Exam Flashcards
(137 cards)
1
Q
Where is the endogenous rhythm generator
A
Sinoatrial node - where depolarisation is initiated & electrical pulse is generated
2
Q
How is heart rate controlled by the autonomic system
A
SA node is stimulated by:
1) sympathetic NS = release of noradrenaline = stimulation by binding to beta-1 adrenergic receptors = activate PKA which causes increase Ca2+ entry into nerve terminal via L-type Ca channel = greater contraction = increased heart rate
2) parasympathetic NS = release of Ach = stimulation by binding to M2 receptors = decreases HR
(There’s a balance bw systems - when you sleep PNS releases more Ach to decrease HR)
3
Q
Whats the myocardium
A
Muscular wall of the heart (made up of cardiomyocytes - which can’t divide in adults but can in kids)
4
Q
Know the M line, Z line arrangements thingy
A
5
Q
As tension (force generated) increases…
A
Muscle length increases up until a maximum where thick and thin filaments have no overlap
6
Q
What does
a) more preload
b) more afterload
Mean
A
a) increased filling of the ventricles
b) more resistance that the heart must overcome to eject blood (could lead to heart failure)
7
Q
Whats preload and afterload
A
Preload = The initial stretch of the heart muscle fibers at the end of diastole, just before contraction. Known as end-diastolic volume, EDV
Afterload = The resistance the heart must overcome to eject blood during systole (contraction) - represents how tight or relaxed the blood vessels are
8
Q
Whats Frank-starling curve
A
illustrates how the heart’s stroke volume increases in response to an increase in the volume of blood filling the heart (the preload) — up to a certain point.
9
Q
Whats LVEDP
A
Left ventricular end diastolic pressure = measure of preload
10
Q
What are the 3 subtypes of troponin
A
Troponin C
Troponin I
Troponin T
11
Q
How does contraction occur in heart muscle
A
The heart as a pump - green section
12
Q
Where is Ca2+ stored
A
The sarcoplasmic reticulum
13
Q
What inhibits SERCA
A
Phospholamban
14
Q
What occurs during a myocardial infarction
A
Blood clot blocks one of the CORONARY arteries = myocardium no longer receives oxygen = ischemia = mitochondria can’t generate ATP = all ATP dependant pumps will be inhibited
Ca accumulates in cardiomyocyte = heart muscle can’t relax = cell death and cardiomyocyte dies due to Ca2+ overload (can induce arrhythmia)
15
Q
What are the 3 main stages of cardiac cycle
A
1) isovolumetric ventricular contraction
2) ventricular ejection
3) ventricular filling
(The heart as a pump pink section)
16
Q
How does depolarisation work in the heart
A
AP generated by SA node which causes a wave of depolarisation that travels from the atrium to the ventricles and back up again (apex to septum to apex again)
17
Q
Why does pressure continue to increase in isovolumetric ventricular contraction even after the aortic valve opens
A
Because the ventricles contract to push blood out into the aorta
18
Q
What are the 4 sounds of the heart
A
S1 closure of AV valves
S2 closure of aortic and pulmonary try valves (splits in young adults but its normal)
S3 blood filling the ventricles, tensing if chordae
S4 atrial systole
19
Q
Whats stenosis and what does it cause
A
Narrowing of (usually referring to a blood vessel)
Causes turbulence
20
Q
What disease can the pressure volume loop identify
A
Go over the pv loops - heart as a pump green
1) dilated cardiomyopathy
2) left ventricular hypertrophy
3) aortic stenosis
4) aortic regurgitation
21
Q
Whats the equation for cardiac output
A
O2 consumption / arteriovenous O2 content difference
22
Q
What does the area of the pv loop graph tell us
A
Amount of work the ventricles put in to achieve cardiac output
23
Q
What resistance vessels are responsible for bp regulation
A
arteries and arterioles bc they contain higher amounts of smooth muscle which regulates diameter of blood vessels
24
Q
1) Where is flow velocity greatest and 2) where is vascular resistance the greatest and 3) what makes capillaries efficient for gas exchange
A
1) Arteries
2) arterioles
3) cross sectional area and SA is the greatest here
25
Whats
a) Darcy’s law
b) MABP (mean artarial bp)
a) force = change in pressure/resistance
b) MABP = diastolic bp + (systolic bp-diastolic bp)/3
26
Whats laplaces law
As radius increases, pressure decreases (this means vessels with smaller diameter require less tension and thickness in the walls to maintain pressure - thats why arterioles have thinner walls than aorta)
27
Whats the iliac artery
Located at the hips and extends to the thighs
And due to the drastic pressure changes it is highly susceptible to disease especially in old people
28
What vessel has the largest pressure drop
Arterioles
They are highly resistant vessels
29
Where is velocity highest in the cross sectional the blood vessel
Centre and lowest around the walls due to friction
30
When blood vessels narrow the laminar flow ..
