Quick Cardio physiology Flashcards
superior mediastinum
aortic arch
anterior mediastinum
thymus
lymph nodes
internal thoracic vessels
thyroid tissue
middle mediastinum
heart and pericardial sac
ascending aorta
SVC
IVC
pulmonary vessels
trachea and main bronchi
phrenic
vagus
LRLN
all the good stuff
posterior mediastinum
descending aorta
oesophagus
azygos (right) and hemiazygos (left)
layers of heart
epicardium, myocardium, endocardium
epicardium - adipose tissue, vessels and nerves
myocardium - muscle
endocardium - inner endothelial cells
ventricle muscle ridges
trabeculae carneae
where are pectinate muscles?
atria
first branch from aorta
coronary arteries
left and right
borders of the heart
right - right atrium
inferior - left and right ventricles
left - left ventricle and some left atrium
superior - L and R atria and great vessels
what does the RCA supply
right atrium
right ventricle
what does the RMA supply?
right ventricle
apex
what does the PIV supply?
AVN
posterior third of IV septum
AVN blood supply
PIV always
what does the LAD supply?
anterior 2/3 IV septum
R and L ventricle
what does the LMA supply?
left ventricle
what does the Cx supply?
left atrium
left ventricle
heart dominance
PIV from RCA only - 70%
PIV from LCA only - 10%
PIV from both - 20%
be careful to see how it is worded!
SAN blood supply
60% RCA
40% LCA
apex beat
left 5th intercostal space midclavicular line
auscultation points for:
aortic valve
pulmonary
mitral
tricuspid
right 2nd IC sternal border
left 2nd IC sternal border
left 5th IC MCL
right 5th IC sternal border
only the mitral valve is mid clavicular line
you would think aortic valve would be on left since left ventricle is on left but it pumps to the other side
right phrenic nerve
travels along pericardium of right atrium
descends anterior to lung root
where does RIGHT phrenic pierce diaphragm?
T8 with IVC
left phrenic nerve
descends anterior to lung root
travels along pericardium of left ventricle
does not pass diaphragm at T8
vagus nerve relative to lung root
posterior
where does vagus pass through diaphragm?
T10 with oesophagus
where do the left and right RLN loop back up?
left - under arch of aorta
right - under right subclavian
which chemoreceptor does vagus innervate?
carotid sinus
truncus arteriosus
aorta
pulmonary trunk
bulbus cordis
smooth part of ventricles (outflow parts)
primitive ventricle
trabeculated parts of ventricles (majority)
primitive atrium
trabeculated parts of atria (auricular appendages)
entire left atrium
anterior right atrium
sinus venosus
smooth part of right atrium (posterior)
coronary sinus
oblique vein of left atrium
vena cavae
smooth part of right atrium
sinus venarum
which layer does the heart develop from
mesoderm
cardiac embryology stages
formation of primitive heart tube
cardiac looping
cardiac septation
layers of primitive heart tube, superior to inferior
truncus arteriosus
bulbus cordis
primitive ventricle
primitive atrium
sinus venosus
formation of primitive heart tube
mesoderm
cells from cardiogenic region form endocardial tubes
endocardial tubes fuse to form primitive heart tube
20-21 days
cardiac looping
bulbus cordis moves inferiorly and anteriorly
primitive ventricle moves superiorly and posteriorly
primitive atrium and sinus venosus move superiorly and posteriorly
only bulbus cordis moves differently
cardiac septation
forming the septum
at this point, there is one atrium and one ventricle connected by atrioventricular canal
endocardial cushions grow from sides of AV canal
cushions fuse to form left and right atrioventricular canal
first aortic arch
maxillary artery
second aortic arch
stapedial artery
third aortic arch
proximal internal carotid artery
common carotid artery
fourth aortic arch
right side - right subclavian artery
left side - aortic arch
5th aortic arch
regresses
sixth aortic arch
right - pulmonary trunk
left - left pulmonary artery and ductus arteriosus
layers of arteries, out to in
tunica adventitia
external elastic lamina
tunica media
internal elastic lamina
tunica intima
basement membrane
lumen
what are blood vessels inside blood vessels, and in which layer are they?
vaso vasorum
tunica adventitia
muscular artery examples
coronary arteries
femoral artery
radial artery
usually peripheral
difference between elastic and muscular arteries
elastic
- media larger than adventitia
muscular
- media = adventitia
types of capillary
continuous, fenestrated, discontinuous
how many muscle layers do arterioles have?
