Physiology Flashcards
Pacemaker potential in SAN/AVN(slow depolarisation to threshold) is from ___ to ___ mV
It is due to ___ + ___
-60 to -40mV
slow Na+ influx - If and Ib - funny current and background Na current
ICaT - transient Ca2+ influx
decreased Ik - less K+ efflux
The action potential in SAN/AVN(rapid depolarisation) is from ___ to ___ mV
It is due to ___
-40 to +10mV
Voltage-gated Ca2+ channels open for rapid influx of Ca2+ - ICaL
Repolarisation in SAN/AVN is from ___ to ___mV
It is due to ____ + ____
+10mV to -60mV
K+ channels open (efflux - increase Ik) and Ca2+ channels close
Electrical impulse travels between myocytes through ____
gap junctions
3 stages of SAN/AVN electrical activity
pacemaker potential - spontaneous slow depolarisation
action potential - rapid depolarisation
Repolarisation
____ and ____ allow rapid conduction of AP to ventricles
Bundle of His, its branches and the Purkinje fibres
Resting potential in cardiac myocytes is
-90mV
Phase 0 of cardiac myocyte AP is from __ to __mV
Due to ___
-90 to +30mV - depolarisation
Fast Na+ influx
Phase 1 of cardiac myocyte AP is due to ___
transient K+ efflux (Ito)
closure of Na+ channels
Phase 2 of cardiac myocyte AP =___
Due to ___
Plateau phase
Opening of voltage-gated Ca2+ (influx - ICaL)
INaL (late Na influx) w. NCX1 (1Ca in:3Na out)
Phase 3 of cardiac myocyte AP = ___
Due to ___
Repolarisation
K+ channels open (efflux) Ik
closure of Ca2+ channels
Phase 4 of cardiac myocyte AP =
maintained at -90mV
______ is the dominating ennervation of the SAN at rest
Vagal tone (parasympathetic)
Normal HR at rest =
60-100bpm
Vagal nerve causes release of __ to ___ receptor in the _____
ACh to M2 receptor
SAN and AVN
Parasympathetic effect on pacemaker potential in SAN
hyperpolarisation, threshold increases = -ve chronotropic
Increases perm. to K+ and decreases perm. to Na+ & Ca2+
Parasympathetic NS has a chronotropic+/ionotropic effect on the heart
-ve chronotropic
NO IONOTROPIC
Sympathetic nerves supply _____ in the heart
SAN, AVN and myocardium
Parasympathetic effect on the AVN
increases delay
Sympathetic nerves causes release of __ to __ receptors in the heart
noradrenaline beta1 adrenoceptor
Effect of sympathetic NS on SAN
threshold decreases, decreased perm to K+ increased perm to Na+ and Ca2+ - increases slope of pacemaker potential
=> +ve chronotropic effect
Sympathetic NS has a chronotropic+/ionotropic effect on the heart
+ve chronotropic and ionotropic effect
QRS complex =
ventricular depol.
masked atrial repol.
T wave =
ventricular repol.
PR interval =
mainly AVN delay
ST interval =
ventricular systole
TP interval =
diastole
P wave =
atrial depolarisation
Desmosomes are located in ___ and provide ___ allowing ___
the intercalated discs
mechanical adhesion
tension development between myocytes
In the heart: Myosin + ___ -> + ___ = ____ formation allowing for binding to _____
ATP ; Ca2+ ; cross-bridge ; actin
In the heart: actin + myosin -> ___ + _______ -> ____
ADP, Pi + energy released ; powerstroke as myosin bends ; A + M detach
Excitation-contraction coupling in cardiac myocytes
systolic Ca2+ influx at Phase 2 stimulates CICR from SR so binding site on actin available for myosin
location of SR
covers myofibrils in muscle cells
effect of increased intracellular Ca2+ in actin myosin binding
Ca2+ binds to troponin on tropomyosin and pulls it away from the binding site on actin
Long refractory period in cardiac myocytes is from ___ to ___
depolarisation to repolarisation
Stroke volume definition =
blood vol ejected from each ventricle per heart beat
EDV-ESV
Intrinsic control of stroke volume =
change in diastolic length of myofibrils (EDV/preload determined by venous return)
Staling’s law of the heart
increased EDV/venous return => increased stroke volume
stretch in cardiac myocytes ____ troponin affinity for Ca2+
Stretch increases troponin affinity for Ca2+
Optimal fibre length in cardiac myocytes =
stretched
Starling’s law partially compensates for a decreased SV as ____
heart doesn’t eject full volume so EDV increases => SV increases by Starling’s law
Extrinsic control of stroke volume =
sympathetic NS to ventricular myocytes
Hormones - adrenaline and noradrenaline
How does the symp. NS cause +ve ionotropic effect on ventricular myocytes?
