Flashcards
Physiology Exam #2
Cards in this deck (160)
- 1Cardiac Muscle vs. Skeletal Muscle Cells (Similarities)1. RMP = -90 mV
2. "fast response action potentials"
3. depolarization = increase in [Ca2+] intracellularly --> cell contraction and chamber contraction - 2Cardiac Muscle vs. Skeletal Muscle Cells (Differences)1. stimulation = conduction system (SA, AV, PKJ fibers)
2. AP in cardiac myocytes travel through gap junctions to adjecent cell - 3EKG Concept*Graphic record of heart’s electrical activity,
*Conduction of impulses through atria & ventricles
*Records electrical events that precede heart’s contractions.
*summation of individual myocardial AP in the atria and ventricles:
Atria depolarize = ventricles repolarized,
Ventricles depolarize = atria repolarize. - 4Conduction of AP in myocardium1. Conduction system – depolarizes cardiac myocytes
*SA node – stimulates atria,
*AV node/bundle – stimulates ventricles
2. When one cell is depolarized; all cells eventually become depolarized,
*Ions--> gap junctions in intercalated disks; depolarize adjacent cells,
**Faster than chemical synapses - 5Mechanism of Cardiac Myocyte Potential*phase 0
Fast Na+ channels open then slow Ca++ channels (depolarized by cardiac conduction system)
*phase 1
K+ channels open (early repolarization)
*phase 2
Ca+ channels open more (plateau or sustained depolarization)
*phase 3
K+ channels open more (repolarization)
*phase 4 RMP (requires depolarization) - 6L-type Ca2+ channels*membrane-bound voltage-gated slow Ca+2 channels (L-type channels)
(L=long lasting)
*Voltage peak (~+20 - +30 mV) results in, ↑open probability (Phase 2):,
*Ca+2-inward current =
Increases Ca+2 release from SR through ryanodine channels (maintaining depolarization - plateau)
*partially blocked by medications/drugs/toxins - 7EKG Recording*3-12 Electrode patches connected to a lead (wire),
*Voltage changes are recorded from skin
(Magnitude < < in heart)
*represent changes in heart’s total electrical activity,
*Characteristic EKG is recorded from lead II, by convention is from right arm (-) to left leg (+),
*EKG recorded from other leads ‘looks’ differently due to the heart’s dipole - 8Bipolar Limb LeadsBipolar= recorded from 2 electrodes
EKG is a recording of a collection of AP
Lead I: (-) terminal connected to RA;
(+) terminal to the LA
Lead II: (-) terminal connected to RA,
(+) terminal to the LL
Lead III: (-) terminal connected to LA,
(+) terminal to the LL - 9Einthoven’s Trianglestates that the electrical potential of any limb equals the sum of the other two (+ and - signs of leads must be observed).
E.g. QRS complex (ventricular depolarization):
If lead I = 0.5 mV,
Lead III = 0.7 mV, then
Lead II = 0.7 + 0.5 = 1.2mV. - 10Principles of Vectorial Analysis of EKG’s*current flows from depolarization to polarization (depolarization wave)
*Electrical potential generated = vector, arrowhead pointing in (+) direction.
*vector length is prop. to voltage of the potential
*generated potential @ a point = instantaneous mean vector.
*normal mean QRS vector = 59 degrees - 11Mean Vector Through the Partially Depolarized Heart*Lead II @ 59 degree angle (QRS vector)
*vector of depolarization
*Size of vector = magnitude of depolarization (# of normal myocytes) - 12Waves on EKGelectrical events from isoelectrical line (0 millivolts)
represents electrical activity in a cardiac chamber - 13Segments on EKGisoelectrical events between waves
- 14Intervals on EKGinclude a segment and a wave(s),
*R-R interval = one cardiac cycle
*P-Q Interval (P-R Interval) = Atrial systole (~0.16 sec - 0.2 sec)
*S-T Segment (R-T Interval) = Ventricular systole (~0.36 sec) - 15P Wave*depolarization of atria
(atrial myocytes undergo depolarization),
*Begins when SA node fires.
