Download - Cardiovascular Physiology VI
Cardiovascular Physiology VI.
50. Pulmonary circulation.32. Biology of the airways. Metabolic and endocrine functions of the lung.40. Cardiac work and metabolism. The coronary circulation.51. Skeletal muscle blood flow, the cardiovascular adaptation to work and exercise.
Ferenc Domoki, November 24 2021.
Characterization of the circulation in specific regions
Quantitative data: % of cardiac output, tissue blood flow (ml/g/min), O2-consumption etc.
Organ specific morphological features: arteries, microcirculation, veins
specifics in capillary transport
regulation of local blood flow!
Pulmonary circulation
The organ with the HIGHEST blood flow! (= CO)
Low pressure – low resistance circulatory bed!
Pulmonary circulation Systemic circulation
PA systolic pressure 24 mmHg Aorta systolic pressure 120 mmHg
PA diastolic pressure 9 mmHg Aorta diastolic pressure
80 mmHg
PA mean pressure 14 mmHg Aorta mean pressure 93 mmHg
Pulmonary capillary mean pressure
10 mmHg Systemic capillary mean pressure
25 mmHg
Left atrial pressure 6-8 mmHg Right atrial pressure 0-2 mmHg
PVR 1.5 mmHg×min/l
TPR 16 mmHg×min/l
Anatomical features
Arterial compliance is similar to venous, thus ~10% of blood volume is evenly distributed between the pulmonary arteries and veins, the capillaries contain ~80 ml of blood.
The bronchial arteries (from aorta) provide NUTRITIVE blood flow to the larger airways (1-2% of CO), physiologic shunt flow.
PVR is affected greatly by PASSIVE mechanisms due to the low pressure and large compliance values. Major aspects: 1. the force of gravity in upright humans, 2. increase of PA pressure / CO, 3. changes in lung volume.
alveolar pressure
dis
tan
ce f
rom
bas
eperfusion
The effect of gravity: vertical gradient of transmural pressure develops in standing position
pressure inpulmonary artery
pressure inpulmonary vein
No flow
Intermittentflow
Continuous flow
Fortunately in healthy people there is no Zone I flow
Bedrest is putting every lung region in Zone III. People with pulmonary infections, shock MUST stay in bed!
Effect of gravity on pulmonary circulation
3-fold gradient!
PVR decreases if blood pressure and/or CO increases, because
Due to the enormous compliance, small increases in transmural pressure lead to the dilation of extralveolar vessels
The alveolar capillary network has multiple branching (net-like, sheet like flow), so increases in flow passively opens new passageways (capillary recruitment)
Vascular resistance is affected by lung volume
Quiet, tidal breathing
Inflation of alveoli is pulling (distending) the blood vessel in the lung parenchyma (extraalveolar vessels), but the inflation will compress the septal capillaries
Optimal resistance: around the FRC volume!
It is of importance how artificial ventilation parameters are set!
Pulmonary microcirculation
VERY thin (0,3 mm!) capillaries, that are permeable to fluid
Edema entering the alveoli can be lethal!
From the Starling-forces, especially the LOW capillary hydrostatic pressure limits fluid filtration
Rich lymphatic vascularization also protects from pulmonary edema
Alveolocapillary barrier
Control of pulmonary circulation
the ventilation/perfusion ratio V/Q 1 Chiefly passive, no autoregulation Unique hypoxic pulmonary vasoconstriction
(HPV aka Euler-Liljestrand rfx) to regulate the DISTRIBUTION of blood flow within the lung
The function of this regulation to optimize gas exchange (oxygenation). Blood will be directed to well-ventilated lung regions from worse ventilated parts.
HPV at work…
In a radical, two compartment lung model (left lung has no ventilation in panels B and C), the advantage is obvious: with HPV (Panel C) oxygenation is less reduced in arterial blood
Hypoxic Pulmonary Vasoconstriction
J. T. Sylvester, Larissa A. Shimoda, Philip I. Aaronson, Jeremy P.
T. Ward
Physiological Reviews 2012 92:367-520
HPV is a feature of pulmonary arterial smooth musce cells
PVR: Pulmonary Vascular Resistance
PH: Pulmonary hypertension
ROCK: RhoA/Rho kinase
(Curr Opin Pharmacol 9:287-296, 2009)
We don’t know the mechanism yet.
Long-lasting hypoxia leads to pulmonary hypertension (PH)
Pulmonary hypertension can damage both the pulmonary vessels and the right ventricle.
In ICU-s, NO (~ 20 ppm) added to the ventilatory gas mixture can alleviate PH.
Metabolic and endocrine functions of the lung.
The ~100 m2 surface area microvascular bed that is connected to the systemic circulation in series, will affect the composition of the blood in addition to the blood gases.
Many of the vasoactive substances that are washed out of the organs will be degraded by the pulmonary microvascular endothelium, so they would NOT have a hormonal effect (see next slide)
This is the site of angiotensin II hormone synthesis from angiotensin I (by ACE)
Metabolic clearance by pulmonary endothelium
Serotonin > 95%
TxA2, PGE2, LTB4 >90%
Bradykinin >80 % (also by ACE!)
