L2: Anatomy & Physiology Of The CV system Flashcards
What is the biggest part of the heart?
The left ventricle - thicker wall than the right
Atria structures are thin
What is the role of the valves in the heart?
stop blood going the wrong way
increase efficiency of blood pumping through heart
Myocardial structure
- What 2 things does intercalated disks contain?
- Gap junctions- for cell to cell ion movement (rapid spread of electrical signal) –> contraction of heart
- Desmosomes - transfer force from cell to cell (end to end), when cells contract, heart contracts
What is the role of cardiomyocytes?
Consume lots of O2 in heart - most dense tissue for mitochondria
What is the structure of cardiomyocyte sarcomeres?
I band: actin (thin filaments)
H band: myosin (thick filaments
Titin: 2 way spring : helps cell relax after contracting
What is the cardiomyocyte length-tension relation?
- increase in myofilament (actin + myosin) overlap = increase in force
- more stretch (return of blood) = produces bigger contraction (increase in output of blood)
What is systolic and diastolic?
Systolic: contraction of heart
Diastolic: relaxation of heart
How is action potential conducted throughout the cardiomyocytes?
T-tubules allow conduction of rapid action potential
- releases calcium from Sarcoplasmic reticulum –> triggers synchronous contraction
What is the big structural difference btwn cardiac and skeletal myocytes?
Heart has much more mitochondria than skeletal - bc need to continuously move
Explain the cardiac excitation-contraction coupling process
- Ca enters cell during AP plateau
- Triggers release of more Ca from SR
- Ca binds to myofilaments (troponin-C)
- Activates cross-bridge cycling
- Cell shortens
- Most Ca pumped back in SR
- Some Ca exits cell by Na-Ca exchanger and sarcolemmal Ca pump
What is the role of the Troponin complex in the contraction and relaxation of cardiomyocytes?
Troponin complex = TnT + TnC + TnI
- Ca2+ binds to TnC
- TnC changes conformation
- TnI moves away from actin myosin binding site
- Actin binds to myosin and contraction occurs
- As [Ca2+] falls - Ca2+ dissociated from TnC
- TnI again blocks actin myosin binding site
- Relaxation occurs
What happens when TnI is phosphorylated by Beta adrenergic signalling?
Promotes dissociation of Ca2+ from TnC and myocyte relaxation
What is the difference btwn Cardiac and skeletal ECC?
- no. of AP’s
- Excitation
- Regulation of force
- Metabolism
Cardiac
- One plateau (refractory period where heart cant contract again - prevent arrhythmia)
- gap junction spread
- Ca entry
- oxidative only
Skeletal
- many spikes
- motor unit
- AP freq and summation
- oxidative and glycolytic
What happens during isovolumetric contraction?
The heart contract, there is no change in volume but there is change in pressure
How can we measure cardiac function?
Echocardiography - systolic function
- assessed by looking at cross sectional view of heart
How can we measure systolic function?
Echocardiography - systolic function
- assessed by looking at cross sectional view of heart
how can we measure diastolic function?
Echocardiography
- assessed by looking at longitudinal view of heart
How can we measure diastolic function?
Echocardiography
- assessed by looking at longitudinal view of heart
What does the doppler flow (mitral inflow) measure?
and what do the E and A waves represent?
- measures blood flow velocity through mitral valve
- E wave = blood flowing into ventricle by passive filling (due to pressure gradient)
- A wave = blood flowing from atrium into ventricle by active filling (due to atrial contraction)
Doppler flow (mitral inflow)
- what is normal E/A?
- What is impaired relaxation E/A?
normal: E/A > 1
- E wave bigger than A wave
Impaired relaxation: E/A < 1
- as heart stiffens, impaired diastolic function so E wave is similar to A wave
What does tissue doppler (mitral valve movement) measure?
What is E’ wave and A’ wave represent?
