Physiol Exam 3: Chps. 13-14, & 16 Flashcards
Describe inflammation, define the purpose of inflammation & name the 4 signs of inflammation
Inflammation: complex of tissue responses to trauma or infection serving to ward off a pathogen & promote tissue repair; “-itis”; (involves leukocytes)
— Purpose: Protect the body and required for health
~NOTE: Can also damage the body
— Characteristics: redness, heat, swelling, pain
Name the 3 types of plasma proteins, name the structure or organ that synthesizes each protein & describe each protein’s function
- Globulins
— α & β globulins: Made by liver
*Function: transports lipids & fat-soluble vitamins
— gamma globulin: Made by (B) lymphocytes
* Function: secrete antibodies / immunoglobulins (used for immunity); B lymphoctye → Plasma cell (secreting antibodies) notify the immune system to get rid of bacteria - Albumin: Made by liver
* Function: Provides osmotic pressure to draw water from interstitial fluid into capillary
~ helps hold fluid in BV; help with blood vol. and BP - Fibrinogen: Made by liver
* Function: becomes fibrin (mesh part of a clot)
Distinguish blood plasma from serum
Blood plasma: contains H2O & dissolved solutes (ions, metabolites/lactic acid, hormones, enzymes, antibodies & plasma proteins)
Serum: plasma without clotting proteins (fibrinogen)
Differentiate the following terms: hematopoiesis/hemopoiesis, erythropoiesis, leukopoiesis
Hematopoiesis/hemopoiesis: blood cell formation
Erythropoiesis: form RBCs
Leukopoiesis: form WBCs
Name the organ that secretes the hormone erythropoietin & describe the function of the hormone
- Erythropoietin: secreted by kidneys
- Function: stimulate erythrocyte production in bone marrow
Name the element in the heme of hemoglobin that binds to oxygen
Iron
Differentiate anemia vs. polycythemia
Anemia: abnormally low red blood cell count
Polycythemia: abnormally high red blood cell count
Define hemostasis
Hemostasis: cessation/ending of bleeding
- Broken endothelium (inner layer of BV’s) exposes collagen proteins
- Process:
1. Web of fibrin proteins
2. Platelet plug formation
3. Vasoconstriction
Describe the function of von Willebrand’s factor
von Willebrand’s factor (VWF) binds to both
collagen & platelet
Describe the effect that clotting factors, that are activated by platelets, have on fibrinogen
Activated platelets help activate plasma clotting factors (proteins); Fibrinogen → fibrin
Explain the purpose of fibrin (as well as clot retraction)
Web of fibrin protein = Strengthens platelet plug to form blood clot (platelets and fibrin)
* Clot retraction: mass contractions to make more compact & effective (prevent blood loss)
Name the final protein (& its precursor) produced in the common pathway
Fibrin
- Precursor: Fibrinogen (Factor I)
Name the enzyme (& its precursor) that catalyzes the production of fibrin
Thrombin
- Precursor: Prothrombin
Identify the ion & the vitamin essential to clotting
Vitamin K and Ca2+ (+ phospholipids from platelets)
Name the protein (& its precursor) that performs fibrinolysis to dissolve clots
Plasmin
- Precursor: Plasminogen
Distinguish thrombosis vs. thrombus vs. embolism vs. embolus
- Thrombosis: abnormal clotting of blood in an UNBROKEN blood vessel
- Thrombus: the clot within the intact blood vessel
— MORE COMMON IN VEINS than arteries (slower blood flow = doesn’t dilute fibrin & thrombin as quickly) - Embolism: OBSTRUCTION of a blood vessel by an embolus
- Embolus: an abnormal object (dislodged thrombus/thromboembolus, foreign object/air bubble or bodily substance/wrong blood type) that travels in blood
— If it gets lodged in a small vessel, that could block blood flow from that point on
Distinguish thrombocytopenia vs. thrombocythemia
Thrombocythemia: HIGHER than normal number of platelets in blood
Thrombocytopenia: LOWER than normal number of platelets in blood
Memorize the duration of ventricular systole & ventricular diastole
Ventricular systole = 0.3 sec
Ventricular diastole = 0.5 sec
Memorize the details of each of the 5 phases of the cardiac cycle (focus on the phase name, ECG, pressure, volume, valve status & heart sounds)
*NOTE: Focus on the L ventricle
1a. Rapid filling; blood from L atrium → L ventricles
* ECG - None
* Pressure - L Ventricular pressure < L atrial pressure
* Volume - Blood vol. in L ventricle increase; fills to ~80%
* Valve status - AV valves open; Semilunar valves close
* Heart sounds - “dub”
1c. Atrial systole/Atrial contraction; AV valves still open
* ECG - P wave (atrial depol.) → atrial systole
* Pressure - L ventricle slightly increase
* Volume - Blood vol in L ventricle increases; fills remaining ~20%
* Valve status - AV valves open; Semilunar valves close
* Heart sounds - “dub”
- Isovolumetric contraction; “same volume”
* ECG - QRS complex (ventricular depol.) → ventricular systole
* Pressure - L ventricle increase; L ventricle begins to contract
* Volume - No change
* Valve status - AV valves and Semilunar valves close
* Heart sounds - “lub” - Ventricular ejection
* ECG - ST segment (ventricular systole cont.)
