CVS Flashcards
what are the 3 steps of the cardiac cycle
- ventricular SYSTOLE (contraction)
- ventricular DIASTOLE (relaxation)
- atrial SYSTOLE (ventricular refilling)
what happens during ventricular contraction (4)
- ventricular pressure > atrial pressure
- AV valves close
- isovolumetric contraction - vP increases, no change to ventricular vol pre-ejection
- ventricular pressure > aortic pressure –> aortic valve opens and EJECTION BEGINS
what happens during ventricular relaxation (4)
- reduced ventricular ejection bc of ventricular relaxation
- aortic blood flow maintained by aortic distensibility (aortic volume decreases while aortic pressure remains constant)
- aortic pressure > ventricular pressure –> aortic valve closes
- isovolumetric relaxation - ventricular pressure decreases, no change to ventricular volume post-ejection
what is aortic blood flow maintained by
aortic distensibility (aortic vol decreases while aortic pressure remains constant)
what happens during ventricular refilling (3)
- atrial pressure > ventricular pressure –> AV valves open
- when atrial pressure = ventricular pressure, filling stops TEMPORARILY
- atrial booster (contraction) resumes filling
what is Starling’s law
stroke volume increases as end diastolic volume decreases
what is stroke volume
volume of blood pumped from the left ventricle per beat
what is the duration o systole
0.2-0.3 secs
what is the duration of diastole
0.5-0.6 secs
what is the ratio of time of systole:diastole
1/3 : 2/3
what is the effect of SNS on cardiac output
increases it by:
- increasing heart rate
- increases force of contraction
what is the effect of PNS on cardiac output
decreases it by:
- decreasing heart rate
- decreasing force of contraction
what are heart sounds: valves opening or closing
closing
what is excitation-contraction coupling?
the conversion of a chemical stimulus to a mechanical response
what are the 3 steps of excitation-contraction coupling
- motor neuron connects with muscle at NMJ
- ACh diffuses across synaptic cleft - depolarises sarcolemma
- depolarisation of sarcolemma causes calcium ions to be released, stimulating muscle contraction
what is a sarcolemma
cell membrane of muscle cell (separates sarcoplasm from extracellular surroundings)
what does the sarcomere run btwn
2 z lines
which band does the z line bisect
i
what does the a band have
myosin and actin
what is myosin made of
2 heavy chains (dual head)
4 light chains (made of alpha and beta myosin)
what is actin
double heli globular protein
where is f acts present
contractile proteins
what is tropomyosin
double peptide chain occupying groove btwn actin strands
what does tropomyosin do
regulate interaction of other 3 proteins
what are the 3 troponin’s
I, T, C
what is diff btwn troponin I, T, C
troponin I = inhibits myosin/actin interaction
troponin T = binds troponin complex to tropomyosin
troponin C = has high affinity to calcium and causes muscle contraction
what are the 7 steps of muscle contraction (sorry it’s so long)
- calcium ions released by excitation-contraction coupling
- calcium ions bind to troponin C, causing tropomyosin to move
- movement of tropomyosin causes myosin binding sites on actin filament to be exposed
- myosin heads bind to actin molecule, forming actin-myosin cross bridges
- ADP is released from myosin head, causing myosin head to nod forward/be pushed along (contraction)
- ATP attached to myosin head to detach it, causing cross bridges btwn myosin/actin to break down
- ATPase hydrolyses ATP –> ADP + Pi, causing myosin head to return to original position
- Continues until there is no more Calcium ions
what are myocytes connected by
gap junctions that form channels to allow ion flow btwn cells (to enable electrical coupling of neighbouring cells)
what does tropomyosin do when the muscle is relaxed
blocks the cross bridge binding sites on actin
what displaces tropomyosin
binding of calcium ions to troponin
where are calcium ions stored in a muscle
sarcoplasmic reticulum
what is a t tubule
extensions of the cell membrane that penetrate into the centre of skeletal and cardiac muscle cells
they conduct impulses from sarcolemma down into the sarcoplasmic reticulum
what are the smallest branches of artery
terminal arterioles –> capillaries
what is the diameter of a capillary
3-40 micron
what is blood flow in capillaries regulated by
pre-capillary sphincters
wha are the 3 types of capillaries
- continuous (normal)
- fenestrated (kidneys, s intestine)
- discontinuous (liver sinusoids)
what is the structure of arteries/veins (internal to external, [5])
- tunica intima (endothelium and basement membrane)
- tunica media (vascular smooth muscle cells)
- internal elastic lamina
- tunica adventitia (fibroblasts)
- external elastic lamina
what are 3 differences btwn pulmonary vs systemic circulation
- thin vs thick walls
- minor vs substantial muscularisation
- low vs high BP
equation for SV (Stroke vol)
EDV-ESV
what’s left ventricular filling pressure
diff btwn L atrial and L ventricular pressure
what is the precise equation for MAP
CO x TPR
= BP
what is the approximate equation for MAP
diastolic pressure + 1/3 (SP-DP)
remember: PP = SP - DP
so DP + 1/3 PP
what is pulse pressure
SP - DP
if resting BP is 120/80 mm Hg, what is the PP?
