The Heart and Circulation ( 25% ) Flashcards

Question

Which of the following is false regarding physiological ECG intervals * The duration of the P wave is normally \< 0.1s * The duration of the QRS complex is normally \< 0.1s * The duration of the PQ interval ranges between 0.12-0.2 s and is dependent on the frequency * The QT interval starts with the end of the Q and ends with the beginning of the T wave and has an average duration of 0.4s * The average duration of the ST interval is 0.32s

Answer 1

**The QT interval starts with the end of the Q and ends with the beginning of the T wave and has an average duration of 0.4** QT is start of the Q to end of the T, average duration 0.4, up to 0.43

Answer 2

**In LBBB the mean QRS vector is \> +110.** LBBB causes LAD, so vector is \<-30

Answer 3

**LAD, highest QRS lead I, negative QRS lead II** * LAD - +ve I, -ve II, III * Any negative II = LAD * RAD - +ve III, aVF, -ve I, +/- II * Positive aVF, negative I

Answer 4

**V1-2** **as per Nick** But V1-4 seem to be known as the anteroseptal leads

Answer 5

* **The U wave is believed to be due to papillary muscle repolarisation** * The PR interval is the time taken for *atrioventricular conduction* * Lead _II_ is the vector between the right arm and left leg * III is left arm to left leg * LBBB is defined by cardiac axis _\< -30_ degrees * Lead V5 is placed in the *5th* ICS * V1-3 4th ICS, 4-6 5th ICS

Answer 6

**There is no Q wave in V1** * The average QT is *400ms (up to 430ms)* * The normal axis is between _-30_ and 110 degrees * T wave coincides with *late systole - contraction lasts longer than the AP* * P wave *immediately precedes the venous a wave (which correspons to the atrial systole) - electrical activity slightly precedes the corresponding mechanical activity*

Answer 7

**Inability of damaged myocardium to depolarize if ST segments are elevated** * Delayed depolarisation can cause ST elevation (systolic current of injury), as this causes a moment of the exterior of infarcted cells to be relatively more positive than healthy cells (but depends on their classification of 'inability' vs 'delayed'. An _inability to polarise_ can also cause TQ depression, which manifests as an ST elevation on ECG.* * Thus, STE can be due to _delayed_ depolarisation, or an _inability to polarise_ (ie RMP close to 0). They cannot get stuck in a polarised state.* or **Current flow if other than on zero potential line** *This is a basic tenet of ECGs I'm fairly sure.* * No current flow, all myocardial membranes positive outside, negative inside * *ST represents the plateau phase of the AP - maintained by Ca2+ influx to balance the K+ efflux which is aiming to repolarise the cell, so there is current flow, it is just balanced.* * Normal current flow of repolarisation * *See above - ST is plateau phase, T-wave represents current flow of depolarisation* * If elevated, current flow during diastole * *ST segment occurs during systole (diastole is the T-P segment), so it has nothing to do with diastolic current flow*

Answer 8

Na influx QRS = ventricular depol = Na influx T-wave = ventricular repol = K+ efflux

Answer 9

* an atrial rate *much faster* than the ventricular rate *(2:1 or 3:1)* * **flutter waves with a saw tooth appearance** * an atrial rate between *200 to 350 (usually 300)* * *Almost always occurs with AV block* * carotid sinus massage *can sometimes* convert atrial flutter into the normal SR. * ACh release at vagal nerve endings depresses conduction of atrial myocytes

Answer 10

Can by caused by ***_Hyper_**thyroidism*

Answer 11

**3rd degree block**

Answer 12

3rd degree block is caused by a complete block of electrical impulses in one bundle branch and an intermittent block in the other bundle branch *Is a constant complete block of all bundles*

Answer 13

The ventricular rate is lower than the atrial rate

Answer 14

QT interval is prolonged in low K \> 2.5

Answer 15

ST elevation of \>0.5mm in chest leads is considered significant for MI Criteria varies but usually about 2-3mm in V2-3 depending on age and gender

Answer 16

***Low* K enhances digitalis toxicity** Digoxin binds to the **extracellular K+ site** of Na-K-ATPase, so hypokalaemia reduces potassiums antagonistic effects on digoxin. Likewise hyperkalaemia can reduce the risk of toxicosis. Note digoxin toxictiy can *cause hyperkalaemia* (due to reduced intake into cells due to Na-K-ATPase inhibition). Magnesium suppresses digoxin-induced ventricular arrhythmias

Answer 17

* **Phase I represents atrial systole** * The aortic valve opens at the *end* of phase II. * Phase 2 = isovolumetric ventricular contraction * The T waves of the ECG occur during *phase III (ejection)* * The 2nd heart sound is due to *Aortic valve closure* * The C wave is due to *Tricuspid bulging into the RA during isovolumetric contraction*

Answer 18

**Transmitted pressure due to tricuspid bulging in isovolumetric contraction** a = atrial sysole V = rise in atrial pressure before triscupid opens in diastole

Answer 19

**When the glottis is opened and intrathoracic pressure returns to normal** Initial rise in BP due to brief increase in venous return, but then raised intrathoracic pressure causes the venous return to fall -\> reduced BP -\> tachycardia + baroreceptor mediated vasocontriction. Once glottis is opened, the venous return and CO return to normal, but the vasoconstriction is still in place -\> hypertension. This is sensed by baroreceptors -\> bradycardia.

Answer 20

**Isovolumetric contraction starts with the opening of the aortic and pulmonary valves** starts with closing of mitral and tricuspid valves

Answer 21

**The diastolic pressure in the vascular system refers to the peak pressure reached during diastole** Refers to low point (or maybe stable pressure)

Answer 22

**The v wave is caused by the rise in atrial pressure due to the closing of the tricuspid valve** V wave = release of the slow rise in atrial pressure during diastole due to *opening* of the triscuspid valve

Answer 23

**Ventricular filling** 1st = closure of AV valves 2nd = closure of aortic/pulmonary valves 3rd = rapid ventricular filling causing vibrations 4th = ventricular filling when atrial pressure is high or ventricle is stiff (not usually normal)

