Midterm Flashcards
Anion gap
(Na+K) - (Cl + HCO3)
Osmolarity
2(Na) + 0.055(glucose) + 0.36(BUN)
Calculating partial pressure of gas (outside body)
multiply % by atmospheric pressure
PiO2
(760-47) x FiO2
PAO2
[FiO2 x (Pb-47)] - CO2/0.8
Total O2 content
(1.37 x Hbg x sat) + PO2(0.003)
Dissolved CO2
PaCO2 x 0.067
A-a gradient
PAO2- PaO2
Alveolar MV
(TV-DS) x RR
Calculating Dead space
PaCO2-EtCO2/PaCO2 (apply % to TV) or 2 mL/kg of IBW
Compliance
TV/PIP-PEEP
Calculating CO
HR x SV (MAP-CVP)/SVR x 80
SV
EDV-ESV
EF
EDV-ESV/EDV x 100
Which has the LEAST negative threshold- SA node, neuron, or myocyte?
SA node
In the SA node, what permeability do we alter to achieve threshold?
potassium
What causes the plateau phase of the action potential in the myocyte?
influx of calcium
normal aortic valve area
2.5-3.5 cm squared
What aortic valve area is severe aortic stenosis?
<1 cm squared
Normal PCWP
<12 mmHg
Normal LAP
4-12 mmHg
normal LV pressure
100-140/3-12 mmHg
normal aorta pressure
100-140/60-90 mm Hg
normal RAP
0-8mmHg
normal RV presure
15-28/0-8 mmHg
normal pulmonary arterial pressure
15-30/3-12 mmHg
normal CO
4-6 L/min
normal CI
2.5-4 L/min
Forces that push or pull fluid OUT of vessel
capillary hydrostatic, interstitial hydrostatic, interstitial oncotic pressures
Pressures that push/pull fluid INTO vessel
plasma oncotic pressure
Net pressures at arterial vs. venous side of capillary
Higher net OUT on arterial side, higher net IN on venous side
Valsalva Maneuver
-forced expiration against closed glottis -mediated through baroreceptors -SNS inhibited, PNS activated - decreased HR, contractility, BP, vasodilation
Baroreceptor Reflex
-response to stimulation/stretch of baroreceptors -afferent signal via Hering’s nerve (glossopharyngeal) or vagus nerve -signal to medulla -efferent response to decrease BP (vagus) -decreased HR and SNS outflow
Occulocardiac Reflex
traction of EOM, conjunctiva, or orbital structures cause reflex bradycardia -treatment- remove stimulus, antimuscarinic
Bainbridge/atrial reflex
increase in HR due to increase in blood volume (stretch receptors in RA) -prevents sequestration of blood in veins, atria, pulmonary circulation
celiac reflex
traction on mesentery/gallbladder/vagus nerve stimulation causes bradycardia, apnea, hypotension -can be elicited by pneumoperitoneum
Cushing reflex
physiologic response to CNS ischema from increased ICP -intense vasoconstriction to restore cerebral perfusion -Cushing’s triad- HTN, irregular breathing, bradycardia -may indicate herniation -may be seen after IV norepinephrine
Chemoreceptor reflex
sensory receptor that transduces chemical signal into action potential -central- located on medulla, stimulated by increased H -peripheral- carotid arteries, aortic arch, stimulated by decreased O2 -results in increased MV, SNS stim, increased BP
Bezold Jarisch reflex