40 mmHg
what is the equation for cardiac output
SV x HR
remember SV = EDV - ESV
what is the equation for Ohm’s law (resistance)
flow = pressure gradient/resistance
what is the equation for Pouiselle’s law (resistance)
flow is proportional to radius^4
what is preload
EDV at the start of systole (how much sarcomeres are stretched)
what is afterload
ventricular pressure at thhe end of systole
define contracility
ability of the heart to contract more to incr BP
define elasticity
ability of the heart to return to normal shape post systolic stress
define compliance
ability for ventricles to expand to accommodate increasing blood volume
define resistance
opposition to the passage of a substance eg blood
why do we need peripheral circulation control (3)
- maintain blood flow n arterial pressure
- distribute blood flow
- homeostsis/autoregulation
what is the main site of resistance to vascular flow
arterioles
why are arterioles the main site of vascular resistance (googled)
cross-sectional area increase in the arterioles is not enough to make up for the increase in resistance going from aorta to arterioles.
This is different in capillaries since their total cross-sectional area is huge, and the change in resistance is smaller since the change in diameter going from arterioles to capillaries is smaller compared to going from aorta to arterioles.
what is myogenic autoregulation
smooth muscle contracts and relaxes in response to local BP change to ensure constant flow rate
what are 2 local vasoconstrictors
- BP (myogenic auto regulation)
- endothelin 1 (stimulated by angiotensin/ADH, released from endothelial cell –> binds to smooth muscle receptors and causes calcium release)
what is endothelin1 stimulated by
angiotensin and adh
how does endothelin 1 work
- released from endothelial cell
- binds to smooth muscle receptors and causes calcium release
what are 3 local vasodilators
- hypoxia
- nitrous oxide
- pH decrease (incr H+ and CO2)
what are neural factors in BP
- BP deviates from norm
- baroreceptors detect changes in BP
- baroreceptors send impulse to brainstem
- brainstem causes change to cardiac output and vessel diameter
name 3 hormonal vasoconstrictors
adrenaline (a1)
angiotensin I
adh
name 2 hormonal vasodilators
ANP
adrenaline (b2)
what is ANP
hormonal vasodilator
what does beta-2 receptor adrenaline do
vasodilates
what does alpha-1 receptor adrenaline do
vasoconstrict
which adrenaline receptors are found in the heart a lot
b2
what is hyperaemia
incr in blood flow
- active when met activity is increased
- reactive following an occlusion
- compensate by myogenic auto regulation (good in coronary, poor in skin) with local vasdilators
what is diff btwn short and long term BP change
short - baroreceptors
long - volume change (ADH, renin angiotensin)
what do baroreceptors detect
changes in BP (sense pressure changes by responding to change in the tension of the arterial wall)
what are primary baroreceptors
arterial
what are secondary baroreceptors
cardiopulmonary
where are primary baroreceptors found
- carotid sinus (more sensitive)
- aortic arch (less sensitive)
where is the carotid sinus
dilated area at base of the internal carotid just superior to bifurcation of intrernal/external carotid at level of superior border of thyroid cartilage
how do primary baroreceptors work
- increase in BP
- inhibition of SNS causes vasodilation
- increased PNS to heart to - - decrease CO
how do secondary baroreceptors work
- increase BP
- inhibition of medullary vasoconstrictive area
- BP falls
- inhibit release of ADH, renin & angiotensin = lower bloodd vol
where are secondary baroreceptors found
systemic and pulmonary veins
atria
what is the afferent nerve supply to the heart
glossopharyngeal (IX)
what is the efferent nerve supply of the heart
vagus (X)
what are the components of central circulation
blood vessels (vasoconstriction/dilation)
heart (cardiac output)
kidneys (fluid control)
what are the effector vessels of the heart
arterioles
what is total peripheral resistance the same as
total arteriolar resistance
what do central chemoreceptors detect (and here)
- CO2 levels
- medulla
what do peripheral chemoreceptors detect (and where)
- O2 levels
- carotid/aortic body
what is the frank-starling mechanism
EDV increase = SV increase (thus increased CO)
what is the length-tension muscle relationship
muscle stretches for more volume - must contract more to push blood out
what does increased EDV result in
increased contraction = increased SV = increased CO
what does the p wave mean
atrial depolarisation
how long is atrial depolarisation (p wave)
80-100ms
what is the PR interval
slow conduction from AV node to His-Purkinje system
how long is PR interval
120-200ms
what is the QRS complex
ventricular depolarisation
how long is QRS complex
60-100ms
what is atrial depolarisation masked by
QRS
what is ST interval
time btwn vent depolarisation and repolarisation
what is the T wave
ventricular repolarisation
what is the QT interval
ventricular depolarisation and depolarisaion
how long is QT interval
200-400ms
what timeframe does each ecg square rep
0.04s (or 40ms)
*****what are the 5 steps of cardiac/myocyte action potential
is 2 de or re????