* Pressure - L ventricle increase/high; > aortic pressure
* Volume - Blood vol. in L ventricle decrease (blood is being pump/ejected into aorta)
* Valve status - AV valves closed; Semilunar valves open
* Heart sounds - “lub” - Isovolumetric relaxation
* ECG - T wave (ventricular repol.) → ventricular diastole
* Pressure - L ventricular pressure decreases; < Aortic pressure (Aortic= 80 mmHg vs. L ventricle = 0 mm Hg)
* Volume - No change
* Valve status - AV valves and Semilunar valves close
* Heart sounds - “dub”
Name the type of blood vessel that causes the greatest resistance but can also produce the greatest BP drop & describe how for each situation (greatest resistance vs. greatest BP drop)
Arterioles: More smooth m., less elastin
* When smooth m. layer relaxes (vasodilation)…
— ↓ Resistance (R)
—↑ Blood flow
* When smooth m. layer contracts (vasoconstriction)…
—↑R
— ↓ Blood flow
Name the 3 types of capillaries
- Continuous capillaries: Cells with intercellular clefts
— Muscle, lung & adipose tissue - Fenestrated capillaries: Cells with wider intercellular clefts & fenestrations
— Kidneys, endocrine glands & intestines - Discontinuous capillaries: (AKA sinusoids); larger clefts and fenestration
— Liver, bone marrow & spleen
Compare the 5 major blood vessels (arteries, arterioles, capillaries, venules & veins)
(focus on diameter, number & total cross-sectional area)
*IGNORE the specific numbers, FOCUS on ordering them from smallest to largest or least to greatest
Diameter (smallest to largest):
Capillaries, Arterioles, Venules, Arteries, Veins
Number (smallest to largest):
Arteries & Veins, Arterioles, Venules, Capillaries
Total Cross-Sectional Area (smallest to largest):
Arteries, Veins, Arterioles, Venules, Capillaries
Name the structure in veins that aid in venous return
Venous valves
Distinguish cholesterol (the molecule) from carriers of cholesterol in the blood
There’s ONLY ONE cholesterol molecule in the body ; but there are DIFFERENT carries of cholesterol in the body (LDL,HDL)
Distinguish the function of LDL vs. HDL & explain why one of these lipoproteins is considered “good cholesterol” & one is considered “bad cholesterol”
LDL: carries lipids; called “bad cholesterol” from the liver to the body’s tissue
— Considered “bad” since its delivering cholesterol to the body’s tissue (arterial wall), which could implicate some things
HDL: carries lipids; called “good cholesterol” from the body’s tissue to the liver
— Considered “good” since we remove the cholesterol from the body’s tissue
Describe the 3 functions of the lymphatic system
- It transports interstitial (tissue) fluid, initially formed as the blood filtrate, back to the blood
- It transports absorbed fat from the small intestine to the blood
- Lymphocytes (its cells) help provide immunological defenses against disease-causing agents (pathogens)
Explain why the SA node is considered the pacemaker & not the other parts of the cardiac conduction system (4)
SA node:
* Contain autorhythmic cells (able to set the beat, and beat spontaneously)
* Normal sinus rhythm (responsible for HR)
* Makes pacemaker potential: spontaneous depol.
