week 5 physio Flashcards
cardiac arrest and its consequences
-when the heart stops
-no pulse, loss of consciousnesss,
-irreversible brain damage 4-6 min
->10 mins survival unlikely
normal frequency range of heart and contractions
60-100 beats/min and 100,000 contractions each day
cardiac output
5-6L/min, around 10,000 L per day
mean arterial pressure
90-95 mmHg (under resting conditions)
functional anatomy of heart
1-deoxyblood enters from sup and inf vena cava
2-blood flows to right atrium to tricuspid valve to right ventricle
3-through pulmonary valve (semilunar) out through pulmonary artery to lungs
4-oxyblood from lungs enters to left atrium through pulmonary veins
5-enters left atrium through bicuspid (mitral) valve to left ventricle
6-blood leaves through aortic valve to aorta
what are the 2 pumps of the heart
systems and pulmonary circulation
idk how to write this
-rhythmic contractions of isolated heart
-ventricular contraction is delayed compared to atrial
lala
what is the mechanism of spontaneous rhythmic contractions
-high frequency excitation comes from SA node (pacemaker) or (venous sinus in frogs) but atria and ventricle also generate spontaneous contractions but at a lower frequency
-different issues in the heart generate excitation but at different frequencies
what excitation
production of cardiac action potentials, depolarisation can spread among tissue
Spontaneous generation of excitation
-occurs in SA node (right atrium) and excitation spreads to AV node where delay of excitation occurs, after delay reaches bundle of hiss and then purkinje fibres to the ventricular wall
what’s intrinsic pacemaker frequency
-if we remove all the external regulatory influence from heart then different regions of heart produce a different frequency or excitation so what the intrinsic frequency is without regulation
intrinsic frequency for:
-SA node ~100 beats/min so regulation of SA node is to inhibit as normal is 70 beats/min
intrinsic frequency for:
-atrial and ventricular myocytes
-No, muscle responsible for contraction under normal conditions will not produce spontaneous excitation
intrinsic frequency for:
-AV node, bundle of his
-40-60, intrinsic frequency is lower than that of SA node
what happens of SA node is damaged
-heart won’t stop as AV node will produce excitation but at a lower frequency
intrinsic frequency for:
-bundle branches and purkinje fibres
-20-40, they can and cannot produce, if they do produce its at a very low frequency
under what condition will the atrial and ventricular myocytes produce spontaneous electrical activity
pathological conditions
what response does the nodal tissue have
slow response AP
what response does the myocardium tissue have
fast response AP
don’t forget graphs ***
compare both graphs for SA node and ventricular muscle
-resting membrane potenital for ventricular muscle is constant -80mV so won’t generate AP and requires arrival of excitation of another region to evoke AP, for SA node its minimum value of membrane potential is more positive like -65mV, also not stable resting membrane potential
ion channel of human SA node:
-I f (funny current)
-channel = HCN4 (HCN1)
-ion = Na+
-direction = in
-function = pacemaker potential activated by hyper polarisation -> -50mV & cAMP
ion channel of human SA node:
-I Ca, T
-channel = T type VDCC
-ion = Na+, Ca2+
-direction = in
-function = initial depolarisation (-50, -60 mV), transiet (channel deactivates), tiny (small channel conductance)
ion channel of human SA node:
-I Ca, L
-channel = L type VDCC
-ion = Ca2+
-direction = in
-function = depolarisation (-20 ~ -30 mV), long lasting
ion channel of human SA node:
-I K
-channel = several voltage-gated types
-ion = K+
-direction = out
-function = repolarisation
ion channel of human SA node:
-I K,ACh
-channel = GIRK1/GIRK4
-ion = K+
-direction = out
-function = hyperpolarisation in response to ACh (vagus N)
sequence of channels
1-repolarization (less than -50mV)
2-Na reflux (If current open)
3-depolarisation: prepotential
-reaches -55mV –> T channel for Na+ and Ca2+ influx
4-depolarisation
–50mV If current stops
–25mV L ch: Ca2+ influx (open)
5-further depolarisation
-T ch inactivated (closed) (transient)
6-K+ channels open and K+ outward current
7- repolarisation
-L ch close
-T ch recovers from inactivition
-If current increases
inhibitors of current
-If current inhibited by ivabradine
-T ch inhibited by verapamil
if someone is treated with ivabradine what happens to heart rate?
-heart rate decreases
what are chronotropic effects
-effects that increase or decrease the heart rate
regulation of heart rate
sympathetic:
supplied by and chronotropic effect
-cervical and upper thoracic ggl.
-positive chronotropic effect so increase
regulation of heart rate
parasympathetic:
supplied by and chronotropic effect
-vagus nerve
-negative chronotropic effect so decrease
what does the vagus nerve innervate and what part of the heart does it not innervate?
-right vagus - SA node, -ve chronotropic effect
-left vagus - AV node, in healthy heart does not effect the heart rate but decreases speed of conduction
-vagus does not innervate ventricles
what changes by regulation of the heart
-value of minimum diastolic potential (most -ve value of Em)
-slope of prepotenital (rate of diastolic depolarisation)
what does the post ggl neuron of the sympathetic system release? and what is its receptor? and effects on
-NE
-B1 receptor
-increase cAMP, If, Ica,L
what does the post ggl neuron of the parasympathetic system release? and what is its receptor? and effects on ????????skip
-Ach
-M2 muscurinic receptor
decrease cAMP, If, Ica,L
2 properties of HCN channel
1- activated by hyperpolarisation
2-activated by cAMP binding
difference between Ca dependant voltage T type and L type channel
-L type has higher (more positive) threshold for opening
what happens if pacemaker activity of SA node fails?
-the other cells containing HCN channel that produce funny current take over excretory activity
-region with highest rate of depolarization can take over pacemaker activity -therefore second highest frequency region takes over
which regions become a pacemaker if SA node activity fails?
-AV node
-AV bundle of his
-tawara branches
-purkinje fibres
add gNa
add gCa
add gK1
gTO
gK
flowchart of ventricular myocyte
read diagram ****
1-conducted stimulus
2-depolarization at -60mV
3-Na+ ch open, o Na+ flux
4-causes further depolarisation
5-IRK K+ ch close
- Na+ ch inactivates
6- -30mV reached, L type VDCC opens with maintains Ca2+ influx
7-further depolarisation
8- 20mV reached early depolarisation
9-plateau
what is the L type voltage dependent Ca2+ channel depend regulated by
Protein Kinase A activates it
importance of activation of B1 receptor of cardiac myocyte
-production of cAMP
-activation of PKA
-phosphorylation of L type channel
what does larger calcium influx result in
-stronger contraction
what stimulates B1 receptor
isoproterenol
what happens if the voltage gated K+ channels (responsible for depolarisation in cardiomyocyte AP) are mutant in some individuals?
-may have fatal cardiac arrhythmia
when Em larger than Ek, is direction of current inwards or outwards
-outwards
