cardiovascular system Flashcards
what is the pericardium?
- outer casing of the heart
- protective fluid-filled sac surrounding the heart
- outermost layer = fibrous pericardium
where is the heart located?
- between lungs to the left
- twisted to the back
- harder to access the left side of the heart
how many borders does the heart have?
4
what are the borders of the heart?
- superior border = great vessels enter and leave
- interior border = lies on the diaphragm / in line with it
- right border = faces right lung
- left border = faces left lung
the apex
where the ventricles join up
what is the mediastinum?
- central compartment of the thoracic cavity
- area between the lungs
what does the mediastinum contain?
- heart
- great vessels
- thymus
- oesophagus
- trachea
what are anterior (front) landmarks of the heart?
- coronary sulcus
- anterior interventicular sulcus
- auricles
the (anterior) coronary sulcus
- marks division between the atria and the ventricles (right atrium & right ventricle?)
- continues posteriorly
- right coronary artery (RCA) in sulcus anteriorly
- grove for veins & arteries
- RCA sits in within a “line of fat”
the anterior interventricular sulcus
- marks division between ventricles (left & right ventricle)
- continues posteriorly as posterior interventriculary sulcus
- Left anterior descending (LAD) from left coronary artery (LCA) in sulcus anteriorly
- LAD sits within this sulcus
auricles
- atrical appendages
- increase capacity -> extra “spaces” for atria to expand
- used when the heart is working really hard
what are the posterior (back) landmarks of the heart?
- coronary sulcus
- posterior interventricular sulcus
the (posterior) coronary sulcus
- division between atria and ventricles
- continous anteriorly
- coronary sinus in sulcus
the posterior interventricular sulcus
- marks division between ventricles
- continues anteriorly as anterior interventricular sulcus
- posterior descending artery (PDA) from LCA or RCA in sulcus
how can you identify the left atrium?
- 4 pulmonary vein vessels
- found in the back of the heart
layers of the heart wall
- epicardium (outer) = the visceral layer of the serous pericardium
- myocardium (middle) = cardiac muscle
- endocardium (inner) = continuous with endothelium of large vessels of the heart
what are the 2 types of the pericardium?
- fibrous
- serous
fibrous pericardium
- tough & inelastic
- rests on / attached to diaphragm
- open end fused with great vessels
- physically attached to diaphragm
serous pericardium
- parietal layer (fused to fibrous pericardium)
- visceral layer (continuous / part of epicardium)
- pericardial cavity (space between parietal and visceral layers contains pericardial fluid)
what is the role of pericardial fluid? and where is it found?
- in the pericardial cavity
- to reduce friction bc layers rub against each other
- helps the heart expand and contract easier
why is the fibrous pericardium physically attached to the diaphragm?
- to allow synchronised movement when breathing in and out
- prevents heart and diaphragm from hitting each other
what are the chambers of the heart?
- right atrium (RA)
- right ventricle (RV)
- left atrium (RA)
- left ventricle (RV)
right atrium
gets deoxygenated blood from the vena cavae (biggest vein in body) & coronary sinus (at the back of the heart)
right ventricle
pumps deoxygenated blood to the lungs (pulmonary circulation)
left atrium
gets oxygenated blood from lungs via pulmonary veins
left ventricle
pumps oxygenated blood in aorta (systematic circulation)
blood to rest of the body
pulmonary circulation
- the system of transportation
- de-oxygenated blood from the heart to the lungs to be re-saturated with oxygen before being dispersed into the systemic circulation
systematic cirulation
provides the functional blood supply to all body tissue.
what are the types of valves of the heart?
- atrioventricular (AV) valves (tricuspid valve, bicuspid valve)
- semilunar (SL) valves (pulmonary valve, aortic valve)
is the right AV tricuspid or bicuspid?
tricuspid = 3 leaflets / cusps
is the left AV tricuspid or bicuspid?
