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Cardio Flashcards

1
Q

What is haematocrit

A

the percentage of blood volume occupied by red blood cells

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2
Q

what causes a high haematocrit - i.e. Polycythaemia?

A

Excessive production of RBCs and dehydration (which reduces plasma volume)

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3
Q

what causes low haematocrit?

A

anaemeia

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4
Q

sites of haemolysis

A

spleen, bone marrow, lymphnodes

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5
Q

which leukocytes are the most abundant

A

neutrophils

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6
Q

neutrophils - function and appearance

A

phagocytosis - they are the first line of defence during acute inflammation
they have multi lobed nuclei with relatively translucent cytoplasm

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7
Q

function of basophils + appearance

A

responsible for anaphylaxis - produces histamine

multi lobed and has so many purple/bluey granules you can barely see the nucleus

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8
Q

eosinophils - function and appearance

A

Combats parasitic infection and neutralises histamine.

Double lobed nucleus with bright pink eosinophilic granules.

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9
Q

what do monocytes differentiate into? and where? give some specific examples
what is their function? what do they look like?

A

they are monocytes in blood and differentiate into macrophages in tissue.
Examples: microglial cells (CNS), Kupffer cells (Liver), tissue macrophages, alveolar macrophages
Function is phagocytosis of foreign material
Large, fine white granule-looking-things, kidney shaped nucleus, kinda wobbly round the edges

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10
Q

Name the 3 types of lymphocytes and give some extra info e.g site of production and function.

A

T cells: progenitors originate in bone marrow but they migrate to and mature in thymus - have many functions but naive t cells identify specific antigens; helper t cells help activate other immune cells, produce cytokines and help B cells with antibody production; cytotoxic cells kill cells by releasing cytotoxic granules; there are also memory t cells
B cells: originate and mature in bone marrow - plasma cells produce antibodies and memory cells remain in case of reinfection
Both have large round nucleus and are agranular

Natural killer cells - kill virus infected cells
Has large round nucleus but is granulated

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11
Q

platelets: structure, function, production

A

structure: anucleate and discoid - becomes spiculated (spikey) with pseudopodia (temporary protrusions) when activated
function: produce platelet plug along with clotting factors for haemostasis

produced as fragments of cytoplasmic material derived from megakaryocytes and modulated by thrombopoeitin

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12
Q

haemostasis? primary? secondary?

A

Haemostasis is the process to prevent and stop bleeding.
Primary involves platelet plugs and the 3 As after vessel injury: Adhesion, Activation, Aggregation
Secondary: coagulation cascade and fibrin clot formation

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13
Q

What happens when vessel injury occurs?

A

Endothelial wall becomes exposed
Smooth muscle contracts to limit blood loss

Mechanisms of contraction:

  • Endothelin release
  • Nervous stimulation
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14
Q

what happens in the adhesion phase of primary haemostasis?

A

Subendothelial collagen becomes exposed

Platelets bind to collagen via vWF (von Willebrand’s factor) using their receptor GP1B

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15
Q

what happens in the activation phase of primary haemostasis?

A

Once bound to the subendothelium, platelets change shape

Platelets release alpha and electron dense granules, to escalate haemostasis process

Alpha:
vWF, Thromboxane A2, fibrinogen and fibrin-stabilizing factor

Electron-dense:
ADP, Ca2+, Serotonin

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16
Q

Aggregation

A

Lots of platelets binding to each other using GP2b/3a receptors and fibrinogen - forms platelet plug

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17
Q

The important parts of the coagulation cascade

A

Prothrombin (II) -> Thrombin (IIa) (catalysed by Xa and/or Va)
Thrombin converts Fibrinogen (I) -> Fibrin (Ia)
Fibrin is stablised by Fibrin-stabilising factor (XIIIa)
this causes a cross-linked fibrin clot to be formed

factor IV (Ca2+) is also important

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18
Q

Which factors in the coagulation cascade are Vitamin-K dependant?

A

X (precursor to what activates thrombin), IX, VII, II (Prothrombin)

Remember 1972

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19
Q

fibrinolytic pathway

A

plasminogen -> plasmin which then mediates fibrin -> fibrin degradation products (important in PE and DVT - D-Dimer??)
can be inhibited by thrombin activatable fibrinolysis inhibitor

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20
Q

types of blood transfusion.

