Lecture 1 - Anatomy/Atherosclerosis Flashcards
describe the anatomy of the heart (where the borders are, what is the point of maximum impulse, what part lies on the diaphragm, are atria or ventricle walls thicker?)
- The heart a bit larger than size of fist
- 2/3 of mass is left side of midline
- Heart angled a bit
- Borders of heart: a base (above - formed by 2 atria – base at level of 2nd intercostal space), and apex (formed by L ventrical – found at 5th intercostal space at mid-clavicular line)
- Anterior surface (at sternum) we have the right ventrical bc heart is turned a bit on its axis
- L ventrical oriented towards clavicular line
- Point of maximum impulse = when the heart contracts, the apex hits against the chest wall and this is called POMI
- Inferior portion of heart that is lying on diaphragm is primarily the R? ventrical (a bit of the L?)
- R atrium next to R lung, L atrium and part of L ventircal next to L lung
- Ventricals thicker walls than atrium – because ventricals move the blood, more muscular
- Intraatrial septum and intraventricaular septum
- Sometimes a communication btw l and r side of heart in certain diseases = bad bc oxygenated and deoxygenated blood mixes
name the valves of the heart
Inlet valves = btw atria and ventricals (tricuspid on R, mitral on L)
Outlet valves = btw heart and vessels (pulmonic on R, aortic valve on L)
Mitral ad bicuspid have cordae tendinae (connected to palpillary muscles) – prevents the valve from bulging out (bc highest pressure is here when blood is being pushed out – prevents regurgitation of blood back)
what are the 3 layers of the heart?
Epicardium = outside (connective tissue and epithelium, aka visceral pericardium)
Myocardium = middle (heart muscle, pretty thick, many capillaries and nerves)
Endo – mesothelial/endothelial connective tissue, continues on the lining of blood vessels
Pericardium = fibrous connective sac, encloses heart – in order to prevent heart from expanding too much
describe the layers of the heart WRT the pericardial layers
The sac is a double layer (think of the heart being pushed into a balloon like with the lungs = 2 layers)
Visceral = inner, parietal = outer
Visceral+parietal together = serous, 10-20 ml of fluid btw the 2 layers which helps reduce friction
Fibrous tissue attached to Pericardial L hemidiaphragma and diaphragm – therefore heart moves with diaphragm during periods of more than normal quiet breathing (vasalava maneuvre)
name the large blood vessels of the heart
what are the layers of the blood vessels and how do arteries/veins differ?
2 main differences btw art and veins:
Elastic lamina
Thicker smooth muscle
- Bc in arteries higher pressure in vasculature, helps to contain vessels and generate the pressure
- Venus pressure = much lower, veins are the capacitors of the vasculature, meaning it is where most of the blood volume stays – for circulation we have the valves which allows 1-direction flow (not backwards)
- Blood pressure is controlled in the smaller vessels (peripheral resistance, sphincters)
- The smaller arterioles have tone and can control distribution of blood to organs but the smaller ones, (arterioles) control the vascular resistance
describe the blood supply to the heart (also which artery is larger?)
- L ca = larger than right
- 70% of oxygen is extracted by heart muscle of the oxygenated blood going to heart
- When demand of heart increases (needs more oxygen) – coronary artieries dilate to increase blood flow to heart during exercise (NOT via extraction – bc extraction is already at 70%, not much more to improve)
- The bloodflow to heart is not constant (when contracting, blood is being pused into coronary arteries – during systole, but muscle cannot extract the oxygen until it is relaxed -during diastole)
describe the 2 types of myocytes
Categorized into 2 groups based on function
–important for the muscles to be fatigue resistance bc it cannot rest!