These effects are specific: histamine, prostacyclin for instance are not inactivated
Organs of the systemic circulation
Today: coronary circulation and muscle circulationRenal circulation: renal physiology (55)Splanchnic circulation: GIS physiology (68)Cutaneous circulation: thermoregulation (86)Fetal circulation: reproductive physiology (91)Cerebral circulation: CNS physiology (93)
Distribution of cardiac output in the systemic circulation
brain
heart
liver +splanchnic
kidney
muscle
skin
other
total
Organ weight % flow ml/min CO% O2 uptake (ml/min) %
+ 1200 +20
2
0,5
2
0,5
50
3
42
Simplified distribution of resting CO
Cerebral + coronary blood flow = 20%
Renal blood flow = 20%
Skeletal muscle blood flow = 20%
Splanchnic blood flow = 20%
Skin blood flow and the rest = 20%
Coronary circulation
Anatomical considerations
Left and right coronaries (85-15 % of blood flow, respectively)
in the left ventricle, blood vessels are compressed during systole, most blood flow in this region occurs during diastole.
This effect is not homogenous in the venticle: the SUBENDOCARDIUM is most vulnerable!
Left
CoBF
Right
CoBF
Aortic
pressure
Systole diastole
MABP
Mean flow
Mean flow
Zero flow
Zero flow
Transmural pressure!
brain
heart
liver +splanchnic
kidney
muscle
skin
other
total
Organ weight % flow ml/min CO% O2 uptake (ml/min) %
+ 1200 +20
2
0,5
2
0,5
50
3
42
5% of CO, 10% of Oxygen consumption, AVDO2 is more than double of body average: Metabolic challenge!
Regulation of coronary circulation
The resting tone of the arterioles is determined by basal tone, there is NO sympathethic vasoconstrictor TONE
Pronounced autoregulation of blood flow
Blood flow is regulated by metabolitesreleased from cardiomyocytes (includingadenosine), important role for endothelial NO
Since oxygen extraction is maximal (up to 80% instead of average 25% elsewhere), increased metabolism MUST be supported by increased flow
rest exercise
Pyruvic acid,
ketone bodies
amino acids
Free fatty acids
Free fatty acids
Substrates of cardiac energy metabolism
Adaptation of coronary circulation to exercise
The increase in CO is chiefly produced by the increased cardiac pump function stimulated by in sympathethic activity.
The increased sympathethic stimulation leads to increased metabolic activity that is eliciting vasodilation through the increased release of metabolites. The coronary blood flow increases proportionaly with the CO (~5%)
Role for a direct autonomic vascular effect is unimportant
Cardiac work
Two components:1. Pressure-volume work (PxV) – the heart
makes form the low pressure blood (stroke volume) high pressure blood – 85%
2. Kinetic work – (1/2 m x v2) -15% increases momentum of blood
W = 1.182 Nm (J) every systole Power: P ~ 1.4 W (J/s) Efficiency: 15-40 %
Circulation in skeletal muscle
brain
heart
liver +splanchnic
kidney
muscle
skin
other
total
Organ weight % flow ml/min CO% O2 uptake (ml/min) %
+ 1200 +20
2
0,5
2
0,5
50
3
42
At rest, the oxygen consumption is a tiny fraction (2%) of the heart muscle per unit weight, also the blood flow (4%)
Skeletal muscle blood flow: quantitative data
The skeletal musculature is ~ half of body weight
15-20% of resting CO, <1 l/min,
80% of CO during physical exercise: up to 20-22 l/min
Responsible for 20% resting oxygen consumption, 80% of maximal oxygen consumption, can increase by 50-75 fold during work! (catches up with heart muscle)
skin
Heart, brain
Splanchnic and renal
flow
Skeletal muscle
Oxygen consumption (l/min)
Cardiac output
Regulation of skeletal muscle circulation
Sympathetic vasoconstrictor tone: systemic MABP regulation
Sympathetic cholinergic vasodilation: anticipatory vasodilation?!
Active hyperemia: metabolic regulation (K+, acidosis, adenosine, PGE2)
Significant capillary recruitment during exercise
Active hyperemia in working skeletal muscle
To observe: initial (anticipatory) flow increase, vascular compression by contractions (transmural pressure!), the developing active hyperemia in between the contractions that diminishes after the stop of the exercise.
Central venous pressure
Mean arterial pressure
Heart rate
Stroke volume
Cardiac output
TP resistance
Splanchnic blood
flow
Venous tone (symp)
Adaptation to physical exercise
Sympathetic tone increases, and arterioles dilate in active muscles.Net effects:TPR decreasesCO increasessystolic and mean arterial pressure increases, diastolic barely changes if any. Redistribution: splanchnic (and skin) flow decreases to limit decrease in TPR
exercise
These factors also affect baroreceptor sensitivity
Guyton diagram at work: cardiac output change during exercise
Sympathetic stimulation of the heart
Sympathetic venoconstriction
Decreased total peripheral resistance