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BIOM2012 (1, 2, 3, & 6) > 2 - cardiovascular > Flashcards

2 - cardiovascular Flashcards

1
Q

formula for cardiac output

what is the minimum cardiac output?

A

cardiac output = heart rate x stroke volume

CO = HR x SV

minimum is at least 5L per minute

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2
Q

compare cardiac and skeletal muscle

A

both skeletal and cardiac:
– straited appearnace
– electrically excitable
– similar contractile response

cardiac cells are interlocked by intercalated discs. cardiac cells are both mechanically (desmosome) + electrically (gap junctions) connected
∴ heart cells function together = contract in sequence = “functional syncytium”
cardiac cells generate own AP = autorhythimcity

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3
Q

draw a diagram representing AP and contractile response in a cardiac cell

include flow of ions

include definitions and values for ARP and RRP

what do these values mean for the function of cardiac cells?

A

ARP = absolute refractory period
= period where second AP cannot be generated
= 0.25 - 0.30 s

RRP = relative refractory period
= interval immediately after ARP where initiation of second AP is inhibited but no impossible
= 0.05 s

summation and tetanus is prevented

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4
Q

describe the flow of electrical conduction in the heart

A

pacemakers in SA node of right atrium generate AP

spreads through right atrium and into left atrium

conducting pathways spread to AV nodes and through to ventricles

spread to apex of heart

purkinje fibres spread up sides of ventricles

pathway allows rapid propagation of AP

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5
Q

draw a diagram and table representing APs in different areas of the heart:
– autorhythimcity
– conduction speed
– function

what is responsible for these differences

A

Differences due to ion channel subtypes present in each cell

SA + AV nodes have unstable resting MP due to slow influx of Na+ and entry of calcium from T-tubules

SA NODE:
autorhythimcity = yes
conduction speed = slow
function = pacemaker
ATRIAL MUSCLE:
autorhythimcity = no
conduction speed = fast
function = atrial contraction
AV NODE:
autorhythimcity = yes
conduction speed = slow
function = secondary pacemaker
PURKINJE FIBRES:
autorhythimcity = yes
conduction speed = very fast
function = conduction of electrical signal / tertiary pacemaker
VENTRICULAR MUSCLE:
autorhythimcity = no
conduction speed = fast
function = ventricular contraction
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6
Q

draw a diagram representing a typical ECG wave

A

P wave = depolarization of the atria

QRS complex = represents depolarization of the ventricles

T wave = repolarization of the ventricles

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7
Q

how is cardiac output regulated?

A

vagus nerve innervates pacemaker regions of SAN and AVN via ACh

sympathetic nerves innervate whole heart (wide-spread)
• pre-ganglionic neurotransmitter = acetyl choline
• post-ganglionic neurotransmitter = noradrenaline

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8
Q

how does the parasympathetic nervous system effect cardiac output?

A

In PNS, ACh acts on muscarinic receptors in cardiomyocytes to:
• slow pacemaker depolarisation and weaken contraction
• slow closure of K+ channels
• resting K+ leakage is increased → hyperpolarisation → slower depolarisation
• slows opening of Ca2+ channels → slower depolarisation

  1. acetylcholine decreases activity of I(f) channel to slow depolarisation
  2. acetylcholine opens GIRK (G protein inward rectifying K+) channels. potassium conductance increases resulting in hyperpolarisation
  3. acetylcholine reduces calcium influx to slow depolarisation. this also reduces calcium availability to weaken atrial + ventricular contraction

OVERALL:
SA node = overall slows pacemaker activity = ↓HR
AV node = decreases node excitability = longer AV delay
Atria = weakened contractions
Ventricles = “ “

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9
Q

how does the sympathetic nervous system effect cardiac output?