* Depolarizes FASTER than other parts of the conduction system
For the pacemaker potential, describe the effect it has on the membrane potential, name the ion involved & name the direction that ion diffuses (into vs. out of the cell)
- Start: Cell HYPERPOLARIZES to approximately –60 mV, causing cell membrane (of autorhythmic cells) HCN channels (Hyperpolarizing cyclic nucleotide) to open
- NOTE: HCN channels can also open due to cAMP/cyclic AMP (from sympathetic stimulation)
- Na+ enters → depolarization to -40 mV (threshold)
- Leads to: AP
For the SA Node’s AP’s depolarization phase, describe the effect it has on the membrane potential, name the ion involved & name the direction that ion diffuses (into vs. out of the cell)
- Voltage-gated Ca2+ channels open (due to hitting threshold) & Ca2+ enters from outside
- This extracellular Ca2+ causes more Ca2+ from SR (which stores Ca2+) to enter (into cytoplasm) ~ AKA Ca2+ -induced Ca2+ release
- Contraction (of cardiac muscle)
For the SA Node’s AP’s repolarization phase, describe the effect it has on the membrane potential, name the ion involved & name the direction that ion diffuses (into vs. out of the cell)
Voltage-gated K+ channels open →K+ diffuses out
Describe how the signal from the SA node spreads to the cardiac muscle fibers
SA node spreads AP via GAP JUNCTIONS to surrounding cardiac m. fiber in order to be a stimulus
— SA node AP causes voltage-gated (VG) Na+ channels to open, Na+ diffuses in & membrane potential reaches threshold
For the cardiac muscle’s AP’s depolarization phase (2&3), describe the effect it has on the membrane potential, name the ion involved & name the direction that ion diffuses (into
vs. out of the cell)
AP: 2. Depolarization phase: MORE VG Na+ channels open, Na+ diffuses = rapid upspike
AP: 3. Depolarization phase: VG Na+ channels close, membrane potential +15 to +30 mV
For the cardiac muscle’s AP’s plateau phase, describe the effect it has on the membrane potential, name the 2 ions involved & name the direction that each of those ions diffuse (into vs. out of the cell)
AP: 4. Plateau Phase: Prolonged depolarization due to Ca2+ influx (via VG Ca2+ channels) vs. K+ efflux (via leakage channels; MORE K+ goes out)
— ST segment (Ventricular systole) of ECG coincides w/ plateau phase in AP of cardiac m
For the cardiac muscle’s AP’s rapid repolarization phase, describe the effect it has on the membrane potential, name the ion involved & name the direction that ion diffuses
(into vs. out of the cell)
AP: 5. Rapid Repolarization Phase: Due to rapid K+ efflux (via VG K+ channels opening); reaching -85 mV quickly
— VG Ca2+ channels close
Describe why there is no summation when cardiac muscle fibers contract
Absolute refractory period and relative refractory period takes up time when cardiac muscles are relaxing and contracting, preventing cardiac m. from summating = NO repetitive contraction
Define CO (definition & equation) & be able to calculate CO when provided relevant information
Ex. For a patient with a SV of 70 ml/beat & HR of 75 bpm, what is their CO?
Cardiac output: volume of blood pumped/min by each ventricle
— Cardiac output mL/min OR L/min (CO) = Stroke volume mL/beat (SV) x Heart rate beat/min (HR)
Ex. For a patient with a SV of 70 ml/beat & HR of 75 bpm, what is their CO?
