Physio Flashcards
Explain the pacemaker potential
Phase 4: resting membrane potential. membrane is -60 mv opening of slow Na channels that give inward current which causes depolarization
Opening of T-type Ca channels with Ca inflow, reaches -40 mV
Phase 0: firing level. closure of slow Na and T Ca channels. Opening of L-type Ca channel giving slow AP response and opening of delayed rectifying K+ channels
Phase 3: repolarization
Opening of delayed rectifying K+ channels, closure of LCa channels and in activation of delayed rectifying K+ channels and activation of slow Na channels restarting a new phase 4
Factors affecting rate of discharge of SA node?
Body temp: for every degree 10 heart beats
Autonomic activity:
Sympathetic: tachycardia
Parasympathetic: bradycardia
Catecholamines: adrenal medulla releases adrenaline and noreadrenaline which increases HR
Extracellular K level: hypokalemia is tachycardia and hyper is bradycardia
Ca channel blockers: in activation causes bradychardia
What are the factors affecting inotropic state of cardiac myocytes
Positive inotropic:
increasing sympathetic or catecholamines which increases Ca in cells
Glucagon: increases c-AMP in myocytes
Increase ECF Ca which makes more inter the cell
Drugs: digitalis and caffine
Negative inotropic:
Ischemia: hypoxia to cardiac muscle
Increase parasympathetic: release acetylcholine which decreases c-AMP
Adenosine: — c-AMP
Drugs: Ca channel blockers and anesthetic drugs
Explain myocyte action potential
Phase 4: RMP
K+ slowly moves out (Ik1) through inward rectifying potassium channels IRK to reach RMP (-90 mV)
Phase 0: Depolarization goes to +20 mv
fast Na channel op and Na influx
IRK close
Fast Na channels close
Phase 1: rapid small initial repolarization
Fast Na are inactivated
transient outward channels op
Phase 2: plateau
L Ca open, inward Ca current
Na and Ca exchanger active
Op of delayed rectifying K
Phase 3: rapid repolarization
Long lasting Ca channels closed
K outward current and then closer of DRK
op of IRK
Describe the excitation contraction coupling
Membrane depolarization–> op of L type Ca–> Ca enters below sarcolemma which open ‘ryanodine Ca channel” which cause SR to release Ca
❶ Ca++ binds to Troponin-C → removes blocking action of tropomyosin. Myosin binding sites become exposed allowing myosin to bind to actin.
❷ Ca++ release decreases when AP ends.
❸ Relaxation: Ca++ is removed from the cytoplasm by:
a. Ca++ pump into SR
b. Ca++ is transported into ECF by:
• Na+ -Ca++ exchanger
• Ca++ pump
Effect of changing afterload on cardiac muscle performance
Effect of changes in afterload on muscle shortening:
+++ afterload → —- degree of shortening
Effect of changes in afterload on velocity of shortening:
• +++ afterload → —- velocity of shortening
velocity can be zero if load greater than max tension
Effect of changing preload on cardiac muscle performance
Effect of changes in preload on muscle shortening:
+++ preload →+++ degree of shortening
b. Effect of changes in preload on velocity of shortening:
• +++ preload → +++ velocity of shortening
Describe the effect of changes in heart rate on cardiac output
+++ HR alone from 70-140 beat/min → no change in CO (because of —– ventricular filling → —–SV → thus no change in CO)
+++ HR alone above 150/min → —- CO (marked —- in SV can’t be compensated by the +++ in HR)
—- HR alone below 60/min → —- CO (marked —- in HR can’t be compensated by the +++ in SV)
During muscular exercise, +++ HR (doubled) → +++ CO (more than double) because of the associated +++ in SV (+++sympathetic)
Describe the effect of changes in afterload on stroke volume
At constant preload, +++ afterload → —- SV
At constant preload & afterload, +++ inotropy → +++ SV
Describe the effect of changes in preload on stroke volume
+++ preload → +++ SV
Several factors can affect ventricular preload:
- +++ venous pressure & VR → +++ ventricular filling → +++ preload
- Strong atrial contraction → +++ preload.
- +++ HR (with constant VR) → —- preload (no enough time for ventricular filling)
- —- ventricular compliance (hypertrophy or myocardial infarction) → —- preload
Describe the venous return curve and describe the factors affecting it
Effect of changes in right atrial pressure on venous return curve: +++ RAP → —- VR —–RAP→+++ VR
Effect of changes in MSFP on venous return curve:
+++ MSFP→ shift of VR curve up & right
—–MSFP→ shift of VR curve down & left
What are the mechanisms that help venous return against gravity?
Muscle pump
Venous valves
Thoracic pump: During inspiration it sucks up VR
Heartbeat effect: atrial suction and ventricular suction
Define Edema, mention its causes
Abnormal large accumulation of ISF in lower limb
Causes:
Inadequate lymph flow, like elephantiasis
Decrease osmotic pressure gradient: decrease plasma protein level.
-accumulation of osmotically active substance in the interstitial space
Increased filtration pressure: high venous pressure
Increase capillary permeability, histamine
What is meant by autoregulation? Explain it’s types
Intrinsic capacity of vascular beds to compensate for moderate changes in perfusion pressure by
changing vascular resistance so that blood flow remains constant
Myogenic autoregulation:
Aim: maintain constant blood flow to an organ in spite of increase in its perfusion pressure
Mechanism: +++ perfusion pressure–> increase in blood flow and makes blood vessels distended which causes Ca to enter and cause VC increasing the resistance.