A

SNS acts on adrenergic receptors (particularly β1-adrenoreceptors) in cardiomyocytes to:
• innervate SA and AV nodes and non-pacemaker contractile cells
• decrease K+ permeability
• noradrenaline increases inward calcium current
• noradreanline decreases K+ permeability → accelerates inactivation of K channels → rapid drift to threshold → increased depolarisation rate

  1. adrenaline/noradrenaline oppose ACh by increasing activity of I(f) channel = faster depolarisation
  2. adrenaline/noradrenaline oppose ACh by increasing activity of I(Ca) channel = faster depolarisation

** adrenaline/noradrenaline do not effect maximum diastolic potential

SA node = overall increases pacemaker activity = ↑HR
AV node = increase node excitability = shorter AV delay
strengthens ventricular and atrial contractions

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10
Q

draw a diagram comparing the parasympathetic and sympathetic regulation on CA by acting on different receptors

A

PARASYMPATHETIC:
ACh binds to M2 receptor (GPCR)
G-protein inhibits adenylyl cyclase

SYMPATHETIC:
noradrenaline binds to beta-1 receptor (GPCR)
G-protein stimulates adenylyl cyclase

active adenylyl cyclase —> ATP to cAMP —> activates PKA
activation of PKA increases calcium influx to modulate both heart rate and force of contraction

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11
Q

formula for stroke volume

what is stroke volume at rest?

A

stroke volume = ventricular end-diastole volume - ventricular end-systole volume

SV = EDV ESV

EDV = volume when fully relaxed = 125mL

ESV = volume when fully contracted = 55mL

∴ SV = 125 - 55 = 70mL

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12
Q

how is EDV intrinsically controlled?

A

FILLING PRESSURE
• ↑ blood flow = ↑ return to atria = ↑ atrial + ventricular pressure
• ↑ pressure causes ventricular walls to expand a greater extent
• ↑ EDV

FILLING TIME
• more time to fill up
• ↑ EDV

VENTRICULAR COMPLIANCE
• state of cardiomyocyte contraction i.e. how easy it can expand
• ventricle can expand and fill more at same pressure
• ↑ EDV

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13
Q

what does the “frank-starling law” state?

A

amount of blood pumped out of the heart is proportional to the amount pumped in

the larger EDV, the larger SV (less ESV)

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14
Q

how is ESV intrinsically controlled?

A

PRE-LOAD
• increase of the EDV increases the stretch on the cardiac muscle
• increases contractility (greater stretch = greater ejection)

AFTER-LOAD
• increased pressure at ventricular outlet
• increases the force of the contractility required to pump the same volume

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15
Q

how is contractility extrinsically controlled?

A

contractility is extrinsically controlled by iontropic agents

POSITIVE CONTROL:
• catecholamines act on β-adrenoreceptors to ↑Ca2+ influx = stronger contraction
• cardiac glycosides block Na-K ATPase

NEGATIVE CONTROL:
• beta blockers block adrenoreceptors
• diltiazem/verapamil blocks calcium channels
• = weaker contraction

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16
Q

list some factors that effect resistance to blood flow?

A

vessel radius

vessel length

viscosity of blood

type of blood flow / geometry of blood vessel

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17
Q

relationship between flow and resistance

A

flow inversely proportional to resistance

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18
Q

relationship between flow and pressure

A

flow directly proportional to pressure

19
Q

why doesn’t arterial pressure drop to 0 mmHg during diastole (no flow into arteries)?

A

elastic properties of arterial walls prevent pressure from dropping to 0mmHg

artery walls contract during diastole = provides driving force which continues to project blood forward

20
Q

how is arteriolar diameter controlled intrinsically (locally)?

A

METABOLIC FACTORS
• O2 = constriction
• CO2 = dilation

LOCAL SIGNALS
• nitric oxide = dilation
• histamine = dilation 
• endothelin = constrict 
• prostaglandins = both

LOCAL TEMP
• heat = dilate
• cole = constrict

INCREASED STRETCH
• myogenic response (muscle)

21
Q

TRUE OR FALSE

extrinsic factors override intrinsic factors in the control of arteriolar diameter

A

FALSE

intrinsic (local) factors override extrinsic factors in the control of arteriolar diameter

22
Q

how is arteriolar diameter controlled extrinsically?