A

homologous (emergency transfusion from other person - have to test safety, recipient serum mixed with donor blood to check for reaction)

autologous (self-transfusion)

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21
Q

blood types? how are they classified? presence of antigens and antibodies?

A

classified by presence of specific antigens and antibodies
A - A antigens and Anti-B antibodies
B - B antigens and Anti-A antibodies
AB - A and B antigens but NO antibodies (universal recipient)
O - NO antigens but has anti-A and anti-B antibodies (universal donor)

focus on antibodies for recipients, and antigens for donor suitability

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22
Q

Rhesus factor (D protein presence)

A

Rh+:

  • contains D-antigen (most immunogenic), no antibodies
  • can receive from both Rh+ and Rh-
  • only donates to Rh+

Rh-:

  • contains no antigens, and anti-D antibodies
  • can donate to both Rh- and Rh+
  • only receives from Rh-

the antibodies are not naturally occuring unlike anti-a and -b. anti-d will only be made if RH- blood comes into contact with Rh+ blood

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23
Q

formation of primitive heart tube

A

during week 3/4 the visceral mesoderm forms 2 heart tubes which then fuse. There is some craniocaudal folding which makes it look kinda like a funky shrimp. It has 5 divisions.

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24
Q

divisions of heart tube

A

truncus arteriosus: ascending aorta and pulmonary trunk
bulbus cordis: smooth outflow portion of ventricles
primitive ventricle: majority of the ventricles
primitive atrium: both auricular appendages, all of left atrium, anterior portion of right atrium
sinus venosus: smooth part of right atria where VC connects, the Vena Cava, coronory sinus

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25
Q

septation

A

(formation of atrial septum - occurs after looping of heart tube to make something kinda c shaped and more like a heart)

  1. septum primum starts developing from top - the open part is foramen primum
  2. septum primum has a bit at top and a bit in middle - top hole is foramen secundum, below is foramen primum
  3. septum primum is only at top and bottom with septum secundum forming at the top on right side of primitive heart - foramen primum completely closed
  4. septum secundem is at top and bottom now but the top part is partially going over the foramen secundum (in between the two bits of septum primum) - the part between the 2 parts of septum secundum that blood can actually flow through is the foramen ovale
  5. foramen ovale closes
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26
Q

aortic arches - time period, names , what they form

A

weeks 4-6
symmetrical, sprouts from aortic sac - 6 of them (but 6th one is actually pulmonary arteries from the pulmonary trunk)

I - maxillary
II - stapedial
III - common carotids and proximal part of internal carotids (distal part made from extensions of dorsal aortae)
IV - aortic arch and right subclavian (both sides join with 7th intersegmental)
V - regresses completely
VI - pulmonary arteries and ductus arteriosus on left
7th segmental arteries (not an aortic arch) form the left subclavian and part of right subclavian

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27
Q

extra embryology facts

A

Heart appears in 3rd week (starts beating ~day 23)

Constriction of ductus arteriosus > ligamentum arteriosum 10-15 hours after birth

Obstetrical climbing = constriction of umbilical vein > ligamentum teres

Increase L atrial pressure & decreased R atrial pressure due to first breath causes foramen ovale to close > fossa ovalis

Ductus venosus constricts > ligamentum venosum shortly after birth

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28
Q

membrane potential definition

A

the difference in electrical potential between the interior and exterior of a cell

e.g. if inside is +1 and outside is 0 the membrane potential is +1
if inside is 0 and outside is +1 the membrane potential is -1

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29
Q

membrane potential of cardiac myocyte at rest

A

-90mV

more positive outside cells

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30
Q

is a cardiac action potential longer or shorter than in skeletal muscle

A

cardiac action potential is around x100 linger than in skeletal muscles. Voltage gated Ca2+ channels open more slowly and stay open longer than Na+ channels (sometimes called L-type Ca2+ channels i.e. long lasting or dihydropyridine - target of amlodipine treatment - antihypertensive)

skeletal muscle action potential is a spike, cardiac myocyte action potential is more like a wiggly water slide that peaks lower and slightly after the skeletal action potential

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31
Q

action potential/cardiac cycle phases

A

phase 4: resting phase - -90mV. SAN generates an action potential which causes depolarisation. If it reaches the threshold, phase 0 starts.

phase 0: depolarisation - threshold (-60mV) reached and Na+ channels open.

phase 1: partial repolarisation - at +30mV Na+ channels close and there is transient K+ channels open allowing K+ out of the cells

phase 2: plateau - L-type Ca2+ channels open to allow an influx of Ca2+ into the cell to balance the efflux of K+

phase 3: repolarisation - Ca2+ channels close allowing repolarisation

there is a bit of overshoot and over polarisation which is when the refractory periods happen

phase 4: resting

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32
Q

In what phase of the cardiac cycle does contraction occur?