*Result in atrial systole - 16P-Q Interval (Segment)*isoelectrical line following P wave
*atrial systole (contraction) takes place *blood moves from atria to ventricles - 17QRS complex*depolarization of ventricles and repolarization of atria
*Begins when AV node fires,
*Results in atrial diastole and ventricular systole. - 18P-R Interval*atrial depolarization --> ventricular depolarization (~0.16 – 0.20 sec),
*beginning P wave to beginning R wave,
*Is time for atria to contract (Systole) and begin to relax (Diastole),
*Is the time for AV node to conduct AP to AV bundle - 19Q-T Interval*Beginning QRS complex to end of T wave
*Time for ventricles to contract (Systole) and begin to relax (Diastole)~0.36 sec - 20Heart Rate on EKG*count time from R-R-peak in a minute
*Each EKG cycle = cardiac cycle
*e.g. HRof 80 bpm = 80 cardiac cycles pm - 21Excitability in Cardiac Myocytes*ability of inward current to bring cardiac myocyte to threshold
*Not always constant,
*Due to molecular characteristics of ionic channels
(Have a period in which ‘gate’ cannot be opened) - 22Effective Refractory Period (ERP)↓‘open’ Na+ channels,
Inactivated gates prevent 2nd AP
*2nd AP only produced in this membrane patch, requires larger stimulus
*AP cannot propagate
*prevents tetanus of cardiac muscle (equivalent to absolute refract. period) - 23Relative Refractory Period (RRP)action potential can be produced only if stimulus is large enough
- 24Heart Sounds1st sound = AV valves close
Louder > 2nd sound, Low pitch
2nd sound = SL valves close
3rd sound = in rushing of blood into ventricles, very low pitch
4th sound = atrial contraction late in ventricular diastole, hard to hear except in HTN pts w/ thick left ventricle - 25Cardiac Cycle Pressure*L ventricle & aorta pressure highlighted
*Equivalent events in R heart,
*R heart pressure usually lower < L heart (thicker L ventricular myocardium)
*Aortic pressures ~ 120 systole, 80 diastole
*Pulm trunk pressures ~ 24 mmHg systole - 9 mmHg diastole - 26Cardiac Cycle Phases1. Systole = Isovolumetric Ventricular Contraction, Blood Ejection
2. Diastole = Isovolumetric Ventricular Relaxation, Passive Ventricular Filling
(Rapid inflow, diastasis)
Active Ventricular Filling – Atrial Systole - 27Ventricular Systole Isovolumetric contraction phase*Begins when AV valves close
(ventricular P > atrial P)
*Ends when Aortic valve opens
(L ventricular P > aortic P)
*AV and SL valves are closed
*Lasts as long as the systolic heart sound
*onset of systole = R wave - 28Ventricular Diastole - Isovolumetric Relaxation Phase*lasts about the time of 2nd heart sound
*Begins when SL valves close
(Aortic P > L ventricular P)
*vent. blood v. = end systolic volume
*dramatic fall in intra-ventricular pressure due to diastole and decreased blood V
*AV valves open and initiate next phase - 29End-diastolic volume vs. End-systolic volumeEDV = preload
is 120-130 mL of blood at rest
ESV = after-load
50 mL of blood remain - 30Ventricular Systole Blood Ejection Phase*continued vent. contraction, SL valves open, ends when AV valves close
(Aortic P > L ventricular P)
*Rapid ejection: initial, short phase, rapid decrease in vent. vol. and rapid increase in aortic P
*Reduced ejection: slow decrease in ventricular Volume
*End coincides with the T wave (ventricular repolarization) - 31Aortic Pressure Curve*Aortic P starts increasing during systole after aortic valve opens
*decreases toward end of ejection phase.
*After aortic valve closes an incisura occurs b/c of sudden cessation of back-flow toward L ventricle
*Aortic P decreases slowly during diastole b/c of aorta elasticity + slow blood flow to the periphery - 32Ventricular Diastole Ventricular Passive Filling Phase* Begins when AV valves open
(atrial P > ventricular P)
*no sig. change in vent pressure once AV valves open
*Rapid inflow-increase in vent. volume (0.1 sec)
*Diastasis, longer period, slow filling
(0.2 sec)
*gradual increase in ventricular P & V
*At this point the ventricles are ~70% - 80% filled with blood. - 33Ventricular Diastole Ventricular Active Filling Phase*AV valves remain open, and SL valves remain closed,
*Begins w/ P-wave of EKG followed by contraction of atria,
*An additional 25% of blood moves into the ventricles from the contracting corresponding atria
*Ventricles are relaxed and filling with blood. - 34Blood Ejection FractionEDV = 120 ml
ESV = 50 ml
Ejection/stroke volume= 70 ml
Ejctn fract. = 70 ml/120 ml = 58% (normally 60%)
HR =70 bpm
CO= HR x stroke volume
CO = 70/min x 70 ml = 4900 ml/min
(~ 5 L/min on average at rest) - 35Calcium Blockerse.g. Nifedipine, Diltiazem, and Verapamil
Rx for HTN:
Block/inhibit L-type Ca+2 channels
= ↓Ca+2 inward current,
↓[Ca+2] intracellular results in:
↓Ca-induced Ca release,
↓[Ca+2] intracellularly for troponin binding,
↓Cardiac myocyte strength of contraction & decreased CO - 36Cardiac Glycosidese.g. Digoxin, Oabain
Rx for CHF:
Block/inhibit cardiac Na+/K+-ATPase
=decreased Na+/Ca+2 exchanger activity,
↑[Ca+2] intracellular results in:
↑Ca+2 available to bind troponin,
↑ Cardiac myocyte strength of contraction & increased CO - 37Propagation of Local Currents*Opening of Na+ channels => local current circuit that depolarizes adj. membrane => opening more Na+ channel.
*Local depolarization in skeletal muscle depolarizes the fiber in all directions
****BUT not in neurons or NORMAL cardiac muscle. - 38Kinesinmotor molecule involved in anterograde transport
- 39Dyneinmotor molecule involved in retrograde transport – toxins (tetanus), viruses (rabies, herpes simplex, polio)
- 40Regulation of Cardiac OutputCO = HR * SV
HR influenced by parasym & symp nerves
SV influenced by contraction strength, stretch, and end diastolic volume (Frank-Startling) - 41Sarcome Optimum Length for Cardiac Contraction*Same opt. sarcomere length for contraction in skeletal & cardiac muscle
*BUT Tension (force) is generated by different sized skeletal muscles,
*In skeletal muscle, max active stress is developed at normal resting length of a sarcomere ~ 2 micrometers
*longer /shorter lengths = force declines
*Cardiac muscle (no exercise) normally operates below ~ 2 micrometers,
*EDV increases (e.g. exercise) ventricular myocyte sarcomeres are stretched to optimum length to increase force (like a rubber band) (Frank Starling Law) - 42Starling Law of the Heart – EDV and SVOtto Frank and Ernest Starling
(Physiologists in 1940’s)
Increased Ventricular (EDV) = increased Stroke volume
Amnt of blood in ventricle at ED =
Amnt of cardiac sarcomere stretch (force generated by ventricles to eject blood). - 43Normal Cardiac OutputCO = 70 beat/min * 75 ml/beat
CO = 5,250 ml/min
CO ~ 5 to 5.5 Liters/min (on average at rest) - 44Arteriescontain elastin and collagen
Can almost 2x diameter (high pressure), undergo passive recoil,
Called conduit vessels
have low & unchanging resistance to blood flow - 45Arterioles**most important in regulation of blood flow to organs
Thinner walls, more smooth muscle per diameter than arteries.