3 or fewer
end diastolic volume
100ml
stroke volume
70ml
end systolic volume
30ml
equation for ejection fraction
stroke volume/ end diastolic volume x 100
percentage of blood pumped out of the left ventricle during systole
normal value for ejection fraction
70%
duration of cardiac cycle
0.8s
duration of diastole
0.5s
duration of systole
0.3s
parts of systole
isovolumic contraction
ejection
parts of diastole
isovolumic relaxation
rapid filling
passive blood flow
atrial booster
isovolumic contraction
AV valve closes when ventricular pressure exceeds atrial pressure
but pressure is not high enough to open aortic valve
therfore isovolumic contraction increases pressure but does not affect the volume
this increase in pressure causes the aortic valve to open leading to ejection
ejection
aortic valve opens
only 70% blood is pumped out
passive blood filling
rapid filling at first
then diastasis reached
atrial booster
atrial walls contract to fill ventricles
the closure of which valve = dub
semilunar valves
window maker
LAD
are the heart sounds made by the valves opening or closing?
closing
what do pulmonary arteris divide into?
lobar arteries
how many pulmonary veins?
4
what do subclavians supply?
arms
what do carotids supply?
face and neck
mean arterial pressure
diastolic volume + 1/3 (pulse pressure)
average arterial pressure during one cardiac cycle
pulse pressure
systolic - diastolic
blood pressure
cardiac output x TPR
TPR is exerted by vascular walls
myogenic autoregulation
increased stretch of vessels during blood flow can stimulate contraction
local vasoconstrictors
endothelin-1 produced by endothelial cells
local vasodilators
hypoxia
adenosine and bradykinin
NO from endothelial cells
increase in K, CO2 and H
release of NO and endothelin-1
NO is a vasodilator produced continuously
endothelin-1 is released in response to stimuli
what are baroreceptors and where are they located?
peripheral pressure sensing receptors
arterially in
- carotid sinus
- aortic arch
venously in
- veins
- myocardium
- pulmonary vessels
what must we do in exam questions?
give units
be specific .g not CO2 level, say PaCO2 for arterial carbon dioxide partial pressure
differentiate between bundle of his, left and right bundle branches and purkinje fibres
what must we do when talking about blood transport in the pulmonary system?
talk about how pulmonary artery splits into left and right
what do central and peripheral chemoreceptors respond to?
central
increase in PaCO2
peripheral
increase in PaCO2
fall in PaO2
cardiac preload vs afterload
preload
stretching of cardiac muscles before contraction
i.e caused by EDV
afterload
force myocytes coontract against
preload is a volume
afterload is a force
effect of increase in EDV
increased stretch of myocardium
increase in sarcomere length
increased length of overlapping filaments
increased force of contraction
increased stroke volume
what is a sarcomere?
basic contractile unit of a myocyte (muscle fibre)
a sarcomere is composed of two main protein filaments (thin actin and thick myosin filaments)
sarcomere physiology
increased stretch opens stretch sensitive calcium channels
stretch enhances affinity of troponin C for Calcium
increased force of contraction as a result
when maximum stretch reached
little overlap between actin and myosin
lots of unbound myosin heads
decreased stroke volume
factors affecting preload
ventricular compliance
heart rate
venous return
ventricular compliance
valvular resistance
atrial contractility
myocyte action potential - look at graph!
phase 0 - fast depolarisation and overshoot
- AP of adjacent cell induced due to movement of ions between gap junctions
- voltage gated sodium channels open
- rapid depolarisation
- channels close immediately afterwards
phase 1 - notch
- opening of transient K+ channels
- efflux of potassium
- small repolarisation
- +10mV to 0mv
phase 2 - plateau
- L-type Ca2+ channels open
- influx of calcium balanced by K+ efflux
- less duration in atria than ventricles as ventricles need greater contraction
phase 3 - repolarisation
- closure of calcium channels
- opening of more potassium channels for K+ efflux
phase 4 - baseline
- resting membrane potential achieved by action of Na/ K+ ATPase pump
- also achieved by membrane being more permeable to K+
remember it starts on 4, then 0, then 1…
how long is the delay at the AVN?
0.1s
to allow ventricles to fill fully
where is the Bachmann’s bundle?
left atrium
how many libres of blood?
