Lecture 1 - Anatomy/Atherosclerosis

Question 1

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?)

Answer 1

• 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

Question 2

name the valves of the heart

Answer 2

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)

Question 3

what are the 3 layers of the heart?

Answer 3

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

Question 4

describe the layers of the heart WRT the pericardial layers

Answer 4

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)

Question 5

name the large blood vessels of the heart

Answer 5

Question 6

what are the layers of the blood vessels and how do arteries/veins differ?

Answer 6

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

Question 7

describe the blood supply to the heart (also which artery is larger?)

Answer 7

• 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)

Question 8

describe the 2 types of myocytes

Answer 8

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

Question 9

describe the conduction system of the heart

Answer 9

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

Question 10

describe the neural control of the heart

Answer 10

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)

Question 11

what is the overall role of artieries/veins/capillaries/heart?

Answer 11

Veins = capacitors, lactic acid production on the venus side

75% of TBV sitting in our veins at any given time

Question 12

what are circulatory movements driven by?

Answer 12

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

Question 13

what valves open/shut during systole/diastole?

Answer 13

Question 14

describe the cardiac cycle (what is the isovolumetric contraction and relaxation period?)

Answer 14

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

Question 15

what is cardiac output? what does it depend on? know formula!

Answer 15

CO depends on HR and SV

Point 4 – when demand goes up (during ecercise), hr and stroke volume incr and therefore CO increases

Question 16

what can cause a change in HR? what are normal, high and low HR values?

Answer 16

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

Question 17

what 3 factors contribute to stroke volume?

Answer 17

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)

Question 18

what factors affect preload?

Answer 18

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)

Question 19

what is the difference btw intrinsic and extrinsic control?

Answer 19

Sympathetic increases venous return, this increased end diastolic volume, increasing contractility and increases SV, incr CO

Extrinsic control woks with contractility and increases SV

Question 20

describe contractility intrinsic control (frank starling curve)

Answer 20

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)

Question 21

describe contractility extrinsic control

Answer 21

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

Question 22

describe the ejection fraction WRT contractility (what are normal vs abnormal values?)

Answer 22

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

Question 23

describe afterload and factors that affect it

Answer 23

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

Question 24

cardiovascular disease epidemiology

Answer 24

CVD = atherosclerosis or coronary artery disease

Question 25

what is atherosclerosis and coronary artery disease?

Answer 25

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%...

Question 26

describe the process of CAD

Answer 26

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

Question 27

what are controllable and uncontrollable risk factors to CAD?

Answer 27

Red = contribute most of all

Question 28

how does age and gender affect CAD?

Answer 28

”silent” but will show up on ecg

Question 29

how does family history affect CAD?

Answer 29

1st degree = father, brother etc Athlerosclerosis incr risk of dying from CAD but also incr risk of stroke

Question 30

how does smoking affect CAD and the cardiovascular system?

Answer 30

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

Question 31

what is normal BP vs hypertension? what 2 things does incr. BP increase?

Answer 31

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!**

Question 32

describe hypertension WRT CO and systemic vascular resistance

Answer 32

2 things control hypertension Renal disease – fluid retention, incr bp Atherosclerosis\* prof pointed out

Question 33

define: dislipidemia

Answer 33

abnormally high levels of cholesterol and possibly triglycerides in the blood

Question 34

what is cholesterol and what is it necessary for?

Answer 34

2 – its is necessary to have it, just bad If you have an imbalance

Question 35

what are normal cholesterol levels for adults?

Answer 35

Note if people have had a heart attack or history of diabetes, levels recommended are more stringent then people who don’t have this

Question 36

what are possible causes of high triglycerides/cholesterol levels in the blood?

Answer 36

Alcohol causes incr in triglicerides

Question 37

describe obesity WRT CAD (know the normal BMI ranges)

Answer 37

Increased risk for low body weight too!! Pear shaped or apple shaped (greater risk for apple shape)

Question 38

describe prediabetes WRT CAD (know glucose ranges)

Answer 38

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

Question 39

describe stress WRT CAD

Answer 39

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

Question 40

describe physical inactivity and CAD

Answer 40

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

Question 41

what are the benefits of regular physical activity?

Answer 41

-Can delay the progression

Question 42

what is an aneurism? location/ S&S?

Answer 42

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

Question 43

what are the 3 types of aneurism?

Answer 43

Saccular/giant = typically seen in brain – try to clip off in a surgery? Fusiform in rest of body

Question 44

whats the treatment of an abdominal aortic aneurism?

Answer 44

Dialationthat is 50% greater than normal = aneuism More than 3 cm in abdominal = abmornal Either can remove it or out in the mesh thing

Question 45

what is a dissecting aneurism? causes? types?

Answer 45

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.

Question 46

what is peripheral artery disease? risk factors?

Answer 46

* 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

Question 47

mortality risk associated with PAD?

Answer 47

Intermittent claudication (reduction in circulation to tissues) Critical limb ischemia = large occulion = complete blockage to limb

Question 48

overlap in different vascular diseases

Answer 48

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

Question 49

pathogenesis of PAD?

Answer 49

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

Question 50

prevalence of pad?

Answer 50

Incr prevalence with age, a bit more with men than women

Question 51

how do you classify PAD/stenosis?

Answer 51

_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

Question 52

how to measure ankle brachial index

Answer 52

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

Question 53

what is the treatment for PAD?

Answer 53

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

Question 54

what are exercise recomendations for PAD?

Answer 54

Pt 1 – or walking over the ground Repeat until symptoms are resolved

Question 55

what are characteristcics of PVD?

Answer 55

- 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

Question 56

risk factors for chronic venus insufficiency?

Answer 56

Heredity Female gender Obesity Age Prolonged standing \*Add smoking and sedentary lifestyle

Question 57

symptoms of chronic venus insufficiency?

Answer 57

Could be swelling in Le too – at the end of the day from prolonged periods of standing

Question 58

pathophysiology of chronic venus insufficiency?

Answer 58

CVI can lead to the skin changes shown in prev slide

Question 59

therapy for chronic venus insufficiency?

Answer 59

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