respiratory path iii dr rotimi adigun hemodynamics, vascular disturbances
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Respiratory Path IIIDr Rotimi Adigun
Hemodynamics, Vascular disturbances
Topics Covered In ThisLecture1.Pulmonary Edema
2.Acute respiratory distresssyndrome (ARDS)3.SARS (Severe acuterespiratory syndrome)4.Pulmonary Embolism5.Pulmonary Hypertension
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Alveolar wall microscopy
Case History
• 72 yr old extremely pleasantCaucasian male with a past medicalhistory of CABG and multiple stents,unstable angina and myelodysplasticsyndrome, presented with left armpain
• He was admitted, but died within 24hours• A post mortem was performed.
Post mortem findings
• Right lung weighed 1,100 g and theleft lung weighed 750 g• Severe coronary atherosclerosis wasnoted• There was evidence of acutemyocardial infarction and massivepulmonary edema
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Causes of PulmonaryEdema
• Hemodynamic disturbances- Increased hydrostatic pressure
• Left sided congestive heart failure
– Heavy wet lungs (basal regions of lower lobes)- Alveolar capillaries engorged
- Intra-alveolar granular pink precipitate- Heart failure cells; brown discoloration- Impairs pulmonary function and predisposesto infection
S. 52
Pulmonary Edema- Causes
HemodynamicIncreased hydrostatic pressure• Left ventricular failure (common)• Excess IV fluids, Excess blood transfusion.Decreased oncotic pressure• Severe hypoproteinemia, Liver disease,Nephrotic syndrome
Other• Lymphatic obstruction (carcinoma, rare)
S. 53
Pulmonary edema--Causes
Microvascular Injury• Damage to vascular endothelium• Leakage of fluid and proteins intointerstitium and lumen• Diffuse edema is a contributor to
acute respiratory distress syndrome
S. 54
Microvascular injury
• Infections: Pneumonia, septicemia• Inhaled gases: Oxygen, smoke• Liquid aspiration: Gastric contents• Drugs and chemicals:Chemotherapyagents, heroin, cocaine, paraquatpoisoning• Shock, trauma• Radiation• Transfusion related
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Adult(Acute) RespiratoryDistress Syndrome (ARDS)
Syn. Shock Lung Syndrome, Diffusealveolar damage (DAD), Acute lunginjury (ALI)
(cf. RDS in neonates due todeficiency of surfactant)
Clinical syndrome caused by diffusealveolar damage
Mechanism of ARDS
• Imbalance between pro-inflammatoryand anti inflammatory cytokines• Toll like receptors activate NF-kB, atranscription factor controllingexpression of pro-inflammatorygenesUltimately pro-inflamatory mediators such as IL-1,IL-8,TNF and thrombin are produced inExcess compared to the production of anti-Inflammatory mediators such as IL-10.Neutrophils play a major role in this process.
ALI, Early ARDS
ARDS morphology
Endotheliumnecrosis
Type I alveolarcells necrosis
Fibrin
Edema
Waxy Hyalinemembranes
Diffuse Alveolar Injury
Shock lung
• Endothelial damage, damage to type 1pneumocytes• Exudate, impaired gas exchange• Hyaline membrane (necrotic debris from
epithelial cells plus edema fluid coagulate)• Type II pneumocyte necrosis=>loss
of surfactant-=>microatelectasis
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What Causes ARDS?
• Infections*• Sepsis*• Head injuries*• Gastric aspiration*• Pancreatitis• Burns• Trauma
• Fractures with fat embolismInfection, sepsis, head injuries and gastric aspirationAccount for more than 50 %of cases.