A

AUTONOMIC NERVOUS SYSTEM
• SNS releases NA which acts on ⍺1-adrenoreceptors to induce vasoconstriction
• SNS releases A from medulla which acts on β2-adrenoreceptors to induce vasodilation

ENDOCRINE
• angiotensin/vasopressin = vasocontriction
• bradykinn = vasodilation

23
Q

how is fluid exchange across capillaries facilitated?

A

exchange achieved by passive diffusion and bulk flow

passive diffusion of solutes down concentration gradient

bulk flow of extracellular fluid between vascular and interstitial compartments

24
Q

what is an oedema?

A

abnormal accumulation of interstitial fluid

reduced plasma proteins:
e.g. renal disease or liver cancer
→ favours filtration → oedema

increased permeability of capillary walls
e.g. local inflammation, allergies
→ more plasma protein in ISF → increased osmotic pressure (outward pressure gradient) → favours filtration → oedema

increased venous pressure
e.g. congestive heart failure
→ favours filtration → oedema

blockage of lymph vessel
e.g. surgical removal of lymph nodes in cancer
→ reduced capacity of lymph drainage → accumulation of ISF → oedema

25
Q

what are the consequences of oedema?

A

excess interstitial fluid

increased distance between blood and cells

decreased rate of diffusion

inadequate nutrient supply/removal of waste

26
Q

what type of receptors detect high pressure in order to regulate blood pressure?

A

baroreceptors are mechanoreceptors which detect changes in pressure

located in carotid sinus (detect pressure of blood entering brain) and aortic arch (detect pressure of blood entering systemic circuit)

baroreceptors involved in moment-to-moment (short-term) regulation of blood pressure

regulate HR, SV and resistance to maintain relatively constant arteriol pressure

27
Q

where is the “cardiovascular control centre”?

afference and efference?

how does it regulate CO?

A

cardiovascular control centre located in medulla

afference = baroreceptors
efference = both parasympathetic (vagus nerve) + sympathetic neurons change to correct situation

increase in mean arterial pressure = detected by baroreceptors = efferent pathway activated = CO decreased

28
Q

draw a flow diagram of the baroreceptor reflex

A
  1. blood pressure elevates
  2. ↑ receptor potential in aortic arch and carotid sinus
  3. ↑ rate of firing in afferent nerves
  4. cardiovascular centre
  5. ↓ sympathetic cardiac/vasoconstrictor nerve activity
    ↑ parasympathetic nerve activity
  6. ↓ HR, ↓ SV
    vasodilation
  7. ↓ CO and ↓ resistance
  8. blood pressure decreased towards normal
29
Q

briefly describe the brain-bridge reflex and the chemoreceptor reflex

A

BRAIN-BRIDGE
• low volume/stretch receptors in atria (and vena cava) detect blood flow coming back to heart and increase HR to compensate
• prevents damming of blood in veins, atria & pulmonary
circuit

CHEMORECEPTOR
• occurs in aortic arch and carotid bodies (like baroreceptors), but also centrally in medulla
• detect low O2, high CO2, high H+
• increase respiratory drive + MAP

30
Q

briefly describe how hormones can regulate blood pressure

A 
noradrenaline/adrenaline:
– from adrenal medulla
– vasoconstriction
– increase HR and CO
– increase veinous return

ADH (vasopressin):
– released from posterior pituitary gland
– regulate water retained in kidneys
– ↑ water retension = ↑ blood volume = ↑ CO

angiotensin:
– potent vasoconstrictor
– increase CO

31
Q

what is hypertension?

describe the causes, symptoms and treatments

A

high blood pressure > 140/90 mmHg

caused by:
• essential hypertension = genetics, diet, salt intake, obesity, insulin resistance, ageing, stress, sedentary lifestyle
• secondary hypertension = occurs due to a primary problem = renal - vascular – endocrine system disorders, obstructive sleep apnea

treatments include diuretics (thiazides), beta blockers, angiotensin converting enzyme inhibitors or receptor blockers, dietary and weight management

32
Q

why don’t baroreceptors resolve high blood pressure in hypertension?

