PHYSIOLOGY

Hemodynamics
MAP = SVR x CO
 Pulse pressure- created by SV on top of a DBP within a compliant vascular tree → aorta is responsible for most of compliance
 ↑ pulse pressure d/t increased SV or poor compliance of aorta
Systemic vascular resistance

80 converts dyne/s/cm5
SVR = 80 x (MAP-CVP)/CO
from mmHg and L/min
 Most drugs ↓ SVR
 Inversely proportional to 4th power of radius
 Most of resistance is d/t arterioles
 PAC to obtain values to calculate SVR
Cardiac Output
CO = HR x SV
 ↓ CO more difficult to treat
 Measure with thermodilution and TEE
Heart rate
 Tachy or brady leads to hypotension
 Excessive Bradycardia  ↓ CO
 Tachycardia  ↓ filling time for LV→ ↓ CO and hypotension
Ejection fraction
 End diastolic volume
 Normal 60-70%
Preload
 ie. EDV
 measure with TEE or LA pressure, PCWP, pulmonary artery diastolic pressure
 CVP measures filling pressures on Right side  correlates with left side if no Pulmonary dz
 Stiff heart → steeper rise of pressure with increased volume
 Low preload caused by venodilation and hypovolemia; others: tension ptx, cardiac tamponade ( manifested by pulsus paradoxus),
pulmonary embolism
Frank-Starling mechanism
 Increased pumping action of heart with increased filling
Afterload
 Largely determined by SVR
 ↑ SVR → ↑ cardiac filling pressure, ↓ SV, EF, and CO
 ↓ SVR → ↑ emptying time and ↓ filling pressure
Contractility
 Force of contraction independent of preload and afterload
 Causes of ↓ contractility:
o Myocardial ischemia, anesthetic drugs, CM, prior MI, valvular heart dz
Cardiac reflexes
 Autonomic nervous system
o SA and AV nodes
o Sympathetic stimulation → ↑ HR through beta1
o Parasympathetic suppression →↑ HR
 Baroreceptors
o Carotid sinus and aortic arch
o Activated by ↑ SBP → stimulates stretch ® → signal thru vagus and glossopharyngeal n. → CNS
o Altered by HTN
o Typical response: ↓ HR
o Vagal stimulation → ↓ inotropy and reflex vasodil.
o Bainbridge reflex: atrial stretch → ↑ HR to match CO to venous return
 Chemo®:
o Carotid sinus
o Arterial hypoxiemia → SNS stilumation
o Oculocardia reflex, bradycardia w/ stretch of abdominal vescera; cushing reflex: brady w/ ↑ICP
Coronary blood flow
  60-70% extraction of O2
 Cannot ↑ extraction as reserve mech
 Primary compensation: Vasodilatation to ↑ blood flow
 Coronary reserve: ability to ↑ flow over baseline (adenosine, NO, adrenergic stim)
 Diastole: heart perfusion → DBP – LVEDP [RV is perfused in diastole and systole]
Pulmonary circulation
 Pulmonary artery pressure {2-12 mmHg}
o ↓ than SBP b/c of ↓ PVR
 Pulmonary vascular resistance
o Resistance in larger vessels, small arteries, and capillary bed
o Phys model: distension and recruitment of capillaries
 ↑ PAP → distention and recruitment → ↑ cross-sectional area and ↓ PVR
o Hypoxic pulmonary vasoconstriction
 Response to low PaO2
 Divert blood away from poorly ventilated areas →↓shunt
o Pulmonary emboli- ↑ PVR
o Arterial thickening- primary pulm HTN, cirrhotic liver
 Zones of the lung
o Zone 1: no blood flow despite ventilation; usually doesn’t exist; occurs with PPV or low PAP
o Zone 2: flow is proportional to difference b/w PAP and airway pressure
o Zone 3: flow is proportional to difference b/w PAP and venous pressure

 Pulmonary edema
o Hydrostatic pulm edema from ↑ LV pressures
o Capillary leak
Pulmonary gas exchange
 Oxygen
 Arterial hypoxemia- reflects gas exchange
o Measurements of oxygenation
 Oxygemoglobin dissociation curve
 P50 = 26.8 mmHg
 Right shift: acidosis, hypothermia, ↓ 2,3 DPG
→ facilitate unloading
 Normal PvO2 40 mmHg ~ 75% SaO2

