Heart and Circulation (26-29)

Question 1

What is the function of the heart and circulation system?

Answer 1

To deliver nutrients and remove waste
→ delivers O2 and sugar to respiring tissues
→ removes CO2 and products of metabolism
→ delivers hormones to site of action
→ central to homeostasis (e.g. body temperature - blushing when hot as blood pushed to surface to remove excess heat)

Question 2

How big is a human heart?

Answer 2

Size of your fist
→ 200 - 425g
→ beats ~100,000/day, pumps ~7,000 litres of blood/day

Question 3

Does heart beat depend on size?

Answer 3

Yes
→ smaller size = faster heart rate
→ smaller size means bigger SA:V ratio, therefore more heat loss, higher metabolic rate and heart beats faster

mouse 450/min, man 70/min, elephant 28/min

(chicken and rabbit excretion due to different body temps)

Question 4

Where does the heart sit in the human body?

Answer 4

Centrally
→ apex is situated on the left in the 5th intercostal space

Question 5

What is the vena cava?

Answer 5

The major vein that returns blood back to the heart
Superior → from shoulders, arms, head
Inferior → from rest of body

Question 6

What is the function of the pulmonary artery?

Answer 6

Takes blood away from heart to the lungs
→ only artery that carried deoxygenated blood

Question 7

What is the function of heart valves?

Answer 7

Control blood flow - ensure its stays in one direction, prevent backward flow
→ tricuspid & bicuspid: shut in systole, open in diastole
→ pulmonary & aortic: open in systole, shut in diastole

Question 8

Why is the wall of the right ventricle thinner?

Answer 8

Has to pump blood around a very short circuit (heart and lungs are close)
→ so requires less pressure

Question 9

Is the duration of diastole of systole longer?

Answer 9

Diastole
→ the heart spends 300ms in systole (ventricular contraction) and 550ms in diastole (relaxation)

mean arterial pressure = 1/3 systole + 2/3 diastole

Question 10

What gives rise to heart sounds?

Answer 10

Closing of valves (lub dub bub)
→ caused by changes in pressure
→ left side much louder

Question 11

What does cardiac output depend on?

Answer 11

The number of beats and their volume
→ cardiac output = stroke volume x heart rate
→ amount of blood you pump per minute
e.g. 70 beats min^-1 x 70ml beats^-1 ~ 5L min^-1

Question 12

What is stroke volume?

Answer 12

The volume of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction

Question 13

What is Starling’s Law of the Heart?

Answer 13

Energy of contraction is a function of the length of the cardiac muscle fibres
→ link between length of myocardial fibres and force generated by contraction
→ stroke volume is governed by filling and stretching of muscle
→ due to an increased sensitivity of the contractile proteins to Ca2+

Question 14

What type of activity does the heart show?

Answer 14

Myogenic → initiated within the heart itself, generates its own beat

Question 15

How is heart contraction co-ordinated?

Answer 15

Electrical impulse starts at the sinoatrial node (found in RA, pacemaker)
→ travels to the atrioventricular node
→ trails to the ventricles through Purkinje fibres, bundle of His
→ spreads throughout myocardium

SA node → AV node → P fibres & His → myocardium

Question 16

Where is there a pause in the heart conduction pathway?

Answer 16

At the AV node
→ inserts delay to wait for atrial contraction and insure maximal filling of ventricles

Question 17

What does ionic pacemaker potential depend on?

Answer 17

Calcium
→ generated by reduced K+ and increased Na+ permeability
→ depolarisation mostly produced by increased Ca2+ permeability

Question 18

What does the sinoatrial node pacemaker potential depend on?

Answer 18

Sodium
→ slow leak of Na+, constant move towards action potential threshold
→ no need for stimulus

Question 19

What does the long refractory period of ventricular myocytes prevent?

Answer 19

Ventricles don’t have rapid depolarisation due to calcium (entry via L-type channels)
→ prevents repeated action potential, tetanus in cardiac muscle
→ if the heart stays constantly contracted - can’t fill with blood

Question 20

What are myocytes?

Answer 20

Branches muscle cells with a single nucleus
→ striated appearance under microscope

Question 21

How are myocytes electrically coupled?

Answer 21

Through intercalated disks
→ connected through tight junctions, coupled through connexins
→ contraction activated by entry of Ca2+

Question 22

What do ECG recordings detect?

Answer 22

Change in ionic charge
→ the spread of the heart beat
→ can be used to diagnose cardiac disease

Question 23

Why does the circulatory system have different vessels?

