenestrated internal elastic lamina only in small arteries
Tunia media
- 3 to 8 layers of circulatory arranged smooth muscle in small arteries, and 1 to 2 layers in arterioles
- Some collagen fibres, elastic fibres, and ground substance in small arteries, and very little in arterioles
Tunica externa/adventitia
- Thin layer of connective tissue
47
Describe the structure of capillaries
- 8-10 um
- Just big enough for single file erythrocytes
- Composed of a single layer of endothelial cells surrounded by basement membrane
48
What are the 3 types of capillaries and provide examples of these
Continuous capillaries - e.g., ,muscle, lungs, CNS
Fenestrated capillaries - e.g.,wherever capillary absorption or filtrate formation occurs e.g., endocrine gland, sites of metabolic and fluid absorption e.g., the gallbladder, kidney, and intestinal tract
Discontinuous capillaries (sinusoidal capillaries) - e.g., liver, spleen, bone marrow
49
Describe the structure and function of continuous capillaries
- Adjacent endothelial cells that are held together with tight junctions that provide an uninterrupted lining
- Intracellular clefs of un-joined membranes - allow the passage of fluids
50
Describe the structure and function of fenestrated capillaries
Have tight junctions, but perforations/pores (fenestrations) in endothelium allow greater permeability to solutes and fluids. This leads to greater exchange across the endothelium
51
Describe the structure and function of discontinuous (sinusoidal capillaries/sinusoids)
- Wider diameter than the other types
- The endothelial cells have multiple large fenestrations and form a discontinuous layer and are separated from one another by wide spaces
- The basement membrane/basal lamina is discontinuous
- Allows large molecules (proteins and blood cells) to pass between the blood and surrounding tissues
52
Describe the function and structure of veins
- Collect blood from all tissues and organs and return it to the heart
- The intima usually has a thin sub-endothelial layer
- The media consists of small bundles of smooth muscle cells intermixed with reticular fibres and a delicate network of elastic fibres
- The collagenous adventitial layer is well developed
- Large lumen
- Valves --> project from the tunica intima to prevent back-flow of blood
53
Describe the two main special features of veins
Valves --> protect from the tunica intima to prevent back-flow of blood
Muscular contraction --> aids the return of blood to heart in conjunction with veins
54
Describe the difference between arteries and veins
Arteries
- Relatively narrow lumen
- Thicker tunica media
- Intima is separated from media by internal elastic lamina
Vein
- Larger lumen
- Tunica externa is the thickest
- Tunica intima is folded to form valves
55
What are the 3 walls if the heart
Internal - Endocardium
Middle - Myocardium
External - Pericardium (Fibrous, Parietal and Visceral/epicrdium)
56
Describe the 3 layers: endocardium, myocardium and pericardium (parietal and visceral)
Endocardium
- Endothelium and aveolar tissue that covers the inner surfaces if the heart
Myocardium
- Muscular wall of the heart consisting primarily of cardiac muscle cells
Parietal pericardium
- The serous membrane that forms the outer wall of the pericardial sac
- Consists of: dense fibrous layer, areolar tissue, mesothelium
Visceral pericardium (epicardium)
- Covers the outer surface of the heart; also called visceral pericardium
- Consists of: mesothelium, areolar tissue
57
a) What is the fibrous heart skeleton?
b) Where is it located?
c) What is it formed of?
d) Describe 5 functions of the fibrous heart skeleton
a) The fibrous central central region of the heart
b) Between the atria and ventricles
c) Formed of dense connective tissues
d)
1. Separates atria and ventricles
2. Anchors heart valves by forming supporting rings at their attachment points
3. Provides electrical insulation between atria and ventricles
4. Insulation ensures that muscle impulses are not spread randomly throughout, thus prevents all the heart chambers from beating at the same time
5. Provides a rigid framework for the attachment of cardiac muscle tissue
58
What is the membrane potential?
Defined as a difference in electric potential (a voltage) between the outside and inside of a cell across a membrane
59
What is the difference in electric potential due to?
It is due to an unequal distribution of ions between the inside and outside of the cell
60
Most cells have. resting membrane potential (RMP) between -30 and -100mV
a) What is the RMP of cardiomyocytes?
b) What is the RMP of cardiac pacemakers?
a) Between -80mV and -90mv
b) between -50mV and -70mV
61
What are the two things resting membrane potential is generated by?
1. The semi-permeable nature of the cell membrane
2. Presence of ion channels and pumps (active transport)
62
Cardiomyocytes express mainly 3 ion channels. What are these?