+ what happens when Re is less than 200
Turns into turbulent flow
This is measured using Reynold’s no. (Re)=
When Re < 200 = there is laminar (smooth streamlined flow)
31
What can cause turbulence in blood vessels
Stenosis
32
Why are elderly people more susceptible to hypertension (as we age)
Blood vessels become stiffer and narrower they become less elastic = causing pressure to increase
33
Does alterations in flow of one organ greatly affect the system as a whole
No because individual organs are arranged like parallel circuits
34
Whats active hyperemia or hyperaemia
process where blood flow to a tissue increases in response to its increased activity or metabolic demand and accumulation of metabolites e.g when you exercise
35
App this may come up as a SAQ
- RAAS system and autoregulation
Turn over
Upload the image on circulation slide 2 onto chatgpt and let it explain bc what is going on mate and it might even come up as a big one
36
Which cornary artery is more predominantly involved in MI
LEFT bc its prone to plaque development
37
How is coronary blood supply re oxygenated
The cardiac veins empty into the coronary sinus which returns to the right atrium
38
Which one is longer diastole or systole
Diastole (relaxation) is twice is as long as systole (contract)
39
Equation for oxygen extraction rate
Oxygen extraction rate = oxygen consumption / oxygen delivery
It increases during exercise
40
What atherosclerosis
Arteries become narrow due to build up of plaque which causes stenosis = reduced blood flow = pt may experience angina in chest area due to increased oxygen demand & reduced supply (complete blockage = ischaemia/MI)
41
Whats a important role of arteriolar vessels
Matching myocardial blood flow to oxygen demand
42
Whats the frontline treatment for heart conditions
ACE inhibitors bc they inhibit the conversion of AG1 to AG2 - AG2 causes vasoconstriction
And in heart conditions we want vasodilation to occur
43
What does EDHF do
Endothelium derived hyper-polarising factor - as it says it hyperpolarises the cell via K+ channels
44
How does metabolic regulation in intramyocardial coronary arterioles occur
Via metabolite mediated dilation (via adenosine release which causes vasodilation)
45
What are 1) functional end arteries and 2) anatomic end arteries
1) Sole supply of oxygenated blood to myocardium - if blocked = ischaemia and MI
2) where tissue is supplied blood - if blocked = ischaemic necrosis (loos fo blood flow to bone tissue)
46
47
Whats anastomosis
When2 blood vessels connect and this occurs when an functional end artery becomes blocked, a nearby one connects and supplies the tissue with oxygenated blood but this is usually insufficient = ischemic necrosis
48
What are the arteries that do not anatomise with their neighbouring arteries
End arteries (2 types - anatomical and functional) there is NO collateral circulation with these boys
49
Is the ability to form collateral variable
Yes highly - it is used minimise effects of occlusions (blockages) due to collaterals filling the vessel
50
Whats coronary cathiterisation
Used to visualise the inside of the coronary arteries
51
What vessel contributes most and least to flow regulation
Arterioles - most(40%)
Epicardial coronary arteries - least (10%)
52
Is vascular resistance in the coronary bed series or parallel
Both depending on the layer of the myocardium
53
Domino effect of atherosclerosis
Atherosclerosis = coronary artery disease = ischaemia = plaque rupture = infarction = loss of contractility = remodelling = heart failure
(= meaning “can lead to” in this context)
54
Equation for coronary flow reserve
CFR = coronary flow(max vasodilation)/coronary flow (basal)
55
Whats coronary flow reserve
refers to the capacity of the coronary circulation to increase blood flow to the heart muscle beyond its normal resting - gives an indication to the recruitment of collaterals during ischaemia
56
what can you do to treat blockages of the coronary arteries
PCI
57
what factors increase the risk of heart failure
1) hypertension 2)lipids
3) hyperinsulinemia (too much insulin) 4)diabetes 5)smoking
non-modifying factors = sex, genetics, ethnicity,...