- C fibers will decrease HR to allow ventricles to fill - see this when sitting patient up during/after anesthesia
Phase 4 of Action potential (myocyte)
resting membrane potential -K inside cell (slow leak out) -Na and Cl are outside -remain in this stage until stimulated
Phase 0 of Action Potential (myocyte)
rapid depolarization (fast Na channels) -rapid influx of Na into cell (more positive membrane) -gates open between -70 and -65, go up to +20 mV
Phase 1 of Action Potential (myocyte)
rapid repolarization -Na gates close -K gates open, K moves out -Cl influx -slow influx of Ca
Phase 0 &1 of action potential make up what part of the EKG?
QRS complex
Phase 2 of Action Potential (myocyte)
plateau phase -Na channels close (no AP at this time- absolute refractory period) -Ca influx- delays quick repolarization -K efflux
What does phase 2 make up on the EKG?
ST segment
Phase 3 of Action Potential (myocyte)
rapid repolarization -Ca channels close -K channels still open (efflux) -when Ca close, allow efflux of K to keep moving back to RMP -Na channels reset
What part of the EKG is phase 3 of the action potential?
T wave
What phase do LA’s work on?
phase 4 (prevent spontaneous depolarization/Na gated channels from opening)
What phase do CCB’s work on?
phase 2 (affect Ca channels)
Smooth muscle characteristics
spindle shaped, nonstriated, uninucleated, involuntary
Cardiac muscle characteristics
striated, branched, uninucleated, involuntary
Skeletal muscle characteristics
striated, tubular, multinucleated, voluntary
Contractile proteins of skeletal muscle
myosin, actin, tropomyosin, and troponin
What electrolyte disturbances cause skeletal muscle weakness?
hypocalcemia, hypermagnesemia
Byproducts of ACh hydrolyzation
choline and acetate (choline is repackaged)
NMJ Steps
1) synthesis and storage of ACh in presynaptic terminal 2) depolarization of presynaptic terminal and Ca uptake 3) Ca uptake causes ACh release into synaptic cleft 4) diffusion of ACh to postsynaptic membrane and binding of ACh to NICOTINIC receptors 5) end place potential in postsynaptic membrane 6) depolarization of adjacent muscle membrane to threshold 7) degradation of ACh
Intercalated Discs
Present in cardiac muscle, helps heart work in unison
Calcium in smooth muscle
comes from plasma/blood, not SR
Somatic Nervous System NT
ACh- always stimulatory
NT of ANS
preganglionic- ACh postganglionic- ACh (PNS) or NE (SNS)
SNS fiber/ganglia characteristics
-origin of fibers- thoracolumbar (T1-L2) -short pre, long post -ganglia close to spinal cord
PNS fiber/ganglia characteristics
-origin of fibers- craniosacral -long pre, short post -ganglia in visceral effector organs
Accelerator Fibers (SNS)
T1-T4
CN of PNS
3,5,9,10
Phases of LV Pressure Volume Loop
Isovolumetric Contraction Ejection Isovolumetric Relaxation Diastolic Filling