Metabolic auto-regulation: maintain constant blood flow to organ despite decrease of perfusion pressure
—- perfusion pressure → initial —- in blood flow
→ +++ VD metabolites → relaxation of arterioles & pre-
capillary sphincters → — resistance →+++ blood flow
Give an account of the diff vasoactive substances secreted by endothelium.
NO: stimulated by acetylcholine and its action is VD of coronary, cerebral and pulmonary vessels
Endothelin-1: Stimulated by Hypoxia, catecholamines, stress. Inhibited by NO, prostacyclin
VC of veins, renal VC, pulmonary VC and coronary VC, positive chronotropic and inotropic effect
Prostacyclin: Action: VD, decrease platelet aggregation and facilitates NO release.
Explain natriuretic peptides types, synthesis, stimulators and action
a. Atrial natriuretic peptide (ANP) → by atrial myocytes
b. Brain natriuretic peptide (BNP) → by ventricular myocytes & brain.
c. C-type natriuretic peptide (CNP) → endothelial cells, brain, kidney
Secretion is increased by:
❶ Stretch of atrial muscle fibers
❷ +++ Na+ concentration in ECF.
❹ Angiotensin-II.
❸ +++ sympatheticß-adrenoceptors.
❺ Endothelin.
Actions: counters ABP raising affects; decreases blood volume
Describe the role of atrial baroreceptors in arterial blood pressure regulation
Found in left and right atrium as well as pulmonary vessels.
Stimulation:
❶ Distension of atrial walls.
❷ +++ blood volume → +++ their discharge.
❸ — blood volume (hemorrhage) → — their discharge.
Stimulation leads to VD and increase HR
Prevents accumulation of blood in atria and pulmonary vessels.
Describe the role of peripheral chemoreceptors in arterial blood pressure
found in carotid and aortic bodies,
Stimulation:
❶ Primarily concerned with respiratory regulation
❷ Marked — in ABP → — blood flow in carotid, aortic bodies → hypoxia → +++ of peripheral chemoreceptors
Response: +++ Peripheral chemoreceptor → tachycardia and VC to increase ABP
Describe the role of the kidney in regulation of arterial pressure
I-Renal pressure naturesis: Basic and most important mechanism for long-term regulation of ABP:
a) +++ ABP → +++ renal excretion of Na+& water → pressure natriuresis → — – ECF volume & ABP. Pressure natriuresis continues until — ABP to normal level.
b) — ABP (hemorrhage) → — renal Na+ & H2O excretion → minimize the —- of ABP.
II- Renin-angiotensin-aldosterone system:
❶ — ABP → +++ rennin → angiotensin II → long-term regulation of ABP through:
a) — Na+ and water excretion by the kidneys.
b) +++ aldosterone → +++ Na+& H2O reabsorption → +++ ECF volume → +++ ABP
❷ +++ ABP → — angiotensin II & aldosterone → +++ Na+& H2O excretion → — ECF volume → —- ABP back to normal.
III- atrial natueratic peptide secretion
When ECF increases, it causes stretch on atrial muscle—>secretes ANP—> +NA excretion —> -ECF
IV- Vasopressin secretion: decrease of ECF —> atrial receptor inhibition —> +vasopressin —> - H2O excretion
Describe rapid compensatory reaction to hemorrhage.
❶ — ABP → — arterial baroreceptors
❷ — blood volume → — atrial volume receptors
❸ — blood flow rate → +++ peripheral chemoreceptors
VC of skin, renal vessels and arterioles and veins
increase HR and inotropic state of heart
Release of catecholamines like adrenaline
Angiotensin II: VC, thirst sensation
ADH: increase water retention 1
Describe the long term compensatory reaction to hemorrhage
Correction of plasma volume: tissue fluid shift, thirst sensation aldosterone (for Na and H2O reabsorption and ADH secretion to decrease water waste.
Correction of plasma proteins: 4 days and formed by liver, enters blood from extra vascular stores. Mainly albumin.
Correction of RBC by increasing erythropoietin. Takes 4 weeks.
Regulation of coronary vascular resistance
Factor controlling diameter of coronaries
Myogenic autoregulation:def
Metabolic regulation: high exercise makes coronary VD and increase coronary flow to match.
endothelial regulation:
VD substances like NO
VC like endothelin
Sympathetic and parasympathetic: cause VC and VD
Factors controlling coronary blood flow
During systole: contraction of myocardium causes VC of coronaries and increase the resistance sub endocardium area is mosey susiptable to ischemic injury
During early diastole: Ventricular relaxation and increase perfusion pressure in aorta which is the most important factor for coronary perfusion and greatest on the left ventricle.
Define intra-pleural pressure value causes and importance
normal expiration: -3 Normal inspiration: -6
forced inspiration: -40 Forced expiration: +50
Function of IPP: helps lung expansion and VR
Causes of the negativity of IPP
Recoil tendency of the lungs due: elastic tissue and surface tension of alveoli
Expansion tendency of chest wall due: Elasticity of muscles tendons of chest
Discuss nature/ functions of surfactant/ causes of surfactant deficiency
Formed of lecithin
it decreases surface tension by
① Facilitate lung expansion during inspiration (↓effort)
② Prevent alveolar collapse during expiration
③ Prevent pulmonary edema