cAMP mediated Ca2+ channels activated = increase force
Shifts Starling curve to the left (contractility at a given EDV is greater)
Aortic area on the chest =
2nd intercostal space
R of sternum
Pulmonary area on the chest =
2nd intercostal space
L of sternum
Tricuspid area on the chest
4th intercostal space
L of sternum
Mitral area on chest
5th intercostal space
Mid-clavicular line
a wave in JVP =
atrial contraction
c wave in JVP =
tricuspid valve bulges into R atrium as ventricles contract
v wave in JVP =
atrial filling
The dicrotic notch in aortic pressure occurs at ____ due to ____
the end of ventricular systole
closure of the aortic valve
isovolumetric ventricular contraction and relaxation occur when
the AV valves and the aortic/pulmonary valves are shut
Ib background Na current in the pacemaker potential is due to ___
“leaky cells” = influx of Na
If (funny current) is mediated by _____
HCN channels
hyperpolarisation-activated cyclic nucleotide gated channels (influx Na and efflux K)
beta 1 stimulation in AVN causes _____ by increasing ____
increased conduction velocity
If and ICa
beta 1 stimulation in SAN causes ____ by ____
increased HR
steeper pacemaker potential slope by If+ ICa increase
lowers threshold by increasing ICa
beta 1 stimulation causes +ve ionotropic effect by ____
increase Ca2+ influx and sensitise tropomyosin to Ca2+
beta 1 stimulation causes an increase in _____ activity which speeds up ___
NaKATPase
repolarisation
Sympathetic enervation of the heart causes the length of systole + diastole to _____
Both shorten
ACh to M2 receptors in SAN+AVN cause ____ subunits to open ____ causing ______
βγ ; GIRK (K+ channels) hyperpolarisation
Parasympathetic NS increases SAN threshold by ____
decreasing ICa
Parasympathetic NS does not supply the _____ in the heart
ventricular myocytes
AVN delay is increased by the parasympathetic NS by ___
decreased Ca2+ channel activity and GIRK hyperpolarisation
Parasympathetic NS ____ atrial refractory period and may => ____
shortens
atrial arrhythmias
HCN channels are activated by
hyperpolarisation
cAMP
SERCA =
Its role is to ____
SR Ca2+ATPase
sequestration of Ca2+ into the SR so cardiac myocytes relax
CICR is caused by Ca2+ activating ____ receptors
ryanodine type 2 (RyR2 receptors)
greatest p.d. detected when lead is _____ to dipole
parallel
Limb lead I goes from ___ to ___
R arm (-ve) to L arm (+ve)
Limb lead II goes from ___ to ___
R arm (-ve) to L leg (+ve)
Limb lead III goes from ___ to ___
L arm (-ve) to L leg (+ve)
Depolarisation towards a +ve electrode causes
upwards deflection in ECG
P wave’s normal duration=
0.08 - 0.1s
normal duration of QRS =
less than or equal to 0.12s
Q wave = ____ depol of ___
L->R depol of intraventricular septum
R wave = depol of ____
main ventricular mass down towards the apex
S wave = depol of ___
ventricle from apex upwards
T wave = repol of ventricles from ___ to ___
epicardium to endocardium towards the apex
normal PR interval =
0.12 - 0.2s
aVR lead electrodes =
L arm and L leg (-ve) to R arm (+ve)
aVL lead electrodes
R arm and L leg (-ve) to L arm (+ve)
aVF lead electrodes
R and L arm (-ve) to L leg (+ve)
V1 is placed ____
4th intercostal space R of sternum
V2 is placed ___
4th intercostal space L of sternum
V4 is placed ____
5th intercostal space L midclavicular line
V5 is placed ____
5th intercostal space L anterior axillary line
V6 is placed ___
5th intercostal space L mid axillary line
V1 and V2 look at the ____
septum
V2-4 look at the ____
anterior of the heart
V5-6 look at the ____
lateral border of the heart
1st Korotkoff sound =
peak systolic pressure
5th Korotkoff sound =
no sound! diastolic pressure
MAP equations
2dbp+sbp/3
dbp + 1/3(sbp-dbp)
COxTPR
normal MAP =
70-105mmHg
___ MAP = can’t perfuse heart brain and kidneys
less than 60mmHg
Short term control of bp is by ___
baroreceptor reflex
baroreceptor firing increases if ___