-Can conduct current (ie nerve impulses)
Cant be replaced! So when someone has a heart attack and cells die, they stay dead and muscle in that area cannot contract OR conduct
describe the conduction system of the heart
Pacemakers initiate the electrical activity
SA node discharges at an intrinsic rate, internodal fibres go to AV node and other side of atrium as well – atria contract when the sa node discharges - blood pushed into ventricles
Delay btw SA node and AV node firing which allows as much blood as possible to be pushed into ventricles
AV node discharges – current transmitted to budle of his, then to right branches to r ventricle, the L bundle branch into L ventricle, and purkinje fibres that are embedded into the ventricles and transmit the current
When current passes to purkinje fibres, the ventricle apices contract and the current is distributed upwards through ventricals so they start squeezing from the bottom to top and enables blood to get pushed from ventricles to pulmonary artery or aorta
describe the neural control of the heart
These systems control Rate and contractility
Vagal and sympathetic in medulla
Para:
cholinergic = acetocholine
Vagal – vagus nerve
Para controls the heart during rest
Sympa:
adregenic = adrenalin and noradrenalin, during exercise
Via stimulation of receptors causes constriction or dialation
Constriction of periph blood vessels helps bring blood back to body/ increase circulation/blood flow
B receptors in the heart/coronary arteries and increase blood flow through heart by dilation of coronary arteries
- Baro and chemoreceptors send signals back to medullary centres
- They respond to blood pressure (link btw HR and bp, when BP goes down, HR increases and vice versa)
what is the overall role of artieries/veins/capillaries/heart?
Veins = capacitors, lactic acid production on the venus side
75% of TBV sitting in our veins at any given time
what are circulatory movements driven by?
Peripheral muscles – blood pools in peripheral veins (In legs for example) so out ms contribute in helping that pooled blood go back to the heart – therefore syncope can happen in soldiers who are standing still long periods
Breathing assists in blood circulating: if you breathe and have neg interthoraccic pressure helps pull blood back into the heart
what valves open/shut during systole/diastole?
describe the cardiac cycle (what is the isovolumetric contraction and relaxation period?)
ECG – electrical tracing in the heart, p wave represents depolarization of atria, QRS = depolarization of ventricles, t wave = repolarization of ventricles
Stage 1
Starts with atria contracting then increased volume of ventricle
pressure within the atria and ventricle = the same bc AV valve is open so it is one big cavity
Point a: increased p in both bc atria squeezing blood from one part to another
Stage 2 (IVCP)
Current goes through purkinje fibers and ventricles contract
- when they contract pressure in ventricles increase and as soon as p starts to increase AV valves shut (S1) and atria and ventricular pressure now dissociate
- the outlet valve does not open immediately bc pressure in aorta is currently much higher than that of the ventricle
- isovolumetric contraction period = when ventricle is contracting but hasn’t reached same pressure as within the aorta the blood is still not being pushed out – volume in the ventricle REMAINS the SAME = so volumetric contraction period, volume line straight
- this period goes until the pressure reached is the same as the pressure within the aorta – this is when the aortic valve opens up – blood within ventricle gets pushed out into aorta – then:
Stage 3/4
LVEDV starts to go down bc it is being pushed out of ventricle into aorta – ventricle and aorta pressure the same bc they are like one chamber
Between 3 and 4 get repolarization of the ventricle, pressure starts to come down, ventricle starts to relax
Stage 5 (IVRP)
End of systole point – output valve closes (S2) and ventricle continues to relax, so no change in volume happening here (isovolumetric relaxation period) pressure coming down in ventricle, and ventricle is relaxing – av valve doesn’t open until pressure is equal to pressure in atrium)
Stage 6/7
LVESV = AV valve opens then opening and filling of ventricle and volume starts to increase – volume fills until atrium contracts again and gives that final push of blood from atrium unto ventricle and the whole thing starts again
what is cardiac output? what does it depend on? know formula!
CO depends on HR and SV
Point 4 – when demand goes up (during ecercise), hr and stroke volume incr and therefore CO increases
what can cause a change in HR? what are normal, high and low HR values?
Sympa increases HR, para decr
When someone is on a beta blocker – beta receptor increases hr so if we block that it decreases hr
Won’t see same increase in HR with exercise in someone on a beta blocker as someone without
Hr increases with someone on bronchodialator
Someone with low hemaglobin increases hr bc not enough oxygen and response is to increase HR
Other factors contributing to incr HR:
Emotions (fear anxiety, sadness, anger) all increase HR and CO
Someone with a fever: they will have incr HR bc for every degree incr in temp (deg C), there is a 6-7 bmp increase in hr
Someone with a very low HR (say <40 bmp) becomes dangerous in terms of the CO – may not be able to make up for it with SV when hr drops below 40 and therefore may become hazardous
If with pt and HR not increasing with exercise or it decreases with exercise, then STOP – this is not a normal response – maybe they have an arrythmia or heart block
what 3 factors contribute to stroke volume?
