LO Cardiovascular

Question 1

Trace the blood flow as it moves through the heart

Answer 1

Blood from body comes in through IVC or SVC into right atrium where it goes through tricuspid valve into right ventricle and out through semilunar valve into pulmonary arteries that go to the lungs, coming back from the lungs is the pulmonary veins into the left atrium through the mitrovalve into the left ventricle where it goes out through the semilunar valve into the aorta

Question 2

Differentiate between Atri-ventricular and semilunar valves

Answer 2

between ventricles and ones that close shut to prevent anything from coming back.

Question 3

Describe the role of papillary muscles and chordae tendinae

Answer 3

They are tendonous and prevent flipping of the valves

Question 4

match heart chamber or valve pressures with valve position

Answer 4

pressure has to be greater in the previous cavity to open it.

Question 5

Identify diastole and systole and relate L ventriuclar pressure, L ventricle volume, L atrial pressure, valve position to the four phases of the cardiac cycle (ventricular filling, isovolumetric contraction, ventricular ejection and isovolumetric relaxation

Answer 5

diastole: filling and relaxation
Systole: contraction and ejection

Explain the Wigger’s diagram

SYSTOLE
isometric contraction: all valves closed, ventricular pressure rising
ventricular ejection: semilunar valves open, ventricular volume decrease

DIASTOLE
isometric relaxation: all valves closed, ventricular pressure decreasing
ventricular filling: AV valvesopen, SL valves closed, ventricular volume increasing

Question 6

define 2 heart sounds and splitting of s2

Answer 6

1: closure of AV valves early in systole
2: closure of semilunar valvues (during expiration as one sound, inspiration as two sounds)

splitting of 2: more blood to right heart, prolongs RV ejection, delays PV closure
less blood to the left heart, shortens LV ejections, AV closes earlier.

Question 7

Identify 3 causes of heart murmurs

Answer 7

1. Normal flow narrowed valve (aortic stenosis)
2. Valve that doesn’t close right (mitral regurgitation)
3. FLow through a hole from high-> low pressure ventrical septal defect

Question 8

Ventricular septal defect

Answer 8

hole in the heart’s ventricles, causes a shift of blood from the left into the right. the left now has more blood to pump so it gets bigger, the right one does not because the new blood flows right into the valve.

high heart rate to compensate for low output
persistent state of exercise.

need to repair the defect percutaneously or invasively. the condition gets worse with age.

Question 9

nodal and ventricular muscle cell action potentials (stability of RMP, principle ions, major roles in determining heart function)

Answer 9

Pacemaker AP: fires on its own

• sinoatrial node (SA node)
• where SVC enters RA
• RMP -60 and NA comes in (slow depolarization)
• fires at threshold potential -40
• upstroke is due to calcium (not Sodium)
• fires SPONTANEOUSLY

Contractile AP: lots of force, needs stimulus from the pacemaker

• typical myocyte is 100 mc long
• ventricular or atrial (mostly ventricular)
• stable RMP at -90 mV
• threshold at -70 (from pacemaker region)
• sharp fast rising phase dependent on sodium
• plateau phase dependent on calcium and potassium
• falling phase K out.
• absolute refractory period 250ms twitch = AP so -open-inactivated-closed (means that it cannot summate or tetanus)

propegates through the heart via gap junctions

Question 10

autonomic nervous system how does it generate faster/slower HR

Answer 10

SYMPATHETIC
- Noradrenaline acts on B1 receptors on SA node to INCREASE slope of PP

PARASYMPATHETIC
- Acetelcholine acts on muscarinic 2 receptors on SA node to DECREASE slope of PP

Question 11

describe pathway of action potential

Answer 11

Starts at SA node, goes through atrium to AV node, and other side to other atrium so that they can contract together, then goes to bundle of his, then exits atria to the ventricles where it goes to left/right bundle branch to the tip of the ventricle and spreads through conduction fibres and goes to purkinjie fibres

Question 12

explain why the SA node is the rhythm generator of the heart

Answer 12

Because the SA node can beat on its own and the AV node is slower (it can beat on its own) but the SA node usually overrides it cause its slower (40bmp compared to 70bmp)

Question 13

why is there an abolute refractory period in venricular AP

Answer 13

so that it cannot summate or tetnus

Question 14

using triangle of leads, predict whether ecg deflection would be up or down

Answer 14

when depolarization moves to the positive end of a lead, the pen deflects upwards. depolarization moves from upper left (when looking at a body) to lower right.