- measures velocity of tissue movement at mitral valve
- E’ wave = passive LV filling
- A’ wave = filling due to atrial contraction
Diastolic function
- what happens to E/e’ ratio with increased severity of heart failure?
E/e’ ratio increases with severity
correlates with HF biomarkers
E/e’ ratio declines when heart failure improves
How does electrical activation of myocardium/heart occur?
- Pacemaker in heart - SA node depolarizes the atria
- depolarizes septum (left to right)
- depolarize ventricular walls towards apex and up towards base
What route does an AP travel through the conduction system of the heart?
Action potential travels from SA or AV node –> common bundle –> bundle branches –> purkinje fibres –> myocytes (cause contraction)
ECG: what is… (refer to slides for diagrams)
P wave
QRS wave
T wave
P - due to atria contracting (depolarisation)
QRS - ventricles contracting (depolarisation)
T - ventricular repolarization
What are the biomarkers of heart damage?
What is the process of their release?
Enzymes such as CK-MB, Troponin I (troponin free in cytoplasm, troponin complex released from actin filament), myoglobin
- used to diagnose myocardial infarction
- onset of myocardial infarction
- plasma membrane of necrotic (dead) myocytes become leaky
- mlcs leak out of cell and into circulation
What is the difference in pressure btwn arterial and venous circuit?
Arterial circuit:
- high pressure
Venous circuit
- low pressure to deliver nutrients and O2 and remove waste
Describe the venous return to the heart via calf muscle + role of valves
- the calf muscle acts as pump for deep leg veins
- calf muscle relaxed: valves prevent backflow, valves closed
- calf muscle contracted : valve open, blood flow caused by muscle contraction
What are the characteristics of the diff. blood vessels?
- large arteries
- small arterioles
- capillaries
- large veins
(refer to slides)
- large arteries - pressure reservoir
- small arterioles - resistance vessels
- capillaries - exchange
- large veins - volume reservoir
Where is there the most blood volume distribution?
Most volume in systemic veins and venules
What is distribution of cardiac output through vascular tree and organ beds?
Vascular tree: perfused in series
Organ beds: perfuse in parallel
At rest: highest flow to gut and kidney
Arterioles: control flow through each bed - by local and central signals
What do the lymphatic vessels contain?
excess interstitial fluid, white blood cells, also transports fats from gut
What is the role of the lymph nodes? How does lymph enter the blood?
Role: important in adaptive immune response
Transport: enters blood via lymphatic duct (right side), thoracic duct (left side) - aided by smooth muscle contraction + valves
What happens to the venous and interstitial fluid during oedema?
Oedema: accumulation of interstitial fluid
- increase in venous pressure
e. g. with congestive heart failure - venous pooling
- fluid accumulation in lung
- increase in interstitial pressure
e.g. lymph vessel blockage, parasitic infection, gross oedema of limbs
caused by poor lymph drainage (not capillary dysfunction)
What is blood pressure?
the driving force to push blood through circulation
Role of pressure in resistance of vessels - systemic and pulmonary resistance
Resistance systemic (narrower vessels) >> pulmonary resistance largest overall resistance in arterioles + biggest pressure drop
How to calculate MAP (mean arterial pressure)?
MAP = DP + 1/3 PP PP = SP - DP
How does vasoconstriction and vasodilation occur?
Vasoconstriction: smooth muscle cells contract + increase resistance of vessel
Vasodilation: smooth muscle cells relax and decrease resistance of vessel
Equation for:
Blood flow (velocity)
Cardiac output
Blood flow = pressure gradient (P2-P1)/ resistance
- blood flow decreases with increased resistance
- blood flow increases with increased pressure gradient
Cardiac output = mean arterial pressure / total peripheral resistance (TPR)
CO = HR x SV
Role of Noradrenaline and Adrenaline in Sympathetic NS activation
Noradrenaline: - at smooth muscle cells
Receptor - alpha AR
Response - constrict
Adrenaline - at smooth muscle cells
receptor - beta 2 AR
response - dilate muscle