bp increases
baroreceptors are found in ___
and enervated by ___
carotid sinus (CN IX) aortic arch (CN X)
Reflex that prevents postural hyypotension
baroreceptor reflex
Parasympathetics decrease MAP by
decreasing HR => decreased CO
Sympathetics increase MAP by
increase HR and SV => increase CO
increase TPR and venous return
Long term regulation of MAP is by ____ adjusting ___
hormones
blood volume
Hormones involved in MAP regulation =
RAAS - Angiotensin II and aldosterone
ANP
ADH/vasopressin
Renin is released from ____
juxtaglomerular apparatus (macula densa (monitor tubular Na) extraglomerular mesangial cells and granular cells (release renin))
Renin is released in response to ___ (3)`
renal artery lbp
stim of renal sympathetic nerves
decreased Na concn in renal tubular fluid
___ is made up of ___ +___ and controls MAP by __
___ makes up 1/3 of total body fluid
extracellular fluid (ECF) = plasma (PV) + interstitial volume PV controls MAP ECF =1/3TBF
Angiontensinogen is produced in the ___ in response to ___
liver
renin
ACE is produced by ____
the lungs - pulmonary vascular endothelium
Angiotensin II stimulates ___
aldosterone release
systemic vasoconstriction
ADH release and thirst
Aldosterone is released from ___
acts on the ___ causing ___
adrenal cortex (a steroid hormone) kidneys - Na and H20 retention
RAAS increases MAP by increasing __ + ___
plasma volume and TPR
ANP is synthesised in ___
atrial myocytes
ANP is released when ___ and causes ___ and___
atrial distension occurs (hypervolaemia)
kidneys excrete more Na and H20
vasodilation
ADH is synthesised in ___ and stored in ___
hypothalamus
posterior pituitary
ADH is released when ___ receptors located ___ sense ___
osmoreceptors ; in brain close to hypothalamus ; ^ plasma osmolarity
ADH effects:
reabsorption of H2O from kidney tubules
vasoconstriction
vasodilating substances eg. __
activate ___ on endothelial membrane ->^_->___ activates __ to turn ___ into ___+___
bradykinin, ADP, 5-HT
GPCR > ^Ca2+ > eNOS = l-arginine + O2 -> citrulline + NO
NO activates ___ and ___
End result = vasodilation
Ca2+ dependant K+ channel (K+ efflux)> hyperpolarisation
guanylate cyclase catalyses gTP>cGMP activates protein kinase G
Endothelin causes ___ by acting on ___ causing ___
vasoconstriction (most potent vasoconstrictor)
ETa receptors on SM => ^Ca2+
Increase synth of endothelin
adrenaline, angiotensin II, ADH
decrease synth of endothelin
NO, A/B/CNP, sheer stress
pulse pressure =
sbp-dbp
TPR =
Mainly controlled by
blood viscosity x length of vessel/radius^4
arteriolar radius
Intrinsic control of vascular SM=
metabolic changes (chemical and humoural), temperature, myogenic stretch response
main control of brain bp by effect on vascular SM
myogenic response to stretch
Factors that increase venous return:
sympathetic nerves, contraction of skeletal muscle
increased respiratory pump, increased blood volume
Exercise causes a ___ pulse pressure by ____
wider - increasing sbp and decreasing dbp
local metabolic changes that cause vasodilation
increased CO2, H+, extracellular K+, osmolarity of ECF, adenosine (from ATP)
decreased O2
local vasodilators =
histamine, bradykinin, NO (serotonin)
local vasoconstrictors =
endothelin, leukotrienes, thromboxane A2 (serotonin)
hydrophobic core of lipoproteins =
cholesteryl ester and triglycerides
hydrophilic coat of lipoproteins=
monolayer of amphipathic cholesterol
phospholipids
more/=1 apoprotein
HDL has apo
A1 and A2
LDL has apo
apoB100
VLDL has apo
apoB100
chylomicrons have apo
ApoB48
Function of apoB containing lipoproteins
deliver tri.s to muscle/adipose tissue
ApoB lipoprotein involved in exogenous pathway=
formed in ____
transports ____
chylomicrons
intestinal cells
dietary tri.s
ApoB lipoprotein involved in endogenous pathway=
formed in ___
transports ___
VLDL
liver
tri.s synthed in liver