Clinical features
• Serious disorder• Respiratory difficulty- acute• Gasping for breath
• Severe hypoxemia, cyanosis, unresponsive tooxygen(Diffusion defect-intrapulmonary shunt)• Bilateral infiltrates on chest X-ray• Absence of clinical features of LVF• High mortality: 40% in 190,000 ARDS cases/yr• Patchy distribution
• Healing may result in diffuse interstitial fibrosis
Phases of ARDS
• Exudation- 0-7 days• Proliferation - 1-3 weeks
macrophages phagocytose deadcells and hyaline membrane, typeII pneumonocytes proliferatemature in to type I cells
• Fibrosis- TGF-β, PDGF
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SARS(Severe acute respiratory syndrome)
• First appeared in China in Nov 2002; last case 2004• Cause -- Corona virus; 8000 cases; 774 deaths• 2-10 day incubation period;begins with dry cough,
malaise, myalgia, fever, chills• 1/3rd fight infection, but 2/3rd progress to severe
respiratory disease, shortness of breath, tachypnea,and pleurisy• 10% of patients die from illness
• First transmitted through wild masked palm civets• Patho-physiology unknown; how virus moved from
animals to humans unknown
S. 64
Wild masked palm civet
Pulmonary embolismPulmonary Infarction
• Causes more than 50,000 US deaths/year• Large pulmonary embolus is a cause of sudden instantaneous death• Blood clots that occlude large pulmonaryvessels are embolic arising mainly from the
deep veins of the leg
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Pulmonary embolism
• 95% from deep leg veins• Sick, bedridden patients with
pulmonary, cardiovasculardisease, atherosclerosis ,OCP use
• BIG embolus -> bifurcation of PA, sudden
death from acute right heartfailure - no time to develop anychanges in lungs
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Pulmonary embolism
• MEDIUM -> hemorrhage, infarctiononly if circulatory status alreadycompromized
• SMALL -> usually no infarct becauseof dual supply, resolve ( lysis),
- if recurrent- pulmonary hypertension
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Saddle embolism
Pulmonary Infarction
Infarction
• Clinically resembles myocardialinfarction - chest pain, dyspnea,shock
• Gross: Wedge shaped, hemorrhagicinfarct, may be multiple
• Micro: coagulation necrosis
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Pulmonary hypertension• When pulmonary pressure reaches
1/4thof systemic levels(usually not more than 1/8 of Systemic
Five distinct groups.• Pulmonary arterial hypertension• PH with left heart disease• PH with lung disease• PH with chronic thrombotic or embolic disease• Miscellaneous
Pulmonary hypertension Underlying pathogenetic mechanism usually related
to any of• Increased pulmonary blood flow/pressure• Increased pulmonary vascular resistance• Increased left heart resistance to blood flow.Common etiologic factors includes: COPD or
interstitial lung disease, Congenital heart disease, Recurrent thrombo-embolism, Connective tissue disease, obstructive sleep apnea.
Idiopathic pulmonary arterial hypertension is a rare cause of pulmonary hypertension.
Pulmonary hypertension• Idiopathic pulmonary arterial hypertension/Primary PH•Familial PH - BMPR2 locus mutations
• Rare, young women,recurrentdyspnea ,syncope
• Raynaud’s phenomenon (vasopasmof peripheral vessels)
Characterised by obstruction to the lumen of Pulmonary vessels caused by proliferation of Endothelial cells,smooth muscle and intimal fibrosis.
••
S.
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BMPR2
• bone morphogenetic protein receptor, type 2 (BMPR2)
• a cell surface molecule that binds to a variety of TGF-β pathway ligands
• It is normally inhibitory to vascular proliferation.• Hence Loss of function mutation affecting the
gene would lead to excessive vascular proliferation.
• Implicated in 50 % of cases of Primary pulmonary hypertension.
Figure 15-28 Pathogenesis of primary pulmonary hypertension. See text for details.
Primary pulmonary hypertension-clinical
• Symptoms appear late• Fatigue, dyspnoea• Syncope on exercise• Chest pain• Respiratory insufficiency, cyanosis• Cor pulmonale
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Pulmonary hypertension
• Secondary PH-endothelia dysfunction due to• COPD - Chronic bronchitis,
emphysema, diffuse fibrosis• Congenital L-R shunts- VSD• Recurrent pulmonary
Thrombo-embolism in small sizedvessels•Drugs-appetite suppressant(aminorex)•Crotalaria spectabilis(Bush tea)
S. 74
Pulmonary hypertension
Morphology:• Irrespepective of etiology, all PH have the
following morphologic changes in common:-Medial hypertrophy affecting muscular and
elastic arteries-Atheromas of pulmonary artery-Right ventricular hypertrophy
Pulmonary hypertension
Mild -
ElasticNormalpulmonaryartery
Severe –Medial hypertrophy,intimal fibrosis
duplication
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Pulmonary hypertension
S. 76
Plexiform lesions
S. 77
Plexiform Lesions
Extreme changes. Seen in:• Idiopathic and Primary PH• Drug use• HIV Characterised by the presence of a tuft of
capillaries producing a web like network that spans the lumina of dilated arteries.
Morphology of pulmonaryhypertension
• Plexiform changes in severevarieties only (primary)
• Necrosis of wall (fibrinoid)• Thrombosis
• Rupture, bleed• Dilation lesions, angiomatoid
lesions
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