Answer 24

* Systole is the period of ventricular contraction (ie between the 1st and 2nd heart sounds). * 2nd heart sound is just after the beginning of diastole, as momentum keeps blood flowing for a split second after contraction finishes so the valve is still open. * The SV is increased by increasing the EDV, not the EF * can be increased by either (increased inotropy -\> increased contraction -\> increased EF) * **Ventricular contraction commences at the R wave and is not completed until the end of the T wave** * Diastole is the period between opening and closure of the AV valves * Systole begins a fraction before closure of the AV valces * JVP waves occur at – a atrial systole, c ventricular systole, v just prior to opening the AV valves. * Notes that v 'mirrors the rise in atrial pressure just before the tricuspid valve opens during diastole' * Incorrect part could also be they want c to be isovolumetric contraction of ventricles, rather than systole in general

Answer 25

* Right ventricular contraction occurs *after* the left * Phase II commences with the *closing* of the AV valves * II = isovolumetric contraction * **Phase IV is isovolumetric relaxation** * During inspiration the pulmonary valves close *after* the aortic * increased pulmonary resistance in inspiration causes a slight delay in pulmonary valve closure, the same reason splitting can occur in PE * The duration of systole is more *consistent* than diastole

Answer 26

* **The 3rd heart sound is heard 1/3 way through diastole in many normal young individuals** * A 4th heart sound can be heard in some individuals with *high* atrial pressure, *or stiff ventricles (eg LVH)* * The 1st heart sound is *soft* when the heart rate is slow * Because ventricles are well-filled and the AV valve leaflets float together before systole * The interval between the aortic and pulmonary valves is *increased* during inspiration * Because of increased resistance in pulmonary circuit (same as PE) * The 2nd heart sound is normally *higher* pitched and *shorter* than the first

Answer 27

**None of the above** * the start of systole *is just after* the P wave * the PR interval represents atrial *contraction* * *Atrial repolarisation (ie the atrial t-wave) is buried in QRS complex* * the ST segment represents absolute refractory period of the ventricles. ARP is from the start of the QRS to the apex of the T-wave * the T wave is *well before* the third heart sound * T-wave is just before diastole begins, third heart sound is 1/3rd through diastole * T-wave ends just before 2nd heart sound

Answer 28

* Sleep - No change * Eating - Increases * Pregnancy in the 1st trimester - Increases * **Sitting from a lying position -** Due to reduced venous return

Answer 29

**glucagon.** *Activates adenylyl cyclase -\> increased cAMP -\> therefore increases magnitude of calcium release* Tachycardia increases inotropy due to reduced diastolic time creating less time to remove calcium from cytoplasm -\> higher cytosolic calcium -\> increased inotropy (*Force-Frequency Relationship)* Bradycardia would have the opposite effect of above Though CO could remain similar if EDV was raised through increased diastolic time

Answer 30

**All of the above** Acidosis, hypercapnia, hypoxia through reduced ATP -\> impaired SR Ca release + downregular of beta receptors Quinidine is a Class Ia anti-arrhythmic -\> blocks voltage-gated calcium channels (like verapamil)

Answer 31

**ESV is ~ *70mL*** SV in AF can be reduced up to 20% - Atrial contraction contributes up to 30% of ventricular filling, and this may be partially lost in AF

Answer 32

**RAP is *~ 5mmHg.*** Same as CVP (approx. 5mmHg)

Answer 33

Diastolic pressure in the left ventricle is *\< 10mmHg*

Answer 34

Pregnancy *increases* CO.

Answer 35

**32L/min** LV output = O2 consumption (ml/min) / [AO2] - [VO2] =1800mL/min / 56ml/L = 32L/min

Answer 36

**Explains the increase in the CO that occurs when venous return is increased** 'states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant' or 'the heart will pump all blood returned to it'

Answer 37

**SV/EDV**

Answer 38

Is shifted upwards and to the left during increased afterload. This is false, the rest are true

Answer 39

**Is decreased when standing** **As per Nick** **However AF will reduce ventricular filling by the atria and hence EDV** **EDV only reduces upon standing from sitting/lying, not if you are already standing.** Is decreased in *septic or hypovolaemic* shock. Is *increased* by an increased CVP or total blood volume

Answer 40

The afterload is greater

Answer 41

* May fall to as little as -10mmHg at rest, but rarely more * **May be 6*mmHg* of blood normally** * Will tend to *rise* with venoconstriction. * Increases with exercise * Cannot find anything on RAP in exercise - LAP will initially rise before falling to normal or subnormal values * *Decreases* with inspiration (as increased intrathoraic pressure reduces venous return)

Answer 42

Compliance is reduced by scarring resulting in reduced heterometric response to preload Heterometric = changes in CO regulated by changes in cardiac muscle fibre length Homometric = changes in CO due to increased contractility independent of length * Starlings law of the heart explains *heterometric* regulation of CO * Afterload promotes sarcomeres shortening while preload opposes it * ?? * β1 receptor stimulation results in further sarcomeres shortening and ultimately to increased CO * ?? * increased venous tone *increases* the myocardial sarcomeres length * Due to increased venous return

Answer 43

The % of ventricular volume ejected with each stroke

Answer 44

*_Homometric_* regulation is changing contractility of the heart muscle fibres independent of length. Heterometic = changing length, ie Frank-Starling law

Answer 45

Standing Reduced length of cardiac fibres seems to be another way of saying reduced EDV / preload

Answer 46

* SV is normally *70ml* * Contraction of the left atrium *follows* the right atrium * **The c wave of the JVP corresponds to movement of the closed tricuspid valve** * LVP immediately falls after opening of the aortic valve * Wrong, increases slightly then falls a bit, but only really falls once the aortic valve closes (needs to be at least 80mmHg to keep it open) * At rapid heart rates, systole shortens *much less* than diastole

Answer 47

* Is responsible for the venous *C* wave * **Causes rapid rise in intraventricular pressure** * Lasts *about 0.05sec* * Causes the *closing* of the AV valves * *Slightly increases* the atrial pressure by causing a bulging of the valves into them

Answer 48

is correlated with body surface area About 3.2L / min / m² BSA * is a product of the HR and *SV* * can be calculated by using *radioactive isotopes or themodilution* * is *unchanged* during sleep * is *increased* during eating

Answer 49

Standing up Blood pools in legs and reduces venous return -\> reduced EDV

Answer 50

* increased volume of work is the product of *MAP* and stroke volume * cardiac work is the product of *MAP* and SV * **the heart in its resting state gains 60% of its caloric requirements from FFAs** * the work of the left ventricle is _6-7x_ that of the right due to higher pressures in the systemic circulation * increased *afterload* has a greater effect on O2 consumption of the heart than increased *preload* * *For unclear reasons, pressure-work produces a greater increase in O2 consumption than volume-work*