SV = amount of blood pushed out when ventricle contracts
Preload = amount of blood that comes back to heart (more = more SV)
Contractility = contractility of heart
Afterload = resistance to the blood flow (increased vascular resistance = decr CO)
what factors affect preload?
2 – venous return is reduced when someone stands up or legs over bed – why bp can drop and go into syncope with pts with bed rest for long perods of time
3 – neg interthoracic pressure increases from prev slide, positive airway pressure from ventilators would therefore decrease VR
4 – if not much tone in vasculature (or pooling happening) = decr
5 – if you have hemmoraged = decr, someone in fluid overload = increased
6 – venus insufficiency, if valves in veins are not good = increased pooling in vasculatire
Diuretics can also reduce blood volume and more susceptible to hypertension bc they are dehydrated (low bv)
what is the difference btw intrinsic and extrinsic control?
Sympathetic increases venous return, this increased end diastolic volume, increasing contractility and increases SV, incr CO
Extrinsic control woks with contractility and increases SV
describe contractility intrinsic control (frank starling curve)
Cross bridging action of actin/myosin fibre
Mysoin fiber = there is an optimal length to it
Looking at end diastolic volume, as it increases, SV increases = the more blood comes back to the heart, the more it will be stretched and the higher the contractility and SV (instrinsic control to heart)
describe contractility extrinsic control
As venous return increases, amount of blood coming back to heart increases, therefore SV incr.
Increased sympathetic stimulation – for any given end diastolic volume – incr contractility, amount of ejected blood incr = incr SV via incr contractility of heart
describe the ejection fraction WRT contractility (what are normal vs abnormal values?)
Single best measure of contractility!
SV = diff btw when Heart completely relaxed and end of its contraction when emptied completely
Stroke volume – what percnt of blood that is in the heart when it is at rest? gets ejected
Normal = 55-65%
Lower ejection fraction = worse an individuals progosis
Less than 20% = considered candidates for heart transplant
30-40% = patients need to be monitored with exercise, heart may not be able to keep up with demand (ie you are increasing circulation, but not maintaining CO, so this is a form of heart failure, will end up with congesion, interstitial or pulm edem in the lungs = congestive heart failure)
55-65% at rest in healthy individual
Someone may not be in pulmonary edema when sitting, but when demand goes up (exercise) there is an accumulation that starts in the lungs and can go into congestive heart failure, so they have to pace themselves
describe afterload and factors that affect it
Stenosis of aorta = constriction of the aorta, ventrical has to push against this resistance and will have decr in CO
Point 2 – atheroclerosis can incr periph vasc resistance, = increased afterload and vascular resistance, inacreased viscosity = heart has to work harder to pump thicker blood
cardiovascular disease epidemiology
CVD = atherosclerosis or coronary artery disease
what is atherosclerosis and coronary artery disease?
Fat hardens and forms plaques – causes damage to the wall itself and blocks it further
Only CAD when it is a heart artery
Can have Cad from vasospasm (ie due to drugs like cocaine which cause sustained vasospasm) – however 95%…
describe the process of CAD
Initially what occurs is point 1 – can be hypertension that causes the trauma
There is a damage to the intima, filled with cells which harden and produce plaques – when thes harden, point #4
Anoxia leads to necrosis
what are controllable and uncontrollable risk factors to CAD?
Red = contribute most of all
how does age and gender affect CAD?
”silent” but will show up on ecg
how does family history affect CAD?
1st degree = father, brother etc
Athlerosclerosis incr risk of dying from CAD but also incr risk of stroke
how does smoking affect CAD and the cardiovascular system?
Smoking - Or if there is an environmental exposure to tobacco smoke! – incr risk
Risk reduces rapidly when you quit – 1 year after, risk drops to half, the longer the more beneficial the effect
Risk is 2-6 times higher in smokers than in non-smokers
Hemo carriage – carbon monoxide contributes to that (binds to hemoglobin and also is highly toxic and damages epithelial cells)
Constricts coronary arteries – nicotene is a potent vasoconstrictor = also contributes to increaased BP
Blood clot = Elevated fibrinogen levels
what is normal BP vs hypertension? what 2 things does incr. BP increase?