P and QRS measure depolarization.

Question 15

relate the ECG waveforms P QRS T with heart function

Answer 15

P: atrial depolarization QRS: ventricular depolarization (inital down, more complex)
T: ventricular repolarization: last cells to depolarize are the first to repolarize. is it the opposite direction compared to depolarization?

Question 16

define normal sinus rhythm

Answer 16

roughtly 75 bpm, 1:1 p and qrs ratio, 60/0.2*# of squares, regular rhythm

Question 17

someone who has paroxysmal atrial fibrillation

Answer 17

depolarization and repolarization are disorganized, AV node gets random APs from SA node. keep the pateint overnight
the danger is that it decreases cardiac output, blood flow can become stagnant and produce embolisms

Question 18

describe the three layers of arteries

Answer 18

lumen
endothelium (intima)
smooth muscle and elastic tissue (media)
connective tissue fat (adventitia)

Question 19

describe and give examples of factors that effet arteriolar diameter (neural, humoral, tissue metabolites)

Answer 19

Neural control: SNS (not pns)

• Noradrenaline in smooth muscles of arterioles causes vasoconstriction on alpha receptors (Gq protein) that goes to PLC which releases 1p3, 1p3 receptors, release clacium which binds calmodulin to MLCK and contraction!
• Adrenaline: on beta receptors and inhibits MLCK causing vasodilation via cAMP

Vasoactive hormones 
- Constrictors 
- Angiotensin 2 -from kidney 
-Arginine Vasopressing (AVP) -brain
DIlators
- Atrial natriuretic peptide (ANP)-from heart

Tissue Metabolites

• released by active cells
• LOCAL
• when decrease o2=increase co2, increase adenosine, increase K+. these all cause vasodilation on their own.

Question 20

describe the actions of noradrenaline and adrenaline on vascular smooth tissue

Answer 20

• Noradrenaline in smooth muscles of arterioles causes vasoconstriction on alpha receptors (Gq protein) that goes to PLC which releases 1p3, 1p3 receptors, release clacium which binds calmodulin to MLCK and contraction!
• Adrenaline: on beta receptors and inhibits MLCK causing vasodilation via cAMP

Question 21

what distinguishes regulation of coronary and cerebral blood flow from ther regulation of peripheral aerial blood flow

Answer 21

Cerebral and coronary blood flow are autoregulated to ensure constant blood supply over ranging pressures. sometimes the heart reduces/increases blood pressuers and the vessels change due to that.

Question 22

what causes angina?

Answer 22

from a coronary artery spasm, or narrowing (plaque formation or complete occlusion)
- the drop in 02 causes afferent endings to go to the brain which send painful stimuli perception and you have the heart attack

Question 23

What happens when you have a plaque

Answer 23

BLood supply does not equal heart demand
it grows in the intima and can project to the lumen. heart has to work harder to get it out, supply is less than the demand!!
- she will have a stress test
angioplasty (PCI) (open with stent)
CABG (replace artery )

Question 24

what is systemic vascular resistance?

Answer 24

the blood volume in arterioles and how relaxed/contracted they are

Question 25

Relate CO, HR, and SV in an equation?

Answer 25

CO = heart rate x stroke volume

cardiac output is influenced by extrinsic and intrinsic factors.

Question 26

Different effects of SNS and PSNS on heart rate

Answer 26

SNS: noradrenaline/adrenaline act on beta 1 receptors on nodal cells to increase the slope of p4 and increase heart rate

PSNS: acetylcholine acts on muscarinic receptors on nodal cells and decreases slope of p4 and decreases HR

Question 27

Intrinsic vs Extrinsic control of stroke volume?

