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what factors affect diffusion?
- AREA - area per unit volume is determined by capillary density
- DIFFUSION RESISTANCE - affected by the nature of the molecule, the barrier and the capillary density
- CONCENTRATION GRADIENT - the large the gradient the faster the diffusion rate, to maintain concentration gradient flow must be sufficient
- SUPPLY & DEMAND - increasing metabolism > increased flow this is know as the perfusion rate.
what must the CVS supply to the different tissues of the body?
- brain -750 ml/min
- kidney - 1200 ml/min
- heart - 300-1200 ml/min
- skeletal muscle - 1000-16000 ml/min
- skin - 200-2500ml/min
- gut - 1400 -2400ml/min
in total - 5 - 25 l/min
how is blood flow regulated?
- arterioles - resistance vessels
- veins - capacitance vessels
structure of large arteries?
- elastic to permit recoil > maintaining blood pressure during diastole
- tunica intima: endothelium, narrow subendothelium with discontinuous elastic lamina
- tunica media: 40-70 fenestrated elastic membranes with smooth muscle cells and collagen between lamellae
- tunica adventitia: thin layers of fibroelastic connective tissue containing vasa vasorum, nerves and lymphatics
structure of muscular medium arteries?
- tunica intima: endothelium, thick subendothelium - with internal elastic lamina
- tunica media: 40 layers of smooth muscle joined by gap junctions to give co-ordinated contraction
- tunica adventitia: thin layer of firbroelastic connective tissue with some vasa vasorum, nerves and lymphatics
structure of arterioles?
- resistance vessels
- endothelium wrapped in smooth muscle cells
- tunica adventitia is layers of fibroblasts
structure of meta-arterioles?
the smooth muscle is not continuous and instead forms pre-capillary sphincters
structure of capillaries?
what are the three types of capillaries?
- diffusion vessels
- single layer endothelium and basement membrane
- pericytes are a branching outer layer that divide into smooth muscle cells and fibroblasts
- there are three types of capillaries: fenestrated, sinusoids and continuous
- continuous are most common and have tight cell junctions
- fenestrated are found in the gut, endocrine glands and glomerulus
- sinusoids are found in the liver, spleen and bone marrow they allow cells to move between blood and tissue
structure of venules?
- post capillary venules are just endothelium and pericytes they are more permeable than capillaries
- venules contain valves and gradually accumulate smooth muscle fibres which are the start of the tunica media
structure of medium veins?
- tunica intima: thin
- tunica media: 2-3 layers of smooth muscle cells
- tunica adventitia: well developed
structure of large veins?
- capacitance vessels
- thin walls more connective tissue than muscle
- larger diameter then associated arteries
- well developed aadventitia
what are ateriovenous shunts?
miss out capillaries
what are vasa vasorum?
small blood vessels that supply large blood vessels with blood
what are venacomitantes?
veins that accompany arteries helping with blood temperature and return to the heart
what are varicose veins?
- swollen enlarged veins
- caused by dysfunctional valves which allow back flow of blood
describe the location of the heart
- inferior middle mediastinum
- between the sternum and the oesophagus
describe the pericardium
- inextensible sac
- inner serous layer which itself is formed of an inner visceral layer and an outer perital layer - between these layers is a space with a few drops of lubricating fluid
there is then also a outermost fibrous layer
describe the features of cardiac muscle
- 3 layers - endocardium, myocardium, epicardium
- low electrical resistance between the cells of the myocardium means they all contract together during systole
what are the pacemaker cells
found in the SA node control the rate of the heart
describe the cardiac cycle
- at rest the pacemaker cells in the SA node produce approximately one action potential per second
- this produces a short atrial systole followed by a longer ventricular systole (280ms)
- this is followed by diastole (700 ms)
- in diastole the ventricles relax and the pressure falls causing opening of the AV valves - blood can then flow from the atria into the ventricles throughout diastole
- atrial systole pushes the remaining blood into the ventricles and then about 150 ms the ventricles contract - the rise in pressure forcibly closes the AV valves and once the pressure exceeds the diastolic pressure in the arteries the outflow valves open
what are the normal heart sounds?