Called resistance vessels
high and changing resistance to blood flow. - 46Venulesvery small amnt of smooth muscle
Wall slightly thicker than capillaries,
Tunica interna (inner most layer) is specialized to form one-way valves to prevent backflow - 47Veinshave one-way valves
Have very little smooth muscle - 48capacitance vesselsVenules and veins store majority of blood in cardiovascular system (>50%)
Together called capacitance vessels
Venous fluid volume is an important determinant of cardiac output (CO). - 49Exchange Vessels*Capillaries have the thinnest walls,
*Lined by only simple squamous epithelium (one-cell, flat cells).
*Thin wall separates blood from IF by only 1 um.
*Found within tissues in the billions,
*Allows diffusion of gases (cell memb), of fluids (fenestrations), and some cells (leukocytes) (extravasation) - 50Cross-sectional area of a vessel typedetermined by multiplying the average diameter of the vessel-type times the number of vessels of that type
***capillaries have the highest cross-sectional area - 51Blood VelocityDistance/second
How fast 1 ml moves from point X - point Y.
Important in capillaries where the velocity is slowest to ‘allow’ sufficient time for gas and nutrient exchange. - 52Blood Flow(volume/unit time)
mL blood / second,
How much fluid arrives per second,
Important in determining concentration of gases and nutrients that arrive to capillaries.
**fastest at arteries, slowest in capillary beds - 53Why Different Velocities?*Blood Vol. same btwn arteries, veins, capillaries
*different cross-sectional area =
velocity change (accommodate)
*Maintenance of blood vol. in cardiovascular section = maintains hydrostatic pressures in fl. compartment
*Hydrostatic pressure + blood velocity determine capillary exchange (Starling Law of capillary exchange). - 54Formula for Blood Velocityv = Q/A
Q = flow (ml/sec)
A = cross sectional area - 55Principles of Blood Flow*Blood flows b/c of a pressure gradient (ΔP = P1- P2)
*e.g. Blood leaves L ventricle (100 mmHg) & returns to R atrium (0 mmHg)
*opposed by resistance due to vessel diameter, viscosity,
distance traveled before returning
Rate of blood flow = ΔP/R - 56Average Blood Pressure Profile in Cardiovascular SystemHigh pressures in the arterial tree
Low pressures in the venous side of the circulation
Large pressure drop across the arteriolar-capillary junction - 57Pressure Gradient*In normal CV system P1 > P2
*fluid flows from H pressure to L pressure.
*Pressure affected by:
HR, vessel diameter, elasticity & compliance of vessels - 58Arterial Blood Pressure*Can be measured clinically with a manometer:
Within blood vessels,
Within the heart.
*Most commonly, measured externally:
Arterial Blood Pressure (brachial artery),
with a sphyngomanometer (sphyng=pulse) called ‘pressure cuff’. - 59Laminar Blood FlowNormal blood flow through a blood vessel,
Concentric circles flow at diff. speeds,
Fluid moves against arterial wall - ↑resistance,
Layers of blood traveling against layers of blood - ↓less resistance, - 60Turbulent blood FlowConstricted vessel disrupts laminar blood flow,
Layers ‘crash’ against each other and against arterial walls
produce a sound called Korotkoff sound
e.g. abnormal arterial narrowing (stenosis) - 61Sytolic Korotkoff SoundFirst sound heard
Caused by collapsed artery expanding enough to allow blood to flow during systole,
Measurement of pressure necessary for blood to flow (Maximum arterial pressure)
range from 110 – 130* mmHg - 62Diastolic Korotkoff SoundLast sound heard
Caused by artery being completely open and not posing any resistance to blood flow during systole or diastole,
minimum arterial pressure
range from 60 – 80* mmHg - 63Resistanceimpediment to blood flow in a vessel
R = ΔP/Q = mmHg/ (ml/min)
Effecting factors:
Diameter (radius) of blood vessel
Length of blood vessel
Viscosity of blood (hematocrit) - 64Poiseuille's LawR = 8ŋl/πr4
ŋ = viscosity
l=length of tube
πr4 = diameter of tube - 65Flow + Poiseuille's LawF = πr4(P1 –P2) / 8ŋl
- 66Effect of Vessel Diameter on Blood FlowConductance (blood flow) is very sensitive to change in diameter of vessel.
conductance increases in prop. to the 4th power of the radius
increased diameter = increased flow
**arterioles = most ability to change diameter - 67ViscosityHematocrit (% erythrocytes in blood) and albumin
increased hematocrit, increased visc., increased vascular resistance, decreases blood flow - 68Mean Arterial Pressure (MAP)Overall pressure in CV system
Diff. over time btwn systolic & diastolic pressures
**arterial elasticity = main contributor to BP
**arteriole resistance = main contributor to blood flow
*MAP decreases = blood further away from L ventricle
*MAP Highest @ aorta and lowest @ vena cava,
*Pressure gradient most significantly contributes to blood flow - 69Mean Arterial Pressure InfluencesInfluenced by (directly proportional):
1. Volume of Blood: fluid intake, fluid loss, hormones that retain fluid vs. Diuretics cause fluid loss
2. HR: symp (adrenergic – Beta 1), parasymp (cholinergic – Muscarinic 2)
3. SV: amnt of blood that leaves left ventricle each time heart beats (dependent on adrenergic effect – B1),
4. Cardiac output: stroke volume/minute,
5. Venous return: amount of EDV Starling Law
6. Venous tone: partial contraction due to symp (adrenergic – alpha) - 70Average Arterial Pressuremathematically calculated from clinically measured systolic and diastolic pressures. Indication of cardiovascular stress.