Answer 51

Moderate increase in environmental temperature

Answer 52

CVP *falls* during negative pressure breathing NPB seems to be akin to an iron lung - ie negative extrathoraic pressure. This would presumably cause dilation of the IVC etc and reduce CVP. PEEP -\> increase in CVP

Answer 53

* the extent of *?stroke volume* is proportionate to end diastolic volume. * cardiac muscle fibres are lengthened by *?increased* ventricular compliance * **contractility of myocardium is increased on standing** * Drop in preload/EDV -\> drop in BP -\> decreased baroreceptor stimulation -\> decreased inhibition of RVLM -\> increased sympathetic response -\> increased HR and contractility * sympathetic stimulation shifts the length/tension curve *upward and to the left* * increased negative intrathoracic pressure increases *venous return to the heart/EDV/preload* * *This increases CO through the F-S mechanism but does not change the contractility of the myocardium per se.*

Answer 54

* a) hypernatraemia is associated with *high* voltage complexes * b) the first change in hyperkalaemia is *peaked T-waves* * c) with hypokalaemia, the resting membrane potential *increases (hyperpolarises)* * d) in *hypercalcaemia*, the heart stops in *systole* * *due to being unable to relax (calcium rigor)* * *Hyperkalaemia causes the heart to stop in diastole as the fibres become unresponsive to excitation* * **e) in hypercalcaemia, myocardial contractility is enhanced**

Answer 55

**c) atrial premature beats produce an ‘A’ wave** A = wave produced by atrial contraction (occurs in late diastole) C = bulging of triscupid during contraction (early systole, at end of isovolumetric contraction) V = slow rise in atrial pressure due to inflow of blood, release once AV valves open (peaks at end of isovolumetric relaxation / end of systole)

Answer 56

b) sleeping

Answer 57

**Venules and veins = 50%** Heart chambers = 12% Pulmonary circulation = 18% Aorta = 2% Arteries = 8% Arterioles = 1% Capillaries 5% Following transfusion \<1% is distributed into the arterial system

Answer 58

Poiselle-Hagen formula relates resistence to viscosity and tube diameter. The main point to take away is that small changes in vessel diameter have large effects on resistence/flow as it is inversely proportional to the radius^4 * Longer tubes *cannot* sustain high flow rates - *More resistance so more energy losses* * Flow is *inversely* proportional to resistance * **Flow will be doubled by a 20% increase in vessel diameter** * Turbulent flow is predicted in high velocity vessels -\> this is Reynolds formula

Answer 59

Oncotic pressure gradient This only explains interstitial fluid movements/gradients

Answer 60

* Proportional to the radius *(r^4)*. * *Directly* proportional to the pressure difference between the arterial and venous end. * **Inversely proportional to the length**. * Proportional to the *radius^4* * *Inversely proportional* to the viscosity.

Answer 61

* Pulse pressure is the difference between *Systolic and diastolic BP* * In the _lying_ position the arterial pressure in the foot is *lower* than the arterial pressure in the head. * Will be lower as further from heart and no effect of gravity * **Dicrotic notch is causes by the closure of the *aortic* valve** * **Low-point in BP curve between systole and the elastic effects of the aorta** * Dicrotic notch is not present in the pulmonary circulation. * Pulmonary arterial pressure is approximately 25/10 mmHg

Answer 62

**Alveoli collapse in the absence of surfactant because their diameter decreases in expiration and the wall tension increases.** * P=T/r, or T=P x r* * Where T tends to be constant, so if r decreases, you will need more pressure to balance the tension to prevent collapse (and that doesnt happen - the smaller alveoli tend to collapse into the larger ones once the tension overcomes whatever pressure is inside them, as pressure and tension should be roughly equal for all alveoli)* * Resistance is inversely proportional to *Radius⁴* * The wall tension necessary to balance transmural pressure is *directly* proportional to the radius (P = T/r) * Velocity is equal to flow for any given diameter. * Velocity is speed (distance/time), flow = volume/time * Flow is related *directly to the radius to the power of 4; resistence reciprocally.*

Answer 63

**Blood flow and resistance in vivo are markedly affected by small changes in the caliber of vessels** * In the blood vessels is normally *Laminar* * Turbulent flow is *Loud* * The small arteries and arterioles are referred to as *Resistance vessels* * *Venous system is known as capacitance vessels* * The average velocity of blood is highest in the *Aorta* * *Flow is greatest in the capillaries*

Answer 64

**The failure of alveoli to collapse in expiration.** * In a sphere, P = 2T/r (where P = distending (intraluminal pressure) and T = tension)* * If T does not reduce when r reduces, tension overcomes the distending pressure causing collapse.* * The only reason they do not is alveolar surfacant.* * The equation is viewed from a differing point with regards to capillary rupture - T = Pr, so for a smaller radius, there is less tension in the walls for a given pressure, reducing risk of rupture* * Increased myocardial work in dilated cardiomyopathy * as increased wall tension is needed to generate a given pressure if the radius is increase * The protection of capillaries against rupture * smaller radius means less wall tension is needed * The relationship between transmural tension and wall tension * I guess this is the general point of the law * The pattern of intravesical pressure/volume curve

Answer 65

are *only* slightly *thicker* than capillaries They are thin and easily distended, with relatively little smooth muscle Considerable venoconstriction is caused by the activity in the NA nerves to the veins and by circulating endothelins.

Answer 66

Critical closing pressure occurs when capillary pressure *falls below* tissue pressure

Answer 67

The law of LaPlace explains the *relationship between tension in the wall of a cylinder, the transmural pressure, and the radius of the cylinder/sphere* *P=T/r*

Answer 68

oncotic and filtration pressure gradients are the same for all capillaries Varies tissue to tissue

Answer 69

The 2 types of lymph vessels are *initial* and collecting.