Hypertension Can contribute to shearing forces in the vessels
Sadness bp goes down, other bad states goes up
Risk of hypertension is when you have the hypertension, not prehypertension
Someone may have normal bp but they are on meds so it is brought down to normal range – being on these meds in itself is an increase drisk factor
*increased BP = increased 1) incidence of CAD proportionate to level of SBP 2) incidence of heart failure proportionate to level of hypertension and age!
describe hypertension WRT CO and systemic vascular resistance
2 things control hypertension
Renal disease – fluid retention, incr bp
Atherosclerosis* prof pointed out
define: dislipidemia
abnormally high levels of cholesterol and possibly triglycerides in the blood
what is cholesterol and what is it necessary for?
2 – its is necessary to have it, just bad If you have an imbalance
what are normal cholesterol levels for adults?
Note if people have had a heart attack or history of diabetes, levels recommended are more stringent then people who don’t have this
what are possible causes of high triglycerides/cholesterol levels in the blood?
Alcohol causes incr in triglicerides
describe obesity WRT CAD (know the normal BMI ranges)
Increased risk for low body weight too!!
Pear shaped or apple shaped (greater risk for apple shape)
describe prediabetes WRT CAD (know glucose ranges)
Don’t need to memorize!!
Type 2 = adult onset, type 1 = juvenile onset
Type 2 = 2-fold increased risk of CAD
Diabetes = incr risk of morbidity and mortalty bc they tend to have more blocked vessels, don’t have same feeling of heart attack due to lack of sensation, tend to have more small vessle disease (peripheral vascular disease)
Poor controlled diabetes = level of blood sugar control is important
Sometimes confuse symptoms with hypoglycemia
describe stress WRT CAD
Direct influence: they all are intertwined, one controls another etc
Hereditaty: there is a debate about family history – maybe it is a lifestyle link more than genetic link
describe physical inactivity and CAD
Anyone not doing that level is deemed inactive = incr risk
Ie if it has been 3 months since pa, not good, but 1 month = ok
what are the benefits of regular physical activity?
-Can delay the progression
what is an aneurism? location/ S&S?
Congenital = it just happens
Aorta bc that is the vessel with the highest pressure in it – also it is quite long, so can have abd aortic aneurisms
S and s depends on the size of it
An aneurism ruptures can bleed out and be fatal
Thrombi can brak off and produce emboli elsewhere, blocking off smaller vessels causing ischemia
what are the 3 types of aneurism?
Saccular/giant = typically seen in brain – try to clip off in a surgery?
Fusiform in rest of body
whats the treatment of an abdominal aortic aneurism?
Dialationthat is 50% greater than normal = aneuism
More than 3 cm in abdominal = abmornal
Either can remove it or out in the mesh thing
what is a dissecting aneurism? causes? types?
Starts as a tear, then it starts creating a pouch – can descend down far – there is a false and a true lumen
Causes: Hypertension, trauma, Marfan’s syndrome
- Marfans = long limbs and joints/bones, they tend to have weak vessels = more susceptible to aneurisms
- Can result in devastating consequence in organ perfusion
- Lethal if not recognized.
Types:
- Most common are proximal dissections occurring in the ascending or aortic arch - require surgery.
- Distal dissection to the (L) subclavian artery requires medical therapy consisting of aggressive BP reduction.
what is peripheral artery disease? risk factors?
- Systemic complication of atherosclerosis
- Reduced blood flow to the extremities (i.e.. thoracic aorta, femoral artery, and popliteal artery)
- Males affected more than females
- Diabetes mellitus, smoking and sedentary life style are risk factors
Athlerosclerosis in the peripheral arteries = PAD
All the factors for CAD are also risk factors for PAD
mortality risk associated with PAD?