- 71Total peripheral resistanceResistance exerted by blood-vessel wall (most important contributors arterioles)
Decreased vessel compliance (ability to expand, most important contributor veins and venules)
R = (viscosity, vessel length, vasoconstriction) - 72Calculation for MAP and Pulse PressueMAP = Diastolic pressure + 1/3 (pulse pressure)
PP = systolic pressure – diastolic pressure - 73Pulse PressureDifference between systolic and diastolic blood pressures,
Indication of pressure being ‘experienced’ by the arteries:
can be calculated by subtracting diastolic pressure from systolic pressure - 74Parallel and Serial Resistance Sites in the CirculationBlood vessel-types (arteries, arterioles, capillaries, etc.) are arranged in series
Organs are arranged in parallel to ensure each organ receives blood of same composition and pressure. Blood flow can then be controlled independently at each organ - 75Sympathetic System on CO(adrenergic) ‘diverts’ blood from GI (alpha-adrenergic) to skeletal muscle (beta-adrenergic)
moderate exercise CO = 17.5 L/min - 76Parasympathetic System on CO(cholinergic) ‘diverts’ blood to GI from skeletal muscle
5 L/min - 77Individual organ perfusionis dependent on specific blood vessel (arranged in parallel):
*Each organ receives blood of same pressure and composition (gas content, glucose content, etc),
*Flow is controlled by arterioles to each organ,
*As blood goes through an organ it contributes only a fraction to the overall resistance (1/R) experienced (contributed to MAP),
*Changes in blood flow to one organ contribute minimally to total peripheral resistance,
*Resistance in parallel is added in fractions (1/R1 + 1/R2 + 1/R3 ……….) - 78Overall perfusion of all organsis dependent on overall resistance of blood vessels, (arranged in series):
*Resistance in series is added as whole numbers (R1 + R2 + R3………..)
*Total peripheral resistance (TPR) influenced by systemic vasoconstriction. - 79Brain and Hearts are Privileged SitesBlood supply is not diminished during cardiovascular stress, such as exercise, standing up, etc.
ANS ‘shunts’ blood to areas of physiological need by regulating
1. Arteriole diameter,
2. Cardiac output (HR, SV)
%of blood flow to other organs varies - 80La Place’s Law*Blood Vol Determines Vessel diameter
↑Resistance = ↑force against blood,
Blood places equal force against vessel:
Arteries expand w/ ↑ volume, recoil w/ ↓ volume.
Force against arterial walls is clinically measured as arterial BP
Blood vessel diameter is determined by:
*Blood volume
*Vessel compliance
*External pressure (smooth/skeletal muscle contraction) - 81Veins are the most compliant blood vesselsVeins have smaller tunica media,
Allows them to expand more than arteries,
Veins can ‘fit a larger volume of fluid per unit of space’, at the same pressure.
Majority of blood is contained within venules and veins (>50%).
Compliance = Volume (mL) / Pressure (mmHg) - 82Mechanism of Venous ReturnVenous blood returning to heart contributes to pre-load (EDV) and therefore to cardiac output,
Two mechanisms serve as venous pumps:
Blood-pumping action of skeletal muscle contractions ‘milks’ blood towards heart,
Venous valves prevent backflow of blood
Respiratory ventilation facilitates venous return
↓thoracic pressure during inspiration ‘pumps’ blood into heart from peripheral veins (outside thoracic cavity) to central veins within thoracic cavity. - 83Venous PressureMuch less than arterial pressure:
Thinner tunica media than arteries
Veins are the most compliant blood vessels,
Have a great capacity to store blood.
At rest, when the body is at heart level:
Pressure in capillaries is ~25 mmHg,
Pressure in the venules is ~5 mmHg,
Pressure in vena cava at the right atrium is 0 mmHg. - 84Changes in PostureAffect venous pressure:
Gravity exerts a force that diminishes (prevents) venous blood returning to heart.
During standing (if no sympathetic compensation or skeletal muscle contraction):
Pressure in capillaries ↑ to 115 mmHg,
Pressure in veins ↑ to 95 mmHg.
