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Physiology, Neurobiology > Heart and Circulation (26-29) > Flashcards

Heart and Circulation (26-29) Flashcards

1
Q

What is the function of the heart and circulation system?

A

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)

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2
Q

How big is a human heart?

A

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

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3
Q

Does heart beat depend on size?

A

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)

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4
Q

Where does the heart sit in the human body?

A

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

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5
Q

What is the vena cava?

A

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

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6
Q

What is the function of the pulmonary artery?

A

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

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7
Q

What is the function of heart valves?

A

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

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8
Q

Why is the wall of the right ventricle thinner?

A

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

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9
Q

Is the duration of diastole of systole longer?

A

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

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

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10
Q

What gives rise to heart sounds?

A

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

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11
Q

What does cardiac output depend on?

A

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

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12
Q

What is stroke volume?

A

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

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13
Q

What is Starling’s Law of the Heart?

A

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+

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14
Q

What type of activity does the heart show?

A

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

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15
Q

How is heart contraction co-ordinated?

A

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

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16
Q

Where is there a pause in the heart conduction pathway?

A

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

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17
Q

What does ionic pacemaker potential depend on?

A

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

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18
Q

What does the sinoatrial node pacemaker potential depend on?

A

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

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19
Q

What does the long refractory period of ventricular myocytes prevent?

A

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

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20
Q

What are myocytes?

A

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

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21
Q

How are myocytes electrically coupled?

A

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

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22
Q

What do ECG recordings detect?

A

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

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23
Q

Why does the circulatory system have different vessels?

A

To accommodate different pressures

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

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

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24
Q

What is the common structure of blood vessels?

A

(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

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25
Q

Do elastic arteries store energy?

A

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

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26
Q

What is the Windkessel effect?

A

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

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27
Q

How is blood flow pulsatile?

A

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

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28
Q

What is resistance determined by?

A

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

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29
Q

What does blood flow depend on?

A

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

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30
Q

Is blood flow laminar?

A

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)

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31
Q

What happens to flow at high velocity?

A

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

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32
Q

What are capillaries?

A

Smallest vessels comprised of only tunica intima
→ site of exchange

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33
Q

What are precapillary sphincters?

A

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

34
Q

How do capillaries optimise diffusion?

A

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

35
Q

How is permeability of molecules in capillaries determined?

A

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

36
Q

What is Starling’s forces?

A

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)

37
Q

What determines the equilibrium between plasma and interstitial fluid?

A

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)

38
Q

What does filtration/reabsorption depend on?

A

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

39
Q

Where does excess fluid from capillaries go?

A

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

40
Q

What are veins?

A

Veins are capacitance blood vessels
→ provide a reservoir of blood

41
Q

How do muscle pumps enhance venous return?

A

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

42
Q

What part of the nervous system innervates the heart?

A

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

43
Q

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

A

Sympathetic → drives heart through noradrenaline, increased rate increased conduction

Parasympathetic → slows the heart through acetylcholine, decreased rate decreased conduction

44
Q

How are chronotropic effects exerted?

A

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

45
Q

What innervates ventricular muscles?

A

Sympathetic nerves only

46
Q

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

A

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)

47
Q

Do sympathetic nerves have vasoconstrictor action?

A

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

48
Q

What neurotransmitter do sympathetic nerves release onto smooth muscle?

A

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

49
Q

How do sympathetic nerves cause vasodilation?

A

Decreasing noradrenaline release
→ dilation increases flow to capillaries

50
Q

How does noradrenaline work on smooth muscle?

A

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

51
Q

What is the baroreceptor reflex?

A

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

52
Q

Where are the baroreceptors?

A

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

53
Q

What determines mean arterial blood pressure (MAP)?

A

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

Baroreceptor reflex alters CO and TPR

54
Q

What is the long term adjustment of blood pressure?

A

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

55
Q

What does angiotensin II do that affect circulation?

A

Rapid: powerful vasoconstricter → increase in peripheral resistance and venous tone

Slow: secretion of aldosterone → retention of Na+, thirst

56
Q

What part of the heart senses filling pressure?

A

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

57
Q

What is the endocrine function of the atria?

A

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

58
Q

How can blood flow to a particular tissue be modified?

A

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

59
Q

What counters increased vasomotor tone?

A

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

60
Q

Overall what controls vessel diameter regulation?

A

Vasoconstriction → sympathetic tone, angiotensin II, ADH

Vasodilation → adenosine, K+, NO, adrenaline

61
Q

How do vessels in the pulmonary circulation differ?

A

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

62
Q

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

A

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

63
Q

How is vessel dilation in the pulmonary circuit governed?

A

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

64
Q

What does hypoxia induce?

A

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

65
Q

What are the reflexes induced by haemorrhage?

A

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

66
Q

What does haemorrhage lead to?

A

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

67
Q

During haemorrhage where do initial corrections come from?

A

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

68
Q

Why is interstitial fluid recruited during haemorrhage?

A

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

69
Q

How is loss of blood volume corrected?

A

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

70
Q

How is loss of red blood cells corrected?

A

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

71
Q

What are the classes of haemorrhage?

A

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

72
Q

What clinical intervention is used for haemorrhage?

A
  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
73
Q

What is needed for exercise?

A

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

74
Q

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

A

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

75
Q

What is the effect of adrenaline during exercise?

A

Sympathetic drive increases adrenaline

alpha receptors → vasoconstriction
beta receptors → vasodilation in skeletal muscles

76
Q

What local effects override any sympathetic vasoconstriction during exercise?

A

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

77
Q

What would occur if filling pressure increased during exercise?

A

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

78
Q

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

A

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

79
Q

How is the increased blood pressure during exercise countered?

A

Reduced total peripheral resistance

80
Q

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

A

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)

81
Q

When does blood flow to myocardium occur?

A

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

Physiology, Neurobiology (6 decks)

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