Answer 70

**The cross sectional area of the capillary bed** (though note that *Ganongs* mentions 'number of active capillaries' as an important factor) All other factors listed are directly quoted from Ganongs

Answer 71

**arteriolar constriction and venular dilation.** This would *reduce* the hydrostatic pressure in the capillary lumen

Answer 72

**contractions of skeletal muscle** * fluctuations in negative pressure during *Inspiration* * *Intra-abdominal pressure rises in inspiration as the diaphragm flattens. This promotes venous return to the heart as the valves in the leg veins prevent retrograde flow* * the absence of valves in the system - *Do not increase blood flow, just prevent retrograde flow* * the high cross-sectional area of the great veins - *relatively low compared to total CSA of the capillaries and venules etc*

Answer 73

**CVP *falls* during negative pressure breathing *(inspiration)*** *Negative intrathoracic pressure allows the IVC to open a bit (less interstitial pressure) so the pressure inside falls.*

Answer 74

**proportional to interstitial fluid pressure** *True if they are talking about flow in lymphatic vessels, rather than flow of fluid from blood vessels -\> lymph* * on average *124*mL/h into the circulation. * 3L per 24 hrs = 125mL/hr * *decreased* with decreased interstitial fluid protein * Will reduce flow into interstium * *increased* with contraction of muscles. * Same as veins (muscle pump) * *increased* with raised capillary pressure. * Will promote increased diffusion from capillary -\> interstitium

Answer 75

**mean capillary pressure is normally greater than plasma colloid osmotic pressure** * Net outward force *changes between capillaries* * *Typical net filtration pressure might be 11mmHg _out_ at the arterial end and 9mmHg _inward_ at the venous end* * the filtration co-efficient describes the rate of plasma proteins being filtered from the microcirculation. * *Is something to do with the way the capillary wall acts as a filter* * rate of filtration *varies wildly* in the different tissues of the body * lymphatics play *a large* role in maintaining equilibrium of the forces - *increased interstitial fluid pressure leads to increased lymph flow to balance it*

Answer 76

**Viscosity multiplied by flow is proportional to the pressure gradient** Flow is proportional to r⁴, and is inversely proportional to the length of the tube. nF = (Pa - Pb) x stuff Where n=viscosity

Answer 77

**capillaries have the largest cross-sectional area** * arterioles have a *higher* ratio of smooth muscle to diameter than have large arteries. * capillary flow is regulated by *arterioles* * capillaries contain *5*% of the total blood volume

Answer 78

**Have a continuous basement membrane** A lot of capillary beds are collapsed at any one time in resting tissue Are frickin small - not 10-20mm Most have intracellular fenestrations but some (?CNS) do not, and have a tight barrier to diffusion.

Answer 79

**its protein content depends on the area it is from**

Answer 80

**pressure gradient** Inversely proportional to viscosity and length

Answer 81

All of the above

Answer 82

Causes focal ischaemia

Answer 83

Sodium retention

Answer 84

* s equal to increase in pressure divided by increase in volume – C = ΔV/ΔP * is the same as vascular distensibility - Compliance is a measure of the tendency of a hollow organ to resist recoil toward its original dimensions upon removal of a distending or compressing force. It is the reciprocal of "elastance". Distensibility is simply the ability to stretch and hold more volume. They are related, but not the same. * is 24 times greater in a vein than a corresponding artery * is increased by sympathetic stimulation in the arterial system - decreased * is increased by sympathetic stimulation in the venous system – decreased

Answer 85

* Capillary pressure at the arteriole end *depends but around 30mmHg* * Hydrostatic pressure exceeds oncotic pressure *at the arterial end* * *Example oncotic pressure is 25mmHg, hydrostatic might be 37 at arterial and 17 at venule* * Capillary pressure at the venule end *depends but around 15mmHg* * **Interstitial colloid osmotic pressure is usually negligible** * Capillary filtration coefficient *increases* with capillary permeability.

Answer 86

* venule constriction *increases* filtration pressure * hypoproteinaemia *increases* fluid shift out of capillaries * Reduced plasma oncotic pressure; hypoalbuminaemia -\> oedema * lymphoedema fluid has a *high* protein count * caused by inadequate lymph draininage * **substance P increases capillary permeability** * **after noxious stimuli, via the axon reflex** * *histamine and bradykinin increase* capillary permeability

Answer 87

**barcoreceptor stimulation causes bradycardia and a drop in BP** Afferents from the aortic arch (X) and carotid sinus (IX) terminate in the NTS -\> CVLM -\> RVLM (inhibited by GABA from CVLM) -\> drop in BP and bradycarida Used for short-term changse in BP (eg standing up)

Answer 88

**Systemic hypoxia** Hypoxia of the RVLM will cause an increase in BP as it tries to increase blood flow to itself Local hypoxia will cause vasodilation also

Answer 89

**Adenosine** Adrenaline causes vasocontriction most places except the hepatic, skeletal, and brain where it dilates

Answer 90

**Increases diastolic BP** *Increases water intake and increases retention of sodium and water -\> increased plasma volume* * Has *the same* aldosterone effects as angiotensin III * (Angiotensin III has 40% of the pressor activity of angiotensin II, but 100% of the aldosterone-producing activity) * Has *more* pressor activity than angiotensin I * Angiotensin I does not seem to have any biologic activity and exists soley as a precurser to Ang2

Answer 91

* **Increased Baroreceptor discharge causes increased X discharge *to* *and from*the vasomotor area** * **X carries afferents to the vasomotor area. Increased baroreceptor discharge causes increase firing of X -\> CVLM, which then releases GABA to inhibit the RVLM.** * **X carries parasympathetic efferents to the heart, which causes ACh release and via M2 (Gi linked -\> reduce cAMP-\> K influx -\> hyperpolarisation and bradycaria)** * A decrease in vasomotor discharge causes an *decrease* in systemic vascular resistance. * Neurons synapse with the preganglionic neurons in the *Intermediolateral gray column* of the spinal cord. * Axons of the RVLM descend in the lateral column of the spinal cord to the thoracolumbar intermediolateral gray column * Is *stimulated* by input from the carotid chemoreceptor. * Is *inhibited* by input from the aortic baroreceptors.

Answer 92

**Expiration.** Inspiration causes increased venous return to the heart briefly, which causes increased atrial stretch (type B receptors in late diastole) -\> ANP release -\> tachycardia + drop in BP Expiration causes the opposite -\> bradycardia

Answer 93

* **Regional blood flow to the skin remains unchanged** * *Systolic increases, diastolic decreases -\> incresased pulse pressure* * *Incresed inotropy and chronotropy + peripheral vasodilation* * O2 consumption of skeletal muscle usually *much* *more than triples* * Blood flow to the brain is *Constant* * *Blood flow to the brain should remain unchanged throughout any normal homeostatic mechanism* * CO increasess *_something \<50_* fold.