- s1 - lup - closure of AV valves at start of ventricular systole
- s2 - dup - closure of outflow valve at the end of systole
draw the Jugular Venous Pressure
- a = atrium contracting tricuspid valve open
- c = small back flow into atrium as ventricle contracts
- x = atrium relaxing then filling
- v = atrium tense and full
- y = tricuspid valve open
what are the normal pressures in the RA, LA, RV, LV, the pulmonary artery and the aorta
- RA = 0-8mmHg
- LA = 1-10 mmHg
- RV = 15-30/0-8
- LV = 100-140/1-10
- pulmonary artery = 15-30/4-12
- aorta = 100-140/60-90
where does the left anterior descending coronary artery supply?
- anterior left ventricle
- some right ventricle
- intraventricular septum
where does the left circumflex artery supply?
- posteriorlateral left ventricle
- left atrium
where does the right coronary artery supply?
- right atrium
- AV & SA nodes
where does the posterior descending coronary artery supply?
- intraventricular septum
describe simply the formation of the CVS during foetal development
Cephalocaudal folding brings heart into chest region
Lateral folding creates primative heart tube from fusion of endocardial tubes - this tube is suspended in a cavity by a membrane that degenerates
The tube receives blood supply from the caudal pole and begins to pump blood around the first aortic arch into the dorsal aorta
- The tube continuous to elongate and on day 23 looping begins - (cephalic portion bends ventrally,
- caudally and to the right AND caudal portion bends dorsally, cranially and to the left)
This creates the cardiac loop by day 28
- Looping occurs so that the primordium of the RV is by the outflow tract and the primordium of the LV is by the inflow tract and the atrium is dorsal to the bulbus
After looping the atrium and ventricle communicate by the atrioventricular canal
The L and R horns are equal in size but venous return switches to the R – L reseeds and R horn is absorbed enlarging the atria
The RA develops from the sinous venosus and the primordial atrium. The LA develops from a small part of the primitive atrium and the proximal part of the pulmonary vessels
Once looping has occurred we need septation to have two pumps in series
Septation of the atrioventricular canal – growth of endocardial cushins
Atrial septation – septum primum grows down towards endocardial cushins, the gap is called the ostium primum, before it closes apoptosis forms the ostium secundum to replace it. The septum secundum then grows up leaving a crescent shape whole at the bottom called the foramen ovale (fossa ovalis after birth)
Ventricular septation – the muscular septum grows up forming most of the septum the membranous septum is made of CT and grows down from the cushins
Septation of the outflow tract – endocarcial cushins form in the truncus arteriosus as the grow they twist around each other forming a spiral septum
what is different in foetal circulation?
what must happen at birth?
- lungs are non functional
- oxygenated blood come via the placenta from the mother
- blood comes via liver > RA > LA > LV > body
- some blood goes into the RV so the muscle can develop but it by-passes the lungs using the ductus arteriosus
- at birth the ductus arteriosus, RtoL shunt and the ductus venosus must all close
describe 4 acyanotic congenital heart defects
- ASD - osteum secundum defect/patent foramen ovale/ primum atrial defect > increase pulmonary blood flow > RV volume overload > right heart failure - fixed splitting of s2
- obstructive lesions - aortic/pulmonary stenosis > split s1+systolic murmor, coarctation of the aorta > radial femoral delay, mitral stenosis > loud s1
- VSD - LtoR shunt > pulmonary venous congestion > pulmonary hypertension
- PDA - lack of prostaglandins from mother and bradykinins from lungs means DA fails to close > heart failure, continuous murmor
describe 3 cyanotic congenital heart defects
- complex LtoR shunts
- transposition of the great arteries - this is only viable with patent ductus arteriosus or AV shunt
- tetralogy of fallot = pulmonary stenosis + VSD + RV hypertrophy + over-riding aorta
describe the roles of the ANS
- contraction of vascular and visceral smooth muscle
- some endocrine and exocrine secretions
- force and rate of heart contraction
describe the sympathetic innervation of the heart
SYPATHETIC - post ganglionic cardiac nerve from the sympathetic trunk innervates the SA & AV nodes and the myocardium . release of NA acts on B1 receptors inc. HR and force of contraction (in cAMP > phosphorylation of Ca channels > inc Ca entry > inc force of contraction) + increases slope of pacemaker potential
describe the parasympathetic innervation of the heart
PARASYMPATHETIC - 10th cranial nerve/vagus nerve synapses in wall of the heart with SA and AV nodes the post ganglionic cells release ACh with acts on M2 receptors > dec HR (-ve chronotrophic) and dec AV node conduction velocity. it also slows pacemaker potential by opening K channels via cAMP.