bicuspid (mitral) =2 cups
what muscles and tendons are involved in the valve cusps
- chordae tendinae
- papillary muscle (projection of myocardium, pushed down / pull on chordae tendinae & valve closes)
pectinate muscles
- on RA
- myocardium projections
- make surface not smooth = facilitate expansion without tension
trabeculae carneae
- contract and pull on the chordae tendinae
- prevent inversion of the bicuspid and tricuspid valves towards the atrial chambers
the great vessels of the heart
- superior vena cava (back from above the heart)
- pulmonary arteries (split in the lungs)
- pulmonary trunk (splits into the pulmonary arteries)
- inferior vena cava (from the bottom of the heart)
- aortic arch (blood to body)
- pulmonary veins (blood from lungs)
- ascending aorta
- left common carotid (goes up the neck)
- brachiocephalic
- left subclavian (upper limbs)
functions of blood
- transportation (nutrients & waste)
- protection (immune system)
- regulation (hormones, proteins)
haematopoiesis
blood production
haemorrhaging
blood loss
blood components
- red blood cells (erythrocytes)
- white blood cells (leukocytes)
- platelets (thrombocytes)
- plasma (the ECM of the blood)
red blood cells
- produced in bone marrow
- erythropoietin - kidney
- no nucleus
- haemoglobin protein
- haematocrit (40-45%)
- anaemia (low number of erythrocytes, low iron)
- polycythaemia (high number of erythrocytes, viscosity)
white blood cells
- protection
- phagocytosis
- 2 classes:
-> granulocytes (neutrophils…)
-> agranulocytes (lymphocytes…) - leukopenia (low WBC count, infection)
- leukocytosis (high WBC countm inflammation)
platelets
- cell fragments
- control blood loss
- fibrin clot -> help body form clots to stop bleeding
- normal count = 150,000 - 450,000 platelets per microliter)
- thrombocytosis (>450,000)
- thrombocytopenia (<150,000)
plasma
- straw-coloured liquid
- blood cells are suspended in it
- ECM of blood
- half of blood is made of plasma
- composed of:
-> water (92%)
-> proteins -> major proteins = albumin
-> glucose
-> electrolytes
what is included in central control of the cardiac cycle?
anything from the heart
what is included in the peripheral control of the cardiac cycle?
blood vessels from the rest of the body
diastole
filling & relaxation
systole
pumping & contraction
(ventricles contracting & pump blood out)
central venous pressure (CVP)
- pressure in the thoracic vena cava near the right atrium
- how much blood is going back to the heart
mean arterial pressure (MAP)
MAP=1/3 (SysP) + 2/3 (DiaP)
- average arteriol pressure throughout one cardiac cycle (systole + diastole)
does diastole or systole take longer?
diastole lasts longer
in systole only for 1/3 of cardiac cycle
aortic pressure
the difference between diastolic & systolic pressure
what does the aortic pulse pressure show?
- how effective the left ventricle is in pulsing blood into the aorta
- the pulse pressure caused by this
the end diastolic volume
- 120ml
- when ventricles are at their maximum capacity
stroke volume
- 70ml
- the volume of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction
end systolic volume
- 50ml
- the volume left in the ventricle after systolic contraction occurred
why are the ventricles never empty of blood?
because the cardiac muscles are always slightly contracted
what is Starling´s law?
- increase in contractile energy with stretch (diastolic distension)
- a greater stretch of muscle fibres = greater contractile energy
- 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.
what happens when there is increased contractile energy in the wall of the heart´s ventricle?
- able to push more blood out
what happens when you faint?
- low Central venous pressure (CVP)
- blood pools in feet
- fibres in diastole shorten
- weaker contractions
- stroke volume (SV) drops
- arterial pressure drops
what to do when someone faints
- put feet up
- this causes blood to return back to the right atrium
peripheral control of haemodynamic function
- changes in blood vessel diameter (tone) can influence pressure and flow characteristics
- via 2 mechanisms:
-> autonomic
-> metabolic - targets for therapeutics
how is pressure regulated?
by mechanoreceptors / baroreceptor reflex
- able to relay information derived from blood pressure within the ANS
how does the baroreceptor reflex work?
- baroreceptors: stretch in the receptors in walls of major arteries sense stretch which causes change in blood pressure
- brainstem: communicates with nerves which control the heart & blood vessels
- changes occur in cardiac output, peripheral resistance and nevous capacitance
- blood pressure: restores arterial blood pressure to normal levels
what are the normal levels of arterial blood pressure?
85-100mmHg
what are baroreceptors?
- stretch sensitive fibres
- a type of mechanoreceptors
- relaying information derived from blood pressure within the autonomic nervous system
where are baroreceptors found?
- in the aortic arch
- each of the carotid sinuses
what are carotid bodies?
- sensory organs that detect the chemical composition of arterial blood
- chemoreceptors
hypotension
<90mmHg
low blood pressure
hypertension
> 140mmHg
- high blood pressure
- impairs stroke volume
- diuretics reduce overall blood volume -> weak heart doesnt need to pump such a large volume of blood around
what occurs during hypertension?
- thicker arterial walls as a result of vascular remodelling occuring to compensate for high blood pressure
what do thicker arterial walls cause?
- needed due to the increased blood pressure
- narrows the lumen and reduceses blood flow
how to calculate blood flow?
Q=(P1 - P2) / R
Q=blood flow
P1=aorta
P2=vena cava
R=resistance
how is arterial blood pressure regulated?
by the nervous system
what are the arterioles also known as?
the resistance vessels of the body
when can blood flow change?
changes happen locally to redistribute flow to where it is needed e.g. a limb
which “tubes” have higher resistance?
long narrow tubes have a higher resistance than short wide tubes
- arterioles have highest resistance
why do capillaries not have such high resistance even when they are long narrow tubes?