70 ml/beat x 75 beats/min = 5,250 mL/min
5,250 mL/min x 1L/1000mL = 5.25L/min
5.25 L/min = CO
Memorize the average value of CO at rest (in L/min & mL/min)
CO avg. at rest : 5500 mL/min OR 5.5 L/min
Define chronotropic effects & distinguish positive vs. negative chronotropic effects
Chronotropic effect: mechanisms affecting HR
— Positive chronotropic effect = ↑ HR
— Negative chronotropic effect = ↓ HR
Compare the sympathetic to parasympathetic division (focus on the effects on the SA node, AV node, atrial muscle, ventricular muscle) & name the chemical messengers involved in each division
Sympathetic Effects (Epinephrine and Norepinephrine): ↑ HR
* SA node - Increased rate of pacemaker potential; increased heart rate
* AV node - Increased conduction rate
* Atrial muscle - Increased strength of contraction
* Ventricular muscle - Increased strength of contraction
Parasympathetic effects (ACh): ↓ HR
* SA node - Decreased rate of pacemaker potential; decreased heart rate
* AV node - Decreased conduction rate
* Atrial muscle - No significant effect
* Ventricular muscle - No significant effect
Define SV and name the 3 variables affecting SV & describe how each variable affects it and wether it’s directly or inversely proportional
Stroke volume: amount of blood pumped out
- EDV (End diastolic volume); directly proportional: Amount of blood in ventricle immediately before contracting (end of diastole/relaxation)
— Workload of ventricle before contraction (called preload) ~ 120 ml - TPR (Total peripheral resistance); inversely proportional: Blood flow resistance (All arteries in the body)
— Opposes ejection of blood from ventricles, making it harder for SV
— TPR produces afterload (impedance/force against to the ejection of blood from the ventricle)
— Increase TPR→ decrease SV & vice-versa - Contractility; directly proportional:
— Intrinsic control:
* Frank-Starling Law of the Heart
*↑ EDV (fill ventricles w/ blood) → ↑ stretch (of sarcomeres) → More FORCEFUL contraction
- Sarcomeres stretched → ↑ # of crossbridges→ ↑ contraction strength & ↑ SV
— Extrinsic control (consists of nervous system and endocrine system):
* Sympathoadrenal system
- Norepinephrine & epinephrine produce
increases in contraction strength (positive inotropic effect)
- More Ca2+ to sarcomeres = more crossbridges
* Parasympathetic nervous system effect = NO inotropic (contraction effect)
* ONLY chronotropic (heart rate)
Define ejection fraction (definition & equation) & be able to calculate ejection fraction when provided relevant information
Ex. For a patient with a SV of 75 ml & an EDV of 120 ml, what is their ejection fraction?
Ejection fraction: proportion/amt of EDV ejected (for each heartbeat)
— = SV divided by EDV
Ex. For a patient with a SV of 75 ml & an EDV of 120 ml, what is their ejection fraction?
75/120 = 0.625
0.625 x 100 = 62.5%
Define Frank-Starling law of the heart
Frank-Starling Law of the Heart: SV DIRECTLY PROPORTIONAL to EDV
* Intrinsic property of heart
* Ex. ↑ EDV stretches myocardium = ↑ Contractility = ↑ SV
Define inotropic effects & distinguish positive vs. negative inotropic effects
Inotropic effects: mechanisms affecting contractility
* Positive inotropic effect = ↑ contractility
* Negative inotropic effect = ↓ contractility
Name the type of blood vessel that stores most of the volume of blood, explain why & memorize the approximate amount stored
Veins stores the most volume of blood:
* Veins have high compliance (a given amount of pressure will cause more distension/stretch than in arteries)
— Holds more blood than arteries (~2/3 blood volume at rest)
Name the 3 mechanisms that aid venous return & explain how for each mechanism
- Venoconstriction
— Sympathetic nervous system stimulate the veins to contract, where alpha I adrenergic receptors are found → venous pressure → venous return - Skeletal muscle pump
— Skeletal muscle apply pressure on the veins to allow blood to be pushed back to the heart - Negative interthoracic pressure
— When breathing, diaphragm contracts, pushing abdominal viscera = negative interthoracic pressure → pressure goes to thoracic (↑ P→↓ P)
Define net filtration pressure & hydrostatic pressure & describe how these pressures affect fluid movement at the proximal (artery/arteriolar) end of a capillary (including the result)
- Net filtration pressure: Filtering of fluid entering vs. leaving the capillary
- Hydrostatic pressure: “Water not moving”, pressure pushing against BOTH sides (in and out/interstitial fluid) of the blood vessel
