CVS Theoretical Flashcards
What is functional synctium and how is it acheived in the heart?
Activity spread so quickly that it contract as 1 - via intercalated disc and gap jct
Describe myocardial structure
Sarcomere - contractile unit of myocardial cell (z line- z line), contain thick myosin filaments and thin (actin, troponin and tropomyosin filaments), shortening vis sliding filament model
Intercalated discs - end of cells maintain cell-cell cohesion
Gap jct - at intercalated discs, are low resistance path to allow spread of AP
Numerous mitochodia (more than skeletal)
T tubules - continous w/ cell membrane, invag cells at z line and carry AP to cell int, well develop in ventricles
- -tubule with a terminal cistern is known as a diad
SR - sm D tubules near contracile elements, site of ca2+ storage and release for excitation contraction coupling
Specialized excitatory and conductive system of the
heart
SAN > intranodal pathway (intraatrial pathway to other atria) > AVN > BoH > purkinje fibres > ventricular msc
SAN - 100b/min, conduction rate - 0.5m/s
- 100bp/min no resting potential (constant AP), x myocytes (just excitable cells), pacemaker potential, autonomic control
- PS - vagus, increased activity > dec . HR, ACh at M2 R, hyperpolarises cell (open K+ channel), decrease slop of pacemaker potential (harder to reach threshold)
- S - exit T1-l2, increased activity increas HR, NA and Adr on B1 R,
AVN - 40beat/min, conduction rate - 0.05m/s
AP In cardiac msc
Resting membrane potential - -85-90mV
AP - 105 mV (0.2s depol in atria and 0.3s in ventricles)
SAN -
- pre potential - (slow diastolic depolarization) - Increased
Na+ [not VG as would depolarise too quick] and K+ permeability and completes as Ca 2+ T (transient) channels open
- AP - Depolarization (Ca2+ L (long-lasting) channels - inward movement of Ca2+ and closure of K+ channels) + Repolarization – K+ channels move out
Properties of Cardiac musc
Excitability - the ability to give response to a stimulus.
Contractility (inotropism) - innate ability to develop force at given msc length 9related to Ca2+)
COnductivity
Rhythmicity - produce own impulses regularly (autorhythmicity or self-excitation)
- Veins and Their Fct
Low pressure, low resistance vessels w/ high capacitance (distensibilty =vol/P), - can distend with increasing pressure of blood >carry more blood.
COntain valves to prevent backflow
Endothelium, CT, TM (sm msc), tunica ext (CT)
RAP = CVP (normally 0mmhg but increase in heart failure) -responsible for filling RA during ventricular systole
Periph vein - 4-7 mmhg
FCT
Return deoxygenated blood to heart and act as reservoir for blood
Venous Pressure = driving force for heart filling - determined by
- peripheral resistance - inc >dec VP, dec > inc VP
- CO - rate heart pumps out blood - inc > blood is rapidly pumped out of veins> reduces VP, dec CO > blood is slowly pumped out of veins> inc VP
- gravitation P - lying (lower) STanding (VP higher)
CVP - filling pressure of heart (increased CVP > inc periph VP)
Mechanism of blood flow return to heart
1) Valve presence
2) skeletal msc pumps of legs
3) lig. Inguinalae contraction during the movements
4) contractions of the diaphragm during the inspiration (reduce intrathoracic pressure)
5) Compliance – Incr sympathetic > reduce venous compliance > l increase VP and VR (when flow into the veins increases > cannot dilate to accommodate the increased blood so VP inc)
6) Blood Volume – inc vein BV > inc VP veins (heart can accommodate the increased blood volume because of the Frank-Starling mechanism (the greater the stretch, the greater the contractility of the heart))
28 - Rapid control of arterial pressure
Control of arterial pressure Mechanisms:
1) Short term (rapid control) mechanism
2) Long term mechanism
Arterial pressure = cardiac output x peripheral resistance
Rapid control (mediated by NS and Chemicals)
Mediated by nervous system and chemicals
1) ANS ( help control HR and force of contraction)
- Sympathetic activity (CN 9 ) -> increases vasoconstriction ->arterial pressure increases, HR increases and cardiac output increases. [+
- Parasympathetic activity (vagus nerve) increases vasodilation therefore decreases arterial pressure, HR
lower and cardiac output decrease.
There are arterial pressure sensing receptors on the carotid sinus and aortic arch called baroreceptors (carotid to CN9 + aortic to CN10)j. If BP
increases baroreceptors sense the increased pressure and send signals to NTS in medulla -> stimulates cardio inhibitory centre (CIC) -> vagus to SAN -> Ach -> M2 receptors
NTS also inhib cardio accelator nucleus (CAN) (normal sympathetic outflow to SA node inhib -> HR and CO is reduced) AND inhibits vasomotor centre(-> vasodilation of the veins and arterioles)
Reversed in the case of low BP.
Chemoreceptors
Chemosensitive cells found on the carotid body and aortic body respond to changes in pCO2 and pO2 and pH levels
If BP is low, pCO2 and pH are also low and pCO2 is high, -> stimulate respiratory centre, cardioacceleratory centre , vasomotor centre and inhibit caridoinhibitory centre -> CO and HR and vasoconstriction resulting in increased BP.
29 - Long term control of Arterial Pressure
Long term control
When blood flow is low, BP is decreased so the juxtaglomerular apparatus is less stretched so they release renin enzyme. when the renin level in blood is increased liver produces enzyme called angiotensinogen, to which renin
binds and convert angiotensinogen to angiotensin I. Angiotensin I will then pass through the pulmonary circulation
where angiotensin converting enzyme converts angiotensin I to angiotensin II ->cause vasoconstriction, act on hypothalamus to stimulate thirst feel thereby increasing blood volume resulting in increased
BP.
All sympathetic nerve have receptors for renin so upon interaction with renin, norephinephrin. The main course
of action of angiotensin II is its ability to stimulate adrenal gland to release aldosterone. Aldosterone works on the
principal cells in the collecting tubules of the nephron to retain sodium and water thus adding to the blood volume
resulting in increased blood pressure.
