Venous Thromboembolism and Pulmonary Embolism

Venous Thromboembolism

• Pulmonary embolism (PE) is the same as pulmonary embolism (LE)
• In 90% of cases, pulmonary embolism arises from an embolus originating from deep vein thrombosis (DVT) located in the Vena cava inferior
• 80% of all DVTs remain clinically silent.
• Approximately half of all fatal PEs are not diagnosed before death.
• PE often presents with nonspecific symptoms.
• Symptoms of PE include sudden dyspnea (73%), acute, breathing-dependent chest pain (66%), tachypnea (70%), and coughing/hemoptysis (37%)

PE Diagnostics

• Includes assessing pretest probability based on medical history, clinical findings, and using Wells Score or Geneva Score
• D-dimer tests are highly sensitive but lacks specificity, and elevated levels occur in inflammations, infections, and malignancies.
• Negative result can exclude PE if pretest probability is low
• Objective diagnostics: Compression ultrasound for proximal DVT is highly sensitive and specific while a positive CUS indicates VTE; negative CUS does not rule out PE
• CT pulmonary angiography (CTPA) with contrast is the gold standard and available, with high sensitivity and specificity.
• V/Q scintigraphy shows mismatch between ventilation and perfusion, useful in low pretest probability with normal lung X-ray or high pretest probability with negative CTPA.
• EKG may show right axis deviation, negative T waves in V1/2, and S1-Q3-T3 pattern.
• Echocardiography may show right heart dilation in severe PE cases to estimate PAP; Doppler ultrasound used first in pregnant patients, then possibly lung X-ray.
• PE outcome depends on the right ventricle condition and can result in hypotension, shock, right heart failure, or sudden cardiac death.

Risk Stratification in PE

• Risk is stratified/estimated using the simplified Pulmonary Embolism Severity Index (sPESI), which considers factors such as age over 80, cancer, chronic heart or lung disease, tachycardia, systolic blood pressure below 100 mmHg, and oxygen saturation under 90%.
• Assesses a patient's risk of death from PE
• Therapy involves hemodynamic support for shock, thrombolysis/anticoagulation/reperfusion, fibrinolysis using rtPA, streptokinase, urokinase, and low molecular weight heparins.
• Novel oral anticoagulants (NOAKs) (Apixaban, Dabigatran, Ricaroxaban, Endoxaban) are increasingly used as first-line treatment and for long-term prophylaxis of DVT/PE.
• Anticoagulation should continue for at least 3 months, with follow-up after 3-6 months to rule out chronic thromboembolic pulmonary hypertension.
• Atypical DD includes pneumothorax, acute aortic dissection, and acute coronary syndrome.

Pulmonary Hypertension (PH)

• Pulmonary hypertension refers to elevated blood pressure in the pulmonary circulation, with a pulmonary artery pressure (PAP) exceeding 25 mmHg.
• Measured accurately via heart catheter, estimated via echocardiography.
• PH is associated with vasocontriction, remodeling of the pulmonary vascular wall due to inflammation/genetics/hypoxia/lesions, and thrombosis; can develop from various conditions.
• Pulmonary hypertension affects about 1% of the population, with pulmonary arterial hypertension being rarer.
• Patients often experience dyspnea, dizziness, fatigue, syncope, cyanosis, or chest pain.
• Complications of pulmonary hypertension: decompensated Cor pulmonale, right heart failure, and malignant cardiac arrhythmias.

WHO Classification of Pulmonary Hypertension

• Pulmonary arterial hypertension (PAH) can be idiopathic/hereditary or related to HIV, portal hypertension, collagen disorders, or drug-induced by anorexigens like aminorex.
• Pulmonary hypertension from left ventricular heart disease can be systolic, diastolic, or valvular.
• Pulmonary hypertension from lung diseases/hypoxia is linked to COPD, interstitial lung diseases, sleep-related breathing disorders, and abnormalities.
• PH from chronic thromboembolic disease and unclassified factors.
• WHO classification related to survival rate
• Initial findings include auscultation for the 2nd heart sound, lab tests for NT-pro-BNP, blood gas analysis for oxygen therapy needs, and a 6-minute walk test assessing prognosis.
• EKG shows right heart stress markers, p-pulmonale, and right axis deviation.
• Diagnostics involve pulmonary function tests, spirometry for obstructive/restrictive ventilation, echocardiography to find PH causes, and chest X-rays.
• Echocardiography helps diagnose PH depending on suspected cause
• C/P, HR-CT (high resolution CT) scans, lung function tests, and sleep studies can help determine if Emphysema , Fibrosis, or Sleep apnea occur.