- At the proximal end (arterial end) of capillary, plasma pressure (due to BP) > interstitial fluid
- Result: MORE fluid goes to interstitial fluid
Define oncotic pressure & colloid osmotic pressure & describe how these pressures affect fluid movement at the distal (venule/venous) end of a capillary (including the result)
- Oncotic pressure: the difference of pressure between the interstitial fluid vs plasma at the distal end/venous end of capillary
- Colloid osmotic pressure: Proteins (Albumin) in the plasma and the interstial fluid that will be PULLING/RETAINING the fluid from BOTH sides
Result: MORE fluid goes to plasma
Define edema and the 3 causes
Edema: Excessive tissue fluid
Causes:
1. Increased capillary filtration (high BP)
2. Decreased capillary reabsorption (plasma protein leak BV and now part of interstitial fluid)
3. Obstruction of lymphatic drainage (clot or parasite blocks lymphatic vessels = elephantitis)
Describe the role hormones (ADH, RAA system & ANP as a group) serve in regulating BP
ADH, Renin- Angiotensin- Aldosterone (RAA) System & Atrial natriuretic peptide (ANP) regulate LONG-term changes in BP
Memorize the details of the negative feedback loop for ADH & the function of ADH
Function: regulate blood osmolality & volume by reabsorbing H2O (kidney)
1. Stimulus: Dehydration (↓ Blood volume) or salt ingestion → ↑ Blood osmolality
2. Sensor: Osmoreceptors in hypothalamus
3. Integrating center: Osmoreceptors in hypothalamus (normal range: 275-295 mOsm)
4. Effector:
a) Posterior pituitary → ↑ADH → water retension/reabsorb H2O by kidneys
OR
b) Thirst → drinking
5. Response: ↑ Blood volume and ↓ blood osmolality
Memorize the function of aldosterone and what does it maintain
Function: regulate BP by reabsorbing Na & Cl (H2O follows) at the kidney
— What does aldosterone maintain?
* Osmolality
* Blood volume
* BP
Memorize the details of the negative feedback loop involving the RAA system
- Stimulus: ↓ Blood pressure and ↓ Blood flow to kidneys
- Sensor: Juxtaglomerular apparatus in kidneys
- Integrating center: Juxtaglomerular apparatus in kidneys
- Effector: a) Juxtaglomerular apparatus in kidneys → secretes renin (enzyme and hormone); converts Angiotensinogen to Angiotensin I → travels to lungs and becomes Angiotensin II by ACE (enzyme at the lungs) → Angiotensin II can cause vasoconstriction of arterioles OR…
— b) Adrenal cortex → secrete aldosterone → salt and water retention of kidneys - Response: ↑ Blood volume and ↑ blood pressure
What does the RAA stand for?
Renin (R): enzyme and hormone
Angiotensin II (A): also stimulates thirst and secrete aldosterone
Aldosterone (A)
Memorize the details of the negative feedback loop involving the ANP & the function of ANP and what opposes it
Function: regulate blood volume (& BP) by excreting Na+ (natriuresis); (Cl- and H2O follow) at the kidney
* What does ANP oppose? Aldosterone
- Stimulus: Water immersion (going in a pool) or increased blood volume → ↑ Venous return
- Sensor: ↑ Stretch of L atrium
- Integrating center: Brain
- Effector: a) ↑ Stretch of L atrium (effector) → ↑Atrial natriuretic peptide (ANP) →↑ NaCl and H2O secretion → kidneys (effector)
b) Posterior pituitary (effector) →↓Antidiuretic hormone → ↓H2O reabsorption → kidneys (effector) - Response: ↑ Urine volume at kidneys → ↓Blood volume
Describe the effect vasoconstriction vs. vasodilation has on TPR
Flow is INVERSELY PROPORTIONAL to resistance R (Flow = 1/R)
* TPR (all vascular resistance)
— Vasoconstriction = Increase of TPR
— Vasodilation = Decrease of TPR
Explain how each variable in the equation for Poiseuille’s Law affects blood flow
After physical constants added, we get this law…
Blood flow ∝ ∆Pr4(p)/ηL(8)
- (directly proportional/inversely proportional); RESISTANCE (R) is the OPPOSITE: ηL(8)/DPr4(p)
∆P=as pressure increases, blood flow increases. As pressure decreases, blood flow decreases
r4=As the vessel radius increases, blood flow increases. As the vessel radius decreases, blood flow decreases.
n=As viscosity increases, blood flow decreases. As viscosity decreases, blood flow increases
l= As vessel length increases, blood flow decreases. As vessel length decreases, blood flow increases
Compare the blood pressure experienced in the 5 major blood vessels (arteries, arterioles, capillaries, venules & veins)
— IGNORE the specific numbers, FOCUS on ordering them from least to greatest!