58
what are the types of hypertension
primary hypertension (no underlying cause) and secondary hypertension (has an underlying cause)
59
whats (cardiac) hypertrophy
increased density and thickness especially of the left ventricle which can lead to heart failure (its due to cardiac remodelling)
60
whats heart failure
inability of the heart to meet the circulatory demands of the body caused by functional abnormalities
61
whats the 3 main types of heart failure
1) heart failure due to left ventricular systolic dysfunction (LVSD) - reduced HFrEF
2) heart failure with preserved ejection fraction (HFpEF)
3) acute heart failure
62
whats a) systolic dysfunction vs b) diastolic dysfunction
a) pump dysfunction
b) fill dysfunction
63
progression of heart failure process
cardiac output decreases = aortic flow decreases, norepinphrine release causes aterio-constriction + cardiac workload increases and afterload increases = cardiac workload increase
64
continue flow chart after cardoac output decreases...
=reduced blood flow to organs like the kidneys = kidneys detect this and release angiotensin = vasoconstriction = causing b)increased preload and aterioconstriction = causing a)increased afterload a) and b) cause increased cardiac workload = causes aldosterone to be released = increased sodium and water retention = increased preload = leads to cardiac remodelling and heart keeps failing
65
what are some common heart failure treatment options
loop diuretics are often given to help remove excess fluids e.g. furosemide then for HFrEF ACE inhib e.g. ramipril may be given, or ARB for black ppl, SGLT-2 inhibitors (dapagliflozin), nitrates, hydralazine, mineralocortoid receptor antagonist (spironolactone) and resynchronization therapy (pacemaker) but for HFpEF its more complicated as it varies for each individual (some need statins, some antiplatelets,...)
66
whats used as a diagnostic tool for heart failure
naturetic peptides (heart failure purple section)
67
what is first line treatment for STEMIs (which is more severe nSTEMI or STEMI)
PCI given as first line and STEMI is more severe
68
whats acute coronary syndrome and treatment for it
ACS= reduced blood flow to the heart, treatment = ACE inhibitor (vasodilation) and beta blockers
69
whats pitting oedema
swelling in the body e.g. build up of fluid in the ankles that leaves an indentation when pressed = sign of acute heart failure
70
whats jugular venous pressure an indication of
pressure in the right atrium of the heart = clinical sign for assessing function in the right side of the heart
71
whats a sign of heart failure
fluid build up in the body oedema, pt presents with weight gain, which is actually water weight, breathlessness, cold skin, gut complication, kidney failure (last 3 due to reduced kidney,gut and skin perfusion)
72
treatments for acute heart failure
-ECG, FBC (to check for infection), U&E to check for electrolytes and ECHO to measure ejection fraction, CHADVASC to measure stroke risk
73
side effects of common heart failure drugs
cough = ramipril (ACEI), muscle aches (statins), fatigue (bisoprolol), brusing/bleeding (antiplatelet)
74
where does atherosclerosis usually occur + what causes turbulence
where you have branching of larger arteries + stenosis and atherosclerosis causes turbulence
75
what do fibroblasts do
produce extracellular matrix and give the heart its structure (in this context)
76
how do scars form after an MI
during MI cardiomyocytes die , triggering fibroblast proliferation, the dead myocytes are replaced by fibroblasts. The fibroblasts produce lots of collagen and patch up the gap = forming a scar. The fibroblasts leave leaving behind a collagen rich scar (scar isn't as contractile = cardiac output is compromised)
77
have a read of cardiac pathology pink part idk what it rlly means
78
whats calcification (in the vessels)
when calcium deposits build up in the artery walls as people age (made worse by atherosclerosis) + less elastin in the walls = makes the arteries stiffer and less compliant = pulse pressure will be larger
VSMCs differentiate into osteoblasts-like cells which produce calcium phosphate deposits either