Aortic Regurgitation

Aortic stenosis

Mitral regurgitation

Mitral stenosis
Central Chemoreceptors
- located on medulla
- respond to changes in H or CO2 (increase stimulates ventilation)
- surrounded by brain ECF
Peripheral Chemoreceptors
- Located in carotid bodies (glossopharyngeal) and aortic bodies (vagus)
- sense decrease in pO2 and pH (increased pCO2) of arterial blood
- responds intensely to paO2 below 100 mmHg
- responsible for all increase in ventilation due to arterial hypoxemia (<60mmHg)
Intrapleural pressure
- between parietal and visceral pleura
- normally negative (becomes more negative with inspiration)
- becomes positive with forced expiration or Valsalva
intrapulmonary pressure
- zero (same as atmospheric pressure) at end expiration
- becomes more negative during inspiration
Contributors to Stroke Volume
- proload (tension on ventricle at end of diastole)
- afterload (wall tension the myocardium needs to overcome to eject SV- pressure within LV during peak systole)
- mycoardial contractility- state of inotropy independent of preload and afterload
What determines coronary artery dominance?
Crux (where coronary and posterior interventricular sulcus meet)
majority of population is RCA dominant
L main coronary artery
- emerges from behind pulmonary trunk
- divides into LAD, L CFX, diagonal branch
L anterior descending coronary artery
multiple branches -anterior 2/3 of interventricular septum, R and L bundle branches, papillary muscles of mitral valve and anterior lateral and apical walls of LV
Left circumflex artery
- travels posteriorly around L heart
- multiple branches, may include sinus node artery
- supplies LA wall, posterior lateral LV, anterolateral papillary muscle, AV node, SA node
Right coronary artery
- supplies SA and AV nodes, RA and RV, posterior 1/3 of interventricular septum, posterior L bundle, interatrial septum
- in 90% of pop, it travels from R coronary sinus to right AV groove, to crux and onto posterior AV groove
- multiple branches- sinus node artery, AV node artery, proximal bundle branches, posterior descending artery, LA/LV terminal branches
Coronary Sinus
- located in posterior AV groove near crux
- collects 85% of blood from LV, drains into LA
- cath for LV studies
- may be cannulated during bypass to delivery cardioplegia
Anterior cardiac veins
- 2-4 veins drain anterior RV wall
- drain into RV directly or into coronary sinus
Thebesian veins
- transverse myocardium and drain into RA, RV, LV
- may carry 40% of blood returned to RA
Nicotinic Receptors
- MUSCLES, all ganglionic neurons
- effect of ACh is always STIMULATORY
Muscarinic Receptors
- found in PNS target organs
- ACh is either inhibitory (cardiac) or excitatory
Beta 1 Receptors
- heart, kidneys
- NE binding increases HR/strength, stimulates renin release
Beta 2 receptors
- lungs, other sympathetic target organs
- NE binding is inhibitory- dilates BV and bronchioles, relaxes smooth muscle
Alpha 1 receptors
- found in blood vessels, sympathetic target organs
- NE binding constricts vessels, sphincters, pupil dilation
Alpha 2 receptors
- found on membrane of adrenergic axon terminals, pancreas, platelets
- NE binding inhibits NE release- inhibits insulin secretion, promotes blood clotting
Increased plasma osmolarity triggers?
thirst mechanism
Osmosis
- movement of WATER across SPM (solutes do not move)
- H2O moves from low solute concentration to high solute concentration
What are the sensors of the respiratory control system?
chemoreceptors, baroreceptors, lung stretch receptors
What is the central controller of the respiratory control system?
brain (pons, medulla)
What are the effectors of the respiratory control system?
muscles of respiration
Major output of central control (respiratory control system) occurs through what nerve?
phrenic (C3-5)
What are the affector nerves for the respiratory control system?
vagus, glossopharyngeal
Pneumotaxic Center
- located in pons
- fine tunes breathing (controls volume and rate)
- inhibits inspiration
Apneustic Center
- located in pons
- prolonged inspiratory gasps (brain injury)
- excitatory effect on inspiration
Dorsal Respiratory Group (DRG)
- located in medulla
- intrinsic periodic firing
- basic rhythm of ventilation
- can be overriden by pneumotaxic center
Ventral respiratory group (VRG)
- located in medulla
- usually not active during normal breathing
- more active with forceful breathing
Surfactant
- made by alveolar type II cells
- decreases surface tension
Law of Laplace
P= 2T/R (for sphere)
P50
partial pressure where 50% of Hgb is saturated (usually around 27 mmHg)
Shifting of Oxyhemoglobin Dissociation Curve
Right- O2 affinity for Hgb reduced (O2 unloads easier)
- caused by increased H, PCO2, temp, 2-3 DPG
Left- increased affinity for Hgb (less unloading)
- caused by decreased temp, H, PCO2, 2-3 DPG
What PO2 is required to achieve a sat of 90% normally?
60 mmHg
Bohr effect
- change in PCO2 affects O2 dissociation curve
- curve shifts to the left into lungs (facilitate O2 loading)
Haldane Effect
- change in PaO2 affects CO2 dissociation curve
- at tissue, O2 diffuses into tissues so CO2 affinity increases for loading
- at lungs, O2 diffuses from alveoli into blood- CO2 curve shifts to R to facilitate unloading

Hypertonic volume expansion (3% admin)

Hypotonic volume expansion (SIADH)

Isotonic volume loss (diarrhea)