Answer 23

To accommodate different pressures

high partial pressure ~ 100mmHg
→ elastic/muscular arteries - more muscular

low venous pressure ~ 0-8mmHg
→ veins - valves

Question 24

What is the common structure of blood vessels?

Answer 24

(outside - in)
Tunica adventitia (externa) → principally collagen
Tunica media → elastic tissue, smooth muscle
Tunica intima (interna) → endothelium, supporting connective tissue, release of paracrine signals
Lumen

Question 25

Do elastic arteries store energy?

Answer 25

Yes → elastic parties store energy during systole (contraction) and release it in diastole - maintaining blood flow at this time and smoothing it

Question 26

What is the Windkessel effect?

Answer 26

As blood is pumped into the aorta and major arteries they stretch → in systole more floor flows in than out The walls of the aorta and elastic arteries recoil in diastole maintaining blood flow

Question 27

How is blood flow pulsatile?

Answer 27

Elastic parties convert the intermittent pressure into pulsatile flow → follows the pressure of the chambers bit never reaches 0

Question 28

What is resistance determined by?

Answer 28

Length of blood vessels → longer = greater resistance, each vessel remains constant Viscosity of blood → more solute = greater resistance, in normal conditions solutes don't change Radius of blood vessels → can be changed

Question 29

What does blood flow depend on?

Answer 29

Radius of blood vessels - muscular arteries control flow Ohms law: Q = (P1-P2)/R → Q = flow → (P1-P2) pressure difference between two ends → R = resistance resistance will rise if the vessel is narrower, flow will be reduced, the pressure will be increased

Question 30

Is blood flow laminar?

Answer 30

Yes → blood flow is layered Flow is fastest at the centre (provision of blood to organs/tissues) Flow is slowest on the outside - friction (necessary to provide nutrients to blood vessels)

Question 31

What happens to flow at high velocity?

Answer 31

It becomes turbulent - laminar flow disrupted → can't deliver nutrients - tissues start to die → leads to endothelial damage, arterial disease

Question 32

What are capillaries?

Answer 32

Smallest vessels comprised of only tunica intima → site of exchange

Question 33

What are precapillary sphincters?

Answer 33

Segments of smooth muscle that control access to microcirculation → help direct blood flow into capillaries via path of least resistance

Question 34

How do capillaries optimise diffusion?

Answer 34

Thin walled - single layer of endothelial cells → minimises resistance to diffusion → maximum amount of SA contact between blood and capillary wall the exchange of blood gases and metabolites generates an equilibrium between plasma and interstitial fluid

Question 35

How is permeability of molecules in capillaries determined?

Answer 35

By the nature of the molecules itself → lipid soluble molecules (O2, CO2) - diffuse easily through capillary cell membranes → hydrophilic molecules - travel through pores, via a paracellular route → molecules > 60kd - not transferred, retained in circulation important to the equilibrium between plasma and the ecf

Question 36

What is Starling's forces?

Answer 36

Extracellular fluid movements between blood and tissues is determined by differences between hydrostatic pressure and colloid osmotic (oncotic) pressure → loss of fluid from plasma - hydrostatic pressure (tries to move solution out) → reabsorption of fluid into plasma - colloid osmotic pressure (tries to pull solution in)

Question 37

What determines the equilibrium between plasma and interstitial fluid?

Answer 37

Hydrostatic pressure → e.g. 35mmHg at arteriolar end and 15mmHg at venular end Oncotic pressure → large molecules (>60kd) don't cross capillary walls, their osmotic pressure draws fluid back into capillaries (constant 25mmHg)

Question 38

What does filtration/reabsorption depend on?

Answer 38

The difference between hydrostatic and oncotic pressure → filtration pressure = hydrostatic pressure - oncotic pressure e.g. hydrostatic pressure > 25mm Hg, push fluid out hydrostatic pressure < 25mm Hg, draw fluid in

Question 39

Where does excess fluid from capillaries go?

Answer 39

Taken up into lymphatic and returned to the circulation system → capillary beds are associated with lymphatic capillaries

Question 40

What are veins?

Answer 40

Veins are capacitance blood vessels → provide a reservoir of blood

Question 41

How do muscle pumps enhance venous return?

Answer 41

Contraction and relaxation of skeletal muscles opens and closes valves in veins enhancing venous return

Question 42

What part of the nervous system innervates the heart?

Answer 42

Both arms of the autonomic nervous system innervate the heart → parasympathetic (response during rest) and sympathetic (fight or flight) → pacemakers and atrial muscle are innervated by the parasympathetic/sympathetic nerves Blood vessels are only innervated by the sympathetic

Question 43

What chronotropic (change heart rate) effects does the autonomic nervous system have n the heart?

