physio mini 3

-4 to 4

25/0

25/8

7

120/0

120/80

• ~ 5L/min
• = SV x HR = (EDV-ESV) x HR

• normal: 55-65%
• =SV/EDV

CO= VO₂/ (C_A-C_V)

• -VO2: rate of O2 consumption
• -CA: O2 content in peripheral artery
• -CV: O2 content in mixed venous blood (RV, PA or RA)

=Psys - Pdias

~SV/ arterial compliance

• normally around 100
• = Pdias + 1/3(pulse pressure)
• = CO x TPR

• - normal : 8-10 mmHg
• - used as an approximation of pressure in pulmonary veins and left atrium
• - >15= mitral stenosis or regurg, severe aortic stenosis or regurg, ventricular failure, etc.

• - narrowing of the aortic valve
• - ausciltation at right 2 ICS:
• ---mid-systolic murmur(later murmur=later stage of stenosis)
• ---S4 will be present due to LV hypertrophy (differential from mitral regurg)

• -closure of AV valves
• - splitting may be caused by conduction problem, ie right bundle branch block
• - heard at start or isovolumetric contraction

• - closure of aortic and pulmonary valves
• - splitting can be caused by inspiration(inc ven return)
• ---if splitting is not accentuated by inhalation, then pathological (atrail septal defect or bundle branch block)
• - heard at start of isovolumetric relaxation

• - excessive ventricular dilation caused by atrial contaction
• - physiological in younger patients
• - pathological- aortic or mitral regurg
• - heard at start of rapid ventricular filling
• - "SLOSH'--ing-in"

• - low ventricular compliance
• - pathological- aortic stenosis or ventricular hypertrophy due to hypertension
• - heard right before S1 during atrial systole
• - "a-STIFF'--wall"

• incompetent mitral valve causing regurgitation into the LA
• - systolic murmur
• - S3 heard (differential from aortic stenosis)

• - narrowing of the mitral valve
• - causes diastolic murmur because of larger pressure gradient b/t atrium and ventricle

- normal: .12-.20 seconds

• - normal < .10 seconds
• - isovolumetric contraction (mechanical phase)

• - > 1/2 of a complete cardiac cycle (~1/3)
• - ventriclar systole
• - starts IVC and ends after RE

K and adenosine

adenosine and NO

PCO2

• hypoxia, causes vasocontriction
• -this helps redirect blood flow to the areas of the lung that are better ventilated

P_AO2= P_IO2- (P_ACO2/R)

• -Pi= PO2 of inspired air
• -P_ACO2= PCO2 of alveolar air
• -R= respiratory quotient (CO2 output/ O2 uptake)

P_ACO2= (VCO2/V_A) x 863

• -VCO2= vol of CO2 from metabolism
• - V_A= minute alveolar ventilation

V_A= (VCO2/PaCO2) x 863

• - any disease that decreases the alveolus ability to create positive pressure (on expiration)
• - ie, COPD,empysema, asthma, chronic bronchitis

• -any disease that decreases the lungs ability to create a negative alveolar pressure on inspiration
• - ie fibrosis, asbestosis

1/C_RS= 1/C_L + 1/C_CW

CO2 output/O2 uptake

V_aO2= O2 dissolved + (gm Hb x 1.34)

.03 ml O2 dissolved/ 10mmHg PO2

• -FRC
• -PVR increase (and flow decrease) on either side of FRC

• - PO2 and [O2]a are both normal
• -decreased blood flow

• - PO2 normal, [O2]a is decreased
• - decreased [Hb]

• - PO2 and [O2]a are normal
• - poisoning (CN) blocks O2 utilization on cellular level

• - low inspired PO2 (high altitude)
• - hypoventilation

• -diffusion limitation
• - R to L shunt
• - V/Q mismatch

• 1- check PaCO2
• a. high= hypoventilation
• b. low= low PIO2 (high altitude)
• c. normal-> continue to step 2
• 2. Give 100% O2
• a. PaO2<400 = R to L shunt
• b. PaO2>400 continue to step 3
• 3. CO2 diffusion capacity test
• a. normal= V/Q defect
• b. decreased= diffusion problem

• both inspratory and expiratory nuerons and is thought to be the rythm generator
• -ramp signal

• controls TV and breathing rate
• -controls "switch off" point of the inspiratory ramp

-high lung volume (sensed via vagus nerve,via slowly adapting pulmonary stretch receptors in the smooth muscle of the airway) inhibits further inspiration, thus terminatin inspiration and begins expiration

• location- airway epithelium
• nerve- myelinated vagal
• activation- lung distention and irritants
• function- cough reflex, gasp and bronchoconstriction by high activity

• - location- near capillaries
• - nerve- non myelinated vagal
• - activated by increase interstitial fluid and pulmonary embolism
• -function-cause rapid shallow breathing, bronchoconstriction and CV depression(tachypnea and hyperventilation

• - location- SM of airway
• -nerve- myelinated vagal
• -activation- lung distention, breath holding and deflation below FRC
• -function- terminate inspiration and terminate large expiration

• - stimulated by H+ (PCO2 responder)
• - inhibited by cold and anesthetics
• - defects can result in sleep apnea, SIDS, panic attacks, epilepsy and migraines

• - PO2 responder mainly
• - located in the carotid body of ExCa
• - mainly O2 sensitive via type 1 glomulus cells(threshold PO2~80mmHg, significant at PO2 of 65 mmHg)
• - mildly CO2 and H+ sensitive

• - at first increase in CO2 causes increased ventilation via central CR, inc CO2 in CSF-> inc H+ in CSF
• - increased CO2 and H+ increases respiration via peripheral CR as well
• -kidney will compensate for inc H+, which decreases peripheral and central CR stim= dec respiration
• -now only stim for inc resp is PO2, so if pt is given O2, this may cause cessation of breathing

• - dec PO2 causes immedite hyperventilation (good low lower PCO2, thus raise PO2), but causes resp alkalosis
• - resp alkalosis will inhibit P and C CR CO2/pH receptor response thus decreasing ventilation for the first few days
• - once alkalosis is compensated for, ventilation increases

• -cycles of gradual increase in tidal volumes followed by a gradual decrease
• -

• -increased tidal volume seen in DKA anddiabetic coma
• - aka air hunger

60-180 mmHg

180-200 bpm