*****
0 Rapid depolarisation = Na+ inflow
1 Partial repolarisation = K+ outflow
2 Plateau = slow Ca2+ inflow (still K+ outflow)
3 Repolarisation = Ca2+ channels close, K+ outflow
4 Resting potential = still K+ outflow
what are the 3 steps of pacemaker action potential
- Pacemaker potential [-60v]=
- closed K+ channels
- (T-type) Ca channels open [-40v]
- Slow Ca2+ and Na+ influx - Depolarisation =
- AP begins when threshold released
- More Ca2+ influx (L type) - Repolarisation =
- Ca channels close
- K channels open –> EFFLUX
what is the conduction pathway (from SA node to ventricular contraction)
SA node –> atrial contraction –> AV node –> bundle of His –> purkinje fibres (septum) –> l and r branches –> ventricular contraction
do atrial impulses spread faster or ventricular
atrial
how do AP spread from cell to cell
via gap junctions
what is the cardiac axis
overall direction of electrical activity in heart (can be normal, left, or right deviated)
what is blood composed of
cellular component (45%) fluid component (55%)
what is in the cellular component of blood
RBC, WBC, platelets
what are erythrocytes
RBC
what are leukocytes
WBC
how many leads in an ecg
12
what are the diff ecg leads
3 bipolar leads (+ve to -ve)
6 chest leads (unipolar)
3 augmented leads
which waves are positive for all leads apart from AVr
p and t
is QRS positive on LHS or RHS leads
LHS
what is plasma
serum liquid and proteins dissolved (eg globulins, albumin, fibrinogen)
what is haematopoiesis
formation of blood cells n platelets which continues throughout life
what do rbc and platelets share in common
both anucleate
what is the lifespan of rbc
120d
what is the lifespan of platelets
7-10d
where does haematopoiesis (blood cell prod) occur in children and adults
children - all bone marrow
adults - only axial skeleton
do rbc have mitochondria
no
what is rbc prod stimulate by
EPO (erythropoietin) - released by kidneys
where are rbc destroyed
liver n spleen
what kind of env does o2 bind to iron in
aqueous
what is anaemia
decrease in no. of rbc or Hb in blood
what is acute anaemia
bleeding - less rbc in circulation
what is pernicious anaemia
no b12/folate - rbc not prod quickly enough
what are the 5 diff types of wbc
- neutrophils
- monocytes
- lymphocytes
- basophils
- eosinophils
what s replication and differentiation (haemopoeisis) stimulate by
hormonal growth factors that stimulate precursor cells
RBC - epo
WBC - gm-csf
platelets - tpo
what is a young rbc aka
reticulocyte
which way does oxygen dissociation curve shift when pH is decreased
right
what is a normal range of Hb
12.5-15.5 g/dL
where is folate found
fruit/veg n food supplements
where is b12 absorbed
terminal ileum
what can cause b12 deficiency
lack of gastric parietal cells
lack of terminal ill function
name some types of anaemia
- acute (injury) 2. chronic (inflammatory disorders) 3. iron deficiency (chronic blood loss eg bleeding)
describe WBC
- mature cells
- circulate in blood
- formed from immature precursor cells in bone marrow (which are derived from stem cells)
- rate of prod is under hormonal control of G-CSF
what is the most numerous type of wbc
neutrophils
which WBC release chemotaxis/cytokines important in inflammatory responsee
neutrophils
what are 2 types of monocytes
macrophages and dendritic cells
what is diff btwn 2 types of monocytes?
