Pulmonary Circulation Flashcards
differences between pulmonary and systemic circulation
- pulmonary circulation is the only vascular bed to receive the entire CO
- ischemic damage is rare because of multiple supplies:
- pulmonary circulation
- bronchial circulation
- alveolar gas oxygen supply
- minimal basal tone in pulmonary vessels
- passive distension with increased pressure or flow without significant autoregulation
- hypoxic vasoconstriction in lung
- change in pulmonary resistance has same affect as increase in vascular resistance for left ventricle
- pulmonary endothelium synthesizes NO and prostaglandins
pulm circulation and pressures
- smaller than systemic-lesser
- blood pressures are lower because PVR is 10x lower than TPR
- afterload of right ventricle is less than afterload of left ventricle, so right heart does less stroke work than left heart
anatomic and physiologic shunts
- bronchial circulation is a normal anatomic shunt
- left to left shunt
- 1-2% of CO
- bronchial circulation starts at base of aorta, perfuses large airways, vessels, nerves, then drains into bronchial veins and pulmonary vein and left atrium
- responsible for slight drop from Pend cap of 100 to Pa02 95
- accounts for slight difference in right and left ventricle output
lymphatic system
- vessels that drain excess fluid from the interstitial space and return it to the circulation via caudal mediastinal lymph node and the thoracic duct
- valves that are regulated by intrinsic propulsion, mechanical pumping during breathing and SNS
- intrinsic pumping can generate up to 20 mmHg if flow is occluded
physiological shunt
sum of normal anatomic shunts plus any pathological intrapulmonary right to left shunt that occurs when airways are blocked
pathological right to left shunts
-result in hypoxemia without much hypercapnea
features of pulmonary vessels
- pulmonary arteries and veins are both thin walled and highly distensible
- gradation of muscularity from muscular to partially muscular to non muscular with no distinct arterioles
- capillaries surrounded by alveolar air, so external pressure is alveolar pressure, which oscillates during breathing
- changes in lung volume during breathing affect pulmonary vascular resistance
- vessels are gas exchanging if they are less than 1 mm in diameter
- alveolar and extra-alveolar vessels have different mechanical properties and are affected differently by changes in lung volume but do not differ anatomically
pulmonary blood pressure
- low and dissipated gradually along vasculature
- mean Ppa > 20 is pulmonary hypertension
- mean Ppa > 25 gives pulmonary edema, resulting in a diffusion problem
- measured with cardiac catheter 100 cm long and 1 mm diameter inserted through skin in peripheral vein
- advanced to pulmonary artery and inflated to occlude flow
- wedge pressure used as estimate as LA pressure
- not capillary pressure-its pulmonary wedge pressure
- tells you about pre load for left ventricle
- mean pulmonary artery pressure is 12 for systolic and 5 for diastolic
- low resistance means low windkessel effect
pulmonary vascular resistance
- PVR = (PpA-PLA)/CO
- difference in pulm artery pressure and LA pressure over CO
- Ppa measured with other catheter
- 10x less than TPR
- work of right ventricle is 10x less
- right heart failure only problem in extreme obstructed pulmonary circulation
- diastolic pressure n pulmonary artery nearly equal to left atrial pressure
- need to measure carefully
- subject supine and middle of ant/post axis
changes in PVR
- mostly passive
- pulm blood volume is 200-300 ml and can increase 2-3x during exercise but vessels are so compliant that pressure doesn’t increase much
- pressure is inversely proportional to radius and resistance
- decreases as pressure increases
- in body, resistance increases as compensation to increased pressure
inflation
- alveolar blood vessels are stretched and become narrower as the capillaries increase in length
- extra-alveolar blood vessels expand due to the more negative intrapleural pressure increasing their transmural pressure
- vessels near alveoli are exposed to those pressures, others influenced by intrapleural
- interstitial pressure around large vessels becomes more negative when the lung inflates
optimum volume
- lung has optimum volume that minimizes PVR
- alveolar and extra-alveolar vessels are in series, so their resistances are additive
- PVR is at minimum at FRC
- lung volume changes during breathing and affects resistance
- U shaped relationship
- increases as transpulmonary pressure increases or decreases
- at very low, kinked, increased resistance
- U shape is sum of two curves for alveolar and extra alveolar vessels
- corner vessels-in alveolar septum but at junctional corners of alveoli-expand during inflation and lower resistance-extra-alveolar and never close during inflation
normal breathing
- alveolar pressure fluctuates between pos and neg 2
- caps remain open
- mechanical ventilation-alveolar pressure positive-greater tendency for caps to collapse and increase their resistance
- causes Ppa to rise increases the afterload of the right ventricle
- ventilated at low pressure settings
- healthy heart responds to this by augmenting CO
active factors affecting pulmonary vascular resistance
- vasodilators:
- prostacyclin, histamine, calcium channel blockers, NO
- vasoconstrictors:
- hypoxic vasoconstriction shunts blood to better ventilated region of the lung
- increased PCO2, low pH
- norepi
- thromboxane
- angiotensin II
- serotonin, ATP
- neural influence plays minimal role in regulating PVR
- pathological conditions remodel and increase PVR-hypertension, asthma, ARDS, COPD, high altitude, PE, veno occlusive disease, tumors
hypoxic pulmonary vasoconstriction
- regional level
- shunts blood to better ventilated regions of lung
gravity
- makes blood flow greatest at base of lung
- passive distension
- 6x greater
- pressure increases in capillaries gradually from top to bottom due to hydrostatic pressure from intrapleural fluid
- top is Ppa-10, bottom is Ppa+10
- caps at base have high transmural pressure and are wide open, resistance to blood flow lower, so flow increases
three zone model
- top, middle bottom
- top PA >Pa>Pv-not usually in healthy lung
- middle Pa>PA>Pv alveolar in middle, flow depends on alveolar pressure
- hydrostatic pressure increases and intravascular pressure exceed alveolar pressure, opening of caps with increase in flow, partial collapse on low pressure side but flow stays
- determined by differences between Ppa and Palv
- waterfall flow- comes from before the falls
- bottom Pa>Pv>PA-flow increases due to gravity and passive distension
pulmonary edema causes
- increased capillary permeability
- increased cap hydrostatic pressure
- decreased interstitial hydrostatic pressure
- decreased colloid osmotic pressure
- insufficient pulmonary lymphatic drainage
- unknown
clinical problems
- adult resp distress syndrome
- oxygen toxicity
- inhaled/circulating toxins
- increased left atrial pressure resulting from L ven infarction or mitral stenosis
- overadmission of IV fluids
- too rapid evacuation of pneumothorax
- protein starvation
- dilution of blood proteins by IV
- renal problems resulting in urinary protein loss
- tumors
- interstitial fibrosing diseases
- high altitude
- head energy
- drug overdose
right to left shunt
-causes hypoxemia
-Qs/Qt= (CcO2-CsO2)/(CcO2-CvO2)
-difference in cap/shunt over difference in cap veins
-obtained from oxygen dissociation curve
-if Qs=0, no shunt
-if Qs=Qt, no oxygenation
if Qs=1/2 Qt, half oxygenation
shunts
- give more hypoxemia than hypercapnea
- these patients will not respond to O2 because you will just send it into the shunt
- small drop in oxygen makes large drop in partial pressure
- small drop in carbon dioxide makes small drop in partial pressure