Answer 94

**The renin angiotensin system is vital in controlling the effect of excess Na intake** * The stress relaxation mechanism is one of the immediate responses. * Stress relaxation is where the aorta or bladder etc will have a sudden increase in wall stress in response to an increase in volume, but the stress will reduce over time as the wall tension relaxe - is not an immediate response, and does not seem to respond much to pulsatile flow, but more of a contstant increase in radius/volume. * Angiotensin acts by increasing *arterial* tone. * Baroreceptors are activated over the course of *seconds* * *provide beat to beat changes in BP - eg standing from sitting* * Renal responses *follow* capillary fluid shifts.

Answer 95

**Is used to replenish phosphoylcreatine stores and replace oxygen from myoglobin** During exercise PC donates phosphate to ADP to create ATP and is used as a short-term energy store, but must be replenished at rest Myoglobin is a short-term oxygen store in the same fashion, and must be replenished at rest

Answer 96

**Increase in peripheral resistance** *Not specifically mentioned in Moores. Everything else is definitely correct, but foramen ovale - closes as soon as LA pressure \> RA (minutes), so this is the only other possibility.*

Answer 97

**Increased atrial stretch receptor activity** To compensate for increased pre-load, HR will increase as BP drops

Answer 98

**The baroreceptors in the carotid *sinus* are stimulated when the BP increases.** *Aortic and carotid bodies are involved in chemoreceptor response. Aortic have and carotid sinus have baroreceptors* * The Bainbridge reflex causes increases in HR * Bainbridge reflex is an increased HR in response to increase atrial filling / pre-load * The Cushing reflex is a special CNS ischaemic response resulting from raised ICP * Pathological process - ischaemia of RVLM causes peripheral hypertension to try and restore blood flow. This causes a bradycardia due to baroreceptor response. * The maximum firing per change in pressure of the carotid baroreceptors occurs at a MAP of 90mmHg. * At higher MAPs, the receptors are firing nearly constantly, so the change between systole and diastole is less. At low MAPs, there is very little firing, so again the change is very little * IX is involved in the Baroreceptor reflex. * Carries carotid sinus afferents

Answer 99

**All of the above are true** Vagal nerve endings have ACh release -\> M2 stimulation (Gi -\> decreased cAMP) -\> increased K flux -\> hyperpolarisation of the cell membrane also M2 -\> Reduced Ca flux causing a reduced slope of the prepotential, slowing the HR

Answer 100

**Decreased activity of the baroreceptors in the left ventricle.** Ventricular distension results in increased ventricular receptor firing which causes reflex bradycardia and hypotension (comparable to a baroreceptor reflex), so the opposite is also true. The rest cause bradycardia

Answer 101

**circulating Na/K ATPase inhibitor** Whatever that is (Reduced Na/K activity -\> increased K outside of cells -\> lowered membrane potential -\> increased excitability/tone)

Answer 102

**direct stimulation by CO2** This is the response elicited in the Cushing Reflex -\> rise in BP All others listed cause an inhibiton of the vasomotor area (ie act to reduce BP) * inhibitory inputs from carotid and aortic chemoreceptors. * Seem to only have excitatory output in response to hypoxia or hypercapnia (or acidosis) -\> vagal output but multiple pathways including respiration -\> tachypnoea and catecholamine release through other hypoxic mechanisms * (Nicks answer in contrast to my understanding): Would inhibit vasomotor ares - inhibition from receptors occurs due to low CO2 or high O2 * excitatory inputs from the carotid, aortic and cardiopulmonary baroreceptors. * Would inhibit vasomotor area - fire in response to high BP * excitatory inputs from the lungs. * Receptors from the lungs fire during inspiration, travel via IX and inhibit RVLM discharge * inhibitory inputs from cortex via the hypothalamus - wrong * Inputs from higher centres are excitatory

Answer 103

**circulating vasoconstrictors hormones include angiotensin II, *noradrenaline, vasopressin, urotensin-II*** Aldosterone is not a vasoconstrictor

Answer 104

**Iron reabsorption is not increased** Dont know exactly, will probably come up in later study but likely something to do with iron not being reabsorbed in the first place * The haematocrit *decreases but not immediately* * *Need time for extravascular fluid to diffuse back into the vascular space and dilute the haematocrit before it drops* * Equals loss of 35% plasma volume. * Mathematically ~28% of plasma volume is approx. 1L of fluid (3.5L plasma in a 70kg person) however the response to this would be different * Plasma protein synthesis *_is_* increased.

Answer 105

It can increase up to 700% ie 7x resting output

Answer 106

**SV increases less than 200%** Most of increase in CO is due to increase in HR apparently

Answer 107

**increased insulin secretion** Others all cause increase in RBC production (EPO) or maintenence of blood volume / reduce urine output

Answer 108

**In general, tissue blood flow is regulated according to the needs of the tissue, CO is regulated according to the sum of tissue blood flow and BP is regulated independently of either local blood flow or CO** * The Cushing reflex is characterized by hypertension and *bradycardia* as cerebral interstitial fluid accumulates when raised intracranial pressure compromises cerebral blood flow. * Increased Baroreceptor discharge from the carotid sinus and aorta will result in decreased *SNA, HR and BP (as it fires in response to elevated BP)* * NA, A, Angiotensin II and ADH are *all circulating hormones or neurotransmitters, and none are involved in local autoregulation. Local autoregulation involves metabolites and NO* * Increased CVP produces *differing* sympathetic response from atrial stretch receptors *compared to the response* elevated BP produces from carotid sinus baroreceptors. * Discharge of atrial stretch receptors results in vasodilation and a fall in BP but an increase in HR * Baroreceptors cause a bradycardia and reduction in BP

Answer 109

**inhibits tonic discharge of vasoconstrictor nerves** * *stimulates* GABA secreting neurons in the medulla *to suppress the RVLM* * *Stimulates* X stimulation of the heart -\> bradycardia * is inversely proportional to pressure change * passes via *afferent* nerves in IX and X nn.