a) INTIMA calcification (in atherosclerotic plaque)
or b) MEDIA calcification (in the smooth muscle)
79
what are the physiological (this type is reversible) forms of hypertrophy and the pathological (irreversible) ones
physiological = caused by chronic exercise and during pregnancy (due to increased haemodynamic demand due to increase in circulatory volume = heart needs to grow to maintain supply
pathological = caused by hypertension
80
whats CVP + normal range
central venous pressure (usually 3-7mmHg) = reflects the amount of blood returning to the heart (venous return) - normally increased CVP = increased return but in heart failure increased CVP doesn't cause increased return
81
what does chronic heart failure lead to
decreased cardiac output, decreased arterial pressure, increase in blood volume, increased CVP, oedema (+pulmonary oedema)
82
how can hyperkalemia be fatal
ti is 1 of the 3 components of the lethal injection - causes depolarisation of myocytes = interferes with generation and propagation of APs and can cause arrhythmias (you may think it causes hyperpolarisation but i promise it doesnt because it interferes with the diffusion gradient)
83
what are the 3 stages of hypertension
stage 1 hypertension = 140/90 to 159/99mmHg
stage 2 hypertension = 160/100 to 180/20mmHg
stage 3 = >180/120mmHg (immediate referral)
84
what does the bp higher no. and lower one mean
higher no. = systolic, refers to pressure when ventricles contract
lower no. = diastolic, refers to when the ventricles relax
85
systemic effects of hypertension
accelerates atheroscelrosis, affects fibrinolysis, increases risk of stroke, MI and renal dysfunction
86
monitoring requirements for ACEIs, CCBS/beta blockers and diuretics
ACEIs = bp, serum creatinine, serum potassium/sodium
CCBs/beta blockers = HR & bp
Diuretics = bp, serum creatinine, serum electrolytes and uric acid
87
what ethnicity do we NOT give ACEIs to & why
African Americans bc dont respond well to renin-angiotensin system blockers - increased risk of angioedema (fluid build up around eyes, lips or gentials lol)
88
whats white coat hypertension
ppl being scared of us and their bp is falsely high bc of that
89
whats resistant hypertension
when bp is high despite taking anti-hypertensives, low dose spironolactone can be given (can be caused by hyperkalemia/renal dysfunction/gynaecomastia)
90
memorise the bp treatment flow chart (its not that bad we've done it lots <3) -hypertension second page
91
what type of muscle has the longest duration of depolarisation and thus contraction: skeletal, cardiac or smooth
cardiac to ensure the emptying of the ventricles
92
how does Na+ channel depolarisation work
intitially a small no. of channels open = small depolarisation, a few more Na+ channels open = more depolarisation = more Na+ channels open =faster depolarisation
93
how are arrhythmias prevented in terms of Na+ channel depolarisation
Na+ channels switch to inactive state shortly after opening and only return to closed state after repolarisation - 1) Preventing Backward Signal Transmission (Unidirectional Propagation): AP can only move forward because the area behind it is in a refractory state.
2) Control of Action Potential Frequency: Limits how quickly action potentials can fire (prevents over-excitation).
In cardiac cells, refractory periods prevent the heart from contracting too rapidly (preventing arrhythmias)
94
What are the 2 types of refractory peroids
absolute RP = The sodium channels are completely inactivated.
relative RP = The sodium channels are recovering, but some may still be inactivated. A very strong stimulus can trigger an action potential, but it will be weaker.
95
whats a diad
region where calcium channels in the T-tubules and the SR interact
96
how does muscle contraction work
1. The T-tubule carries the action potential deep into the muscle cell.
2.The action potential triggers voltage-gated calcium channels (L-type) on the T-tubule.
3. This causes the Sarcoplasmic Reticulum (SR) to release more calcium (calcium-induced calcium release).
4.The released calcium binds to troponin, cross bridge forms and moves along triggering muscle contraction.