what affects can the ANS have on the vasculature?
- most vessels = sympathetic innervation, A1 receptors sympathetic output normal = vasomotor tone, dec = dilation, inc = constriction
- cardiac muscle, skeletal muscle, liver = sympathetic innervation A1and B2 receptors - circulating adrenaline has higher affinity for B2 receptors > vasodilation
name some (7) drugs that can be used that work due to their affects on the ANS and the three categories they fall in to
sypathomimetics: adrenaline (cardiac arrest & anaphylactic shock), dobutamine (B1 agonist - give in cardiogenic shock), salbutamol (B2 agonist -asthma)
adrenoceptor agonists: prazosin (A1 antagonist - inhibit NA action on smooth muscle - treat hypertension), atenolol (B1 antagonist - slow HR and reduce force of contraction)
cholinergics: pilocarpine (muscarinic agonist - treat glucoma), atropine (muscarinic agonist - inc HR, cause bronchiodilation - dilate pupils for eye exam)
what effect does the ANS (parasympathetic and sympathetic) on the pupil of the eye?
- s: NA acts on A1 receptor > pupil dilates
- p: ACh acts on M3 receptor > pupil constricts
what effect does the ANS (parasympathetic and sympathetic) on the salivary glands?
- s: NA acts on A1 receptors > thick viscous secretion > dry mouth
- p: ACh acts on M3 receptor > watery mucus high enzyme content
what effect does the ANS (parasympathetic and sympathetic) on the airways of the lung?
- s: circulating adrenaline acts on B2 receptors > dilation
- p: ACh acts on M3 receptors > constriction
what effect does the ANS (parasympathetic and sympathetic) on the SA node of the heart?
- s: NA acts on B1 receptors > inc firing > inc HR
- p: ACh acts on M2 rceptors > reduced firing > reduced HR
what effect does the ANS (parasympathetic and sympathetic) on the atrial muscle of the heart?
- s: NA acts on B1 receptors > inc contractile force
- p: ACh acts on M2 rceptors > reduced contractile force
what effect does the ANS (parasympathetic and sympathetic) on the ventricular muscle of the heart?
s: NA acts on B1 receptors > inc contractile force
what effect does the ANS (parasympathetic and sympathetic) on the blood vessels in most tissues?
s: NA acts on A1 receptors > constriction
what effect does the ANS (parasympathetic and sympathetic) on the blood vessels in skeletal muscle?
s: NA acts on B2 receptors > dilation
what effect does the ANS (parasympathetic and sympathetic) on the erectile tissue?
- s: NA acts on A1 receptors > constriction of blood vessels
- p: ACh acts on M3 receptors > dilation of BVs > erection
what effect does the ANS (parasympathetic and sympathetic) on the male sex organs?
s: NA acts on A1/2 receptors > ejaculation
what effect does the ANS (parasympathetic and sympathetic) on adipose tissue?
s: NA acts on A1 & B1 receptors > lipolysis
what effect does the ANS (parasympathetic and sympathetic) on the liver?
s: NA acts on A1/2 & B2 receptors > glycogenolysis
what effect does the ANS (parasympathetic and sympathetic) on the kidney?
s: NA acts on A1 receptor > salt and water retention
what effect does the ANS (parasympathetic and sympathetic) on the sweat glands?
s: ACh acts on M3 receptors > secretion
what effect does the ANS (parasympathetic and sympathetic) on the gut?
s: NA acts on A2 & B2 receptors > constriction of sphincters, NA act on all receptor > decreased motility
p: ACh acts on M3 receptors > inc motilty , inc secretion and relaxation of sphincters
what is flow?
