2 Hemodynamic Disorders Thromboembolic Disease Shock NOT diseases OF blood vessels, but what can go wrong with the fluid INSIDE of them.
3 Overview Edema (increased fluid in the ECF) Hyperemia (INCREASED flow) Congestion (INCREASED backup)Hemorrhage (extravasation)Hemostasis (keeping blood as a fluid)Thrombosis (clotting blood)Embolism (downstream travel of a clot)Infarction (death of tissues w/o blood)Shock (circulatory failure/collapse)Simple definitions, often used incorrectly in medicine.
4 WATER 60% of body 2/3 of body water is INTRA-cellular The rest is INTERSTITIALOnly 5% is INTRA-vascularEDEMA is SHIFT to the INTERSTITIAL SPACEHYDRO--THORAX, -PERICARDIUM, -PERITONUM,(ASCITES)( EFFUSIONS),ANASARCA(total body edema)Can you substitute the word HYDRO- for HEMO- if the substance is blood rather than water? ANS: Yes
5 Fluid Homeostasis Starling’s Law Homeostasis is maintained by the opposing effects of:Vascular Hydrostatic PressureandPlasma Colloid Osmotic Pressure
7 EDEMA Increased hydrostatic pressure: – Impaired venous return Increased fluid in the interstitial tissue spaces or body cavities.Increased hydrostatic pressure:– Impaired venous return– Congestive heart failure (poor right ventricular function)– Constrictive pericarditis– Ascites (peritoneal dropsy; e.g. from liver cirrhosis)– Venous obstruction or compression (thrombosis, external pressure,dependency of lower limbs)Arteriolar dilation (heat; neurohumoral dysregulation)Reduced plasma osmotic pressure (hypoproteinemia)– Nephrotic syndrome (protein-losing glomerulopathies)– Liver cirrhosis (ascites)– Malnutrition– Protein-losing gastroenteropathy
8 Lymphatic obstruction – Interstitial fluids are removed via lymphatic drainage, to thoracic ductand left subclavian vein– Inflammation, neoplasm, surgery, irradiationSodium retention (water follows sodium)– Excess salt intake with renal insufficiency– Increased tubular reabsorption of sodium (renal hypertension;renal hypoperfusion--increased renin-angiotensin-aldosterone secretion)Inflammation (acute, chronic, angiogenesis)
9 CHF EDEMA INCREASED VENOUS PRESSURE DUE TO FAILURE DECREASED RENAL PERFUSION, triggering of RENIN-ANGIOTENSION-ALDOSTERONE complex, resulting ultimately in SODIUM RETENTIONBOTH are EQUALLY IMPORTANT!!!! Please do NOT think overly anatomic or overly physiologic.
10 HEPATIC ASCITES PORTAL HYPERTENSION HYPOALBUMINEMIA Portal hypertension causes edema of organs and tissues with portal circulation.Hypoalbuminemia however, may cause systemic edema.
11 RENAL EDEMA SODIUM RETENTION PROTEIN LOSING GLOMERULOPATHIES (NEPHROTIC SYNDROME)TWO main reasons for edema due to relatively “pure” renal causes.
12 Transudate vs Exudate Transudate Exudate results from disturbance of Starling forcesspecific gravity < 1.012protein content < 3 g/dl,Exudateresults from damage to the capillary wallspecific gravity > 1.012protein content > 3 g/dl,KNOW the difference
13 GENERALIZED EDEMAHEARTLIVERKIDNEYDependent Edema is a prominent feature of Congestive Heart Failure; in legs if standing or sacrum in sleeping patientPeriorbital edema is often the initial manifestation of Nephrotic Syndrome, while late cases will lead to generalized edema.
14 Pulmonary Edema is most frequently seen in Congestive Heart Failure May also be present in renal failure, adult respiratory distress syndrome (ARDS), pulmonary infections and hypersensitivity reactions
15 Pulmonary Edema The Lungs are typically 2-3 times normal weight Cross sectioning causes an outpouring of frothy,sometimes blood-tinged fluidIt may interferewith pulmonary function
17 Brain EdemaTrauma, Abscess, Neoplasm, Infection (Encephalitis due to say… West Nile Virus), etcThe surface of the brain with cerebral edema demonstrates widened gyri with a flattened surface. The sulci are narrowedThe surface of the brain with cerebral edema demonstrates widened gyri with a flattened surface. The sulci are narrowed
18 Brain EdemaClinical Correlation The big problem is: There is no place for the fluid to go!Herniation into the foramen magnum will killAcute cerebral swelling can also often produce herniation of the cerebelllar tonsils into the foramen magnum. Note the cone shape of the tonsils around the medulla in this cerebellum.
23 SEPTIC shock OVERWHELMING INFECTION “ENDOTOXINS”, i.e., LPS (Usually Gm-)Degraded bacterial cell wall productsAlso called “LPS”, because they are Lipo-Poly-SaccharidesAttach to a cell surface antigen known as CD-14Gm+FUNGAL“SUPERANTIGENS”, (Superantigens are polyclonal T-lymphocyte activators that induce systemic inflammatory cytokine cascades similar to those occurring downstream in septic shock, “toxic shock” antigents by staph are the prime example.)
26 CLINICAL STAGES of shock NON-PROGRESSIVECOMPENSATORY MECHANISMSCATECHOLAMINESVITAL ORGANS PERFUSEDPROGRESSIVEHYPOPERFUSIONEARLY “VITAL” ORGAN FAILUREOLIGURIAACIDOSISIRREVERSIBLEHEMODYNAMIC CORRECTIONS of no use
27 Morphologic Features of Shock Brain: ischemic encephalopathylung :DAD (Diffuse Alveolar Damage,)Heart: subendocardial hemorrhages and necrosisKidneys: acute tubular necrosis or diffuse cortical necrosisGastrointestinal tract: patchy hemorrhages and necrosisLiver: fatty change or central hemorrhagic necrosisDICMULTIPLE ORGAN FAILUREEach organ demonstrates different signs of shock to us microscopically.
28 CLINICAL PROGRESSION of SYMPTOMS(linear sequence) Hypotension Tachycardia Tachypnea Warm skin Cool skin CyanosisRenal insufficiencyObtundanceDeathPlease note that this is generally a LINEAR sequence of events, with not too much overlap, and does not usually progress in any other ORDER, except this one. This is how most people die, who do not die acutely.