A

phase 2 - contraction occurs when there is a calcium influx

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33
Q

refractory periods

A

absolute refractory period - when the cell is completely unexcitable (longer for myocytes than skeletal muscle)

relative refractory period - when the cell can be depolarised by a greater than usual stimulus

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34
Q

where is the sinoatrial node located? what does it do? what is it modulated by?

A

in the right atrium - it is the primary pacemaker (rate of discharge: 60-100/min) - vagus stimulation decreases rate, noradrenaline from sympathetic nerves increases rate

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35
Q

pacemaker potential

A

There is no resting baseline line in normal depol/repol. No plateauing.

Phase 4 equivalent - prepotential: slow influx of Na+ through HCN channels (hyperpolarisation activated cyclic nuclotide gated channels - permeable to K+) - slow depol from -60mV to -40mV

Phase 0 equivalent - depolarisation: influx of Ca2+ through voltage-gated t type channels (specifically found in heart condutive cells) - -40mV -> +10mV

Phase 3 equivalent - repolarisation: Ca2+ channels close and voltage-gated K+ channels open - +10mV -> -60mV (at which point f type Na+ channels open again - they open at most negative membrane potential)

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36
Q

which cells act as pacemakers in heart - what do they do

A

pacemakers are responsible for automacity of heart. Nodal cells generate the pacemaking potential (1%?)

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37
Q

sympathetic stimulation of pacemaker potential

A
  • noradrenaline binds to beta-1 receptors - increases Ca2+ channels opening - faster depol
  • steeper phase 0
  • increased heart rate and force of contraction
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38
Q

parasympathetic (vagal) simulation of pacemaker potential

A
  • Ach activates K+ channels - hyperpolarises membrane - takes longer to reach treshold potential
  • reduces influx of clacium so slower depolarisation (shallower slope of phase 0)
  • decreases heart rate
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39
Q

excitation-contraction coupling

A

Wave of depolarization (AP) spreads into myocytes via T tubules.

L-type Ca2+ channels open πŸ‘ͺ Ca2+ enters the muscle cell

Ca2+ binds to Ryanodine Receptor πŸ‘ͺ release of more Ca2+ from Sarcoplasmic Reticulum (Ca2+ induced Ca2+ release.)

Ca2+ binds with Troponin which uncovers active site on tropomyosin

Cross-bridge cycling = Muscle contraction

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40
Q

What causes contraction in excitation-contraction coupling?

A

The presence of Ca2+ in the cytosol. Force of contraction is directly proportional to cytosolic Ca2+ levels.

drugs and chemicals that increase cardiac contractility (like adrenaline, Digoxine, cardiac glycosides) are increasing the levels of cytosolic Ca2+

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41
Q

Electrode and lead (for ECG) definitions

A

Electrode is the object placed on the body to pick up electrical signals
A lead is a specific plane in which you are observing the heart

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42
Q

shapes of ECG graphs

A

+ve going to a positive electrode = curve goes up
+ve to -ve electrode = curve goes down (as in it is inverted/peaking underneath the baseline instead of above it)
-ve to +ve electrode = curve goes down

if the charge is going at an angle and so only part of the vectored charge is picked up (e.g. like how a thrown ball has a horizontal and vertical part that combines to form the final vectored trajectory) - then the curve will just be shorter but the same width and shape

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43
Q

list all the ECG leads

A

6 limb leads:

I - goes from right arm (-ve) to left arm (+ve) - bipolar - (the leaving part is always negative and receiving part is positive)
II - from right arm (-ve) to left leg (+ve) - bipolar
III - left arm (-ve) to leg (+ve) - bipolar
aVR - right shoulder - unipolar
aVL - left shoulder - unipolar
avF - left ankle - unipolar

6 chest leads:
Lead V1 – 4th IC space to right of sternal border
Lead V2 – 4th IC space to the left of sternal border
Lead V3 – midway between V2 and V4
Lead V4 – 5th IC space, mid-clavicular line
Lead V5 – anterior axillary line at same level as V4
Lead V6 – midaxillary line at same level as V4 and V5

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44
Q

Key parts of ECG:

A

P wave - atrial repolarization.
QRS - ventricular depolarisation.
T wave - ventricular repolarization.