 Arterial oxygen content (Normal PaO2 = 100 mm Hg →

SaO2 98%)

CaO2 = SaO2 (Hgb x 1.39) + 0.003 (PaO2)

(normal ~21.15 mL/dL)

 Determinants of alveolar oxygen partial pressure

 Alveolar gas equation (describes the way
inspired PO2 and ventilation determin PAO2)

PAO2 = FiO2 x (Pb-PH2O) – (PCO2/RQ) =

FiO2 x (760-47) – (PCO2/0.8)
(Pb barometric pressure, RQ ratio of CO2 production to O2 consumption)
  Normal O2 consumption 300 mL/min
 No preO2, pt will desat after 30 s to SaO2 90%, with preO2: 7 minutes
 Venous admixture (describes physiologic causes of arterial hypoxemia for which PAO2 is normal)
 Normal A-a gradients 5-10 mmHg

A-a gradient = PAO2 – PaO2

o Intrapulmonary shunt (V/Q = 0)

 Mixed venous blood is not exposed to alveolar gas → still mixes with oxygenated blood from normal lung → ↓ O2
 Giving O2 will NOT help
o Ventilation-perfusion mismatch
 Disparity b/w amount of well-ventilated alveoli and poorly ventilated alveoli → cannot compensate
 Giving O2 will help to achieve a PO2 on plateau
o Diffusion impairment
 On cellular level, easily eliminate w/ O2
o Venous oxygen saturation
 Shunt is a mix of venous and normal → ↓ SVO2 will ↓ PaO2
 Carbon dioxide- exists as bicarb or carbaminohemoglobin
o Hypercapnia
 If >80 → narcosis
o Determinants of arterial carbon dioxide partial pressure

 PaCO2 = k (VCO2/VA)

o Rebreathing
 Exhausted CO2 absorbents, malfunction expiratory valves
o ↑ CO2 production
 Tourniquet, insufflation, thyroid storm, fever, MH
o ↑ dead space
 Anatomic, alveolar, phys
 ↑ in emphysema, cystic fibrosis, PE, hemorrhagic shock, ↑ airway pressure, and ↑ PEEP
 Bohr equation: Vd/Vt = (PaCO2 – PECO2) / PaCO2
 Normal: 25-30%
o Hypoventilation
 PaCO2 = 40, PvCO2 = 46
 PaCO2 ↑ 6 mmHg/1st minute; 3mmHg thereafter
o Ddx of ↑ arterial CO2 partial pressure

Pulmonary mechanics
 Static properties
o FRC is natural balance pt b/w chest wall and lungs
o Static compliance = Vt/(Pplat - PEEP)
 Dynamic properties and airway resistance
o Resistance determined by radius
o Small airways no cartilaginous structure or muscle
o Dynamic compliance = Vt/(PAP – PEEP)
Contol of breathing
 Central integration and rhythm generation
 Central chemoreceptors
o Ventrolateral medullary surface respond to pH and PCO2
 Peripheral chemoreceptors
o Carotid bodies
o Respond to ↓ PO2, ↑ PCO2 and ↓ pH
o Exposed to arterial blood
 Hypercapnic ventilator response
o Central and peripheral
o Brainstem response is slow
  Hypoxic ventilator response
o Peripheral response ↑ventilation with ↓ PaO2 and ↓ SaO2
o Central response: ↓ ventilation
 Effects of anesthesia- depressant effects
o Volatiles ↓ excitatory neurotransmission
 Disorders of ventilatory control
o Primary central alveolar hypoventilation syndrome, morbid obese, sleep apnea
o Periodic breathing: peripheral recetpros activated by mild arterial hypoxemia → continual overcorrection/undercorrection
Integration of the heart and lungs

Fick equation: VO2 = CO x (CaO2 – CVO2)

 O2 delivery

DO2 = CO x CaO2

 O2 extraction
= (CaO2-CvO2)/CaO2

o Anemia
o Metabolic demand