Intermittent claudication (reduction in circulation to tissues)
Critical limb ischemia = large occulion = complete blockage to limb
overlap in different vascular diseases
PAD severity is a significant predictor of increased cardiovascular mortality
CAD and cerebral arterial disease assumed even if patients are asymptomatic
⇒ aggressive risk factor management
⇒ heavy lifting & straining are avoided: incr intrathoracic pressure, ↓ VR, ↓ CO ⇒ incr cardiac strain
notes:
People who have PAD we assume that even if they are asymptomatic for CAD or cerebral arterial disease are at increased risk for both of these
Someone with PAD, we assume immediately that they may have CAD or cerebral arterial disease
If decr CO output – it goes to limbs/muscles as well as coronary artieries! – decr blood to heart and periphery
Avoid strain to decrease risk of decr CO etc
Up to 60-80% of those with PAS have sign athlerosclerosis in at least 1 coronary artery = why this management exists
pathogenesis of PAD?
Pathogenesis of peripheral arterial disease (PAD). Figure outlines the predisposing factors and molecular pathways that convert a health artery (left) into an artery with PAD (right).
- Same as before
prevalence of pad?
Incr prevalence with age, a bit more with men than women
how do you classify PAD/stenosis?
Mild arterial stenosis: asymptomatic
More severe arterial stenosis:
- coldness of the affected leg
- possible numbness
- limb pain on exercise that is relieved by rest
⇒ ⇒ referred to as Intermittent Claudication
- ↓ exercise tolerance
- ↓ function
Very severe stenosis:
- pain at rest
- ischemia related color changes
- skin breakdown
- ulceration
- gangrene ⇒ amputation
Subjective gradation:
1 = Initial discomfort (established, but minimal)
2=Moderate discomfort but attention can be diverted
3=Intense pain (attention cannot be diverted)
4=Excruciating and unbearable pain
notes:
Symptoms depend on severity, may be asymptomatic
Limb pain on exercise bc – lactic acid is formed, muscles are working anaerobically – lactic acid causes the pain! – for example pain on walking and if they stop and rest, it goes away – this is known as intermittent claudication
Colour changes – mauve looking coloured limb
L=skin breakdown = loss of hair/looks shiny
Gangrene – complete blockage
Those with chronic PAD = amputations usually
- Severe claudication = hair loss shininess etc
- Ischemic rest pain = at rest not by effort
how to measure ankle brachial index
How to measure ankle brachial index = measure of arterial occulive ressure – of diffuse athlerosclerosis
Related to cardiovascular risk and overall survival
Measures reduced bp distal to the occlusion, the lower the abi, the greater the decrease circulation occuring to the lower limbs, bc when you have an occlusion = lower measured BP
Measure bp at ankles, (L and R) and at the arms (R and L)
Highest arm/ankle pressure – use whichever is higher! Same with ankle
what is the treatment for PAD?
Exercise programs improve the intermittent claudication
Recommended that people walk until they feel pain, then stop then walk again with decreased pain – in order to increase the endurance
Weight control so it doesn’t add pressure to the vasculature
Skin assessment important bc if perosn with PAD cuts themselves, they have difficulty with wound healing which can start ulcers – foot care, proper shoe fitting, socks, etc is important
what are exercise recomendations for PAD?
Pt 1 – or walking over the ground
Repeat until symptoms are resolved
what are characteristcics of PVD?
- Phlebitis (inflammation of the walls of a vein)
- Venous stasis (a condition of slow blood flow in the veins, usually of the legs)
- Thromboembolus (obstruction of a blood vessel by a blood clot that has become dislodged from another site in the circulation)
- Leg vein valvular incompetence
- Skin lesions
- Poorly healing LE ulcers
A venous insufficiency, not sever – spider veings
B – vericose veins
C – discoloration, blood pools and heme goes into tissues that cause the rust red colour
D – venus ulcure due to venus insufficiency
risk factors for chronic venus insufficiency?
Heredity
Female gender
Obesity
Age
Prolonged standing
*Add smoking and sedentary lifestyle
symptoms of chronic venus insufficiency?
Could be swelling in Le too – at the end of the day from prolonged periods of standing
pathophysiology of chronic venus insufficiency?
CVI can lead to the skin changes shown in prev slide
therapy for chronic venus insufficiency?
Treatment directed towards the cause 0 trying to reduce venus hypertension
Mobilization bc muscle aciton helps reduce swelling and venous pooling
Anticoag = if increased risk of DVT
Venus stripping = removes some of the veins
Cosmetic vein injection reduce appearance of veins cosmetically