PR segment - delay in AVN
ST segment - plateau phase of ventricular repolarization.

PR interval - atrioventricular conduction time - this is when atrial systole happens
QT interval - Total ventricular contraction during systole.

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45
Q

What is a segment in ECG

A

A period of isoelectric neutrality

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46
Q

What is an interval in ECG

A

A region including magnitude

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47
Q

what is the ejection fraction

A

the proportion of the EDV that is pumped out the LV per beat, SV/EDV, provides an indication of the contractility of the heart

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48
Q

what percentage of blood passively fills the lungs?

A

70-80% - during diastole - helps equalise pressure

49
Q

what is the atrial booster?

A

atrial systole - it pushes the remaining blood into the ventricle - PR interval

don’t forget that this is an important part of ventricular diastole

50
Q

what percentage of blood ejected during maximal ejection?

A

65-75% of blood in the ventricles (then reduced ejection happens)

51
Q

What can passive ventricular filling be split into

A

rapid inflow - to equalise pressure - most of the blood entres here
diastasis - the slow ventricular filling that occurs afterwrds when pressure is nearly equalised

52
Q

what factors affect stroke volume?

A

preload, afterload, contractility, (heart rate?)

53
Q

what occurs during the Frank-Starling curve (in the heart)?

A
  1. Increased stretch opens stretch-sensitive calcium channels= increased cytosolic calcium 👺 increased force of contraction
  2. Stretch enhances affinity of troponin C for calcium 👺 increased force of contraction

After maximum stretch reached:

Little overlap between actin and myosin 👺 lots of unbound myosin heads 👺 decreased force of contraction 👺 decreased stroke volue (curve starts going down)

54
Q

factors that affect preload?

A

venous return, heart rate, ventricular compliance, atrial contractility, valvular resistance

55
Q

inotropy meaning

A

relates to force of contraction

56
Q

chronotropy meaning

A

relates to heart rate

57
Q

what happens in increased contractility?

A

+ve inotropy -> Increases Force of Contraction πŸ‘ͺ increases SV

58
Q

what are some positive inotropic agents?

A

Sympathethic nervous system
Hormones: adrenaline, thyroxine
Drugs: e.g. Digoxin

59
Q

decreased contractility

A

-ve inotropy -> decreased force of contraction -> decreased SV

60
Q

negative inotropic agents?

A

Parasympathetic nervous system, Drugs: e.g. Ξ²-blockers

61
Q

factors affecting afterload

A

valvular diseases, TPR, Aortic pressure

SVR/TPR: mainly determined by radius of vessels

Vasodilation πŸ‘ͺ Decreased resistance πŸ‘ͺ decreased afterload
Vasoconstriction πŸ‘ͺ Increased resistance πŸ‘ͺ increased afterload

Aortic pressure:

Increased aortic pressure = increased LV pressure (hypertension) πŸ‘ͺ increased afterload
Decreased aortic pressure = decreased LV pressure (hypotension) πŸ‘ͺ decreased afterload

Valvular diseases:

Mitral valve regurgitation πŸ‘ͺ decreased LV wall stress πŸ‘ͺ decreased afterload
Aortic stenosis πŸ‘ͺ Increased LV pressure πŸ‘ͺ Increased afterload

62
Q

afterload definition

A

ventricular wall stress during sytole

63
Q

blood pressure definition

A

the pressure exerted by blood on a given vessel surface area

64
Q

pressure equation

A

Ξ”P = Pi – Pf

Pi = MAP (mean arterial pressure)

Pf = CVP (venous pressure)

or Ξ”P = Q x TPR

65
Q

systolic pressure definition

A

point when LV pressure during ejection = aortic pressure during ejection

66
Q

diastolic pressure

A

Pressure caused by recoiling of arteries during diastole

67
Q

pulse pressure equation

A

PP = SP - DP

68
Q

Mean arterial pressure equation

A

MAP = 1/3(PP) + DP or MAP = DP + 1/3(SP - DP)

MAP = CO x TPR

69
Q

blood flow definition

A

The volume of blood that flows through the systemic circulation per unit of time

(it is equal to cardiac output)

70
Q

velocity of blood flow equation

A

V = Q/A

71
Q

Types of blood flow

A

Laminar:

