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
Causes of surfactant deficiency
① Respiratory distress syndrome
• in premature infant →↓ Surfactant →↑ surface tension → lung collapse
②Long term inhalation of 100% 02 or use of pump oxygenator in cardiac surgery
③ Obstruction of branch of pulmonary artery
④ Heavy smokers
⑤ Hypothyroidism
⑥ Hypocorticism
⑦ Hyperinsulinsm:
List factors affecting airflow in respiratory passage
Physical factors:
negative intrapleural pressure: During inspiration → more negative intrapleural pressure → more airways distention →↓ airway resistance.
Lateral tension: During inspiration as alveoli expand → exerts lateral traction on small airways →↓ airway resistance.
Nervous: sympathetic and parasympathetic
Chemical factors: cause bronchoconstriction like hitamine
Define dead space, type significance?
Part of respiratory system that doesn’t take part in gas exchange
❶ Anatomical Dead Space: volume of air in the conducting zone = 150 ml
❷ Physiological dead space = anatomical dead space + alveolar dead space. in normal both are the same
Significance:
❶ Difference in composition between inspired, alveolar and expired air: Alveolar air contain less PO2 and more CO2 than inspired/expired
❷ Differences in alveolar ventilation in various breathing patterns: in shallow rapid there is low
ventilation causing hypoxia. In deep becomes high alveolar ventilation
Protective function: humification and warming of inspired air. Removal of foreign particles from air.
Explain causes of regional difference in alveolar ventilation-perfusion
VA/Q = 0.8.
Both alveolar ventilation and perfusion ↓ from lung base toward apex
At apex, perfusion is poor compared to ventilation
At base, perfusion is high compared to ventilation
Cause of the regional difference:
Under the effect of its weight, the lung drop → widen
pleural space more at lung apex
Intra pleural pressure is more negative at apex than base
Cause of regional difference in perfusion is due to the effect of gravity.
Discuss variation of ventilation and perfusion in chronic bronchitis.
At ideal ventilation and perfusion: Arterial PO2 slightly < alveolar PO2 due to venous admixture
At normal perfusion, no ventilation (in bronchial obstruction): VA/Q is 0, capillaries can’t be oxygenated, PO2 in veins=arteries
At normal ventilation, no perfusion (pulmonary embolism) VA/Q is infinite. No gas exchange (no CO2 is extracted or O2 is added)
Mention causes of hemoglobin O2 dissociation curve/significance.
Relationship between PO2 and % HbO2 saturation is S shaped
Plateau part: PO2 from 100 to 60 mmHg the saturation is relatively constant, doesn’t go below 90%. Importance at high altitudes allow easy saturation even if O2 tension is low
Steep part: At 60 mmHg, desaturation is very rapid. At 40 mmHg 27% of O2 is taken by tissue. At 20 mmHg curve becomes vertical.
Name factors that shift curve to the right
Means ↓ Hb affinity to O2 = less O2 bound to Hb
↑ temperature
↑ PCO2
↑ H+ (↓PH)
muscular exercise
↑ (2.3 DBG)
Factors that shift curve to the left
Means ↑ Hb affinity to O2 = more O2 bound to Hb
❶ ↓ temperature
❷ ↓ PCO2
❸ ↓ H+ (↑ PH)
❹ ↓ 2,3 DBG
❺ Carbon monoxide
❻ fetal hemoglobin
Chloride shift phenomenon
At tissues; CO2 diffuse from tissue to blood according to pressure gradient. Inside the RBCs, CO2 gets converted into HCO3- which causes an electric charge and acidity. Some of the HCO3- moved from RBCs to plasma by binding to Na+ to decrease acidity. Chloride diffuses from plasma to RBCs so it can neutralize the change in electrical charge.
At the lungs: Low CO2 tension, HCO3 shifted from plasma to RBC’s and Chloride returns to plasma.
Describe the medullary respiratory centers
Two groups of respiratory centers: Medullary and Pontine respiratory center.
Medullary center can maintain automatic, irregular respiration, modified by pontine center
Medullary has 2 centers: Dorsal respiratory group and ventral respiratory group. Dorsal respiratory group is responsible for inspiration and get excited by apneustic center and inhibited by pneumotaxic center.
Ventral respiratory group ( turned on during respiration) mainly responsible for expiration, works in case of hyperventilation. receive stimulus from dorsal respiratory group.
Apneustic center: in lower pons, stimulate DRG and pneumotaxic and turn on inspiration
Pneumotaxic center: in upper pons, inhibitory to DRG apneustic and switch of inspiration.
Describe the site and stimuli of central chemoreceptors.
Site: under ventral surface of medulla
Stimulus:
↑H+ (primary stimulus)
H+ in CSF & brain interstitial fluid: the only direct stimulus
H+ in blood: has no effect on stimulating central chemoreceptor
b) ↑ PCO2 in blood
indirect effect as CO2 crosses BBB
CO2+H2O → H2CO3→ HCO3- + H+ (acidifying CSF)
Small change in arterial PCO2→ results in large changes in CSF pH
Describe site, innervation, stimuli of Peripheral chemoreceptors:
Site: carotid bodies and aortic bodies
They monitor only PO2
Stimulus:
↓ Oxygen tension (hypoxia) most potent stimulus. At PO2 60 doubles ventilation, PO2 100 no effect on ventilation and at 20 inhibit RC.
H+ concentration:
Metabolic acidosis: stimulate ventilation
Metabolic alkalosis: inhibit ventilation
CO2 tension: when increase it stimulates ventilation
Why hypoxia is a weaker stimulus for respiration than CO2 excess?
↓ PO2 from 100-60 mmHg has a minimal effect on Hb O2 saturation
Stimulatory effect of ↓ PO2 from 100 to 60 mmHg → not affect ventilation
↓ PO2 has Stimulatory effect on peripheral chemoreceptors & inhibitory effects on RC
Define hypoxia, types and characters sign, cause
Hypoxia is O2 deficiency at tissue due to low O2 supply or utilization
Hypoxic hypoxia: due to inadequate oxygenation of arterial blood.
❶ ↓PO2 in inspired air : e.g. high altitude
❷ Shunting of venous into arterial blood
❸ pulmonary disorders:
impaired ventilation: RC depression
Impaired diffusion: edema
ventilation perfusion imbalance
characteristics: ↓ PO2, O2 content, % Hb sat. in
arterial blood and cyanosis
Anemic hypoxia: due to low Hb
❶ ↓ Hb (anemia)
❷ Abnormal Hb: e.g.
Characteristics pf anemic hypoxia: Normal PO2, % Hb sat., ↓ 02 content in arterial blood. No cyanosis
