Cor pulmonale - Comenius University · PDF fileLess surfactant, inefficient perfusion of...
Transcript of Cor pulmonale - Comenius University · PDF fileLess surfactant, inefficient perfusion of...
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Cor pulmonale
Peter Ce lec
petercelec@gmai l .com
www.imbm.sk
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Introduction
2,718281828459045235360287471352
e
Leonhard Euler (1707-1783)
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IntroductionUlf von Euler (1905-1983)
Nobel prize in 1970
neurotransmitters
Göran Liljestrand (1886-1968)
Karolinska Institute
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IntroductionEuler–Liljestrand mechanism
Decrease in ventilation
• COPD
Local hypoxia • Hypoxemia
Pulmonaryvasoconstriction
• Lower blood flow
More blood to better oxygenated– ventilated regions
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IntroductionEuler–Liljestrand mechanism
Oxygen-dependentpotassiumchannels
• are blocked
Depolarisationdue to blocked
channels
• Ca2+ releasefrom ER
Smooth musclecontraction due
to calcumrelease
• vasoconstriction
More blood to better oxygenated– ventilated regions
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Pulmonary arterial pressurePulmonary circulation vs systemic circulation
Lungs are the only organ to receive the entire cardiac output
Same volume of blood, but much lower arterial pressure
Why?
Large cross-sectional area of pulmonary capillaries
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Pulmonary arterial pressureSystolic PAP ◦ 18-25 mm Hg
Mean PAP◦ 12-16 mm Hg
Pulmonary venous pressure◦ 6-10 mm Hg
PAP = (Pulmonary flow x pulmonary vascular resistance) + PVP
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Pulmonary hypertensionMean pulmonary pressure at rest > 25 mm Hg
WHO classification◦ 5 groups
Main cause – COPD
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Pulmonary hypertension
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Pulmonary hypertension
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Pulmonary hypertensionSWOT analysis◦ Strenghts
◦ Weaknesses
◦ Opportunities (internal)
◦ Threats (external)
Causes of pulmonary hypertension◦ Arterial hypertension
◦ Venous hypertension (heart)
◦ Thromboembolism (internal)
◦ Hypoxemia (external)
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Survival
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Survival
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Pulmonary arterial hypertension (PAH)Idiopathic (1/1 000 000/year) and heritable – familial
◦ Bone morphogenic protein receptor 2 (BMPR2)
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CBLN2 (Cerebellin 2 Precursor)
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Pulmonary arterial hypertension (PAH)
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Pulmonary arterial hypertension (PAH)
Genetic predisposition
Risk factors
Altered mediators
Proliferation
Thrombosis
Vasoconstriction
Vascular remodeling
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Pathogenesis – PAH
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Pathogenesis – PAH
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Molecular pathogenesis – PAH
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Where do the cytokines comefrom?
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PH due to left heart disease
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PH due to hypoxiaCOPD
Interstitial lung diseases
Sleep-disordered breathing
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Obstructive sleep apnea
Risk factors for obstructive SAS?◦ Male gender, age > 65 years, BMI > 30, large adenoids, neck size
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Continuous positive airway pressure(CPAP)
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Pulmonary hypertensionRisk determinants
Lower Risk Determinants of Risk Higher Risk
NoClinical evidence of
RV failureYes
Gradual Progression Rapid
II, III WHO class IV
Longer (>400 m) 6 minutes walk test Shorter (<300 m)
Minimally elevated BNP Very elevated
Minimal RV dysfunctionEchocardiographic
findingsPericardial effusion,
significant RV dysfunction
Normal/near normalRA pressure and CO
Hemodynamics High RA pressure, low CO
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Pulmonary hypertension
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Diagnostics
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DiagnosticsPulmonary hypertension◦ Mean pulmonary arterial pressure > 25 mm Hg at rest
Pulmonary arterial hypertension◦ Pulmonary wedge pressure < 15 mm Hg
◦ Normal left ventricular ejection fraction
◦ No left-sided valvular disease
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Diagnostics
William Ganz (1919-2009) Jeremy Swan (1922-2005)
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Swan-Ganz catheter
Pulmonary artery catheter
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Diagnostics
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Swan-Ganz catheter
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EchocardiographyNormal Pulmonary hypertension
RVLV
RA LA
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Pulmonary angiography
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Treatment
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Treatment
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Novel therapies for PAH
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Guidelines
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Guidelines
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Guidelines
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Guidelines
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Guidelines
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Guidelines
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Diagnostic guidelines
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Diagnostic guidelines
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Guidelines for risk assessment
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Follow up guidelines
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Treatment guidelines
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Chronic thromboembolic PH
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Chronic thromboembolic PH
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Pulmonary embolism
Pulmonary embolism is an occlusion or partial occlusion of thepulmonary artery by an embolus – mostly (95%) from deep veinthrombosis.