A

baroreceptors operate around a set point

in hypertension, set point becomes higher i.e. baroreceptors maintain a higher MAP

33
Q

describe the structure, location and function of the cardiac ryanodine receptor (RyR2)

A

cardiac ryanodine receptor (RyR2) is a large tetrameric protein that forms a channel between the lumen of the SR and the cytosol of the myocyte (skeletal muscle)

RyR2 facilitates muscle contraction:
– at rest, RyR2 won’t let calcium out of SR (some can leak out)
– when it’s time to contract, RyR2 lets calcium out into SR
– phosphorylation of receptor causes it to open

cytosolic + SR proteins sit alongside RyR2 to stabilise it

these proteins don’t attach to every single receptor ∴ some receptors more prone to movement

34
Q

TRUE OR FALSE

spontaneous calcium release through RyR2 is triggered by the L type calcium channels

A

FALSE

spontaneous calcium release through RyR2 is NOT triggered by the L type calcium channels

spontaneous calcium release caused by:
– hyperphosphorylation of RyR2
– store overload

35
Q

how does the RyR2 receptor respond to heart failure?

A

during heart failure, heart is becoming weaker

weak heart tries to maintain function

brain sees that heart is not meeting demand ∴ gives heart low-level stress response to increase heart function

PKA phosphorylating RyR2 in many places —> destabilising channel

these phosphorylations remove some of the stabilising proteins

RyR2 receptor becomes more open = calcium leaks out of channel = diastolic Ca2+ leak

36
Q

how does a myocyte respond to calcium store overload?

A

heart failure = calcium elevated for a long time

how to clear calcium from cytosol?
– 3Na+/Ca2+ exchanger
– CIRCA —> back into SR —> uses energy

3Na+/Ca2+ exchanger limited because it must bring sodium in —> cannot put that much sodium into cell when there are high levels of calcium

CIRCA takes extra calcium and pumps it into SR

SR over-filled with calcium = RyR2 receptor leaks calcium = STORE OVERLOAD INDUCED CALCIUM RELEASE (SOICR)

each RyR2 receptor has different threshold to SOICR due to stabilising proteins

37
Q

TRUE OF FALSE

action potential propagates uni-directionally

A

true :P

38
Q

how does triggered arrhythmia differ from normal electrical conduction?

A

in triggered arrhythmia, local calcium leak triggers an electrical impulse between normal contractions

the cells ahead of that impulse are in their refractory period HOWEVER the ones behind aren’t

∴ the signal moves backwards and interferes with the next contraction

39
Q

what is CPVT?

A

catecholaminergic polymorphic ventricular tachycardia

sudden cardiac death:
– induced by stress response
– underlying cause is a mutation of a protein
– type of arrhythmia

associated with mutations in RyR2

40
Q

how does defibrillation work?

A

application of electrical shock ‘resets’ AP of all myocytes

all myocytes depolarise at once to reset and re-coordinate APs

shock must be sufficient to depolarise every cell simultaneously

next stimulated action potential can now propagate normally through the tissue

41
Q

list and briefly describe the classes of anti-arrythmic drugs

A

CLASS 1:
alter AP via Na+ channels

CLASS 2:
block β-receptors to reduce phosphorylation

CLASS 3:
alter AP via K+ channels

CLASS 4:
block Ca2+ channels

42
Q

what is the β-adrenergic signalling cascade?

A

adrenaline binds to and activates β-adreneroreceptor

G-protein activates

G-protein activates adenylate cyclase

adenylate cyclase increases [cAMP]

cAMP activates protein kinase A

43
Q

what are the pros and cons of beta-blockers?

give two examples of beta-blockers

A

PROS
– effective at preventing arrythmias
– e.g. metoprolol and carvedilol (also stabilises RyR2)

CONS
– low compliance
– slow HR does not increase during exercise = reduced quality of life
– people stop taking drug as they “feel better” without it

BIOM2012 (1, 2, 3, & 6) (4 decks)

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