- there are millions of them
- resistance is so spread out due to the increased surface area
flow distribution regulated at rest
- determined by local metabolic rate in tissues
e.g. skeletal muscle 20% oxygen consumption
-> will receive 20% cardiac output
what can affect flow distribution?
- movement = standing, sitting, exercising
- stress
- things that will change how much oxygen skeletal muscles need to receive
how is flow distribution determined?
- by changes in “vascular tone”
- intrinsic and extrinsic mechanisms
intrinsic control - myogenic response
- increase in arterial pressure = increased vascular tone = constriction
- decrease in arterial pressure = decrease in vascular tone = dilatation
what acts together to set the basal level of vascular tone?
- myogenic response
- endothelial secretions
- vasoactive metabolites
- temperature
what is the myogenic response?
- bayliss myogenic response
- myocytes depolarize when they are stretched
- extent of stretchedness depends on how much blood is in the lumen
endothelial secretions
- vasoconstrictors (endothelin-1 (ET-1))
- vasodilators (nitric oxide (NO))
what are myocytes?
smallest subunit of muscular tissues and organs throughout the body
what are the functions of vasoactive metabolites?
- help set basal level of vascular tone
- metabolic activity of myocardium, skeletal muscle…
- blood flow is diverted there within seconds
- H+, K+, ATP, CO2… can be released while exercising and can affect blood vessel diameter
temperature and vasodilatation
- specifically close to skin (organ of temp regulation)
- blood flow here can change >100 fold
- sympathetic vasoconstrictor fibres
-> activity influenced by hypothalamic temp-regulating centre
blood vessels close to the skin
- dilate with heat = contain more blood close to skin= skin “reddens”
- constrict with cold = less blood = pale/bluish skin colour
why do blood vessels constrict in the cold?
to conserve core temperature and warm organs
so blood flow moves to organs and core
raynaud´s syndrome
- spasm of small arteries supplying the extremities in response to
-> cold
-> stress
-> most cases unknown
-> severe = gangrene (skin & tissue death)
extrinsic control
- vasomotor nerves
- vasoactive hormones
- higher level of control = overrides intrinsic controls to meet needs of the whole body
vasomotor nerves
- sympathetic vasoconstrictors = NT (noradrenaline - alpha receptors on vascular myocytes)
- sympathetic vasodilators (NT = NA or ACh)
- parasympathetic vasodilators (NT = ACh)
vasomotor hormones
- adrenaline -> constriction / dilatrion
- vasopressin -> ADH -> constriction
- angiotensin -> constriction
- atrial natriuretic peptide (ANP) -> dilation
- insulin -> dilation
fight or flight & adrenaline
- released by adrenal medulla in adrenal gland
- enters blood stream -> pumped everywhere due to increased heart rate
- adrenaline binds to same alpha receptors on smooth muscle cells in arterioles
- also binds to beta receptors on smooth muscle cells = dilation (instead of restriction) where beta receptors outnumber alpha receptors
- in skeletal muscles, myocardium (heart muscle cells), liver -> needed for fight or flight
- blood redistributed from stomach to areas needed for survival -> digestion suppressed
- body muscles tighten
- f.o.f = sympathetic nervous system
therapeutics for blood flow control
- sodim nitroprusside -> vasodilator that mimicks endothelial NO -> treats: angina
- sildenafil -> vasodilator that boosts cGMP -> no pathway -> treats: pulmonary arterial hypertension
- ACE inhibitors -> block effects of angiotensin II -> treats: hypertension
- antihistamines -> vasoconstrictors
how to calculate blood pressure?
blood pressure = total peripheral resistance x cardiac output
how to calculate cardiac output?
cardiac output = heart rate x stroke volume
what is stroke volume?
the amount of blood being pumped
how can kidney failure cause excess blood volume to rise?
- kidneys filter blood so excess volume is lost here
- if dont work -> the excess blood not lost
causes of hypertension
- smoking
- obesity
- diet
- exercise
- genetic (can be inherited)
chronic hypertension
- high blood pressure
- the resistance is greater, and your heart has to work harder to push blood through your body
- can lead to further cardiovacsular diseases
-> atherosclerosis
-> stroke
-> myocardial infarction
-> heart failure
-> renal failure
-> retinopathy
clinical benefits of reducing blood pressure
- 40% reduction of stroke
- 25% reduction in myocardial infarction
- > 50% reduction in heart failure
how can you lower blood pressure with drugs?