macrophages: phagocytose bacteria n foreign material
dendritic cells: present antigens to immune system
what do basophils do
migrate to tissues –> become mast cells
- mast cells fill w granules containing histamine and express IgE
what are basophils important for
immune repsonse
what do eoisonophils play an important role in
inflammation and allergic response
what is the ratio of B:T lymphocytes
20:80
where do b and t lymphocytes mature
B - Bone marrow
T - Thymys
what do b lymphocytes do
generate antibodies when stimulated by foreign antigens
what do t lymphocytes do
aid B cells - generate cellular immunity (helper cells)
what are the 2 types of t lymphocytes
helper cells (CD4+) suppress/reg immune response
natural killer cells (CD8+) target damaged/infected cells
which 2 WBC are involved in phagocytosing
neutrophils n monocytes
which 2 wbc are involved in allergic response
basophils n eosinophils
what are platelets
small cytoplasmic enucleate cells that block up holes in blood vessels
how do platelets form a thrombus (3)
adhere
activate
degranulate
list 4 proteins found in blood
- albumin
- imunoglobulins
- coagulation proteins
- carrier proteins
what is the most numerous plasma protein
albumin
which protein determines oncotic pressure of blood
albumin
where is albumin produced
liver
what are immunoglobulins produced by
b lymphocytes - generated when stimulated by foreign antigens
when are IG produced
in response to non-self antigens
what are coagulation proteins
series of enzymes that circulate in an inactive form
vitamin k is essential for correct synthesis of WHICH coagulation factors
10
9
7
2
which cells is tissue factor present on
every cell but endothelial cell
what triggers the beginning of the coagulation cascade
bleeding
what type of inheritance pattern is haemophilia
recessively x linked
what type of inheritance pattern is von willebrand disease
autosomal dominant
what is haemophilia
not enough clotting factors in blood
what is VWF
lack of vwf
where is vit k found
green veg
is vit k fat or water soluble
fat
what is vit k necessary for
functional activity of coagulation factors 2, 7, 9, 10
where is the apex beat of the heart
5th intercostal space, mid-clavicular line
what is the mediastinum
area btwn l and r pleura
which plane divides superior and inferior mediastinum
sternal angle n t4/5
how do papillary muscles attach to AV valves
chord tendinae
which ventricle is systemic n why
left - thick walled n muscular
where does coronary sinus drain blood from heart into
RA
what separates smooth n trabeculated portions of RA
crista terminalis
where do coronary arteries arise from
aortic root
what does the left coronary artery divide into
left anterior descending / left anterior interventricular
circumflex
where does LAD run
in anterior IV groove
where does Cx artery run
left AV groove
what dominant are most ppl
right
what is gastrulation
mass movement n invagination of blastula to form 3 layers (outer –> inner)
- ectoderm
- mesoderm
- endoderm
what is a gastrula
trilaminar structure that the embryo blast develops into
what does ectoderm develop
outside skin
nervous systems
neutral crest
pit/mamm/sweat glands
what does mesoderm form
muscle
most systems
kidneys
blood
what does endoderm form
GI tract
endocrine organs
where is most of CVS formed from embryologically
mesoderm
what are the 3 stages of cardiac formation
- formation of primitive heart tube
- cardiac loop
- cardiac septation
when is heart formed in foetus
w3
when does heart begin to beat
day 22
in foetus, which side of heart is there more pressure?
right bc unfunctional lungs so incr vascular resistance in pulmonary circulation
why is blood shunted from right to left atrium
down pressure gradient
describe foetal circulation
- blood enters RA
- blood flows through foramen ovale
- blood pushes valve of foramen ovale to left
- blood enters LA
what happens to pressure in RHS of heart at birth
drops - pressure greater in LHS (blood in LA pushes foramen ovale valve, closing atrial passageway)
how does oxygenated blood from placenta enter foetus
umbilical vein
what is myogenic tone
vascular smooth muscle is never relaxed
what is the resp pump
- diaphragm descends, pushes abdominal cavity and increases intra-abdominal pressure, which is transmitted to abdominal veins
- simultaneously, pressure in the thorax decreases, decreasing RA pressure and intrathoracic veins (net effect of pressure changes btwn thorax n chest enhancing venous return)
this is the basis for the frank-starling mechanism
how does anterior hypothalamus impact BP/HR
increases
what is pacemaker potential
slow pos incr in voltage across membrane that occurs btwn end of 1 AP and beginning of next
where is the AV node located
base of RA
what is PS stim of heart controlled by
ACh - binds to muscarinic receptors
What is S stim controlled by
Ad/NAd
when does contraction of the hear muscle happen
with Ca entry to cells n and finishes before repolarisation
what is resting membrane potential
-55 0 -60 mV
release of what into sarcasm promotes sliding of actin n myosin
Ca2+