Pulmonary Arterial Hypertension (PAH) Details

• PAH involves mechanisms causing increased arteriole resistance, a rare form lacking underlying heart or lung issues, with pulmonary artery pressure over 25 mmHg at rest, and more common in women between 20 and 40 years old.
• Diagnosis secured by excluding Diffential Diagnosis (DD), assessing hemodynamics through vasodilation tests via heart catheter, and evaluating the prognosis using vasoreactivity tests with adenosine/nitrides/epoprostenol.
• Therapy aims to reduce Belastung, dyspnoe, and improve quality of life.
• Training, Diuretics, Digitalis, oxygen if paO2 < 65 mmHg, anticoagulation, prostacyclin, endothelin, phosphodiesterase inhibitors, Vasodilation is used
• Lung transplant is ultima ratio

Pulmonary Hypertension + COPD Details

• COPD progression can cause alveolar hypoxia, which leads to Gefäßremodeling, pulmonary hypertension, Cor pulmonale, and then right heart failure; mortality depends on pulmonary artery pressure with physiological PAP
• Pathophysiology: Endothelial damage ( dysfuntion), Hypoxi, inflimation + stress
• Diagnose by measuring pressure at the lung arteries and it being too high

Spirometry & Bodyplethysmography Basics

• Spirometry measures "small lung function", while bodyplethysmography measures "large lung function".
• Spirometry is the gold standard for suspected obstructive ventilation disorder, with early diagnosis and severity assessment, and for bronchopulmonary conditions like dyspnea/chronic cough/sputum.
• Indications: systemic conditions with lung involvement like HI/collagen disorders/muscle diseases, smokers over 40, exposure to inhaled toxins, abnormal thoracic imaging/lab parameters/blood gas values, and pre-operative risk assessment.
• Absolute contraindications include hemoptysis, pneumothorax, acute cardiovascular issues, aneurysms, while complications involve dizziness, syncope, bronchospasm, chest pain.
• Guidelines: device with bacterial filter and calibration, patient stability, withholding inhaled bronchodilators for 4-12 hours, nicotine abstinence, seated position, and maximal inhalation/exhalation.

Spirometry Key Elements

• The flow-volume loop contains inspiration & expiration curves, with peak expiratory flow (PEF) decreasing at the curve's end indicating small airway issues.
• An indented expiration curve suggests obstructive ventilation disorder.
• Peak flow measurement is recommended for asthma patients and detects exacerbations.
• Volume–time curve assesses lung function, total lung capacity (TLC), and vital capacity (VC) to indicate inspiratory/expiratory reserve volumes.

Spirometry Standard & Issues

• Reference values are relative & based on height/age/gender/ethnicity, obstructive gradiation, unzureichende/unvollständige, fehlende kraftanstrengung, unvollständing verschlossen
• Quality controle: zu geringe Anstrengun, Husterzacke

Ventilatory Disorders

• Obstructive: Due to increased resistance (Überblähung), Empyhsem, tumor, asthma, COPD, FeV1/VC < LLN, reversible with beta mimetics
• Restrictive: Expansion restriction, LungfgewebsVerust, FeV1/Vc normal, VC<LLL, Lungengewebs verlsut
• Empyshm: FeVL<FeVC<TLC<RV and Stenosen extra/intra thoraxtic
• Bodyplethysmography measure gas and resistance with gloschläger + zwerchfellhochstand, +L
• Further tests involve Resketion, provoktion

Blood Gas Analysis (BGA) and Acid-Base Balance

• Blood gas analysis measures pH, pO2, pCO2, base excess (BE), and bicarbonate levels to assess a patient's acid-base balance.
• Acidemia is blood pH below 7.35; alkalemia above 7.45 and acidosis/alkalosis refers to conditions causing acidic or basic blood.
• Acidemia reduces heart contractility and ventilatory pump function, while alkalemia causes arrhythmias and cramps.