- the volume of blood passing a given point per unit time
- Q= P/R
what is velocity?
- the rate of movement of fluid particles along the tune
- V = Q/area
- V is proportional to 1/SA
what are the two types of flow?
- LAMINAR - high central velocity
- TURBULENT - flow resistance greatly increased - hear bruit
what is viscosity?
the property of a fluid that resists the force tending to cause the fluid to flow, the higher the viscosity the lower the velocity
what is poiseulles law?
resistance is proportional to rxrxrxr
why does it matter that blood vessels are connected together?
reduces the resistance of the capillaries as there are so many in parallel
why are distensible vessels useful?
- as the vessel stretches the resistance falls
- as the pressure drops the vessel collapses causing a cease in blood flow before the pressure reaches zero
what happens to the pressures in the arteries during the cardiac cycle?
what would happen if they had rigid walls?
arteries stretch during systole and recoil during diastole maintaining an even pressure
if the walls were rigid then pressure would be very high in systole and zero in diastole
what is reactive hyperaemia?
if the circulation to a part of the body is cut off for a short amount of time when blood flow is restored there is a massive increase in to this area for a short amount of time while metabolites (H, K, adenosine) which cause vasodilatation are washed away once they are washed away the SM of the BV can constrict again
what is autoregulation?
- if supply pressure changes the flow to the tissue changes
- this alters metabolite concentration
- this alters arteriole resistance
- thus correct blood flow to the tissue is maintained
draw a diagram of typical arterial pressure in a cardiac cycle
what happens when CO stays the same but TPR falls?
- arterial pressure DOWN
- venous pressure UP
what happens when CO stays the same but TPR rises?
- arterial pressure UP
- venous pressure DOWN
what happens when CO rises but TPR stays the same?
- arterial pressure UP
- venous pressure DOWN
what happens when CO falls but TPR stays the same?
- arterial pressure DOWN
- venous pressure UP
what is CO?
CO = STROKE VOLUME X HEART RATE
what factors affect CO?
- ventricular filling: starlings law more in = more out
- force of contraction - can be increased by sympathetic activity
what is starlings law?
- stretched muscle contracts harder so if more blood is put into the heart by high venous pressure the harder it will contract and the higher the stroke volume will be
what happens when we eat a meal?
- vasodilation around the gut
- fall in TPR
- rise in venous pressure therefore fall in arterial pressure
- the high venous pressure > increase in CO - Starlings law
- low arterial pressure triggers SNS > Inc HR
- demand met
what happens when we have changes in HR?
- if HR increases initially with no other change
- venous pressure falls
- so SV falls
- so CO is normalised
- - the heart is controlled by the circulation
what happens when we exercise?
- massive increase in demand and muscle pumping > inc venous return
- the increase in venous pressure is a problem as it tends to overfill the heart
- overfilling is prevented by a rise in heart rate as soon as exercise begins from the brain
what happens when we stand up?
- blood pools in superficial leg veins
- central venous pressure falls
- so starlings law causes CO to fall
- - this doesn't work because both arterial and venous pressure have changed in the same direction
- SPECIAL MECHANISM - baroreceptors increase HR as venous pressure falls and TPR increases by minimising perfusion to the skin and gut this defends the arterial pressure
failure of this = postural hypotension
what happens when we haemorrhage?
- reduced blood volume > low venous pressure > low CO >low arterial pressure
- baroreceptors detect and increase HR and TPR
- this helps arterial pressure but further lowers venous pressure
- to raise venous pressure the vessels constrict and fluid moves from extracellular into circulation
what happens when we have a longer term increase in blood volume?