5
blood serum
blood plasma without clotting factors
haematocrit
proportion of erythrocytes
0.45
where is haematopoeisis in
adults
embryo
adults
- bone marrow
embryo
- other sites e.g spleen
platelet life span
6h
blood cell growth factors
erythropoietin - rbc
granulocyte colony stimulating factor - wbc
thrombopoietin - platelet
wbc life span
days to weeks to years
rbc precursor cells located where?
adults
children
in utero
adults
- axial skeleton
- skull, ribs, spine
children
- all bones
utero
- yolk sac
then liver, then spleen
how to remember which factors push o2 dissociation curve right
CADET face right
increase in these causes right shift
- co2
- acidity (decrease in pH)
- DPG
- exercise
- temperature
decrease in affinity
Bohr effect
haldane effect
oxygen displaces carbon dioxide from Hb
haem
protoporphyrin IX and iron
what is anaemia?
hb deficiency
NOT RBC deficiency necessarily
types of anaemia
impaired production
increased haemolysis
iron deficiency anaemia
low iron diet
low mcv - mean cell volume
microcytic
vitamin b12/ folate deficiency anaemia
pernicious anaemia
causes
- autoimmune attack on gastric mucosa
slow onset as LIVER stores B12 for 3-5 years
- lack of folic acid in diet
- lack of b12
both needed for rbc dna maturation and to condense
high MCV - macrocytic
high mcv because dna not condensed
haemorrrhagic anaemia
blood loss
peptic ulcer
gunshot wound
normal mcv of course!
aplastic anaemia
affects all blood cells
caused by destruction of bone marrow e.g chemotherapy
common myeloid progenitor destroyed
causes pancytopenia
- anaemia
- leukopenia
- thrombocytopenia
where are beta 2 receptors
lung
where are beta 1 receptrs
heeart
what is the a band of a sarcomere?
mostly myosin
dark band
thalasseaemia
congenital
alpha or beta depending on which subunit of haemoglobin is reduced/ absent
haemolytic anaemia
hereditary
- G6PD deficiency
acquired
- autoimmune haemolytic anaemia
- infection e.g malaria
agranulocytes
monocytes
lymphocytes
granunocytes
basophils
eosinophils
neutrophils
which cells differentiate into macrophages?
monocytes
macrophage examples
liver Kupffer cells
microglial cells of CNS
tissue macrophages
lymphocytes
B cells
- antibodies
T cells
- bone marrow then thymus
natural killer cells
- kill virus infected cells
platelet structure
anucleat
discoid then
become spiculated with pseudopodia once activated
haemostasis
where is tpo produced?
liver and kidneys
largest white blood cell
monocyte
primary haemostasis
platelet plug formation
vessel injury
- endothelial wall exposed
- smooth muscle contracts to limit blood loss
- mechanisms of contraction are nervous stimulation and endothelin release
adhesion
- subendothelial collagen exposed
- platelets bind to collagen via vWF using their receptor GP1B
activation and granule release
- once bound, platelets change shape
- alpha and electron dense granules released from platelets to escalate haemostasis
aggregation
- more platelets join and they bind to each other using GP2b/3a receptors and fibrinogen
secondary haemostasis
coagulation cascade
fibrin clot formation
contents of alpha dense granules
vWF
fibrinogen
fibrin stabilising factor
contents of electron dense granules
ADP
Ca2+
serotonin
coagulation cascade
intrinsic
12-11-9-8
extrinsic
3-7
both
10-5-2-1
(5x2x1=10)
what triggers intrinsic pathway?
extrinsic pathway?
internal damage to vessel wall
external damage
factor 2
thrombin
factor 1
fibrinogen
factor 1a
fibrin
factor XIIIa
fibrin stabilising factor
factor 4
Ca2+
vitamin K dependent factors
1972
10, 9, 7, 2
types of blood transfusion
homologous
- emergency transfusion
autologous
- self-transfusion
cross matching
mix recipient serum with donor blood
what factors influence haematocrit?
erythropoiesis and haemolysis
site of haemolysis
spleen
bone marrow
lymph nodes
causes of high haematocrit
dehydration
polycythemia
fibrinolysis
by plasmin
intrinsic action by factor 7a and extrinsic action of tissue plasminogen activator converts plasminogen to plasmin
plasmin causes degredation of fibrin
factor 7a is part of thee extrinsic pathway in the coagulation cascade and part of the intrinsic pathway in the fibrinolytic system
heart embryology
week 3/4
- visceral mesoderm –> 2x heart tubes
heart tubes fuse (lateral folding) –> craniocaudal folding –> heart tube has divisions now
primitive heart tube has 5 section
- truncus arteriosus
- bulbus cordis
- primitive ventricle
- primitive atrium
- sinus venosus
septation
cardiac looping
aortic arches
when does heartbeat start
day 23
when does heart appear
week 3
when does the ductus arteriosus close?