↑capillary pressure results
in ↑hydrostatic pressure in capillaries (PC)
resulting in ↑force to move fluid into tissue (edema). - 85Venous Pressure While StandingSympathetic Physiological Compensation includes:
↑HR & SV = ↑ Cardiac Output
↑Venous vasoconstriction (venous tone)
↑Venous return
↑Skeletal muscle contraction (moving around) – ‘milks’ blood back heart
This physiological compensation is reduced by long periods of inactivity (like bed rest), or medications that decrease sympathetic response. - 86Respiratory System Functions1. ventilation (exc. air w/ atm)
2. gas exchange (o and co2 alveoli)
3. host defense (MALTs)
4. metabolism (two blood supplies - alveolar supply and bronchial supply) - 87Lung Blood Supply1. Alveolar (Pulmonary) supply for Perfusion is calculated CO using CV from RIGHT ventricle (HR X SV = CO),
2. Bronchial supply – arises from aorta and supplies lung parenchyma (‘physiologic shunt’-some unoxygened blood travels through the bronchial circulation and bypasses alveolar perfusion – normally ~2% of cardiac output) - 88Pulm Ventilation vs. Gas ExchangePulmonary Ventilation
air in respiratory conduction system is exchanged with atmosphere but gases are not exchanged with blood (physiologic ‘dead’ space’)
Gas Exchange
Gases (O2 and CO2) exchanged with blood in pulmonary capillaries at respiratory bronchi and alveoli only. - 89Conducting Zone of Lungswhere ventilation takes place (trachea, bronchi, bronchioles, terminal bronchioles)
air flow decreased by increased resistance (bronchial diameter)
Circular smooth muscle controls diameter of bronchi:
*Relaxation = bronchodilation (adrenergic Beta-2)
*Contraction = bronchoconstriction (cholinergic muscarinic), histamine, accumulation of mucous, adrenergic B-2 antagonists) - 90Respiratory Zonerespiratory bronchioles --> alveolar ducts --> Alveoli
Gas Exchange takes place
Respiratory bronchi and alveoli – affected by tissue damage - 91Air Ventilationrate is automatic & rhythmic
*on average 6 – 8 L of air/minute at rest
*Respiratory rate – on average 12 – 15 breaths/minute at rest,
*Air exchanged with atmosphere – ~ 0.5 L of air/breath (tidal volume) during ‘quiet’ (at rest) inspiration
*possible due to intrapulm pressure gradients - 92Gas Exchangeair mixes with air in alveoli
gases exchanged through diffusion
0.25 L of O2 is used / min at REST,
0.20 L of CO2 is excreted / min at REST - 93Innervation of Bronchi and Bronchioles – Smooth Muscle1. Cholinergic = bronchioconstriction:
*Muscarinic receptors – many bronchi
directly innervated by parasymp
2. Adrenergic = bronchiodilation:
*Beta - 2 receptors – most bronchi not innervated by symp; respond to circulating epi; stimulate bronchial secretions
*Alpha -1 receptors – inhibit bronchial secretions (decrease mucous production)
3. Other stim = bronchiodilation ; other peptides for ex, vasoactive intestinal peptide (VIP) - 94Sympathetic Effects on Arterioles*Pulmonary – slightly constricted (control primarily blood’s partial pressure of CO2 and blood pH)
*Coronary - Alpha = constriction, Beta-2 = dilation (blood epi), sensitive to blood gases and pH
*Most blood vessels – constricted (prevent orthostatic hypotension - veins)
*Abdominal viscera arterioles – constricted
*Skeletal muscle arterioles – Beta-2 = dilation (circulating epi) - 95Parasympathetic Effects on ArteriolesCoronary arterioles – dilated
Most blood vessels – little to no effect - 96Intra-pleural pressureIntra-pleural space contains pleural fluid for lubrication, cushion interphase of membranes, allows smooth gliding during lung inflation/deflation
Thoracic volume changes are ‘matched’ by lung volume changes
Intrapleural pressure prevents lung collapse during expiration, ALWAYS sub-atmospheric (-3mmHg to -6mmHg) - 97Pleural Recess(space between parietal pleura and lungs) reduced during inspiration
Costomediastinal recess (much smaller)
Costodiaphragmatic recess inferior space that only fills completely during forced inspiration - 98pneumothoraxLungs are elastic and recoil back slightly during each expiration. Negative intrapleural pressure prevents lung collapse.
If pressure in thoracic cavity matches atmospheric pressure lungs collapse - 99Boyle's Lawdecreasing volume increases collisions and increases pressure
P1V1 = P2V2 - 100Inspirationactive, rhythmic, controlled by medulla & pons (also by DRG in nuc. solitarius)
quiet = at rest, not forced, contraction of diaphragm
thoracic cavity increases, decrease Pgas, 0.5 L (tidal volume) moves into lungs
forced = addt'l muscles contraction, lifting ribs, forces 3 L more air in - 101intrapulmonary, intrapleural, alveolar pressures during rest, inspiration, expirationat rest
intrapulm = 760 mmHg
intrapleural = 757 (- 3 mmHg)
inspiration
intrapulm = 757 mmHg
intrapleural = 754 (- 6 mmHg)
alveolar = - 1 cmH2O
Expiration
intrapulm = 763 mmHg
intrapleural = 757 (- 3 mmHg)
alveolar = + 1 cmH2O - 102Expirationquiet = passive, decreased stim from inspiratory centers in brainstem, diaphragm relaxes, air moves out due to decrease in volume (0.5 L)
Forced = VRG in nucleus ambiguous controlled; uses
internal I/C, abs (rectus abdominus) - 103Alveolar Pressures??*is pleural pressure + elastic recoil pressure (at mouth/nose = 0 cm of H2O)
*Pressure in resp bronchi, alveoli < bronchi and trachea (no collapse),
*Air diffuses over larger SA: 70 m2
*Alveoli in parallel to each other decreasing resistance = each alveoli receives ‘fresh’ air
Pressure at alveoli fluctuates:
Inspiration: -1, Expiration: +1 cmH2O - 104Alveolar Elasticity vs. Alveolar Compliance1. elastic – stretch and recoil
*Simple squamous alveoli w/ small basal lamina, elastic proteins,
*↓elasticity in alveolar destruction & scar tissue (emphysema), ↓ability to expand and return to normal size (continued breathing effort alveoli enlarge beyond normal compliance)
2. compliant – normally stretch to ‘contain’ air, as air volume increases
↑compliance due to ‘over-stretch’ (emphysema), ‘holding’ more air than normal, decreased air exchange, ↓compliance due to mucous or fluid also ↓ air exchange. - 105Lung: Abnormal Low Compliance Vs. High ComplianceLung compliance is a measure of the
lung’s stretchability.