Answer 43

Sympathetic → drives heart through noradrenaline, increased rate increased conduction Parasympathetic → slows the heart through acetylcholine, decreased rate decreased conduction

Question 44

How are chronotropic effects exerted?

Answer 44

By altering pacemaker potential → sympathetic and parasympathetic alter the steepness of Na+ influx - the point at which the threshold is hit changes

Question 45

What innervates ventricular muscles?

Answer 45

Sympathetic nerves only

Question 46

What part of the nervous system can alter contractility of the heart?

Answer 46

Only the sympathetic nervous system → increases contractility through NA enhancing Ca2+ release in myocytes → positive inotropic effect - greater force of contraction, increase stoke volume (parasympathetic has no effect)

Question 47

Do sympathetic nerves have vasoconstrictor action?

Answer 47

Yes, vasoconstriction causes: → increase in resistance in arteries → increase in venous return in veins (causes higher blood pressure)

Question 48

What neurotransmitter do sympathetic nerves release onto smooth muscle?

Answer 48

Noradrenaline - increasing causes vasoconstriction → sympathetic nerve in tunica media cause contraction from NA → controls resistance of systemic circulation → regulates flow to organs or tissues

Question 49

How do sympathetic nerves cause vasodilation?

Answer 49

Decreasing noradrenaline release → dilation increases flow to capillaries

Question 50

How does noradrenaline work on smooth muscle?

Answer 50

NA acts on α1 and α2 receptors to mobile Ca2+ in smooth muscle → it alters the activity of myosin light chain kinase: more phosphorylation - more contraction → and myosin light chain phosphatase

Question 51

What is the baroreceptor reflex?

Answer 51

One of the body's homeostatic mechanisms to help maintain blood pressure at a constant level, in spite of changing requirements → sensing of blood pressure → integration by the CNA → correction of error

Question 52

Where are the baroreceptors?

Answer 52

Aorta → that's where BP is the highest, don't want to break the aorta Carotid → ensure brain has enough pressure, skull can't take too much

Question 53

What determines mean arterial blood pressure (MAP)?

Answer 53

Cardiac output (CO) and peripheral resistance (TPR) → MAP = CO x TPR Baroreceptor reflex alters CO and TPR

Question 54

What is the long term adjustment of blood pressure?

Answer 54

Blood volume → secretion of renin by the kidney is an important factor in regulating blood volume → increased frequency of impulses from sympathetic nerve system to kidney (detects quantity of blood) - increased renin secretion

Question 55

What does angiotensin II do that affect circulation?

Answer 55

Rapid: powerful vasoconstricter → increase in peripheral resistance and venous tone Slow: secretion of aldosterone → retention of Na+, thirst

Question 56

What part of the heart senses filling pressure?

Answer 56

Atrial stretch receptors → activation controls output of hormones → rescue ECF (and therefore blood) volume

Question 57

What is the endocrine function of the atria?

Answer 57

Secreting atrial natriuretic peptide/factor (ANP) → atrial stretch receptors help regulate extracellular fluid volume → release of ANP: renal excretion of Na+ and reduction of ECF volume → sends information to hypothalamus to decrease secretion of anti-diuretic hormone (ADH) - reduces ECF volume, removes vasoconstrictor effect

Question 58

How can blood flow to a particular tissue be modified?

Answer 58

Adjusting vasomotor tone → vasoconstriction will reduce blood flow → vasodilation will increase blood flow

Question 59

What counters increased vasomotor tone?

Answer 59

Potassium and adenosine act as paracrine signals → metabolites oppose sympathetic innervation - vasoconstrictor sympathetic nerve fibres are opposed by paracrine effects of metabolites → vasodilator metabolites ensure flow meets metabolic requirements

Question 60

Overall what controls vessel diameter regulation?

Answer 60

Vasoconstriction → sympathetic tone, angiotensin II, ADH Vasodilation → adenosine, K+, NO, adrenaline

Question 61

How do vessels in the pulmonary circulation differ?

Answer 61

They are thin walled (look like veins but arteries) and are highly compliant (always want blood flow to lungs) → pulmonary circulation under low resistance - short distance, large diameter - essential yo stop fluid build up in lungs

Question 62

Is hydrostatic pressure lower of higher than oncotic pressure in pulmonary circulation?

Answer 62

Hydrostatic pressure is less than oncotic pressure in the pulmonary circulation → reabsorption throughout capillary bed rather than tissue fluid formation → don't want to push fluid into lungs

Question 63

How is vessel dilation in the pulmonary circuit governed?