- block sympathetic nervous system
reduce effects on heart (beta blockers)
reduce effecrs on blood vessels (alpha blockers -
constrict blood vessels) - kidney
reduce blood volume (dieretics) - hormones
ACE inhibitors - vasodilation of peripheral resistance arterioles
Ca2+ channel blockers
beta andrenoceptor blockers
- examples: propanolol & atenolol
- competitive reversible antagonists
- lower blood pressure by blocking the beta sympathetic tone on heart and reducing renin released from the kidney
- lower heart rate & stroke volume
- lower cardiac output
- could affect the ability to increase heart rate when exercising
adverse effects of beta adrenoceptor blockers
- exacerbate asthma
- reduced ability to exercise
- hypogylcaemia
- vivid dreams if propanolol goes into the brain
alpha adrenoceptor blockers
- examples: phentolamine, doxazosin, prazosin
- competitive reversible antagonists
- reduce blood pressure via drop in sympathetic tone in arterioles (symp. tone = activation of sympathetic NS)
- reduced peripheral resistance
adverse effects of adrenoceptor blockers
- postural hypotension = loss of sympathetic venoconstriction -> lack of blood and oxygen to the brain
- reflex tachycardia (via baroreceptors)
ACE inhibitors
- examples: captopril & enalapril
- antagiotensin converting enzyme on vascular endothelial surface converts angiotensin I to the active angiotenisn II
- can reduce the activity of an enzyme called angiotensin-converting enzyme -> the enzyme is responsible for hormones that help control your blood pressure.
how do ACE inhibitors lower blood pressure?
- reduced formation of the vasoconstrictor angiotensin II (reduction in peripheral resistance)
- reduced blood volume
adverse effects of ACE inhibitors
- generally well tolerated
- can cause a sudden drop in blood pressure on first dose
- lead to persistant irritant cough -> due to reduced breakdown of bradykinin (peptide that activated sensory nerves in lung tissue)
what percentage of blood is made out of red blood cells?
45% (55%= plasma, remianing 1% are white blood cells and platelets)
arteries
carry blood away from the heart
veins
carry blood to the heart
neurotransmitters of the parasympathetic nervous system? and the effect on heart rate?
acetylcholine
decreases HR
neurotransmitters of the sympathetic nervous system? and the effect on heart rate?
noradrenaline & adrenaline
increases HR
what does a decrease in the firing rate of the sympathetic vasoconstrictor neurotransmitter noradrenaline have on boood vessels?
vasodilation
Which group of receptors are commonly targetted and blocked to lower blood pressure?
beta adrenocpetors are commonly targeted to lower blood pressure
how do beta blockers help lower blood pressure?
they inhibit beta (1) adrenoceptors (which increase hr) and their sympathetic effect on the heart
what is a problem with propanolol?
it blocks beta(2) receptors as well as beta(1)
this can cause bad bronchospasms in patients with asthma
what are the three main types of angina?
- stable
- unstable
- variable
stable angina
- predictable attacks e.g. during exercise
- myocardial O2 demand not met
unstable angina
- attacks unpredictable
- coronary atery occlusion due to platelet adhesion to ruptured atherosclerotic plaque
variant angina
- unpredictbale attacks
- coronary artery occlusion by vasospams
main causes of heart failure
- haemodynamic overload = due to excessive pressure on the heart (hypertension…) or excess blood volume on heart due to leaky valves and obesity due to growing amounts of tissue and heart needs to work harder
- neurohormonal overload = excessive amount of thyroid horomones
- tissue damage = due to myocardial infarction normally
- genetics = hypertrophic cardiomyopathy (heart produces excessive hypertrophic response to pressure within the heart)
role of cholesterol
- helps allow substances to be incorporated into the cell membrane
- membrane fluidity and permeability
- production of steriods and fat-soluble vitamins
what can high cholesterol levels lead to?
atherosclerosis
what is atherosclerosis?
where hard, calcified plaques are deposited in the arteries over time and keep growing and developing
- hardening of blood vessels -> lumen is narrower -> restricted blood flow
- the plaques can also dislodge and float elsewhere
how many deaths a year due to cardiovascular disease?
31%
how does physical activity indirectly reduce the risk of coronary heart disease?
- indirectly = does not improve heart health itslef
- pa helps weight loss, glycaemic control, good bp, lipid profile & insulin sensitivity
- these combined help reduce the risk
How many minutes of moderate intensity exercise is recommended for adults on a weekly basis to keep them active?
150
How many minutes of vigorous intensity exercise is recommended for adults on a weekly basis to keep them active?
75
systolic pressure
- pressure experienced by arteries when heart is beating
- maximum blood pressure when ventricles contract
diastolic pressure
measures the pressure in your arteries when your heart rests between beats
what is angina?
- chest pain
- due to reduced blood flow to heart muscles
- warning sign that at risk of heart attack or a stroke