K+, Na+, Ca2+
63
Give the two types of cardiac muscle cells
1. Cardiomyocytes
2. Pacemaker cells
64
Describe the difference of cardiomyocytes and pacemaker cells when it comes to producing cardiac potential
Cardiomyocytes
- Not auto-rhythmic so do not create action potentials on their own, but do conduct action potentials to adjacent cardiac myocytes via gap junctions
Pacemaker cells
- Auto-rhtyhmic so initiate and conduct action potentials for the adjacent cardiac myocyte cells
65
Describe the role of gap junctions and intercalated discs
The connection between cardiac myocytes known as the intercalated disk contain gap junctions that directly connect myocytes through the intercellular space and their membranes to allow direct current/ion flow between cell
66
Describe the role of gap junctions and intercalated discs in cardiac myocytes
The connection between cardiac myocytes known as the intercalated disk contain gap junctions that directly connect myocytes through the intercellular space and their membranes to allow direct current/ion flow between cell
67
Describe the role of T-tubules in cardiac myocytes
T-tubules penetrate deep into cells and allow very quick conduction of action potential between and into cells
68
Describe the phases of the propagation of a cardiac mycocyte
Phase 4 -resting membrane potential:
Phase 0 - rapid depolarisation phase: influx of Na+ when fast voltage gated Na+ ions open
Phase 1 - rapid repolarisation phase: efflux of K+ (and inactivate of Na+ channels and current)
Phase 2 - plateau: an elongation of the action potential (maintained depolarisation) and mainly depends on he continued entry of Ca2+
Phase 3 - late repolarisation: depends on the outward K+ current via opening of delayed rectifier K+ currents. These return the membrane to the resting membrane potential
69
Pacemaker potential rate can be changed by the autonomic system. Describe the effects of the autonomic stimulation on pacemaker potential
Sympathetic stimulation (adrenaline or noradrenaline) via beta-adrenergenic receptors instantly increase rate until stimulation is removed
Parasympathetic stimulation (vagal stimulation and acetylcholine) instantly decrease rate until stimulation removed
70
Describe the cellular response to muscarinic stimulation in cardiac muscle - acetylcholine
Acetylcholine interacts with the muscarinic receptors and inhibits the attached adenylate cyclase
This causes a reduction in the levels of cAMP and in turn protein kinase A
Reduction in levels of protein kinase A reduces Ca2+ inwards currents and K+ outwards currents
These effects increase the duration of time for pacemaker potential to drift to threshold action potentials
Acetylcholine also has a direct on muscarinic K+ (kACh) channels that allows potassium efflux, and this increase the level of hyperpolarisation of the resting membrane potential
71
Describe the cellular responses to beta-adrenergic stimulation in cardiac muscle - noradrenaline
Noradrenaline interacts with beta-adrenergic receptors and activates the attaches adenylate cyclase
This causes an increase in levels of cAMP and in turn protein kinase A
Increase in levels of cAMP increases pacemaker (funny) inward currents
Increase In level of protein kinase A increases Ca2+ inwards currents and K+ outwards current
72
Describes the 4 factors determined the mean arterial blood pressure (MABP)
1. Blood volume - change in fluid retention/intake can increase or decrease blood volume and thus increase or decrease MABP
2. Cardiac output - primarily increased by sympathetic stimulation or decreased by parasympathetic stimulation, increasing, or decreasing MABP)
3. Resistance of system to blood flow (diameter of arteriole) - arteriole vasoconstriction (e.g., sympathetic stimulation causing release of noradrenaline) increases resistance and thus increases MABP; arteriole vasodilation (e.g., inhibition of sympathetic nervous system) decreases resistance and thus decreases MABP
4. Relative distribution of blood between arterial and venous blood vessels (diameter of veins) - venous vasodilation can increase the amount of volume available for the blood on the venous side of the circulatory and so decrease MABP
73
Where are baroreceptors found?
aORTIC ARCH
Carotid sinus
74
Describe the structure of baroreceptors
Myelinated and unmyelinated sensory fibres entwined in the elastic layers of the arteries
75
Describe the role of the baroreceptor reflex
Nerve endings of baroreceptors (stretch receptors) monitor blood pressure. This is by firing more often when they are stretched as pressure increases.
The receptors send information back to the CNS (medullary cardiovascular control centre) about MABP
76
Describe how the baroreceptor reflex responds to
a) Decrease in MABP
b) Increase in MABP
a) If MABP decreases, the receptors decrease their input, and this results in activation of the sympathetic nervous system and inactivation of the parasympathetic nervous system
b) If MABP increases, receptors increase their input, and this results in activation of the parasympathetic nervous system and inactivation of the sympathetic nervous system
77
Describe the role of of cardiopulmonary reflex
These are baroreceptors found in the atrial walls and monitors atrial blood volume and feedback on hear rate
An increase in stretch (i.e., an increase in venous return) leads to an increase in heart rate (not force of contraction) - this known as the brainbridge effect
78
Describe the role of natriuretic peptides (ANP and BNP)
ANP is released due to atrial stretch from increased blood volume
BNP is released from ventricular stretch and its presence is predominately associated as a marker of heart failure
Natriuretic peptides act on natriuretic peptide receptors (NPRs) and activation of these receptors lead to a net increase salt and water excretion (and decrease central sympathetic output) to reduce blood volume and thus pressure
79
Describe the role of the renin-angiotensin-aldosterone system (RAAS) on MABP
RAAS is a system for controlling circulating blood and this is a determinant of MABP
Angiotensin is a vasoconstrictor and thus will increase MABP and TPR directly
80
Name 2 mechanisms controlling blood pressure that stress can override
1. Vasovagal syncope
2. Fight or flight response
81
Describe how stress can override vasovagal syncope
There is overstimulation of the parasympathetic nervous system and decreases sympathetic output causing a sudden fall in MABP and perfusion pressure to the brain
This results on bradycardia hypotension and apnoea