(relaxation = Ca2+ taken up and blockage on tropomyosin restored)
97
what ATPases are in involved in regulating Ca2+ conc
1) SERCA - on SR membrane - during relaxation it removes Ca2+ from the cytosol back into the SR
2)PMCA - on the cell membrane - modulates Ca2+ channels and phospholamban - increases Ca2+ current but inhibits phospholamban, negatively regulates SERCA = PKA stimulates SERCA
98
what are cardiac glycosides + examples
Cardiac glycosides inhibit the sodium-potassium ATPase pump on the cardiac cell membrane.This causes an increase in intracellular sodium (Na⁺).
The increased Na⁺ reduces the activity of the Na⁺/Ca²⁺ exchanger, which normally removes calcium.
As a result, intracellular calcium (Ca²⁺) increases.More calcium is available for contraction, leading to stronger heartbeats (positive ionotropy). e.g. digoxin, digitoxin but
99
whats a functional syncytium
when a cell depolarises the action potential spreads rapidly to neighbouring cells - this is possible bc these cells are joined together by gap junctions
100
are sinus arrhythmias life-threatening
nope perfectly normal esp in young ppl
101
how do ECGs work
3 leads place in a triangular shape - 2 at the apex and 1 by the lowest rib
102
what are the different types arrhythmias
tachyarrhythmias (increased hr), bradyarrhythmias (decreased hr), AF (irregular), supraventricular (above ventricles), bradycardia (slow hear BEAT)
103
What drug may cause a pt to get nightmares +why
bisoprolol bc it crosses the BBB, if so we can give them atenolol instead bc it doesn't cross the BBB
104
what causes characteristics of AF and what causes it actually
Arises from atrium, electrical signla does not travel down the purkyne fibres to the bundle of his - i.e. not causing ventricular contraction
common causes: infection, stress, diseases and obesity
105
symptoms of af
palpitations, chest pain, dyspnoea, dizziness
106
what do we need to monitor for AF pts
HR, CHADVASC score, INR, HAS-BLED,
107
what does P wave and QRS wave represent
P = atrium contraction
QRS = ventricle contraction
108
what are drug classes 1-4
class I = Na+ channel blocker (phenytoin)
Class II = beta blockers (bisoprolol, atenolol)
Class III = K+ channel blockers (sotalol)
Class IV = Ca2+ channel blockers (verapamil, diltiazem)
109
what is digoxin
Na+/K+ ATPase inhibitor (beware its effects are reduced by hyperkalemia)
110
flow chart begin: ventricular tachycardia
= ineffective pumping = reduced cardiac output = low bp which can lead to death (asystole)
111
what do anticoagulants do
increases the time it takes for blood clots to form - thins the blood
112
how is cholesterol formed
ester goes to aldehyde to alcohol
the reaction uses HMG CoA reductase and involves 2 hydride transfers from the co factor NADPH:
1st one cleaves off CoA moiety
2nd reduces the resulting aldehyde group
113
what are statins and how do they work
drugs that
a)decrease cholesterol production as they are HMG CoA reductase inhibitors preventing the formation of mevalonate (a precursor for cholesterol)
b)The liver responds by making more LDL receptors on its surface. These receptors remove LDL cholesterol ("bad" cholesterol) from the blood, lowering blood cholesterol levels.