- blood volume is controlled by the kidney
- if blood vol is increased for days
- venous pressure increases
- CO increases
- arterial pressure increases
- TPR increases > further rises in arterial pressure > high BP
what is heart rate dependant on?
- heart rate is dependant upon the ANS
- baroreceptors in the carotid sinus and aortic arch detect stretch and send messages to the medulla
bainbridge reflex = if venous pressure rises HR rises
draw a graph and describe what happens in myocardial cells that causes the heart to contract
- in diastole the cell membrane potential is most permeable to K so the membrane potential is close to Ek at around -80mV
- spread of activity raises the cells to threshold by an initial depolarisation this opens voltage gated Na channels so equilibrium moves towards Ena
- Na channels are quickly inactivated but by this point the Ca channels are open
- Ca channels cause a large influx of Ca causing contraction they remain open for the rest of systole and when they close K channels open
draw a graph and describe what happens in pacemaker cells that causes the heart to contract
- pacemaker cells are normally found in the SA node
- the spontaneously generate APs
- the dont have fast Na channels so the upward stroke is dependant on Ca channels that also close quickly
- they have a feature called pacemaker potential - the membrane depolarises at a steady rate until it reaches threshold - HR is dependant on the steepness of the pacemaker potential
what drugs can we use to treat arrhythmias?
- arrhythmias can be tachycardia, bradycardia, atria flutter, atrial fibrillation, ventricular fibrillation
- they can be caused by: ectopic pacemaker activity due to a damaged area of myocardium,
- 4 classes of dugs:
- 1. voltage dependant Na channel blockers - lidocaine - prevents after depolarisations but allows normal HR used after MI if patient shows signs of ventricular tachycardia to prevent VF
- 2. B blockers - atenalol - blocks SNS acting on B1 receptors in the heart > decrease slope of pacemaker potential > dec HR - used after MI to prevent VF reduces O2 requirement of the heart, can also be used to treat slow conductance of the AV node or used in hyperthyroid to reduce affects on the heart
- 3. K channel blockers - prolong AP by lengthening ARP - used to treat tachycardia associated with Wolff-Parkinson-White syndrome
- 4. Ca channel blockers - dec slope of pacemaker potential, dec AVN conductance, dec force of contraction, cause coronary and peripheral vasodilation
what drugs can we use to treat heart failure?
- the idea is the reduce the force of contraction, reduce CO, reduce tissue perfusion and oedoma
- 1. cardiac glycosides - digoxin - block Na/K-ATPase causing a rise in intracellular Na this reduces the effect of NCX and thus more Ca is stored in the SR +ve inotrphic affect and also reduce HR
- 2. ACE inhibitors
- 3. diuretics
- 4. B blocker
what drugs can we use to treat angina?
- reduce workload of the heart - B blockers, Ca channel antagonists, organic nitrates
- improve blood supply to the heart - organic nitrates, Ca channel antagonists
what drugs can we use to treat hypertension?
- ACE inhibitors
- B blockers
- Ca channels antagonists
- A1 adrenoceptor antagonists
what anti-thrombotic drugs are there and when would we use them?
- used in AF, acute MI, mechanical valves
- heparin - inhibits thrombin
- warfrin - antagonises vit K
- asprin - anti platelet
describe an ECG
where do the leads go?
what views do the leads give?
- RA-On the right arm, avoiding thick muscle.
- LA-In the same location that RA was placed, but on the left arm this time.
- RL-On the right leg, lateral calf muscle
- LL-In the same location that RL was placed, but on the left leg this time.
- V1-In the fourth intercostal space (between ribs 4 & 5) just to the right of the sternum (breastbone).
- V2-In the fourth intercostal space (between ribs 4 & 5) just to the left of the sternum.
- V3-Between leads V2 and V4.
- V4-In the fifth intercostal space (between ribs 5 & 6) in the mid-clavicular line (the imaginary line that extends down from the midpoint of the clavicle (collarbone)).