Isotonic volume expansion (0.9 admin)
Static Volumes (Lungs)
TV, RV, ERV, IRV, CV
Dynamic Lung Volumes
FEV1, FVC, FEV1/FVC
Tidal volume
- normal volume of breathing
- 6 mL/kg of IBW
Residual Volume
air left after maximal expiration (1200 mL)
Expiratory Reserve Volume
maximum air from end of normal inspiration to maximal expiration (1100 ml)
Inspiratory Reserve Volume
maximum inspired air from rest (3000 mL)
Closing Volume
volume at which alveoli close at end expiration (normally above residual volume)- absolute voluem of gas in lungs when small airways close
-increases with age, may exceed FRC in supine position
FEV1
forced expiratory volume in one second
-normal 4L
FVC- forced vital capacity
volume of gas that can be exhaled forcefully
-normal 5 L
FEV1/FVC
ratio of parameters that allows distinction of obstructive vs. restrictive lung disease
- normal is 0.8
- restrictive lung disease may have normal ratio (both parameters decreased)
Zone 1 of Lung
- top
- minimal blood flow
- ventilated but not perfused (alveolar dead space)
- PA>Pa>Pv
Zone 2 of Lung
- waterfall zone
- blood flow determined by difference between arterial and alveolar pressures
- Pa>PA>Pv
Zone 3 of lung
- blood flow determined by arterial-venous gradient
- continuous blood flow
- where tip of PA cath should be
- Pa>Pv>PA
- greatest compliance
Zone 4 of lung
- PATHOLOGICAL
- present with pulmonary edema
- low lung volumes, reduced blood flow
- Pa>Pi>Pv>PA
- Pi is interstitium pressure
What is on the x and y axis of the flow volume loop?
y- flow (L/sec)
x- volume

Normal flow volume loop

Fixed upper airway (kinked ETT)

Obstructive lung disease

Restrictive Lung Disease
Semilunar valves
aortic and pulmonic (each have 3 cusps)
AV valves
tricuspid (R side, 3 leaflets)
mitral (L side, 2 leadflets)
Inferior EKG leads
II, III, aVF
RCA
Anteroapical EKG leads
V3 and V4
distal LAD
Anteroseptal EKG Leads
V1, V2
LAD
Anterolateral EKG Leads
I, aVL, V5, V6
Circumflex artery
Extensive Anterior EKG Leads
I, aVL, V2-V6
proximal LCA
True Posterior EKG leads
Tall R in V1
RCA
Average Total Blood Volume
5 L
What % of blood volume is RBCs?
40% or 2 L
What % of blood volume is water?
60% or 3 L
Variations in age with water content
babies- more water
elderly- less water (less muscle mass)

Norepinephrine synthesis
How is NE removed from the synpase?
reuptake or metabolized by MAO and COMT
NE metabolites
DOMA, NMN, MOPEG, VMA
Where is NE synthesized?
nerve terminal
Which has a longer effect, NE or ACh?
NE- takes longer to metabolize
reuptake is how its action is stopped
Limb placements for Einthoven’s triangle
RA (-/-)
LA (+/-)
LL (+/+)
Lead Directions

Which lead follows the electrical direction of the heart?
Lead II
Layers of Pericardium
visceral- covers outer surface of heart
parietal- outer layer
normally 10-25 mL of serous fluid of between
Layers of Cardiac Musculature
epicardium- outermost layer
myocardium- middle/muscle layer- pumping action
endocardium- thin, innermost layer
Simple Diffusion
- passive transport
- nonpolar lipid soluble substances diffuse directly through phospholipid bilayer (gradient)
Facilitated Diffusion
- passive process
- certain lipophobic molecules (glucose, amino acids, ions) use carrier proteins or channel proteins
- proteins are selective, saturable, and can be regulated in terms of activity/quantity
Is coronary blood flow continuous or noncontinuous?
Non-continuous
Functional Residual Capacity (FRC)
air left after normal expiration
RV+ERV
2300 mL
reservoir for O2
Vital Capacity
maximal inspiration followed by maximal expiration
(IRV+TV+ERV)
4500 mL
Inspiratory Capacity
IRV+TV
3500 mL
Total Lung Capacity (TLC)
volume in lungs after maximal inspiration
IRV+TV+ERV+RV
5800 mL
Hypoxic Pulmonary Vasocontriction
determined by ALVEOLAR PO2
inhibition of nitric oxide pathway
shunts blood away from hypoxic areas
Nitric Oxide effects on pulmonary vasculature
- relaxing factor
- increases cGMP- smooth muscle relaxation
- disruption can lead to pulmonary HTN
Prostacyclin effects on pulmonary vasculature
- vasodilator
- activates adenyl cyclase
- inhibits platelet aggregation
Pulmonary vasoconstrictors
- endothelin 1
- thromboxane 2