Embolus with infarction
Embolus without infarction (bronchial circulation)
Massive occlusion
Multiple pulmonary emboli◦ Chronic reccurent embolization
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Wirchow´s triad
Blood
Coagulation
Flow
Stasis
Thrombosis
Vessel
Injury
Estrogens, pregnancy, cancer,
surgery
Atherosclerosis, hypertension,
infections, implants, trauma
Immobilization, obesity,
hospitalization
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Pulmonary embolism
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Pulmonary embolism
Embolization
Neurohumoralsubstances
Inflammatorymediators
Pulmonaryhypertension
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Pulmonary embolismPathophysiology◦ Hemodynamic changes
◦ Pulmonary hypertension, decrease in cardiac output
◦ Changes in ventilation/perfusion◦ Hyperventilation, less surfactant production, alveolar collapse
◦ Hypoxemia◦ Less surfactant, inefficient perfusion of hypoventilated areas, right to left shunts
◦ Bronchoconstriction◦ Histamine from the embolus, wheezing
◦ Pulmonary infarction
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Molecular pathogenesis
Decrease in endothelium-derived vasodilators◦ NO, prostacyclin
Increase in vasoconstrictors◦ Thromboxane, endothelin, VEGF
Functional and later structural changes
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Incidence of embolism
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DiagnosisClassic triad◦ Dyspnea
◦ Pleuritic chest pain
◦ Hemoptysis
◦ Swollen, tender, warm, red calf
◦ ECG, X-ray
◦ Ventilation/perfusion scan
◦ CT angiography
◦ D-dimers – fibrin degradation products – high sensitivity, low specificity
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Chest X-rayWestermark sign – oligemia Hampton hump – pulmonary infarction
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Figure 1. Chest radiograph demonstrating focal oligemia in the right lung (area between white
arrowheads) Westermark sign and a prominent right descending pulmonary artery (black arrow)
– Palla’s sign.
Shiva Sreenivasan et al. Circulation. 2007;115:e211
Copyright © American Heart Association, Inc. All rights reserved.
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Philip Steven Wells, M.D., M.Sc
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Deep vein thrombosis
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Guidelines
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Decision tree algorithm
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Decision tree algorithm
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Decision matrix
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Exotic emboli
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Differential diagnosisPulmonary thromboembolism vs pulmonary hypertension
Pneumonia
Valvular diseases
Acute myocardial infarction
Acute heart failure
Pericarditis
Aortic rupture
Pleural diseases
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Treatment
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TreatmentThrombolysis or surgical thrombectomy
Heparin, warfarin, vena cava inferior filter
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Pulmonary embolism
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Pulmonary embolism
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Cor pulmonale
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Examination1. Definition
2. Classification
3. Epidemiology
4. Etiology
5. Pathogenesis
6. Symptoms & Signs
7. Complications
8. Prevention & Diagnosis & Therapy
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DefinitionCor pulmonale
Pulmonary heart disease
Syndrome with right-sided ventricular hypertrophy, dilation or heartfailure due to vascular resistance in the lung circulation
not due to systemic causes
„Lungs cause the heart to fail“
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Classification
Acute◦ ARDS, lung thromboembolism...
Chronic◦ COPD, sleep apnea, lung thromboembolism...
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Epidemiology10% of all cases of heart failure
5-year mortality 70-80%
In 50% the cause is COPD◦ Chronic bronchitis
◦ Lung emphysema
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EtiologyPulmonary hypertension
◦ Primary pulmonary hypertension
◦ Alveolar hypoxia – pulmonary vasoconstriction (sleep apnea)
◦ Lung disorders – lung tissue damage (COPD, interstitial lung disease, rheumatid disorders)
◦ Blood viscosity (blood clots, polycythemia)
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PathogenesisRight ventricular afterload is increased
Hypertrophy or Dilation?
◦ Acute or Chronic
Mortality predictors◦ Age > 65 years
◦ Bed rest > 72 hours
◦ Tachycardia, tachypnoe
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Symptoms & SignsFatique
Dyspnea
Cyanosis
Chest pain
Hepatomegaly
Ascites
Jaundice
Raised jugular venous pressure
Abnormal heart sounds
Right ventricular hypertrophy
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ComplicationsPeripheral hypoxia
Backward failure of the right heart
Arrhythmias
Polycythemia – stroke
Liver failure
Renal failure
Neurological complications◦ Syncope, cognitive deficits
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Prevention & Diagnosis & TherapyCausal prevention
Prevention and therapy of lung diseases
Discontinuing smoking
Patient history
Auscultation, Chest X-ray, ECG – right axis deviation, echocardiography, BNP, arterial gases
Causal treatment
Diuretics, anticoagulants, oxygen, transplantation?
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PH onlineAnimation of PAH
https://www.youtube.com/watch?v=9a4untSzLzg
Khan Academy
https://www.youtube.com/watch?v=KtkR_NTte4M
Brown University lecture
https://www.youtube.com/watch?v=3bopVnVwPGQ
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PE onlineMEDCRAM lecture
https://www.youtube.com/watch?v=4C6BB56fG1M
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Final notesWithout heparin prophylaxis 84% of patients will have pulmonarythromboembolism after hip or knee replacement.
Pulmonary embolization is the most common preventable cause of death in hospitalized patients.
80% of pulmonary emboli occur without prior symptoms
In 25-50% of autopsies of hospitalized patients pulmonarythromboemboli are found.
They are diagnosed in only 10-20% of cases antemortem.
Most of the cases remain undiagnosed.
2/3 of deaths due to pulmonary emboli occur within 30 minutes.
Early treatment is effective.
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Final notesWe seem to know a lot about the pathogenesis of pulmonaryhypertension.
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Final notesWe seem to know a lot about the pathogenesis of pulmonaryhypertension.
But we are far from understanding the disease processes.
So, how can we maximize the benefits for the patients?
...by following the guidelines.