Answer 63

By oxygen levels and adenosine → principle regulator is O2 - low O2 results in vasoconstriction → innervated by the sympathetic nervous system - plays little role in physiological control of resistance

Question 64

What does hypoxia induce?

Answer 64

Adenosine release causes: → vasodilation in system circulation → vasoconstriction in pulmonary circulation - stops blood flow to areas of dead lung

Question 65

What are the reflexes induced by haemorrhage?

Answer 65

(Rapid loss of blood) → respond to reduction in blood volume → maintain blood pressure and cardiac output → restore circulating fluid volume (become counterproductive)

Question 66

What does haemorrhage lead to?

Answer 66

Fall in blood volume → fall in venous return → decrease in venous and arterial pressure → decrease in cardiac output

Question 67

During haemorrhage where do initial corrections come from?

Answer 67

Baroreceptors → vasomotor centres → ANS → increasing cardiac output: elevating heart rate, enhancing contractility - increases rate of haemorrhage → increasing drive to vasculature: raising TPR (arterioles constrict), arising venomotor tone (veins constrict to push reservoir of blood) - stops blood flow to tissues

Question 68

Why is interstitial fluid recruited during haemorrhage?

Answer 68

Haemorrhage causes drop in hydrostatic pressure → oncotic pressur recruits interstitial fluid → reabsorption of fluid at the expense of viscosity

Question 69

How is loss of blood volume corrected?

Answer 69

Secretion of renin from kidneys → release of angiotensin II short term: constriction of arterioles → increase TP + constriction of veins → restoring filling pressure longe term: secretion of aldosterone → fluid retention + thirst → restoring ECF

Question 70

How is loss of red blood cells corrected?

Answer 70

Secretion of erythropoietin → hormone which induces production of red blood cells

Question 71

What are the classes of haemorrhage?

Answer 71

Class I → 15% bv: no change in vital signs e.g. blood donation Class II → 15-30% bv: tachycardia, blood pressure changes, peripheral vasoconstriction, pale, cool Class III → 30-40% bv: heart rate increase, bp drops, peripheral hyperfusion (shock) Class IV → >40% bv: limit of body's compensation reached, resuscitation required to prevent death

Question 72

What clinical intervention is used for haemorrhage?

Answer 72

1. treat cause of blood loss → prevent further bleeding 2. give fluids → preferably blood, saline with colloid to maintain oncotic pressure 3. monitor oxygen saturation 4. in server situationsm monitor filling pressure of the heart with catheter

Question 73

What is needed for exercise?

Answer 73

Provide skeletal muscle with radically increased blood supply → rase cardiac output and balance changes in peripheral resistance → increase coronary blood flow

Question 74

During exercise how is the blood supply redistributed to skeletal muscles?

Answer 74

Exercise induces sympathetic nervous system → vasoconstriction in peripheral tissue → vasodilation in muscle blood vessels

Question 75

What is the effect of adrenaline during exercise?

Answer 75

Sympathetic drive increases adrenaline alpha receptors → vasoconstriction beta receptors → vasodilation in skeletal muscles

Question 76

What local effects override any sympathetic vasoconstriction during exercise?

Answer 76

Electrical activity release K+ → plasma [K+] rises in exercise, K+ relaxes vascular smooth muscle ATP converted to Adenosine - an important paracrine vasodilator Anaerobic respiration → lactat production, acidification leads to vasodilation → vasodilator metabolites match blood flow to metabolic needs

Question 77

What would occur if filling pressure increased during exercise?

Answer 77

Lead to overstitching cardiac muscle → high filling pressure also leads to oedema - fluid in lung if left atrial pressure too high → at high filling pressures stroke volume no longer increases with increasing filling pressure - hit elastic capacity

Question 78

How is the heart protected from overfilling/stretching during exercise?

Answer 78

Reduction in diastole → cardiac output rises - cannot be sustained through an increase in stoke volume alone so increase in heart rate → increase in heart rate reduces filling time protecting from over filling

Question 79

How is the increased blood pressure during exercise countered?

Answer 79

Reduced total peripheral resistance

Question 80

How does cutaneous (skin) vasodilation contribute to thermoregulation during exercise?

Answer 80

Get rid of excess heat during exercise through sweating and cutaneous vasodilation → however, reduces peripheral resistance and will divert blood from muscles - initially thermoreg wins but if central venous pressure falls then thermoreg abandoned (hot climates: heat stroke)

Question 81

When does blood flow to myocardium occur?

Answer 81

Coronary circulation flows during diastole (ceases during systole - contraction) → heart very good at extracting O2 70% efficient