Pathophysiology of Pulmonary and Visceral Circulation

1
Pathophysiology of Pulmonaryand Visceral
Circulation

• Tatár M.
• Dept. of Pathophysiology
• Jessenius Med. School

2
Pulmonary Circulation

• Anatomy
• arteries gt 1 mm thin wall, media consists mainly
  from elastin and collagen fibres
• arteries 0.1- 1 mm muscular layer represents 5
  of external diameter
• arteriols lt0.1 mm mainly elastic tissue
  connections with capillary system, postcapillary
  venules and bronchial arteries (around the neck
  of terminal bronchioles)
• venules communication with bronchial circulation
  
• veins media rich of muscle cells active
  contraction bronchopulmonal anastomosis 2/3 of
  bronchial blood flows to left atrium

3
Pulmonary Circulation

• Hemodynamics
• high flow with low resistance enormous blood
  volume changes without marked pressure changes
• pulmonary blood flow depends on respiratory
  movements and activity of left ventricle
• marked effect of left atrium pressure
• inspirium improve blood flow into thoracic
  cavity, expirium improve pulmonary blood flow
• main goal of the regulation of pulmonary
  circulation is to maintaine optimal gas exchange
  - ventilation is regulated mainly centrally,
  pulmonary perfusion locally humoral substances
  and respiratory gases
• mean pressure in pulmonary artery 12-16 mmHg
  in pulmonary veins 6-10 mmHg

4
(No Transcript)
5
Pulmonary Thromboembolic Disease

• block of pulmonary artery (P.A.) flow with
  thrombus/embolus
• always associated with dilatation of bronchial
  circulation
• hemorrhagic infarction is relatively uncommon
  (bronchial artery supply)
• classification
• a) acute minor
• b) acute massive
• c) subacute massive
• d) chronic thromboembolic hypertension

6
Pulmonary Thromboembolic Disease

• Effects on the lung
• small emboli no detectable effect
• Hypoxemia with hypocapnia
• - overperfusion of unembolised lung
• - reduced SvO2 due to ? cardiac output (CO)
• - ? ventilation of dead space

7
Pulmonary Thromboembolic Disease

• Effects on the heart and circulation
• normal CO even when embolus effects pulm.
  function
• obstruction of 50 of pulm. circulation is
  compromising right ventricle
• sudden and severe obstruction acute right
  ventricle failure (hypotension, dizzeness,
  syncope)
• subacute massive obstruction during weeks time
  for some hypertrophy of R.V. P.A. pressure
  60-90 mm Hg
• chronic thromboembolic pulmonary hypertension
  generalized intimal and medial hypertrophy
  right heart failure

8
Pulmonary Hypertension (PH)

• 1. Primary PH
• - arteriopathy of unknown etiology
• - all branches of P.A. medial hypertrophy,
  fibrinoid necrosis
• 2. Heart diseases
• a) ? P.A. blood flow (left-to-right shunt)
• b) ? pulmonary venous pressure (left heart
  failure)
• 3. Respiratory system disorders (frequently COPD)
• - alveolar hypoxia
• a) smooth muscle contraction in P.A. through a
  direct
• effect on intracellular calcium level
• b) reduction in NO production
• - muscle hypertrophy in the media
• - loss of capillary bed in areas of severe
  emphysema

9
Splanchnic Ischemia

• rich collateral supply in this teritory
  occlusions result in comparatively little
  disturbances in blood supply
• portal venous system is of large capacity and can
  pool a considerable proportion of blood volume
• muscle vascular plexus in intestinal wall has
  more collateral circulation than mucosal plexus
  in certain types of ischemia mucosa has
  selectively undergone complete necrosis

10
(No Transcript)
11
(No Transcript)
12
(No Transcript)
13
Physiology of Intestinal Circulation

• precapillary resistance vessels site of local
  and remote control system
• precapillary sphincters control of the number of
  perfused capillaries
• exchange vessels place between intravascular and
  extravascular compartments
• postcapillary resistance vessels main
  determinant of mean hydrostatic capillary
  pressure fluid exchange

14
(No Transcript)
15
Physiology of Intestinal Circulation

• autoregulation
• - constant flow with pressures between 80-160
• mmHg to keep hydrostatic pressure
• - precapillary arterioles in villous
  circulation
• postprandial hyperemia
• intestinal counter-current exchanger for oxygen
  is much more involved during hypotension

16
(No Transcript)
17
(No Transcript)
18
Splanchnic Ischemia

• occlusive (embolisation, massive venous
  trombosis)
• - rare
• - transmural infarction
• - loss of circulating volume peritonitis
• non-occlusive and relative
• - common in critically ill patients
• - cardiac failure, hypovolemic shock, sepsis

19
(No Transcript)
20
Mechanisms of Splanchnic Ischemia

• GIT
• - barrier against very noxious intraluminal
  environment
• - nutrients provide optimal conditions for the
  grow of
• microorganisms and helmints
• mucosal circulation
• - essential to sustaine balance between
  agressive
• intraluminal toxins and barrier components
• - compensatory adjustments in capillary surfice
  area and
• oxygen extraction

21
(No Transcript)
22
(No Transcript)
23
(No Transcript)
24
Ischemic Injury to Intestinal Mucosa

• hypoxia
• critical level of blood flow - ? intracellular
  energy stores
• amplification with counter-current exchange of O2
  at the villous base
• intracellular accumulation of hypoxantine

25
(No Transcript)
26
Ischemic Injury to Intestinal Mucosa

• postischemic reperfusion
• free oxygen radicals
• activation of resident neutrophils another
  source of reactive oxygen metabolites
• promotion of conversion of xantine dehydrogenase
  to xantine oxidase via proteolysis
• proteases (pancreas, granulocytes)
• contra
• protease inhibitors (?1- protease inhibitor)

27
(No Transcript)
28
(No Transcript)
29
(No Transcript)
30
(No Transcript)
31
Systemic Mediators of Splanchnic Origin

• ischemic bowel releases toxic agents which, in
  turn, affect the cardiovascular system and lead
  to development of shock and multiple organ
  failure
• bacterial translocation (bacterial leave the
  intestinal lumen) role of macrophages, ischemic
  changes of intestinal architecture
• endotoxins Tr and Leu aggregation, abnormal
  tissue perfusion, ? capillary permeability
• eicosanoids splanchnic region is important
  source and a target, as well

32
Splanchnic Organ Injury Syndromes

• stress ulceration acute non-occlusive ischemic
  erosions
• ischemic hepatitis centrilobular hepatocellular
  necrosis
• ischemic pancreatitis due to circulatory
  disorders without other predisposing factors
• acute intestinal ischemia severe abdominal pain
  and intense peristaltic activity
• focal ischemia of the small intestine edema,
  cell infiltration into the mucosa followed by
  fibrous stricture
• ischemic colitis damage of mucosal and muscular
  layers replaced by scar and stricture
• chronic intestinal ischemia (intestinal angina)
  pain occuring in relation to meals inability to
  produce postprandial hyperemia

33
Gut as the Motor of Multiple System Organ Failure

• uncontrol infection alterations in gut
  adynamic ileus, third space, hypermetabolism,
  loss of barrier function
• - upper gut is colonised by pharyngeal
  microflora
• - aspiration pneumonia invasion of gastric
  flora
• - bowel serves as a reservoir of pathogens, but
  also
• as a modulator of immune responses
• source of endogenous vasodilators in hemorrhage,
  cardiac failure, sepsis
• - damage of mucosal barrier ? bacterial
  translocation
• ? toxins into the circulation

34
(No Transcript)