lipidation of ApoB lipoproteins is performed by ___
MTP - adds ApoB to lipoprotein
Most of the cholesterol in chylomicrons is from __
75% bile salts
25% dietary
ApoB lipoproteins are activated by
apoCII on HDL
allows delivery of tri.s
___ allows ApoB lipoproteins to bind to ___ which ___ tri.s allowing them to ___
ApoCII ; LPL ; hydrolyses ; enter the tissues
LPL is released from ___
capillary endothelium in adipose and muscle cells
Once LPL dissociates from chylomicrons+VLDL ___ is transferred to HDL in exchange for ___ and they =
ApoCII for ApoE
=remnant (cholesteryl ester rich)
after chlomicrons+VLDL become remnants they go to the ___ where they are metabolised by ___
liver
hepatic lipase
Receptor mediated endocytosis in hepatocytes clear __
all apoB48 and 50% of apoB100 remnants
hepatic lipase remove tri.s from ____ to form ____which then becomes ___ as ___ is lost and only ___ remains
50% of apoB100 remnants
IDL>LDL - apoE is lost, apoB100 remains
LDL receptors (esp. in hepatocytes) bind to LDL > _____ > ____ where cholesterol is released by ____ >LDL receptor is
endocytosed>lysosome>hydrolysis>recycled to the membrane
LDL uptake by LDL receptors => (3)
inhibits HMG CoA reductase (de novo chol synth)
storage of cholesterol
less LDL receptor expression
___ is released when vessel endothelium is damaged. It is oxidised to form ___
LDL>atherogenic oxidised LDL (OXLDL)
OXLDL is taken up by ___ and converted to ___
macrophages> cholesterol laden foam cells
inflammatory substances released in vessel damage =>
division and proliferation of SM cells into intima and collagen laid down
ie. plaque and fibrous cap form
Function of HDL
reverse transport of cholesterol
blood->liver
HDL is formed in the ___
liver
cholesterol and cholesteryl ester are taken into hepatocytes when HDL interacts with
SRB1 (scavenger receptor)
In plasma - ___ mediates the transfer of cholestryl ester from HDL to VLDL+LDL
This =
CETP - chol. ester transfer protein
indirect chol. return to liver
High tri.s damage the ____
pancreas
Extra O2 to cardiac tissue is only achieved by ____ as o2 extraction is already at 75% (compared to 25% normal tissues)
increasing blood flow
Intrinsic control of coronary artery blood flow __
Extrinsic control of coronary artery blood flow ___
intrinsic: metabolic hyperaemia causes decreased PO2 -> vasodilation
extrinsic: sympathetics = constriction (overridden by intrinsic) and adrenaline vasodilation
Pulmonary bp normally =
20-25/6-12mmHg
pulmonary capillary pressure =
systemic =
8-11mmHg
17-25mmHg
hypoxia causes pulmonary vessels to
vasoconstrict - to divert blood away from poorly ventilated areas of lung
Blood volume _____ in varicose veins to compensate therefore CO ___
blood volume increases
CO remains the same
Exchangeable proteins pass though capillary endothelial cells by ___
vesicular transport
forces favouring filtration in capillaries
Pc (capillary hydrostatic P)
+
πi (interstitial fluid osmotic P)
forces opposing filtration in capillaries
πc (capillary osmotic P)
+
Pi (interstitial hydrostatic P)
arteriolar end net filtration pressure =
favours ___
+10mmHg
filtration
venular end net filtration pressure =
favours ___
-8mmHg
reabsorption
which is greater in a day filtration or reabsorption in capillaries?
Filtration by 2-4litres
Excess is returned as lymph
Filtration/reabsorption is favoured in pulmonary capillaries as ___ is low and __ is normal
reabsorption ( still is a nett filtration movement though)
Pc is low
πc is normal
Oedema causes
1) increase capillary P =
2) increase venous P =
3) decreased plasma osmotic P =
4) lymphatic insufficiency =
5) changes in cap. permeability =
1) arteriolar dilatation
2) LV failure (pulmonary)
RV failure (peripheral)
prolonged standing (ankles)
3) plasma protein
Isoelectric complex =
The axis lies ____ to the isoelectric complex
positive and negative deflections are equal in size
at 90degrees