*Abnormally low – Ex. Pulmonary fibrosis, ‘work of breathing’ is
increased, decreased air exchange – continuous forced inspirations = barrel-chest (COPD)
*Abnormally high – Ex. Emphysema, damaged scar tissue is ‘heavier’ , less elastic, lungs fail to hold themselves open during expiration, collapse with each breath (crackling sounds) - 106Tidal Volume0.5 L
amount of air exchanged in quiet inspiration - 107Inspiratory Reserve Volume (IRV)3 L men, 1.9 L women
Amount of air inspired after quiet inspiration - 108Expiratory Reserve Volume (ERV)1.1 L men, 0.7 L for women,
Amount of air expired after a quiet expiration - 109Residual Volume (RV)1.2 L men, 1.1 L women.
Air remaining in lungs after maximum expiration - 110Vital Capacity (VC)4.6 L men, 3.1 L women
Calculated from TV + IRV + ERV
Men = 0.5 + 3 + 1.1 = 4.6
Women = 0.5 + 1.9 + 0.7 = 3.1 - 111Inspiratory Capacity (IC)3.5 L men, 2.4 L women
Calculated from TV + IRV
Men = 0.5 + 3 L = 3.5
Women = 0.5 + 1.9 = 2.4 - 112Functional Residual Capacity (FRC)2.3 L men, 1.8 women
Calculated from ERV + RV
Men = 1.1 + 1.2 = 2.3
Women = 0.7 + 1.1 = 1.8 - 113Total Lung Capacity (TLC)5.8 L men, 4.2 L women
Calculated by adding all pulmonary volumes - 114—Total Pulmonary Ventilation and Total Alveolar Ventilation are different values! Alveolar Ventilation is the air exchanged at the respiratory bronchi and alveoli. There is no exchange in conduction system (trachea, first 32-generations of bronchia)
- 115Forced Expiratory VolumeAmount of air that can be exhaled forcefully,
Measurement of air flow through conducting system,
Measured as a rate of vital capacity (VC):
FEV1 – in 1 second ~80% of VC
FEV2 – in 2 seconds ~ 95% of VC
FEV3 – complete VC (may take up to 4 seconds)
Can also use FEV (Forced Expiratory Volume)/FVC (Forced Vital Capacity)
Ex., Obstructive lung disease (asthma) – ratio less than ~.8 or 80% of VC at FEV3. - 116Resistance and AirflowF = ΔP /R
Flow can be decreased by ↑R from ↓elasticity, ↓bronchi radius - 117Factors that Affect Airway Resistance*Upper airways – obstruction
Foreign objects, mucous infection, allergies, irritation.
*Bronchi –↑resistance, ↓flow bronchioconstriction from
Parasymp, Thromboxane & Leukotrines, Angiotensin II (through AT1 receptor)
*Bronchi –↓resistance, ↑flow bronchiodilation from
Increased CO2 in blood plasma (Pco2),
Symp, Epinephrine,
VIP, Bradykinin, Serotonin (5-HT1c receptor) - 118Fluids of Trachea to Terminal BronchiolesTrachea to terminal bronchioles,
Mucous = ‘thick’ fluid mostly glycoproteins secreted by goblet cells into respiratory lumen ‘rides’ on a layer of,
Periciliary fluid = ‘thin’ aqueous fluid allows ciliary movement (ciliated epithelium) to move mucous and trapped substances out respiratory system. - 119Fluids of AlveoliSurfactant a fluid that decreases surface tension due to hydrogen bonding between water molecules and prevents alveolar collapse,
Mostly water containing phospholipids, neutral lipids, fatty acids and proteins that serve as ‘soap’ to reduce the surface tension on alveoli, premature babies – do not produce surfactant). - 120What keeps the very thin alveoli from collapsing?Intra-pleural pressure and surfactant
alveoli are surrounded by capillaries and interstitial fluid.
Starling Law of Capillary Fluid diffusion applies. Hydrostatic pressure in pulmonary capillaries is less than systemic capillaries to prevent pulmonary edema - 121SurfactantLipids produced by Type II alveolar cells, reduces surface tension by breaking hydrogen bonding between water molecules
Most important during exhalation when alveoli normally decrease their radius – prevents alveolar collapse - 122Type I vs. Type II Alveolar CellsType I = structural cells that make up the alveoli. Form simple squamous epithelia that is thin enough to allow for gas exchange, and elastic to expand and recoil.
Type II = synthesize, secrete surfactant - 123Law of LaplacePressure is greater in the smaller bubble, surfactant reduces surface tension, pressure is equalized
Explains why alveoli and blood vessels do not collapse when the volume of their contents decreases (up to a critical point)
Alveoli are ‘protected’ by their elasticity and surfactant, blood vessels are ‘protected’ by their elasticity. Elasticity is due to the property of these tissues (Collagen and elastic proteins) - 124Principles of FlowBlood or air flows because of a pressure gradient (ΔP = P1- P2)
Normal CO ~ 5 L of blood/min,
Normal Alveolar ventilation ~ 4L of air/min
F = ΔP/R
*very slow in capillary bed - 125Partial pressure of O2 and CO2 at alveoliAt alveoli with normal ventilation rate of 4.2L/min
PO2 = 100mmHg
PCO2 = 40 mmHg
hypoventilation = PO2 decreased
hyperventilation = PO2 increased - 126Overview of O2 exchangeO2 in blood plasma = 0.3ml /100 mL
At CO=5L/min at rest is 15ml of O2/min.