Blood pressure from least to greatest:
Vein, Venules, Capillaries, Arterioles, Arteries
Identify the 2 organs that autoregulate
Kidney and brain
Describe how metabolic control mechanisms affect blood flow (focus on O2,CO2, pH/H+, K+, adenosine, NO)
Metabolic Control Mechanisms: Intrinsic chemoreceptors sense “chemicals” from tissue cells →
Vasodilation:
* ↓ [O2]: ↑ local metabolic rate
* ↑ [CO2]: ↑ local metabolic rate
* ↓ tissue pH (inversely proportional): ↑ H+ due to CO2 and lactic acid
* ↑ K+ & paracrine regulators (adenosine, NO & others)
Describe the details of how the sympathoadrenal system affects blood flow & describe how it impacts TPR
Sympathoadrenal System - α1-adrenergic stimulation (NE) on arterioles to skin & viscera (vasoconstriction) & ↑ TPR
Describe the effect (increase, decrease or stays the same) exercise has on CO,HR, SV, contractility & TPR
DURING EXERCISE
* CO ↑: 5 L/min to 25 L/min
— More for elite athletes (over 40 L/min)
* HR could ↑ to max
— Max HR: 08 - (0.7 x Age)
* SV could ↑ to max (100 mL/beat)
* Contractility ↑
* TPR: ↓
— ↓: Skeletal m.
— ↑: GI tract & skin
* Blood flow to brain = same
Name the 2 factors that regulate arterial BP/MAP & explain how for each factor
Arterial BP regulated by:
* CO (HRxSV)
* TPR
— Arterial BP ∝ CO x TPR
* Arteriole (with smooth muscle) = resistance vessels for TPR
Describe the role baroreceptors serve in regulating BP and where it’s found
Baroreceptors (stretch receptors) are found at 1. aortic arch (monitor BP in systemic circuit) & 2. carotid sinuses (monitors BP going to brain; found w/n internal carotid a. and MOST sensitive of the two)
— Tonically active (always send signals as long as stimulus is present)
— Role: regulate immediate (SHORT-term) changes in BP
Describe the effect of increasing vs. decreasing BP has on baroreceptor stimulation
Stimulus: ↑BP
* Causes MORE stretching (of baroreceptors) = MORE AP’s from baroreceptors to medulla oblongata
Stimulus: ↓BP
* Causes LESS stretching (of baroreceptors) = LESS AP’s to medulla oblongata
Memorize the details of the baroreceptor reflex discussed in class
From a lying down position to standing up → ↓ venous return → ↓ End-diastolic volume → ↓ Stroke volume → ↓ Cardiac output →…
1. Stimuli: ↓ Blood pressure
2. Sensor: Baroreceptors at aortic arch and carotid sinus
3. Integrating center: Medulla oblongata (vasomotor and cardiac center); Sensory neurons send LESS AP to integrating center
— ↑ Sympathetic, ↓ Parasympathetic
4. Effector: a) Vasoconstriction of arterioles (effector) →↑ Total peripheral resistance
b) ↑ Cardiac rate (effector) →↑ Cardiac output
5. Response: ↑ Blood pressure
NOTE: BP ∝ CO x TPR
Name the mechanism that drives O2 & CO2 movement at the alveoli and systemic tissues
Diffusion
Describe the movement of O2 & CO2 (to the tissue or to the blood) when blood arrives at the alveoli vs. systemic tissues
At the alveoli/lungs (external respiration):
* Capillary (CO2) → Alveolus
* Alveolus (O2) → Capillary
— Also happens in systemic tissues but reversed…
At the systemic tissues (internal respiration):
* Capillary (O2) → Tissue cells
* Tissue cells (CO2) → Capillary
Describe the function(s) of the following cells: type 1 alveolar cell, type 2 alveolar cell, alveolar macrophage
— Type I alveolar cells: (simple squamous) diffusion for gas exchange
— Type II alveolar cells: secrete surfactant (prevent alveoli from collapsing) and reabsorbs Na+ and water to prevent fluid build up
— Alveolar macrophages: phagocytize dust particles, bacteria, blood cells
Explain Boyle’s law
Boyle’s law: Pressure of gas is INVERSELY PROPORTIONAL to its volume or P = 1/V
* Skeletal m. (of ventilation) contraction changes chest V → changes intrapulmonary P (w/n airway/lungs/alveoli). So,…
— Air goes in because
* ↑ lung V & ↓intrapulmonary P
— Air goes out because
* ↓ lung V & ↑ intrapulmonary P
Describe the function of surfactant
Surfactant: consists of phospholipids & hydrophobic surfactant proteins
* Function: Lower surface tension
— Prevents alveoli from collapsing during expiration → easier for alveoli to inflate
Explain Dalton’s law and what does the atmospheric pressure equal to?