Answer 110

Increase vessel diameter

Answer 111

Regional blood flow to the skin remains unchanged

Answer 112

muscarinic antagonist M2 receptors on heart cause bradycardia when stimulated (vagal nerve is main driver of HR through inhibiton) M receptors on sweat glands are the only acetlycholine receptors in the sympathetic nervous system All vasomotor tone is controlled by sympathetic system Nicotinic receptors are not found in heart or sweat glands alpha blocker could cause tachycardia via peripheral vasodilation but would impair ejaculation and affect BP

Answer 113

**Decreased contractility** *Denervated hearts run at 100bpm.* At rest: * Vagal tone predominates in the heart, lowering the HR. If vagal tone is cut, HR is about 150bpm. If there is loss of all innervation, HR is about 100bpm. * Sympathetic tone increases contractility and constricts blood vessels - if nerves are cut they vasodilate (Parasympathetic nerves have no effect on vasculature or resistence) If dennervated: * Loss of parasympathetic dampening causes the HR to increase to about 100, whilst the loss of sympathetic stimulation will reduce contractility (ie at rest PNS is reducing HR, whilst SNS is increasing contractility from ‘baseline’)

Answer 114

**isoprenaline** Is a non-selective beta-agonist -\> treat bradycardia Norad and adrenaline have alpha effects

Answer 115

**Increased thoracic pumping** Shock -\> increased ADH as there is a desire to maintain the bodys fluid, not loose it in urine

Answer 116

**Vasopressin is released from the supraoptic nuclei –** ***ADH or vasopressin is made in the cell bodies in the SON, but the axons project to the posterior pituitary for release of the hormone.*** * Noradrenaline and adrenaline are secreted in response to a fall in blood pressure * The reninangiotensin system is brought into play * The kidneys bring the blood pressure to near normal * via the atrial reflexes (the volume reflex) -\> dilatation of afferent arteriole -\> rise in GFR. Also signals from atria to hypothalamus -\>ADH causing reduced reabsorption of fluid in the renal tubule, increasing urine output and reducing blood volume. Also, release of atrialnatriuretic peptide increases urine output and thus reduces blood volume. * The baroreceptor mechanism operates best during fluctuations of blood pressure

Answer 117

Noradrenaline – vasoconstriction

Answer 118

neuropeptide Y causes vasoconstriction ## Footnote *others are all opposite*

Answer 119

**a decrease in central bloodpool by 400ml** *Standing causes a reduction in preload (reduced venous return/EDV) -\> reduced SV -\> increased HR to maintain CO (do not need to increase it - just maintain what it previously was)* * an increase in total peripheral resistance by *40%* * Increased peripheral SNS activity stimulates arteriolar vasoconstriction – increasing the TPR by 1:1.4 (i.e. 40%) * an increase in stroke volume by 10% * venous return will drop, thus so will preload and therefore SV. HR increases to compensate for this * *No change in CO - just need to maintain, not increase* * a *increase in* intra-abdominal vascular resistance *as intraabdominal pressure will rise*

Answer 120

**carotid body receptors are strongly stimulated** *they will be poorly perfused and therefore activated by a reduction in PO2 (stagnant anoxia). These receptors are responsible for the Mayer Waves seen in hypotension: 20-40s fluctuations in BP as feedback is looped.* * carotid sinus receptors are *very* *weakly* stimulated * they are stimulated by high pressures not low * central nervous system ischaemia response is *not quite* activated * Only activates \<40mmHg

Answer 121

**Oxygen usage may increase up to 10 times** * Cardiac output *may be up to 20.9L/min* * Stroke volume *has a small range it can increase - increased inotropy but due to increased HR diastolic time shortens and thus EDV has a plateau* * A-V difference is *maybe 3-4x* greater than at rest * Pulse rate is *up to 170+bpm*

Answer 122

**lactate is a vasodilator** * Blood flow is maximal during *Diastole* * *70-80%* of O2 is extracted. * β adrenergic receptors mediated *vasodilation* * *If beta receptors are blocked, noradrenaline causes vasoconstriction through alpha action, but the increased HR and inotropy brought about via beta-receptors -\> increased myocardial O2 demand -\> coronary vasodilation* * the ostia of coronary arteries *are held open throughout the cardiac cycle*

Answer 123

**e) in hypercalcaemia, myocardial contractility is enhanced** * a) hypernatraemia is associated with *high* voltage complexes * b) the first change in hyperkalaemia is *peaked t-waves* * c) with hypokalaemia, the resting membrane potential decreases * Need to clarify this point - hypokalaemia hyperpolarises the cell (ie more negative RMP) - Ganongs has contradictory points in the nerves and cardiology sections on this * Gangongs in Cardiology states that *hyperkalaemia* reduces the RMO * d) in hyperkalaemia, the heart stops in *diastole* * *This is because as the voltage-gated sodium channels begin to close (inactivation gates) and the myocardium becomes unresponsive to stimulation (see notes for full details)*

Answer 124

**c) atrial premature beats produce an ‘A’ wave** * a) the ‘*C*’ wave denotes the increased atrial pressure due to the bulging of the tricuspid valve during isovolumetric ventricular contraction * A=atrial contraction, V=valve opening, C=contraction of ventricles causing AV valve to bulge * b) in tricuspid insufficiency, there is a giant ‘*C*’ wave with each ventricular systole * Presumably C as there will be backflow during ventricular systole * d) the ‘v’ wave occurs during *diastole* * *V=AV valve opening at beginning of diastole* * e) a giant ‘_A_’ wave (‘cannon wave’) may be seen in complete heart block * Occurs when the atria contract against a closed AV valve

Answer 125

**b) sleeping** Standing up reduce CO (reduced preload due to venous pooling) All others increase it

Answer 126

**e) 9ml/100g/min**

Answer 127

**d) the aorta has 2%** * a) the heart has *12%* * b) the pulmonary circulation has *18%* * c) the venous circulation has *54%* * e) capillaries have *5%* * *Arteries 8%, arterioles 1%*

Answer 128

**d) evokes positive inotropic and chronotropic effects on myocardium** Endothelin is the most potent vasoconstrictor known. I cannot find that is has direct myocardial effects, but HR and SV will need to increase to maintain CO in the context of increased PVR. As a vasoconstrictor it should produce a reduced GFR Cannot find information on its extra-vascular effects * \*\*Prostacyclin -\> platelet inhibition and vasodilation* * \*\*TXA2 -\> platelet activation and vasoconstriction*