Avg person ~250 ml of O2/min.
hemoglobin binds O2 cooperatively to carry ~1L of O2/min (at 100% saturation)
Normally, deoxygenated arterial blood enters lungs 75% saturated with O2 - 127Functions of HemoglobinTransport O2 and CO2,
Buffer [H+] in blood – regulate pH,
Erythrocytes carbonic anhydrase
Enzyme in RBCs, catalyzes the reaction:
CO2 + H2O --> H2CO3 (carbonic acid) - 128Carbonic AcidDisassociates into bicarbonate (HCO3-) and H+ ions, HCO3- diffuses out of cell (facilitated diffusion) into blood plasma,
H+ binds hemoglobin and other proteins. - 129Erythrocyte StructureMost numerous blood cell,
Biconcave disk (denucleated),
No organelles,
~280 million hemoglobin molecules/cell:
Oxyhemoglobin = Carries O2
Carbaminohemoglobin = Carries CO2, H+ - 130Hemoglobin StructureAdult - protein subunits:
2 alpha & 2 beta chains
amino acids bind H+,CO2
1 heme group/subunit:
Iron (Fe+2) holds O2
Cooperative binding (75% - 3 sites bound to O2) increase affinity to O2,
At Hb 100% saturation all 4 sites bound to O2.
*men have more hemoglobin due to more testosterone = increases RBCs - 131Oxygen ‘Loading’ and ‘Unloading’Loading = O2 moves from air in alveoli to fluid in blood plasma (carried by blood to tissue)
Unloading = O2 moves from fluid in blood plasma to IF to tissues (oxygen leaves the blood)
*used for oxygen binding to hemoglobin (loading) and unbinding from hemoglobin (unloading).
*Used for CO2 for loading (entering) into blood and unloading (leaving) from blood. - 132PO2 in arterial blood and venous blood*Arterial blood in systemic circulation - PO2 = 100 mmHg
Oxyhemoglobin: carries 98.5% of O2; saturated at alveoli (oxygen loading); at 100% saturation = 20 mL O2/dL arterial blood
O2 dissolved plasma=1.5%
*Venous blood in systemic circulation - PO2 = 40 mmHg
Carbaminohemoglobin: carries less oxygen 75% saturation after perfusion of tissues (oxygen unloading) - 133PCO2*Venous blood in systemic circulation - CO2 = 46 mmHg
CO2 is transported in blood as bicarbonate ion (70% produced by body), bound to carbaminohemoglobin (23% ), and dissolved in plasma as a gas (7%)
*Arterial blood in systemic circulation - PCO2 = 40 mmHg
Decreased carbon dioxide since it was ‘unloaded’ at the alveoli. - 134O2 Pressure in arterial blood, alveoli, and tissueTravel of oxygen
100 mmHg (alveoli) --> 40 mmHg (venous blood) --> 100 mmHg (arterial blood) --> 40 mmHg (tissue) - 135Metabolic Factors that Shifts hemoglobin curve to the rightdecreased O2 affinity
seen in metabolizing cells
↑ Temperature
↑ [CO2], ↑ PCO2
↑ [H+] = ↓pH
↑ [2,3-DPG] - 136Metabolic Factors that Shifts hemoglobin curve to the leftincreased O2 affinity
seen in alveoli
↓ Temperature
↓ [CO2], ↓ PCO2
↓ [H+] = ↑pH - 137O2-Hb Dissociation CurveP50 = P at which Hb is 50% saturated,
Shifting curve to right = PO2 must be higher to maintain 50% saturation,
O2 unloading is increased = hemoglobin’s affinity for oxygen is less,
Hb ability to carry O2 is decreased - 138Critical PO2 value in arterial blood60 mmHg
Steep part of curve
O2-Hb saturation drops below 90% - 139pH effect on O2 binding to HbNormal blood pH = 7.4
↑[H+] (↓pH) shifts curve right
Blood acidosis = ↓affinity for O2
Normally = slighly decreased pH at tissues ↑O2 unloading - 140Temperature effect on O2 binding to HbNormal body temperature = 37 C
↑Temperature shifts curve right
High fever =↓affinity for O2
Normally = increased temperature at tissues ↑O2 unloading - 141CO2 partial pressure effect on O2 binding to HbNormal PCO2 in arterial blood = 40 mmHg
↑CO2 shifts curve right,
Hypercapnia = ↓affinity for O2 binding
Normally = increased PCO2 at tissues ↑O2 unloading - 142O2-Hemoglobin Dissociation CurveAdult Hb is:
50% saturated at PO2=27mmHg,
90% saturated at PO2=60mmHg,
98% saturated at PO2= 100 mmHg
Normal range in arterial blood is 80-mmHg
O2 binding /unloading happens in msec,
Cooperative binding = bound O2 increases Hb affinity for O2 - 143Carbon Monoxide PoisoningHb = high affinity for CO (200X >O2),
When CO binds Hb, it also increases hemoglobin’s affinity for O2,
(O2 is sequestered by Hb & not released to tissue) (shifts to left)
Tissues = bright, red (high O2 content in Hb but since O2 is not released from Hb - tissues are HYPOXIC! - 144Carbon Dioxide LoadingTissues constantly producing CO2
CO2 moves from tissues (P1) --> blood (P2),
Partial pressures of CO2 forces P1 --> P2
in tissue = 46 mmHg (P1)
in arterial blood = 40 mmHg (P2)
Once CO2 in blood plasma it diffuses into RBCs driving CAH to RIGHT to produce bicarbonate ion and H+ - 145Carbon Dioxide Transport in BloodCO2 gas dissolves in blood as a gas (40 times more soluble in plasma than O),
*not enough dissolves to carry all CO2 produced in tissues,
Must be carried as HCO3- (liquid) – 70%
Bound to Hb amino acids – 23%
(carbaminohemoglobin)
Dissolved in plasma as gas – 7% - 146Carbon Dioxide TransportCO2 diffuses through plasma membrane --> RBCs:
CAH catalyzes: CO2 + H2O -->H2CO3
H2CO3 => HCO3- and H+
HCO3- diffuse into blood plasma
*Exchanged by antiport (HCO3-/Cl- exchanger) to ‘prevent’ charge across membrane,
*In blood plasma (serum) bicarbonate is transported as NaHCO3 or H2CO3 (ratio = 20:1) **bicarbonate serves as a buffer for blood pH.