Smooth, streamlined flow

Turbulent:

Disruption to laminar flow (e.g. decrease in vessel diameter)
Produces Korotkoff sounds

72
Q

what affects viscosity of blood

A

haematocrit:
anaemia = decreased viscosity
polycythaemia = increased viscosity

73
Q

resistance equation

A

8nl/pi r^4

74
Q

Poisueille’s equation (this thing seems to change depending on what source I look at so just use whatever’s in the question)

A

change in pressure combined with resistance

Q = (Pi - Pf)pi r^4 / 8nl

75
Q

what mainly determines resistance in a healthy individual

A

vessel radius

76
Q

what is blood volume controlled by

A

RAAS - renin-angiotensin-aldosterone system

77
Q

Intrinsic control of BP

A

Myogenic autoregulation

Self regulation of arterioles based on stretch experienced - if pressure increased in an arteriole, it would constrict to decrease flow and so pressure

Local mediators

Hormones, nerves, local autocrine and paracrine agents.

78
Q

local vasoconstrictors of arterioles

A

Endothelin-1, internal pressure

79
Q

local vasodilators of arterioles

A

Prostacyclin

Hypoxia (only in systemic circulation)

Tissue factor

NO/EDRF (endothelium derived relaxing factors - one of which is nitrc oxide)

H+/K+/Ca2+

Adenosine

Bradykinin

80
Q

Extrinsic control of BP

A

Humoral factors

Baroreceptors

Neural control

81
Q

Circulating hormonal factors - vasoconstriction and vasodilation

A

Vasoconstrictors - adrenaline (ALPHA adrenergic receptors), angiotensin II, ADH

Vasodilators - Atrial Natriuretic Peptide, adrenaline (BETA 2 adrenergic receptors)

82
Q

Baroreceptors - function, location, nerves involved

A

Pressure receptors that control short term change in BP.

Found in carotid sinus and aortic arch

afferent neurons from CN IX and CN X (glossopharyngeal and vagus) travel to medulla oblongata.
efferent neurons (SNS/PSNS) travel to heart and vessels
83
Q

How do baroreceptors work? give an example

A

They are constantly firing and if BP drops then they decrease their discharge rate.

e.g. in a haemorrhage - BP drops

sends signals to medulla which acts through nts and vmc (vasomotor centre) to:

Increase sympathetic activity 
Raise HR (and CO) 
Increase contractility (and CO)
Cause arteriolar vasoconstriction due to innervation and raised angiotensin II (increased TPR)
Decrease parasympathetic activity 
Raise HR (and CO)
84
Q

which nerves involved with baroreceptor reflex

A

vagus (recieves input from aortic arch) and glossopharyngeal

85
Q

What is a universal plasma donor?

2-What ion is responsible for the major depolarization in nodal cells?

3- What is serum?

4-What enzyme is responsible for clot breakdown?

5-Which of the following clotting factors are not vitamin K dependent?

a) X
b) II
c) IV
d) VII

6-Which protein can be measure in the blood as a sign for myocardial infarctions?

7-Which type of vessel is responsible for the total peripheral resistance for the systemic circulation?

8-Which cranial nerve receives input from aortic arch baroreceptors?

9-Which of these is not a factor of cardiac preload?

a) Venous return
b) Atrial contractility
c) TPR
d) Heart Rate

10-Which ECG event corresponds to atrial systole?

A

1-Type AB+

2-Calcium

3-Blood plasma without clotting factors

4-Plasmin

5-C

6-Trop T

7-Arterioles

8-CN X

9-C

10-PR interval

86
Q

Where do the SA and AV nodes lie

A

SA node - upper wall of right atrium

AV - bottom of right atrium on the septum

87
Q

What does right coronary artery supply

A

Right atrium and part of ventricle

SA node in 60% of people and AV node in 90% of people

88
Q

what does right marginal artery supply

A

right ventricle

apex

89
Q

What does posterior intraventricular artery supply

A

part of right and left ventricles
posterior 1/3 of IVS
AV node (PIV always supplys AV node so AV node proportions mirror PIV proportions in the population)

90
Q

What does left coronory artery supply

A

left atrium and ventricle
IVS and part of right ventricle (from LAD)
at least some part of the AV bundles
SA node in 40% of people, AV node in 30% of people

91
Q

what does left anterior descending supply

A

left and right venricles (anterior aspect)

anterior 2/3 of IVS

92
Q

what does left marginal supply

A

left ventricle

93
Q

what does circumflex artery supply

A

left atrium and ventricle

94
Q

percentages of population that has right-, left- and co-dominent coronary circulation

A

70%, 10%, 20% respectively

so 90% of population have PIV coming from RCA and 30% has PIV from LCA

95
Q

where is the apex of the heart/mitral valve sound found?