- V5-Horizontally even with V4, but in the anterior axillary line. (The anterior axillary line is the imaginary line that runs down from the point midway between the middle of the clavicle and the lateral end of the clavicle; the lateral end of the collarbone is the end closer to the arm.)
- V6-Horizontally even with V4 and V5 in the midaxillary line. (The midaxillary line is the imaginary line that extends down from the middle of the patient's armpit.)
what would you look for on an ECG?
Draw a normal ECG
- p wave
- qrs complex
- pr interval
- st segment
- t wave
what would you see on the ECG of a patient with a MI after:
a) 1 hour
b) 24 hours
- a) st elevation
- b) inverted t waves
- c) pathological q waves
what is 1st degree heart block and what would you see on the ECG?
- not itself a problem but may indicate CAD, electrolyte disturbance ...
- prolonged PR interval
what is 2nd degree heart block and what would you see on the ECG?
- some atrial impulses not conducted to the ventricles
- 3 types
- mobitz type 1: progressive lengthening of PR intervals and then a failed conduction
- mobitz type 2: most beats are conducted but occasional missing QRS complex
- 2:1, 3:1... more P waves than QRS complexes
What is 3rd degree heart block and what would you see on the ECG?
- no conduction from atria to ventricles can be caused by MI or fibrosis of bundle of His pacemaker required
- no relationship between P and QRS
- abnormal QRS
What is RBBB and what would you see on the ECG?
bundle branch block no conduction is carried down right side but left is as usual causes a M in lead v1 and a W in lead v6
may indicate atrial septal defect
what is LBBB and what would you see on the ECG?
- v1 = W
- v6 = M
- may also be t wave inversion
may indicate aortic stenosis, ischaemic disease or possibly an MI
what is 2:1, 3:1, 4:1 and what would you see on the ECG?
multiple P waves for each QRS complex
what are ventricular ectopic beats?
- abnormal random QRS can be any shape
- if occur early in t wave of a proceeding beat can lead to VF
what is atrial fibrillation?
- atrial muscle contracts independantly of the SA node
- no p waves
- irregular base line
- irregular QRS
- normal shaped QRS
what is ventricular fibrillation?
- muscle fibres contract independantly
- no pattern
describe the features of the pulmonary circulation
- the lung have two circulations
- the bronchial circulation - part of the systemic and the pulmonary circulation
- the pulmonary circulation works with low resistance and low pressures
- low resistance is due to short wide vessels lots of capillaries and little smooth muscle in the arterioles
- hypoxic pulmonary vasoconstriction ensures ventilation perfusion matching
what is cushing's reflex?
- rigid cranium doesn't allow for volume expansion
- increases in intercranial pressure impair intercranial bloodflow
- impaired blood flow to vasomotor control regions of the brain stem increase sympathetic activity
- increases arterial pressure
- helps maintain cerebral blood flow
describe the features of the cerebral circulation
- brain receives 20% of CO
- meets o2 need by having high density capillaries, short diffusion distance, high basal flow rate and high o2 extraction rate
- neurones are very sensitive to hypoxia
describe the features of the coronary circulation
- arise from aortic sinuses
- blood flow is mainly in diastole
- capillary density is high
- capillaries produce lots of O/NO to dilate vessels
- there are few anastomoses
- prone to atheroma
describe the features of the skeletal muscle circulation
- must be able to increase o2 delivery and nutrient delivery and remove metabolites
- it has a role in regulating arterial BP
- resistance vessels have strong sympathetic innervation
- cap density depends on muscle type postural muscle have very high density
- vasodilators = adenosine K and H
describe the features of the cutaneous circulation
- Main function = body temp regulation
- acral/apical skin has specialised structures called atereovenous anastomoses
- apical skin has a high SA to volume volume ratio
- under neural control
- inc sympathetic tone of AVAs reduce blood flow to apical skin raise core body temp
what is heart failure?
heart fails to maintain adequate circulation for the needs of the body despite adequate filling pressures
what are the causes of heart failure?