Process is reversed in alveoli. - 147Hydrogen BufferingCAH reaction in venous blood shifts to the right = more H+,
1. In blood most effective buffering system = bicarbonate & proteins in blood plasma,
2.In CSF, little albumin compared to blood; ‘ability’ to buffer pH is diminished
3. In cells most effective buffering system = intracellular proteins (hemoglobin in erythrocytes) - 148Oxygen and Carbon Dioxide ExchangeDependent on rate of alveolar ventilation & rate of CO2 production, use of O2:
*Cellular aerobic respiration:
1 glucose = 6CO2 produced& 6 O2 used
*80 CO2 are expired per 100 O2
entering alveoli
respiratory exchange RATIO = 0.80
Respiratory quotient = same exchanged at tissues (at rest) - 149Blood Carbon Dioxide Effect*blood pH (CAH), ventilatory rate (neural physiological compensation)
*Increased blood CO2:
Shifts CAH => more HCO3- and H+,
If not buffered sufficiently - ↑[H+] causes blood acidosis
↑[H+] = decreased pH ‘sensed’ by chemoreceptors of medulla to increase resp rate (increased ventilation) - 150Ventilation*Determined by TV and resp rate
*Minute ventilation – amount of air entering lungs per minute
(5L/breath X 12 breaths/min = 6L/min),
*Alveolar ventilation – amount of air exchanged at alveoli per minute (deduct dead space) = 4.2 L/min. - 151Perfusion in LungsVenous blood is re-oxygenated by the lungs,
R ventricle pumps blood to pulm arteries at a lower pressure (24/9 mmHg) compared to L ventricle to aorta (120/80 mmHg)
Deoxygenated blood travels through pulm capillaries at a pressure of ~10 mmHg (systemic capillaries ~20 mmHg),
*Fluid diffusion through capillaries forces less fluid into IF (~30mL/hr) than in systemic capillaries( which returns through lymphatics) - 152Pulmonary EdemaIf pressure in pulm capillaries increases:
Pulm capillary hydrostatic pressure increases
*more fluid into interstitial space*
Gas exchange is decreased.
If pressure in pulm capillaries decreases:
Pulm capillary hydrostatic pressure decreases
*more fluid remains in capillaries*
Gas exchange is decreased. - 153Pulmonary Edema (Causes and Safety Factor)*Causes of pulmonary edema
left heart failure
(Left atrial pressure > 25 mmHg; should be zero!)
damage to pulmonary membrane
*Safety factor
negative interstitial pressure
lymphatic pumping
decreased interstitial osmotic pressure - 154Dynamics of Pulmonary Capillary (Starling Laws)Outward Forces
Pulmonary capillary pressure 7 mmHg
Interstitial osmotic pressure 14 mmHg
Negative interstitial pressure 8 mmHg
Total = 29 mmHg
Inward Forces
Plasma osmotic pressure = 28 mmHg
Net filtration pressure = +1 mmHg
**Negative interstitial pressure keeps alveoli dry** - 155Ventilation and Perfusion are MatchedRatio of gas diffusion to blood flow (V/Q),
Defined at the lungs or at the alveoli,
Lung – total alveolar ventilation divided by cardiac output (4.2 L/min 5 L/min = ~0.8) - 156Abnormal Conditions (Ventilation and Perfussion) Arterial Hypoxemia, hypoxia, hypercapnia, hypocapnea1. Hypoxemia – PO2 < 80 mmHg
2. Hypoxia – PO2 < 60 mmHg (insufficient to carry normal metabolic demands, will need blood transfusion)
3. Hypercapnia – PCO2 > 40 mmHg
(shifts Hb curve right, less O2 carried)
4. Hypocapnea - PCO2 < 35 mmHg (shifts Hb curve left, more O2 remains bound to Hb– less oxygen unloading) - 157Changes in Gas pressures affect diameter of terminal bronchi (alveolar ventilation) and blood vessels (blood flow)Increased PCO2 = dilate brionchioles and systemic arterioles
Decreased PCO2 = constrict brionchioles and systemic arterioles
Increased PO2 = dilate pulm arterioles, constrict sys. arterioles
Decreased PO2 = constrict pulm arterioles, dilate sys. arterioles - 158Hypoxia (vasoconstrict/vasodilates)*vasoconstricts pulm arterioles (shunts blood to alveoli ventilating properly)
*vasodilates systemic arterioles
(increases blood flow to tissue).
O2 =LARGER effect on blood vssls
CO2=LARGER effect on bronchioles - 159Local Physiological Compensationmost effective for hypoventilation
Hypoventilation (↓PO2, ↑PCO2 in alveoli) ‘locally’ compensated by:
*Terminal bronchi dilation = increase gas exchange (more sensitive to CO2 than O2)
*Pulm arteriole constriction to ↓blood flow to non-ventilating alveoli (more sensitive to O2 than CO2)
*Compare to systemic arteriole dilation (increase blood flow to organs) - 160During Exercise NormallyIncreased CO
‘Decreased transit time’ BUT
Increased diffusing capacity
Opening up of additional capillaries
Better ventilation/perfusion match
Equilibration even with shorter time spend traveling through the capillaries.
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- Physiology Flashcards on Physiology Exam #2 , created by Vy Nguyen on 10/10/2017.
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