A

left midclavicular line - 5th intercostal space

96
Q

where do you hear aortic valve sound, pulmonary valve sound and tricuspid valve sound

A

aortic - 2nd intercostal space - right sternal border
pulmonary - 2nd intercostal space - left sternal border
tricuspid - 5th intercostal space - right sternal border

97
Q

Phrenic nerve: roots, modality of innervation, what it innervates, path through thorax

A

C3, 4, 5
Motor and sensory
diaphragm

Right Phrenic nerve;
Descends ANTERIORLY (phrenic, front) along R lung root
Travels along pericardium of R atrium
Passes through diaphragm at IVC opening (T8)

Left Phrenic nerve
Descends ANTERIOR to L lung root
Crosses aortic arch, bypasses vagus nerve
Travels along pericardium of L ventricle
Passes through diaphragm separately
98
Q

Vagus nerve: roots, modality of innervation, what it innervates, path through thorax

A

CN10
motor and sensory; parasympathetic and sympathetic
Parasympathetic to ALL orgens of thorax and abdomen - gives of superior laryngeal branch to supply thyroid, and recurrent laryngeal loops around aorta or subclavian to supply larynx

Passes behind nerve roots, passes through diaphragm at T10

99
Q

what type of artery is the aorta?

A

elastic artery

100
Q

why are arterioles the main source of TPR? (aka why don’t other vessels contribute as much to TPR?)

A

The media of large arteries are more elastic than the smaller arteries, which have more muscle

Capillaries are fenestrated (have holes) so things can easily flow in/out

Capillaries also have pericytes which are involved in the regulation of blood flow

101
Q

Layers of artery wall (and arterioles), from lumen out

A

Endothelium, basement membrane, intima, internal elastic lamina, media, external elastic lamina, adventitia

arterioles are the same but without the external elastic lamina

102
Q

Layers of vein wall and venule, lumen out

A

Endothelium, basement membrane, intima, media, adventitia

same for venule

103
Q

why are veins capacitence vessels?

A

they hold up to 70% of blood volume - normally

104
Q

pulmonary circulation pressure

A

20/8

105
Q

systemic circulation pressure

A

120/80

106
Q

average cardiac output

A

~5-6L

107
Q

average stroke volume

A

~70mL

108
Q

average heart rate

A

60-100 beats per minute

109
Q

average end diastolic volume

A

~130ml

110
Q

average ejection fraction

A

65%

111
Q

average end systolic volume

A

~50ml

112
Q

Factors affecting cardiac output

A

Anything that affects stroke volume or heart rate

Age, Gender, Pregnancy, Exercise, Emotions, Posture, Sweating

(AG PEEPS)

113
Q

What does the Frank Starling law dictate about force of contraction

A

Within PHYSIOLOGICAL LIMITS, the force of contraction is directly proportional to initial length of muscle fiber.

114
Q

tamponade meaning

A

when pericardium fills with blood or fluid - increased pressure on heart can contract as easily

115
Q

What does venous return depend on?

A

skeletal pump activity, ECF volume, sympathetic activity-venoconstriction

116
Q

what does atrial pump activity depend on

A

Atrial contraction increases due to sympathetic activity

117
Q

What factors affect myocardial contractility?

A

More ventricular muscle mass increases contractility
Sympathetic stimulation increases ventricular contractility, Parasympathetic decreases
Hormones- thyroxine increases left ventricle contractility
Drugs and chemicals- caffeine, digoxin (both increase)

118
Q

Factors affecting heart rate

A

Influence mainly by autonomic activity
Vagal stimulation decreases HR, Sympathetic stimulation increases HR.

Tachycardia does not necessarily mean a proportionate increase in CO as duration of diastole SHORTENS, meaning ventricles have less time to be filled= EDV decreases/does not increases as much AS EXPECTED. vice versa in bradycardia.

119
Q

what is the reason for SA node automacity/pacemaker potentials?

A

spontaneos diastolic depolarisations (Phase 4) - caused by HCN Na+ channels which open when hyperpolarised

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