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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
septation
(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
26
aortic arches - time period, names , what they form
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
27
extra embryology facts
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
28
membrane potential definition
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
29
membrane potential of cardiac myocyte at rest
-90mV | more positive outside cells
30
is a cardiac action potential longer or shorter than in skeletal muscle
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
31
action potential/cardiac cycle phases
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
32
In what phase of the cardiac cycle does contraction occur?
phase 2 - contraction occurs when there is a calcium influx
33
refractory periods
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
34
where is the sinoatrial node located? what does it do? what is it modulated by?
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
35
pacemaker potential
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)
36
which cells act as pacemakers in heart - what do they do
pacemakers are responsible for automacity of heart. Nodal cells generate the pacemaking potential (1%?)
37
sympathetic stimulation of pacemaker potential
- noradrenaline binds to beta-1 receptors - increases Ca2+ channels opening - faster depol - steeper phase 0 - increased heart rate and force of contraction
38
parasympathetic (vagal) simulation of pacemaker potential
- 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
39
excitation-contraction coupling
Wave of depolarization (AP) spreads into myocytes via T tubules. L-type Ca2+ channels open 🡪 Ca2+ enters the muscle cell Ca2+ binds to Ryanodine Receptor 🡪 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
40
What causes contraction in excitation-contraction coupling?
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+
41
Electrode and lead (for ECG) definitions
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
42
shapes of ECG graphs
+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
43
list all the ECG leads
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
44
Key parts of ECG:
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.
45
What is a segment in ECG
A period of isoelectric neutrality
46
What is an interval in ECG
A region including magnitude
47
what is the ejection fraction
the proportion of the EDV that is pumped out the LV per beat, SV/EDV, provides an indication of the contractility of the heart
48
what percentage of blood passively fills the lungs?
70-80% - during diastole - helps equalise pressure
49
what is the atrial booster?
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
what percentage of blood ejected during maximal ejection?
65-75% of blood in the ventricles (then reduced ejection happens)
51
What can passive ventricular filling be split into
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
what factors affect stroke volume?
preload, afterload, contractility, (heart rate?)
53
what occurs during the Frank-Starling curve (in the heart)?
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
factors that affect preload?
venous return, heart rate, ventricular compliance, atrial contractility, valvular resistance
55
inotropy meaning
relates to force of contraction
56
chronotropy meaning
relates to heart rate
57
what happens in increased contractility?
+ve inotropy -> Increases Force of Contraction 🡪 increases SV
58
what are some positive inotropic agents?
Sympathethic nervous system Hormones: adrenaline, thyroxine Drugs: e.g. Digoxin
59
decreased contractility
-ve inotropy -> decreased force of contraction -> decreased SV
60
negative inotropic agents?
Parasympathetic nervous system, Drugs: e.g. β-blockers
61
factors affecting afterload
valvular diseases, TPR, Aortic pressure SVR/TPR: mainly determined by radius of vessels Vasodilation 🡪 Decreased resistance 🡪 decreased afterload Vasoconstriction 🡪 Increased resistance 🡪 increased afterload Aortic pressure: Increased aortic pressure = increased LV pressure (hypertension) 🡪 increased afterload Decreased aortic pressure = decreased LV pressure (hypotension) 🡪 decreased afterload Valvular diseases: Mitral valve regurgitation 🡪 decreased LV wall stress 🡪 decreased afterload Aortic stenosis 🡪 Increased LV pressure 🡪 Increased afterload
62
afterload definition
ventricular wall stress during sytole
63
blood pressure definition
the pressure exerted by blood on a given vessel surface area
64
pressure equation
ΔP = Pi – Pf Pi = MAP (mean arterial pressure) Pf = CVP (venous pressure) or ΔP = Q x TPR
65
systolic pressure definition
point when LV pressure during ejection = aortic pressure during ejection
66
diastolic pressure
Pressure caused by recoiling of arteries during diastole
67
pulse pressure equation
PP = SP - DP
68
Mean arterial pressure equation
MAP = 1/3(PP) + DP or MAP = DP + 1/3(SP - DP) MAP = CO x TPR
69
blood flow definition
The volume of blood that flows through the systemic circulation per unit of time (it is equal to cardiac output)
70
velocity of blood flow equation
V = Q/A