114
importance of cholesterol + risks of elevated levels
it forms a component of biological membranes - immobilises the first few hydrocarbon groups, its used to make steroids, vit D and hormones
But elevated levels = hypercholesterolemia which can lead to coronary heart disease
115
which ones bad LDL or HDL
LDL obvs - it takes cholesterol FROM the liver to other tissues = which can lead to build up in arteries forming plaques (atherosclerosis) = narrow arteries - if the the fibrous cap covering the plaque breaks open, exposing the inner contents (lipid core) to the bloodstream -the body sees this exposed material as an injury and responds by forming a blood clot = partial blockage = chest pains (angina) or full blockage = MI
HDL - transports cholesterol away from cells back to the liver (cleans up cholesterol)
116
what features does a HMG CoA reductase inhibitor need
needs to mimic the transition state, have a hydrophobic group and an ester group that can hydrolyse in the body (as a prodrug)
117
what are the 2 types of beta blockers and the first ever one made
1) non-selective (1st gen) beta blocker (propanolol, timolol, nadolol) - contraindicated in asthmatics bc they act on beta-1 and beta-2 adrenoreceptors (beta-2 antagonism causes bronchoconstriction)
2)selective beta-1 blockers (2nd gen) selectively antagonise beta-1 adrenoreceptors in the heart (bisprolol, atenolol, esmolol)
1st ever beta blocker = propanolol
118
whats the most popular beta blocker and why
bisoprolol because it selectively binds to beta-1 adrenoreceptors doesn't cross the BBB so no CNS effects
119
what conditions come under acute coronary syndrome
unstable angina, stable angina - chest and back/neck pain relieved using GTN spray, NSTEMI and STEMI (most severe)
120
whats ischaemic heart disease
narrowing of the lumen of the coronary arteries = imbalance bw supply of oxygen and myocardial demand = chest pain
121
treatment for stable angina
GTN spray, smoking cessation, beta blockers, calcium channel blockers (can cause ankle swelling), anti-platelets and nitrates (side ffects = flushing and hypotension) and lifestyle = reduced salt intake, exercise
122
treatment for NSTEMI and STEMI
STEMI = pt may need a PCI/STENT or coronary angioplasty but treatment for both is generally he same: aspirin (300mg STAT then 75 OD) with antiplatelet for 1 yr (clopidrogel) and isosorbide mononitrate and beta blocker/CCB
123
whats CABBAGE (CABG)
coronary artery bypass graft = when blood vessel is taken from another area e.g. leg and bypass it in the heart (give antiplatelets and analgesia after and maybe diuretics)
124
what's thrombosis
formation of occulsive thrombi (blood clot that completely blocks flow in small vessel) leading to MI/ischaemic stroke
125
go over the process of haemostasis
1) damage to blood vessel 2)exposure of platelets and vWF in extracellular matrix and later exposure to thrombin 3)platelets adhere and activate 4) release of mediators 5)vasoconstriction + aggregation of platelets 6) formation of soft platelet plug
126
Whats GPVI
receptor protein found of surface of platelets that activate thrombin, TXA2 and ADP leading to platelet aggregation
127
red clots vs white clots
white = arterial thrombosis, associated with atherosclerosis and treated via prophylaxis with anti-platelet drugs red = venous thrombi, associated with the stasis of blood treated via prohpylaxis using anticoagulants
128
what are the 3 classes of antiplatelets
1) aspirin 2) P2Y12 antagonists i.e. - clopidrogel/prasugrel, prevents ADP-mediated platelet aggregation 3)GPIIb-IIIa e.g. abciximab, very potent not for long term use due to thrombocytopaenia
129
how is thromboxane formed
phospholipase causes arachidonic acid to form which gets converted to prostaglandins via COX-1/2/ which gets converted to TXA2 (thromboxane) via prostaglandin isomerases (aspirin inhibits this by IRREVERSIBLY binding - other drugs reversibly bind )
130
what triggers platelet activation and what inhibits it
trigger = TXA2 (thromboxane)
inhibits = PGI2
131
why do we need to be careful when giving antiplatelets
it increases the risk of a hemorrhage so we need to find a balance between preventing clots whilst also not causing hemorrhages
132
what are anticoagulants and thrombolytics
anticoagulants = prevent coagulation of blood to prevent clots e.g. apixaban, warfarin (vit k antagonist) & heparins
thrombolytics = dissolve blood clots that have already formed in blood vessels (rapid removal of thrombus)
133
what are the 2 types of heparin
1) unfractionated heparin
2)low molecular weight heparin
134
what are thrombin inhibitors
factor IIa inhibitors - directly block the active site of thrombin
135
what are factor Xa inhibitors
rivaroxaban, apixaban and edoxaban - they inhibit factor Xa (pro is that they dont require frequent monitoring)
136
DOACs vs other anticoagulants
traditional anticoagulants = monthly blood tests, dietry considerations and possibility of uncontrolled bleeding DOACs = none of these BUT trad anticoagulants have antidotes but most DOACs dont
137
what is fibrinolytics
essentially the same as thrombolytics but they describe diff stages of the same process Thrombolytic emphasizes the "clot-breaking" action
Fibrinolytic emphasizes the "fibrin-dissolving" action - activate plasminogen to break down the clot
