Seven Flashcards
What is the relationship between Q of the right ventricle and left ventricle. What is the normal pressure of the pulmonary artery? Systemic system? What does that mean concerning the resistances of the two systems? What will happen to P(PA) if pulmonary resistance increases? What will be the result in capillaries?
The rate at which the right ventricle pumps blood, its cardiac
output (
.
Q) (L/min), must equal that of the left ventricle
to avoid an imbalanced distribution of blood volume within
the systemic and pulmonary circulations. However, normal
pulmonary arterial blood pressure (PPA) averages just
12-16 mm Hg, or about one-eighth of the average blood pressure
in the dorsal aorta. Because Ohm’s law states that fl ow =
ΔP/R (Chap. 6), total pulmonary vascular resistance (PVR)
normally is also a small fraction of vascular resistance in the
much larger systemic circulation. (Diseases for which PVR
is signifi cantly increased will be presented elsewhere in this
book.) This chapter will focus on factors that affect PVR and
thus PPA, realizing that increases in PPA will increase the work
required of the right ventricle and the gradient for fl uid constituents
of the blood to leak out of alveolar capillaries into the
surrounding interstitium and airspaces.
What happens to PVR when Q increases? Why must this happen? How does this happen?
As required by Ohm’s law (
.
Q = ΔP/PVR), the resistance of pulmonary
blood vessels must decrease as Q increases if pulmonary hypertension is to be avoided. Studies show that when
Q rises, PVR decreases by further distension of previously open arterioles and capillaries, and by recruitment of vessels
that are collapsed when
.
Q is lower. Such changes refl ect the
exceptional compliance of the thin-walled pulmonary vasculature.
Thus when
.
Q is low, many pulmonary arterioles and
alveolar capillaries either are closed or are fl owing at less than
maximal diameters.
Describe the vascular waterfall. What happens in zones 1/2/3? What kinds of things will have an effect on these dynamics and how?
Remember that pulmonary capillaries are compliant
vessels surrounded by a fl uctuating PA while perfused by
a relatively low PPA. In the most widely accepted model of
the pulmonary circulation described in 1963 as the vascular
waterfall (Fig. 7.3), three zones of perfusion can be identifi ed
for the upright lung. In Zone 1, PPA simply is too low to perfuse
the lung apices, while PA exceeds both PPA and PPV . Such
Zone 1 capillaries are collapsed and have fl ow rates of zero.
In Zone 2, PPA exceeds PA but PPV does not. Such Zone 2 capillaries
have fl ow rates proportional to the difference between
PPA and PA, while PPV has no direct effect on their fl ow. Extending
the model, capillaries high in Zone 2 (near Zone 1) will
open or closed with each pulse as PPA rises during systole to
exceed PA, declining during diastole to fall below PA. Capillaries
lower in Zone 2 would remain open longer during each
systolic cycle of pressure than would capillaries above them
within the gravitational gradient. In Zone 3, alveolar capillaries
presumably behave like those in the systemic circulation,
since both PPA and PPV exceed PA throughout the cardiac cycle.
Additionally, alveolar capillary blood fl ow increases slightly
with depth in Zone 3 due to progressively greater capillary
distension (Fig. 7.3).
These zonal boundaries of lung perfusion are not fi xed in
time or space, but fl uctuate depending upon posture and changes
in PA, PPA, or PPV with exercise, disease, etc. For example, it is
unlikely that Zone 1 conditions exist in the lungs of a healthy
adult with normal chest size, cardiac output, and PPA. However,
Zone 1 conditions quickly arise in subjects holding their breath
while swimming, as well as in patients being mechanically ventilated
and in whom PA increases dramatically during inspiration
(Chap. 30). One can also appreciate how Zone 3 perfusion conditions
would exist in the lung apex of a subject doing a handstand,
or would move closest to the bed mattress in a supine patient.
Consideration of these frequent adjustments in transmural capillary
pressures makes the lung’s elegant “vascular waterfall”
an intelligible and useful working model to explain the easily
observed and dynamic differences in regional pulmonary blood
fl ow. Understanding the challenge of maintaining good
.VA/.Q
matching in the face of such fl uctuating regional gradients in air
and blood fl ow is the primary subject of Chap. 8.
Explain starling’s law of the capillaries. What is ultrafiltration? What prevents it from occuring?
All pressures mentioned to this point have been hydrostatic,
whether alveolar, vascular, or intrapleural. Hydrostatic pressures
within blood vessels are only partially opposed by interstitial
hydrostatic pressure of the delicate alveolar parenchyma.
This imbalance would rapidly move blood water out of the
vascular spaces by ultrafi ltration, if capillary hydrostatic pressures
were not opposed by colloid osmotic pressure exerted by
blood proteins (Fig. 7.5). Formally presented, Starling’s law of
the capillary states that:
F = K ∙ [(P(MV) − P(PMV)) − σ (πMV − πPMV)]
where:
F = net extravasation or transvascular fl uid movement
K = fi ltration coeffi cient for permeability of the capillary
endothelium
PMV = hydrostatic pressure within lung microvessels
(~10 mm Hg)
PPMV = hydrostatic pressure in perimicrovascular space
(0 to −10 mm Hg)
σ = protein refl ection coeffi cient, normally 1.0 (in
arbitrary units)
πMV = protein colloid osmotic pressure in the circulation
(~28 mm Hg)
πPMV = protein colloid osmotic pressure in peri-microvascular
space (~20 mm Hg)
Explain what P(MV) is like and what P(PMV) is like? Where does fluid that leaks from the capillary go? What happens if that process doesn’t work well enough?