71
Types of blood flow
Laminar: Smooth, streamlined flow Turbulent: Disruption to laminar flow (e.g. decrease in vessel diameter) Produces Korotkoff sounds
72
what affects viscosity of blood
haematocrit: anaemia = decreased viscosity polycythaemia = increased viscosity
73
resistance equation
8nl/pi r^4
74
Poisueille's equation (this thing seems to change depending on what source I look at so just use whatever's in the question)
change in pressure combined with resistance Q = (Pi - Pf)pi r^4 / 8nl
75
what mainly determines resistance in a healthy individual
vessel radius
76
what is blood volume controlled by
RAAS - renin-angiotensin-aldosterone system
77
Intrinsic control of BP
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
local vasoconstrictors of arterioles
Endothelin-1, internal pressure
79
local vasodilators of arterioles
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
Extrinsic control of BP
Humoral factors Baroreceptors Neural control
81
Circulating hormonal factors - vasoconstriction and vasodilation
Vasoconstrictors - adrenaline (ALPHA adrenergic receptors), angiotensin II, ADH Vasodilators - Atrial Natriuretic Peptide, adrenaline (BETA 2 adrenergic receptors)
82
Baroreceptors - function, location, nerves involved
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
How do baroreceptors work? give an example
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
which nerves involved with baroreceptor reflex
vagus (recieves input from aortic arch) and glossopharyngeal
85
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?
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
Where do the SA and AV nodes lie
SA node - upper wall of right atrium | AV - bottom of right atrium on the septum
87
What does right coronary artery supply
Right atrium and part of ventricle | SA node in 60% of people and AV node in 90% of people
88
what does right marginal artery supply
right ventricle | apex
89
What does posterior intraventricular artery supply
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
What does left coronory artery supply
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
what does left anterior descending supply
left and right venricles (anterior aspect) | anterior 2/3 of IVS
92
what does left marginal supply
left ventricle
93
what does circumflex artery supply
left atrium and ventricle
94
percentages of population that has right-, left- and co-dominent coronary circulation
70%, 10%, 20% respectively so 90% of population have PIV coming from RCA and 30% has PIV from LCA
95
where is the apex of the heart/mitral valve sound found?
left midclavicular line - 5th intercostal space
96
where do you hear aortic valve sound, pulmonary valve sound and tricuspid valve sound
aortic - 2nd intercostal space - right sternal border pulmonary - 2nd intercostal space - left sternal border tricuspid - 5th intercostal space - right sternal border
97
Phrenic nerve: roots, modality of innervation, what it innervates, path through thorax
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
Vagus nerve: roots, modality of innervation, what it innervates, path through thorax
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
what type of artery is the aorta?
elastic artery
100
why are arterioles the main source of TPR? (aka why don't other vessels contribute as much to TPR?)
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
Layers of artery wall (and arterioles), from lumen out
Endothelium, basement membrane, intima, internal elastic lamina, media, external elastic lamina, adventitia arterioles are the same but without the external elastic lamina
102
Layers of vein wall and venule, lumen out
Endothelium, basement membrane, intima, media, adventitia same for venule
103
why are veins capacitence vessels?
they hold up to 70% of blood volume - normally
104
pulmonary circulation pressure
20/8
105
systemic circulation pressure
120/80
106
average cardiac output
~5-6L
107
average stroke volume
~70mL
108
average heart rate
60-100 beats per minute
109
average end diastolic volume
~130ml
110
average ejection fraction
65%
111
average end systolic volume
~50ml
112
Factors affecting cardiac output
Anything that affects stroke volume or heart rate Age, Gender, Pregnancy, Exercise, Emotions, Posture, Sweating (AG PEEPS)
113
What does the Frank Starling law dictate about force of contraction
Within PHYSIOLOGICAL LIMITS, the force of contraction is directly proportional to initial length of muscle fiber.
114
tamponade meaning
when pericardium fills with blood or fluid - increased pressure on heart can contract as easily
115
What does venous return depend on?
skeletal pump activity, ECF volume, sympathetic activity-venoconstriction
116
what does atrial pump activity depend on
Atrial contraction increases due to sympathetic activity
117
What factors affect myocardial contractility?
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
Factors affecting heart rate
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
what is the reason for SA node automacity/pacemaker potentials?
spontaneos diastolic depolarisations (Phase 4) - caused by HCN Na+ channels which open when hyperpolarised

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