Physiological Considerations

• Respiratory and metabolic factors influence pH, with compensation mechanisms.
• Normal blood gas values: pH (7.35-7.45), pO2 (65-100 mmHg), pCO2 (35-45 mmHg), BE (-2-2 mmol/l), and HCO3- (24 mmol/l).

Respiratory Acid-Base Disorders

• Respiratory acidosis occurs with PaCO2 above 45, leading to hypercapnia from increased CO2 production, hypoventilation, or Totraumventilation.

  • COPD exacerbation causes respiratory acidosis due to dynamic hyperinflation, Ventilationstörung, and increased CO2 production.
  • Therapy: Treat OBSTRUCTIVE and ventilation

• Respiratory alkalosis occurs with PaCO2 < 35, causing hypocapnia from alveolar hyperventilation which is not needed.

Overview: Metabolic Acid-Base Disorders

• Base Excess (BE) measures metabolic acid-base status via lactate, electrolytes, albumin, and unmeasured anions, with changes to HCO3-

Electrolyte & Lactic Acid

• Electrolyte imbalances include hyperchloremic acidosis (Cl up, HCO3- down) caused by diarrhea, saline infusion, reversed by infusion and hypochloremic alkalosis (Cl down, bicarbonate up) caused by vomiting, treated with rehydration.
• Lactate levels increase (lactate up, bicarbonate down) in shock, hypoxia, treated by shock

Anion types & Synthesis

• Ungemessene Anioonen UMA causes Bicarbonate down, seen in keto, acidose (KUSME).
• Albumin synthesis (Albumin down, Bicarbonate up) seen in Lberinsuffizienz, Unernährung.

Asthma Bronchiale - Basics, & Pathophysiology

• Asthma is defined as a frequent, heterogeneous condition, with chronisch entzündung and bronchial hyperreagibilität, which effects genes or exterl factors
• Asthma is ALWAYS IMMER Entzündung but COPD is abbauend

Asthma, Diagnosis, T2 vs non-T2

• T 2 ashtma has allergie related beginnings, eosinophils that respond to corticosiderode, but non T2 has no allergie and slower healing.
• Diagnoses by Dyspnoe, sputem etc adn Lungfunciton, and phenyotyp

Asthma GINA Guidelines

• Track1 LAMA Low dose, andTrack 2 higher levels

Asthma Therapy & Differenzierung

• Short acting (SABA) Bricanyl or Long Acting
• Ers diagnois for Asthma is more childhood based
• Airways is hyper sensitive
• Responds to steriods

Chronisch Obstrucitve Pulm Disease- COPD

• Sammelbegriff for chronische Erkankung, not reversible Obstuktion lungemphysem and Inflammation
• Durch Rauschen and Viren anormale lungen
• Diagnosic lunges, sat etc
• FVC<70%
• Hohe exzerbation, comorbid, kardio and Osteoporsis

Therapie bei stabiler COPD

• Medikamten with Beta 2 and Anticholingerics, anti inflamm Apperatibe and Schulung zur Linderung

Infection Atemwege akut

• Akute Broncitis viren
• Nur Temp unter 39
• Keien AB Influenza can akticvatre macrpohagen
• Omirckobilder viren

Chronische Atemwegsinfektion

• Bronchiolekstasen istirreversiebel
• Lungenreinigen
• Gen defekt
• Lungen auswaschen und physio

Pneumonien Basics

• Infketion parenchyms, entzundulg
• Epidemol >3 morte pro JAhr
• Hohes alt immobilimmuno, herz suff
• Impfeung
• Com acquired, no socomial and Immunsuppress

Causes, Diagnostic & Therapie Pneumonien

• Com AC is strep pneumo
• Highers aereu and sonde Riskeo is CB, alters or rater over 24
• Therapy broad bet lact

Thoraxchirg, Radiologie, CT, Sonographie

• Thoraxrontgen
• Ct höhere Belastung

Radiologie importante Diagosen

• Weiße Hemie Thorax
• Pulmoonale oder
• Mehrere
• Raumbefund

Pleural basics Pleura Ergeuss

• Auseinernderteilung Flüsßigkeit zwischen Lunge. Wand mit exsudat vs trasnsudat
• Eiweiß, zell Arm, glukos

Pneumothorax

• LuftAnsammlung was in zu Lunge kollabiert
• Perkurison Hyposeronoher kopf