The hydrostatic pressure PMV within the blood vessel
causing fl uid to extravasate from lung capillaries into the
septal interstitium is mostly unopposed by any rise in PPMV ,
because the delicate alveolar epithelial membranes cannot
resist increases in interstitial volume as can occur systemically
in tissues like skeletal muscle. Rather, the septal interstitial
compartment expands with this capillary ultrafi ltrate
that drains into blind-ended pulmonary lymphatic capillaries.
However, if lymphatic drainage cannot remove the ultrafi
ltrate at a suffi cient rate, interstitial edema will occur that
can progress to alveolar edema accompanied by disruption of
epithelial layers (Fig. 7.6). Maximal lung lymphatic drainage
is probably 2-3 times the normal fl ow rate of 20 mL/h.
What things will alter Pi(MV) and Pi(PMV)? What about K and σ? In what ways?
The protein colloid osmotic pressure πMV of blood in the
alveolar capillaries is relatively constant as in systemic capillaries,
except in diseases like Kwashiorkor or liver failure that reduce plasma [albumin]. Likewise, πPMV is generally
considered constant unless interstitial [protein] declines by
dilution with water from the blood (ie, ongoing edema) or
from within the airspaces (eg, near-drowning in fresh water).
Smoke or fume inhalation, aspiration of stomach contents or
toxic chemicals, and blood-borne diseases like gram-negative
endotoxemia alter the endothelial K or σ such that net fl uid
fl ow out of alveolar capillaries increases and edema occurs,
even if PMV , PPMV , πMV , and πPMV are all normal.
What are the two primary categories of pulmonary edema? What are the causes of each? What are the results of each? What are the vascular conditions in each?
In practice, factors in Starling’s equation are most likely
to become unbalanced in two main ways to initiate interstitial
and then often alveolar edema. The fi rst occurs when PMV
becomes elevated due to systemic hypertension, generally rising
in parallel with increases in PPA and PPV. The resulting leak
is termed cardiogenic edema since its cause is usually congestive
heart failure or mitral valve dysfunction (Table 7.1).
In this type of edema, the endothelial barrier to protein movement
is usually intact (ie, K and σ are normal), and the resulting
edema fl uid has a [protein] lower than that of plasma.
The second major type of pulmonary edema occurs despite
normal hydrostatic forces and is considered noncardiogenic in
etiology. It commonly begins as an increased permeability (K
and/or σ) of the capillary endothelial or alveolar epithelial layers,
often following direct cellular injuries. Plasma proteins can
now leak out directly between adjacent barrier cells, so that such
edema fl uids have a higher [protein]. Indeed in severe cases,
intact formed blood elements can appear within the interstitial
or alveolar spaces as well, yielding a hemorrhagic edema
(Fig. 7.7). Such severe forms of edema are a characteristic
feature of acute lung injury (ALI) and the acute respiratory
distress syndrome (ARDS). How these disruptive changes in
pulmonary endothelial or epithelial permeability occur in the
previously healthy lung, and the impact they have on diffusional
gas exchange will be discussed at length in Chap. 28.
Describe pulmonary edema as it applies to restrictive lung disease and obstructive lung disease.
Pulmonary edema is conventionally viewed as an acute
restrictive lung disease (Chap. 6) because fl uids within the
alveolar septa and distal airspaces reduce the functional
parenchymal volume available for ventilation. However,
such edema also has a propensity to accumulate within the
interstitial spaces surrounding larger airways and blood
vessels (Fig. 7.7). Such edematous cuffi ng creates a sleeve
of fl uid that prevents dilatation along the length of such
vessels, even if smooth muscle cells within their walls are
relaxed. The resulting bronchiolar edema is an acute
obstructive lung disease that will adversely aff ect peak
expiratory fl ow rates and increase dynamic airway resistance.
Thus, a patient with ALI or ARDS would have a mixed
respiratory disorder that clinically has both a complex
etiology and an uncertain outcome (Chaps. 26 and 28).
Explain how high altitude pulmonary edema can occur. What happens in it? What can relieve it?
The specifi c causes of pulmonary edema are multiple
(Table 7.2), and a complete discussion is beyond the scope
of this introduction to the topic. However, it is evident that
perturbations to virtually all terms within Starling’s equation
occur clinically, although not all result in cases of equal
severity or duration. Of interest to the general public is the
sudden and often unpredictable development of high altitude
pulmonary edema, HAPE in some travelers to elevations
above their normal residences. By poorly understood
mechanisms, severe hypoxia reduces active Na+ transport
that normally drives the reabsorption of capillary ultrafi ltrate and thereby keeps alveolar membranes moist but free of
excess fl uid. This uncleared alveolar fl uid, whose formation
is invariably accelerated by the increased PPA and PMV that
are also caused by hypoxia (Chap. 8), leads to acute HAPE in
susceptible individuals. What makes some climbers sensitive
to this serious side effect of even moderate altitude exposure,
while their climbing partners may be unaffected, remains an
intriguing and unsolved question in the fi eld (Chap. 13). In
any case, resolution of their often hemorrhagic edema is
rapid and reversible if a descent to lower elevations can be
achieved in time.