Dalton’s Law: TOTAL P of a gas mixture = SUM of P of EACH GAS in mixture
* One atmosphere = PATM=PN2+PO2 +PCO2+
PH2O + … = 760 mmHg (at sea level)
~ Varies with altitude
Define partial pressure & be able to calculate partial pressure when provided relevant information
- Ex: PO2 (sea level) = ~21%,
Partial pressure: Each gas exerts P independently; (continuing from Dalton’s law)
- ex: PO2 (sea level) = ~21%, so 0.21 x 760 mmHg =159.6 mmHg
Memorize the value (including units) of PO2 & PCO2 in…
1. alveoli
2. arteries entering tissue (systemic) capillaries
3. veins leaving tissue capillaries
4. arteries entering pulmonary capillaries
5. veins leaving pulmonary capillaries
- Alveoli
* PO2: 105 mmHg
* PCO2: 40 mmHg - Arteries entering tissue (systemic) capillaries
* PO2: 100 mmHg
* PCO2: 40 mmHg - Veins leaving tissue capillaries
* PO2: 40 mmHg
* PCO2: 46 mmHg - Arteries entering pulmonary capillaries
* PO2: 40 mmHg
* PCO2: 46 mmHg - Veins leaving pulmonary capillaries
* PO2: 100 mmHg
* PCO2: 40 mmHg
Compare the relative (no specific number) PCO2 of tissue (systemic) capillaries vs. arteries entering tissue (systemic) capillaries
PCO2 of tissue (systemic) capillaries > blood/arteries entering tissue (systemic) capillaries
Describe the 2 methods used to transport O2 in the blood & memorize the % for each method
- Dissolved O2 = PO2 (1.5%)
~ free, w/n plasma of blood - Oxyhemoglobin (98.5%)
~ doesn’t contribute to PO2
~ O2 binds to hemoglobin = more O2
Distinguish oxyhemoglobin from deoxyhemoglobin
Oxyhemoglobin: ≥1 O2 molecule(s) bound to iron of heme
Deoxyhemoglobin: NO O2 attached
Memorize the details of the oxyhemoglobin dissociation curve
Oxyhemoglobin dissociation curve (at rest):
— Sigmoidal curve; Factors can shift the curve R or L, making it easier or harder to release O2 to the tissue
— Powerful curve because of 3 components: Percent oxyhemoglobin saturation (how much O2 is attached to oxyhemoglobin), PO2 in blood (mmHg), and oxygen content (ml O2/100 ml blood) = total O2 content in blood
* Understand how to read the graph! (Slide 25 of Chapter 16)
Describe the effect temperature, pH & exercise each have on the oxyhemoglobin dissociation curve
— Effect of Temperature on Oxygen Transport
* Curve shifts to the left (lower body temp.) = more affinity (bond) for O2 = LESSER unloading of O2
* Curve shifts to the right (higher body temp.) = less affinity (bond) for O2 = GREATER unloading of O2
— Effect of pH on Oxygen Transport
~ Bohr effect: affinity(bond) ↑/↓ due to pH changes
* Curve shifts to the left (High pH) = more affinity (bond) for O2 = LESSER unloading of O2
* Curve shifts to the right (Less pH) = less affinity (bond) for O2 = GREATER unloading of O2
— Exercise: Curve shifts to the RIGHT = ↑ Body temp., ↓pH
Identify the function of the medulla vs. pons in regulating breathing
- Ventral Respiratory Group (VRG; medulla): Primary generator of respiratory rhythm; send signals down spinal cord to lower motor neuron going to muscles involved in breathing
- Dorsal Respiratory Group (DRG; medulla): Modifies; output to VRG
- Pontine Respiratory Group (PRG; pons): Modifies (medulla oblongata); output to VRG and DRG
Name the 2 locations of the peripheral chemoreceptors and name the substances & fluid that these chemoreceptors monitor
Peripheral chemoreceptors (carotid & aortic bodies)
*Monitors: H+, PCO2 (indirectly; PCO2 → H+) & PO2 changes in blood
Name the location of the central chemoreceptor and name the substance & fluid that this chemoreceptor monitors