Answer 27

extrinsic: SNS releasing NA on b1 receptors increase calcium and increase stroke volume. (CICR). Adrenaline does the same things 9 (IN VENTRICULAR MUSCLE CELLS) in vascular its a and b
intrinsic: frank skarling preload thing

Question 28

When presented with a Sarling Curve, identify x and y axes and illustrate law of heart and mention preload.

Answer 28

strength of contraction is related to length of heart muscle. End diastolic volume on x, stroke volume on y. the heart pumps what it recieves. End diastolic volume: preload (volume coming into the heart)

Question 29

relate flow pressure and resistance in an equation

Answer 29

blood pressure = CO x resistance (SVR)
SVR is determined by the radius of the blood vessels. if radius if halved, then resistance increases by factor of 16. flow decreases by 16.

Question 30

define afterload

Answer 30

pressure the ventricle needs to generate in orderto eject the cardiac output. high arterial pressure is high afterload.

Question 31

related capillary hydrostatic pressure, capoillary oncotic pressure and intersitital hydrostatic pressure and interstital oncotic pressure to the net movement f fluid across the length of a normal capillary.

Answer 31

FILTRATION
- move fluid out of capillaries, caused by an increase in Capillary hydrostatic pressure (CHP)

REABSORPTION
- draw fluid into capillaries, caused by an increase in Capilllary Oncotic Pressure (COP)

At the artieral end, CHP > COP (filtration)
At genous end, COP > CHP (reabsorption)
usually equal.
when you have both filtrating, then you get edema.

Question 32

Cardiomyopathy explain it and the consequences

Answer 32

Heart failure. CO is not enough to maintain perfusion to her tissues. her pressure are HIGH. can’t pump the blood enough at the left end of the heart so it builds up causes filtration and edema into the lungs (pulmonary edema) venous pressure is too high. you’d need a heart transplant.

Question 33

what do ANP and AVP do to vascular smooth muscle?

Answer 33

ANP vasodilates by inhibiting MLCK through cyclic GMP

AVP and others lead to vasoconstriction through different receptors with Gq protein

Question 34

How can you measure BP with a cuff?

Answer 34

measure the height of a mercury column relative to atmospheric pressure mm/hG

Question 35

how does your brain know your blood pressure?

Answer 35

• baroreceptors (stretch sensitive) sense it and through afferent nerves send to the medulla and through efferent nerves send to BP controllers (Sympathetic and Parasympathetic Activity)

Question 36

carotid sinus and aortic baroreceptors in terms of anatomical location and afferent nervous connections

Answer 36

carotid in the common carotid artery (base of the neck)
- afferent nerve is the glossopharyngeal nerve

aortic arch in arch of aorta: afferent nerve is the vagus nerve.

Question 37

what is the sequence of events that restores BP which coincides with rise or fall in arterial pressure? What about hormones?

Answer 37

If BP rises: increase stretch of baroreceptors, increase firing to brain, increase inhibition of SNS and incrase PSNS. this goes to the heart to lower heart rate therefor lowering SV and lowering SVR and lowering BP.
Opposite for fall in BP.

PSNS only works on heart not on the vessels.

HORMONES?
- this happens through SNS on the kidney and AVP on the SVR and the kidney. THe kidney absorps na, water, renin A2 and aldosterone.
IF BP goes up, it decreases blood volume which leads to decreased cardiac output. decreased SVR leads to decreased BP. normalization of BP.

Question 38

What is training induced/athletic bradycardia?

Answer 38

AT rest low heart rate:
increased vagal tone
reduced sa node pacemaker activity
Increased stroke volume with no change in co so low heart rate (in athletes)
beta receptors are desensitivved so noadrenalinea and adrenaline MAYBE. CONTROVERSIAL.
max HR for females in 226-age, for males its 220-age.

Adaptations to exercise 
increase left ventricle size
incrase stroke volume 
decreased HR 
increase Blood volume 
BP doesn't change 
CO better distributed: can put out more blood to tissues.