- primary cause is ischaemic heart disease
- other causes = hypertension, dilated cardiomyopathy - bugs drugs and pregnancy, valvular heart disease, pericardial disease, arrhythmias
how is heart failure classified?
NYHA class 1-4
what are the clinical syndromes of heart failure?
- right sided heart failure
- left sided heart failure
- congestive heart failure
- systolic HF- pump failure
- diastolic HF - failure of relaxation
signs/symptoms of left heart failure?
- exertional dyspnoea
- paroxysmal nocturnal dyspnoea
- mitral regurge
- peripheral oedema
- basal pulmonary crackles
causes of right heart failure?
- most common is secondary to LHF
- others = chronic lung disease, PE, pulmonary hypertension, tricuspid valve disease
- isolated right ventricular cardiomyopathy
signs/symptoms of right heart failure?
- raised JVP
- tender smooth hepatic enlargement
- pleural effusion
management of heart failure?
- lifestyle modifactions
- ACE inhibitors
- B blockers
what are the volumes that should be in the heart during the cardiac cycle?
- CO = 5l/min
- SV = 75 ml
- LV end systolic vol = 75 ml
- LV end diastolic vol = 150 ml
- ejection fraction = > 50 %
what is systolic dysfunction?
- inc LV capacity
- reduced LV CO
- thinning of myocardium
- mitral valve incompetence
- neuro-hormonal activation
- cardiac arrhythmias
what structural heart changes can occur?
- loss of muscle
- unco-ordinated abnormal contraction
- changes in ECM - increase in type iii collagen, slippage of myocardial fibre orientation
- changes in cellular structure and function
what neuro-hormonal changes occur in heart failure?
- SNS - early compensation to improve CO > damage
- RAAS - activated by poor kidney perfusion or SNS > elevated angiotension II > LV hypertrophy, myocyte dysfunction and worsens hypertension
- NATRIURETIC HORMONES - balance effects of RAAS on vascular tone
- ADH - inc water retention > inc co > inc stress on walls
what is diastolic dysfunction?
- this is normally in elderly females with a history of hypertension/obesity/diabetes
- normal LV function but concentric LVH
- impaired relaxation of heart > impaired LV filling > raised PA pressure > low CO > triggers neuro-hormonal response
list cardiac and non cardiac causes of chest pain?
- aortic dissection
- aortic aneurysm
- peptic ulcer
- cervical disc degeneration
what is ischaemic heart disease?
characterised by lack of oxygen to heart muscle causing ischaemia main reason is CAD
describe coronary artery disease
- caused by atherosclerlosis
- starts with fatty streak > foam cells + smooth muscle cells > plaque
- risk factors = age, male, family history, high cholesterol . low HDLs, hypertension, smoking, diabetes, LVhypertrophy, obesity, alcohol
describe stable angina
- this is a symptom
- often caused by CAD
- exercise stress test may show ST elevation
describe unstable angina
- no necrosis
- plaque rupture
- > 90 % occulsion
what is a STEMI?
- MI necrosis secondary to interuption of blood supply
- full occulsion
- complications - arrhythmias, LV failure, cardiogenic shock,
what enzymes are measured in a suspected MI and why?
- creatine kinase MB
- troponin 1
- released by dead myocytes
what is the treatment for a MI?
- thrombolysis and angioplasty
- anti coagulants
what is shock?
- acute condition of inadequate blood flow throughout the whole body
- can be due to a fall in TPR or CO
what are the different types of shock?
divide based on whether they cause a fall in CO or TPR
- TPR - anaphylaxis/sepsis > distributive shock
- CO -
- - haemorrhage/burns > hypovolaemic shock
- - MI/ heart failure > cardiogenic shock
- - cardiac tamponade/PE > mechanical shock
how do patients in shock present?
- distributive > tachycardia, warm red extremities, strong pulse
- other > tachycardia, weak pulse, cold and clamy extremities
what is cardiac arrest?
how do we attempt to treat these patients?
- lack of pulse
- can be asytole or VF
- correction by defibrilation and give adrenaline