Central chemoreceptors (medulla oblongata)
* Monitors: H+ changes in CSF & brain interstitial fluid
Describe hypoventilation & its effect on PCO2 & pH
Hypoventilate (inadequate ventilation; relative to metabolism)
* PCO2 ↑ (hypercapnia) ; due to not breathing enough
* Then pH falls
Describe hyperventilation & its effect on PCO2 & pH
Hyperventilation (excessive ventilation; breathing too much)
* PCO2 ↓ (hypocapnia) ; due to exhaling excessive amount of CO2
* Then pH rises
Memorize the Carbonic Acid Reaction
H2O + CO2 ↔ H2CO3 ↔ H+ + HCO3-
Describe how central chemoreceptors can indirectly monitor CO2 levels
Central chemoreceptors ONLY respond to H+ ions, but first…
CO2 must cross blood brain barrier → mixes with H2O at the CSF → = H2CO3 → splitting into HCO-3 and H+ (which can now make its way into brain interstitial fluid to the central chemoreceptors/medulla oblongata)
Describe the 3 methods used to transport CO2 in the blood & memorize the % for each method
- HCO3- ; Bicarbonate ion(70%)
- Carbaminohemoglobin (20%) ; CO2 binds to hemoglobin
- Dissolved CO2 = PCO2 (10%)
Memorize the details involved with the Cl- shift & the other 2 methods involved in transporting CO2 in the blood at tissue capillaries
Chloride shift: at the tissue capillaries (Cl- enters RBC)
CO2 enters the plasma from the tissue cells by…
1. Dissolving in plasma (10%)
2. CO2 binds to hemoglobin (of RBC) to form carbaminohemoglobin (20%)
— CO2 mixes with H2O of the plasma → H2CO3 → seperates into H+ and HCO3-
— H+ binds to hemoglobin, but HCO3 exits RBC (70%) into and Cl- will enter (carbonic anhydrase can speed up the reaction)
Memorize the details involved with the reverse Cl- shift & the other 2 methods involved in transporting CO2 in the blood at pulmonary capillaries
Reverse chloride shift: at the pulmonary capillaries (Cl- exits RBC)
CO2 from the plasma enters the alveoli by…
1. The CO2 dissolved in the plasma diffuses into the alveoli
2. Carbaminohemoglobin dissociates into hemoglobin and CO2 and CO2 travels to alveoli
3. Chloride moves out of the RBC into the plasma and HCO3- move back into the RBC and combine with H+ ion to form H2CO3 → disscociates into H2O and CO2
— CO2 can enter the alveoli
Memorize the normal range for pH
Normal blood pH: 7.35 to 7.45
Name 3 examples of nonvolatile acids discussed in class
- Lactic acids ; from breakdown of glucose
- Fatty acids ; from lipids (triglycerides)
- Ketone bodies
Describe the function of buffers & name the most important buffer in the body
- Function: Stabilize pH by releasing or binding H+
- Most important body buffer: HCO3- (Bicarbonate)
Distinguish acidosis vs. alkalosis
Acidosis: Blood pH is lower than 7.35
Alkalosis: Blood pH is greater than 7.45
Distinguish the causes of respiratory acidosis vs. respiratory alkalosis vs. metabolic acidosis vs. metabolic alkalosis
- Cause of respiratory acidosis: inadequate ventilation (hypoventilation)
- Cause of respiratory alkalosis: excessive ventilation (hyperventilation)
- Cause of metabolic acidosis: due to excess production of nonvolatile acids or loss of bicarbonate
- Cause of metabolic alkalosis: RARE but due to too much bicarbonate or inadequate nonvolatile acids
Describe how each of the conditions are partially compensated for: respiratory acidosis, respiratory alkalosis, metabolic acidosis, metabolic alkalosis
Respiratory acidosis ↔ Metabolic alkalosis
Metabolic acidosis ↔ Respiratory alkalosis