Answer 129

**a) nitric oxide** Is a vasodilator. Endothelin production is managed in the way you would expect - vasodilators inhibit it, vasoconstrictors enhance it. All others listed are either vasoconstrictors (AngII, catecholamines) or have no effect I know of (insulin, GF)

Answer 130

**a) it synthesises nitrous oxide from arginine** As per Ganongs: 'NO is synthesised from argenine in a reaction catalysed by NO synthase' There are 3 isoforms NOS 1 is in nervous system (Ca2+ induced) NOS 2 is in macrophages and immune cells (cytokine-induced) NOS 3 is in endothelial cells (Ca2+ induced) *They thought 'C' but Hb is not mentioned in Ganongs either way*

Answer 131

**e) histamine**

Answer 132

e) carotid body The *carotid arch* is, but the carotid and aortic *bodies* are chemoreceptors

Answer 133

**e) it contains very low levels of cholesterol relative to plasma** **0.2 vs 175 mg/dL** Total volume is 130ml (100ml subarachnoid, 30ml in ventricles) It is *produced* in the choroid plexus and *absorbed* by arachnoid vili Produced at 500ml/day pH is slightly lower than serum Normal pressure is 112mmCSF (measured in mmCSF as that is what is pushing up against gravity in the pressure thing for LPs) \*\*Note that Ganongs states that lipids freely cross the BBB, and that a lot of the bodies cholestrol is in the brain (25% in Myelin), however every other answer is clearly wrong\*\*

Answer 134

**c) Na+** **pCO2 is higher in CSF** **Ca is lower** **K is lower** **Glucose is lower** **HCO3 is equal**

Answer 135

**e) umbilical artery** Carrying deoxygenated blood from the fetus to the uterus (the foetal pulmonary artery, as it were) Uterine vein has 80% saturation (cf 95% equivalent in adults) Systemic venous blood (similar to the umbilical artery) is only 26% saturated

Answer 136

**e) O2 consumption of skeletal muscle may increase 100-fold** Brain blood flow is always constant Diastolic has a small increase, systolic a large one (due to vasodilation of peripheral vasculature) CO increases about ??7x HR takes longer to normalise than BP

Answer 137

**b) causes the ‘A’ wave of the jugular pulse** C=contraction of ventricle causing AV bulge V=AV Valve opening dicrotic notch = small plateau in arterial pressure due to closure of the aortic valve (ie it is dropping into diastole, the valve closes, and the elasticity of the aorta bumps the pressure a little bit) Obviously atrial systole increase the atrial pressure

Answer 138

**c) repolarisation due to K+ efflux through two types of K+ channels** **They said d (definitely wrong), c) seems closest** Phase 0 - Rapid depolarisation due to rapidly opening voltage-gated Na channels Phase 1 - initial rapid repolarisation due to closure of voltage-gated Na channels Phase 2 - plateau due to Ca *INFLUX* thruogh slow-opening voltage-gated Ca channels Phase 3 - slow repolarisation via K efflux through 'multiple types of potassium channels' Phase 4 - resting RMP

Answer 139

**d) the bundle of HIS (1m/s) is not the most rapidly conducting part of the conducting system** The purkinje system is (4m/s) * a) all cardiac cells have the same resting membrane potential * Myocytes -90, pacemakers -55 * b) cholinergic fibres act predominantly by *slowing Ca influx and increasing K efflux to reduce the slope of the pre-potential (mediated via M2 receptors -\> decreased cAMP)* * c) discharge rates of pacemaker tissue *can* change significantly with temperature * *Hypothermia -\> bradycardia* * e) the last parts of myocardium to depolarise *are the posterobasal portions of the LV, pulmonary conus, and uppermost portion of septum*

Answer 140

**b) delayed depolarisation** 1. Rapid repolarisation early with current flow away from infarct due to rapid opening of K+ channels (lasts seconds to minutes) -\> STE 2. Decreased RMP with inward current flow -\> TQ *depression (manifesting as STE)* * Loss of intracellular K+ with reduced Na-K ATPase activity -\> negative RMP* 3. Delayed depolarisation with outward current flow due to infarcted fibres being unable to depolarise properly -\> STE

Answer 141

d) valves in the cerebral circulation

Answer 142

a) serotonin Others all dilate (except K - unsure)

Answer 143

**d) atrial stretch receptors inhibit the vasomotor centre** * a) baroreceptors causes *inhibition* * b) chemoreceptors cause inhibition * c) baroreceptors provide *minimal* input below 70mmHg mean arterial pressure (as baroreceptors are inhibitory, so hypotension -\>less firing -\>more constriction) * e) direct inputs include *pCO2* * Responsible for the Cushing response in increased ICP

Answer 144

**c) has a higher concentration of creatinine than plasma** *1.5 vs 1.2 mg/dL* * a) volume is about *130ml* * b) normal pressure is *112mm* CSF (range 70-180mm) * d) has a *lower* concentration of urea than plasma * 12 vs 15 mg/dL * e) *about 80%* is formed in the choroid plexus

Answer 145

**a) the PR interval is shortened but the QRS normal in length in Lown Ganong Levine syndrome** *Aberrant pathway near AV node which bypasses it but still excites the intraventricular conducting system* Long QT mutations can occur in Na or K channels In AF the atria beat at 300-500bpm and ventricles at 80-160 SVT has atrial rates up to 220/min Atrial flutter has trial rates 200-350/min PVCs can be benign

Answer 146

**b) the concentration of creatinine is approximately equal to that of plasma** 1.5mg/dL vs 1.2mg/dL (ie 1.25x as much in CSF)

Answer 147

**d) blood in the umbilical veins is believed to be about 80% saturated with O2** * a) HbF has a higher affinity for O2 than HbA as it binds 2,3DPG *less* effectively than HbA * b) the sucking action of the first breath in the newborn, plus constriction of the umbilical veins, squeezes as much as *100*ml blood from placenta * c) bradykinin *constricts* umbilical veins and the ductus arteriosus, while *dilating* the pulmonary bed * Bradykinin is released from lungs during the first few breaths into the foetal circulation * e) the placenta is a *less* efficient gas exchange organ than the adult lungs - *hence foetal blood is only 80% saturated in the umbilical vein*