10-15h after birth
obstetrical climbing
constriction of umbilical vein to form ligamentum teres
embryological remnants
ductus arteriosus to ligamentum arteriosum
umbilical vein to ligamentum teres
umbilical arteries to medial umbilical ligament
foramen ovale to fossa ovale
ductus venosus to ligamentum venosum
urachus/ median umbilical ligament - remnant of allantois - foetal bladder drains here - urinary bladder to umbilicus
why does the foramen ovale close?
increased left atrial pressure
decreased right atrial pressure
due to first breath
cardiac myocyte membrane potential
-90mV
is the action potential of the heart longer than skeletal muscle?
is the absolute refractory period longer?
yes
yes
pacemaker potential
3 phases
phase 4
- leaky F type Na channels (permeable to K+) open
- ‘funny’ as open when most negative
- positive Na+ influx causes gradual -60mV to -40mV
phase 0
- T-type Ca2+ channels open
- depolarisation from -40mV to +10mV
phase 3
- +10mV to -60mV
- closure of T type Ca2+ channels and opening of K+ channels
responsible for automaticity of the heart
primary pacemaker
latent (potential) pacemakers
primary - SAN - highest rate of discharge
latent
- AVN
- bundle of his
- purkinje fibres
control of pacemaker potential
sympathetic and parasympathetic
NAd is sympathetic
- increases Ca2+ channel opening
- faster depolarisation
- stepher phase 0
- increases heart rate and force of contraction
ACh is parasympathetic
- decreases heart rate
- activates K+ channels
- hyperpolarises membrane
- longer to reach threshold potential
- decreases calcium influx
- decreases slope of pacemaker potential
excitation-contraction coupling
waves of depolarisation spread into myocytes via T-tubules
L-type Ca2+ channels open
Ca2+ enters muscle cell
Ca2+ binds to ryanodine receptor
release of more calcium from sarcoplasmic reticulum
(calcium induced calcium release)
calcium binds to troponin to uncover active site on tropomyosin
cross bridge cycling = muscle contraction
force of contraction is directly proportional to levels of cytosolic Ca2+
what determins force of cardiac contraction?
cytosolic Ca2+
so drugs that increase myocardial contractility increase cytosolic calcium levels
e.g adrenalin
difference between segment and interval
segment
- period of isoelectric neutrality
interval
- a region including magnitude
PR segment
delay in AVN
because it is between end of P wave (atrial contraction) and start of QRS complex (vent. contraction)
ST segment
plateau phase of ventricular repolarisation
PR interval
atrioventricular conduction time
QT interval
total ventricular contraction during systole
how many leads? how many of each type?
12 leads
6 limb leads
- 3 bipolar
- unipolar
6 chest leads
- all unipolar
one small square and one large square
small - 0.05s
large 0.2s
limb leads
3 bipolar - I, II, III
3 unipolar (augmented) - aVR, aVL, aVF
lead electrode placements
lead V1
- 4th intercostal space right sternal border
V2
- 4th ICS left sternal border
V3
- midway between V2 and V4
V4
- 5th ICS midclavicular line
V5
- anterior axillary line at the same level as V4
V6
- midaxillary line at same level as V4 and V5
Frank Starling Curve
find picture
2 ways stroke volume increases
1. increased stretch opens stretch sensitive calcium channels
increased cytosolic calcium
increased force of contraction
- stretch enhances affinity of troponin C for calcium
increased force of attraction
after maximum stretch reached
- little overlap between actin and myosin
- lots of unbound myosin heads
- decreased force of contraction
- decreased stroke volume
positive ionotrophy
increased contractility
agents
- adrenaline, thyroxine
- drugs e.g digitoxin
- sympathetic nervous system
negative ionotrophic agents
beta blockers
parasympathetic nervous system
poiselles law
.
what controls blood volume?
RAAS
intrinsic blood pressure control
myogenic autoregulation
- arterioles regulate its own blood pressure based on how much it is stretched
- constrict if pressure increases
local mediators
vasoconstrictors
- endothelin 1
vasodilators
- prostacyclin
- hypoxia in systemic circulation
- tissue factor
- NO
- bradykinin
- protons, potassium, calcium
extrinsic blood pressure control
circulating hormonal factors
vasoconstrictors
- adrenaline - alpha adrenergic receptors
- angiotensin II
- vasopressin
dilators
- ANP
- adrenaline - beta 2 adrenergic receptors
baroreceptors
- pressure
- carotid sinus and aortic arch
- afferent neurons are CN 9 and 10
- efferent are SNS or PNS to heart and vessels
neural control
how is blood controlled long and short term
long - RAAS and blood volume
short - baroreceptors