Answer 148

**b) the AV node contains P cells** **as does the SA node** * a) the *left* bundle branch (of HIS) divides into anterior and posterior fasicles * c) myocardial fibres have a resting membrane potential of *-90*mV * d) action potential in the SA and AV nodes are largely due to *Ca2+* influx * e) there are two types of *Ca2+* channels in pacemaker tissue – transient and long acting

Answer 149

**d) the end systolic ventricular volume is about 50mL** isovolumetric contraction is 0.05sec peak pressure is about 120mmHg in LV and 25 in RV EDV is about 130ml, SV is about 70-90ml, hence ESV is about 50ml EF is about 70% Atria only contribute a very small amount to ventricular filling

Answer 150

**e) standing normally decreases the length of ventricular cardiac muscle fibres** ***as venous return falls -\> smaller EDV*** CI is CO vs BSA Sleep has no effect on CO basal O2 consumption is 2ml/_100g_/min * Bainbridge Reflex - increased venous return -\> increased HR * Ficks Law - relationship of diffusion to surface area and diffusion coefficient * Starlings law - compares contraction strength to the initial myocyte length (aka SV to EDV) * Poiselles law - relationship between flow in a tube and radius/viscosity * Laplaces law - relationship between vessel diameter/pressure and wall tension

Answer 151

**e) magnesium counteracts digitalis toxicity** *Magnesium suppresses digoxin-induced ventricular arrhythmias* * a) PR interval increases in *hypo-*kalaemia * b) in hyperkalaemia, the heart stops in *diastole* * c) hypercalcaemia causes *shortening* of the QT segments * Opposite effects to potassium * d) hypernatraemia is associated with *high* voltage electrocardiographic complexes

Answer 152

**b) they are smaller than skeletal muscle fibres** Skeletal muscle is multinucleated, whereas cardiomyocytes are generally mononucleated Ca is released due to DEpolaristion Catechols -\> incresaed SR Ca

Answer 153

**d) the largest drop in energy occurs at the level of the *small arteries and arterioles.*** *The largest drop in pressure is at the small arteries and arterioles. I assume this is what they mean. Otherwise, who knows.*

Answer 154

**b) the volume of blood pumped through the lungs equals the volume entering the heart** c) Poiseville’s Law predicts the effects of pressure and resistance on cardiac output One of these two - they say b) is false, I cannot find anything about it. Poiseuilles law relates flow to radius and viscosity, which would infer resistence (radius) and CO (flow) also apply.

Answer 155

They say d) a) wholse blood is 3-4x as viscous as water - so likely correct b) arteries contain 8%, aorta 2%, aterioles 1%, so b) is correct if they are including all 3 in one but that is confusing c) Correct d) False e) seems false as increasing TPR (constriction) should either reduce arterial volume or have a negligible effect on it

Answer 156

b) Perkinje fibres are ‘fast fibres’, and can conduct a wave of depolarisation at a speed of 4m/sec

Answer 157

They think c) which is wrong - liver and kidneys alone are ~50% CO I would say d) knowing nothing more than the information below. Liver - 28% of CO (1500ml/min) Kidneys - 23% (1260ml/min) Brain - 14% (750ml/min) Skin - 8% Skeletal muscle - 16% Heart - 5%

Answer 158

**e) sounds of Korotkoff occur when velocity of flow through constriction exceeds critical velocity** *Turbulence is determined by* Reynold formula, which essentially gives a maximum speed for laminar flow, all other factors being the same. Above this velocity, flow is turbulent * a) the sounds of Korotkoff when taking blood pressure are caused by *turbulent* flow * b) the diastolic pressure in resting adults correlates to the *disappearance of* Korotkoff sounds * correlates with muffling in adults after exercise and children * c) pressures obtained by palpation of auscultation methods are usually 2-5mmHg higher ??? * d) if cuff is inflated for some time, it can give falsely low BP readings

Answer 159

**d) coronary flow at rest is 250ml/min** * a) left coronary artery has greater flow in *10-20*% of people * *80-90% of people are right dominant* * b) thebesian veins connect *capillaries* to the heart chambers * c) cusps of the aortic valve *never* occlude orifices of coronary arteries - they are always patent * e) at rest, heart extracts *70-80*% O2 / unit of blood delivered

Answer 160

**b) true capillaries are about 5μm in diameter at the arterial end and 9μm in diameter at the venous end** * a) *arterioles* are the major site of resistance to blood flow * c) the aorta wall is *2*mm thick * d) lymphatic endothelium *does not* contains fenestrations * e) angiogenin *?promotes* angiogenesis

Answer 161

**d) the Poiseville-Hagen formula gives the relation between the flow in a long narrow tube, the viscosity of the fluid and the radius of the tube** Whole blood is 3-4x as viscous as water

Answer 162

**e) venous flow may be pulsitile** Varies with respiration and heart beat * a) pressure is higher in the *venules* compared with the *veins (12-18mmHg vs 5.5)* * b) central venous pressure averages *4.6*mmHg and fluctuates with respiration and heart action * c) the drop in venous pressure during *inspiration* aids venous return * d) peripheral venous pressure _is_ affected by gravity

Answer 163

**c) decreased K+** *increased K causes vasodilation*

Answer 164

c) NO synthase inhibition leads to a prompt rise in blood pressure * This question doesnt seem to be in Ganongs, but given NO is a vasodilator is seems reasonable that it will cause a rise in TPR if it is blocked. And all other answers are wrong.* * a) *platelets are recycled and thus replenish their* cyclo oxygen over four days * b) nitrous oxide synthase in immune cells is induced by *cytokines (endothelial and nervous is Ca)* * d) endothelin-1 is a potent vaso*constrictor* * e) angiotensin II *stimulates* secretion of endothelin-1

Answer 165

**d) stimulation of pain fibres in trigenial nerve** **Most other pains increase HR** * a) *Increased* activity of baroreceptors * b) inspiration * Reduced venous pressure during inspiration -\> increased venous return -\> tachycardia * c) Bainbridge reflex * This is a rise in HR in response to increased venous return/atrial stretch * e) increased activity of atrial stretch receptors - increases via Bainbridge reflex

Answer 166

**e) cannon waves are giant ‘A’ waves seen in complete heart block** * Due to the atria contracting against a closed triscupid valve* * b) the ‘C’ wave is the rise in atrial pressure produced by the bulging of the *tricuspid* valve into the atria during isovolumetric ventricular contraction

Answer 167

a) platelet factor IV

The Heart and Circulation ( 25% ) Flashcards

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