hemodynamics part 1 Flashcards
1
Q
define hydrothorax
A
- fluid in pleural space
- like in between lungs
2
Q
defien hydropericardium
A
- fluid in the space between the heart and pericardium
3
Q
define ascites or hydroperitoneum
A
- fluid in peritoneal space
4
Q
What are some causes of edema (5)
A
- elevated hydrostatic pressure
- decreased plasma oncotic pressure (low protein)
- lymphatic obstruction
- sodium retention
- inflammation
5
Q
what can cause elevated hydrostatic pressure
A
- CHF, constrictive pericarditis, ascites from liver cirrhosis, venous obstruction
6
Q
define Edema
A
- increased fluid in the interstitial tissue spaces
- occurs when there is a greater movement of fluid out of the vasculature than is returned by venous absorption or lymphatic drainage, then edema results
7
Q
define transudate
A
protein poor fluid with a specific gravity of < 1.012
8
Q
what causes a decreased plasma oncotic pressure
A
- Low protein due to nephrotic syndrome, end stage liver disease, malnutrition, protein losing gastroenteropathy
- -> low albumin levels
9
Q
what causes lympahtic obstruction
A
- inflammation, neoplastic, surgery, postirradiation
10
Q
what causes sodium retention
A
- renin, angiotensin, aldosterone (sodium reabsorption, renal insufficiency
- water follows sodium causing increase in vascular volume
11
Q
what causes inflammation
A
- acute and chronic, angiogenesis
12
Q
describe how heart failure causes edema
A
- heart failure leads to an increase in hydrostatic pressure which directly leads to edema due to back up of blood
- heart failure decreases renal blood flow leading to the activation of renin-angiotensin system which causes retention of Na+ and H2O that results in an increase in blood volume (edema)
13
Q
what is the cause of reduced plasma oncotic pressure
A
- ALBUMIN is the protein most responsible for maintaining colloid osmotic pressure
EXAMPLES - Reduced synthesis or production of albumin caused by liver failure or cirrhosis
- Loss of protein via glomerular injury caused by nephrotic syndrome
14
Q
define anasarca
A
- severe generalized edema
- due to lack of oncotic pressures
- earliest sign is periorbital edema
15
Q
describe sodium and water retention
A
- increased salt in circulation causes:
- -> shift of fluid in intravascular space
- -> increased hydrostatic pressure due to expansion of fluid volume
- -> increased plasma water content results in decreased oncotic pressure resulting from dilution of albumin (not as much reabsorption on venous end**)
- Secondary to renin-angiotensin- aldosterone system activation
- common in renal failure
16
Q
describe inflammation
A
- edema caused by inflammation is due to increased passage of fluid into the extracellular space
- it is localized unless it is the result of a systemic inflammatory response
- e.g allergic reaction
- OFTEN EXUDATE
17
Q
describe lymphatic obstruction
A
- impaired lymphatic drainage results in lymphedema, therefore it is usually localized
- common result of:
- -> inflammation
- -> neoplasia
- -> surgical removal of axillary lymph nodes during treatment of breast cancer may cause obliteration of lymphatic drainage
18
Q
describe the microscopic appearance of endema
A
- depends on the amount of protein exudate
- just see clearing and separation of the ECM elements
- may see pink-staining if protein content is significant
- edema is most commonly seen in subcutaneous tissue, lungs and brain
19
Q
describe subcutaneous edema
A
- important, but seldom of clinical significance
- edema may interfere with healing because fluid must be removed before healing can take place
- severe edema may compromise venous return and increase the risk of infection and ulceration (pooling fluid is bad and can cause infections)
20
Q
what are the two site of clinically relevant edema
A
- LUNG AND BRAIN
- due to the increased risk of death
21
Q
describe the clinical manifestations of pulmonary edema
A
- Dyspnea; sudden, orthopnea, cyanotic (central), “air hunger”, tachypnea
- Cough: copious sputum, frothy, blood tinged
- Pulse: tachycardic, bounding
- breath sounds: crackles (fine to course)
- Engorged neck vein
22
Q
describe the radiographical findings of the two types of pulmonary edema
A
- Interstitial pulmonary edema
- -> poorly defined pulmonary vessels
- -> visible lung fissures
- -> septal lines
- -> thick bronchial walls
- -> see haziness on X-ray
- Alveolar pulmonary edema (more severe)
- -> bilateral symmetric perihilar lung consolidation
- -> you see densities on X-ray
- also look for enlarged heart and pleural effusion
23
Q
describe cerebral edema
A
- extremely serious condition because when brain swells, skull prevents further expansion so tissue is compressed
- Parenchymal edema may shift brain due to increased pressure and if generalized may push the brainstem down into the foramen magnum (tonsillar herniation)
- if edema is more localized (focal), one part of the brain may herniate into adjacent compartments tearing brain tissue
24
Q
what causes localized cerebral edema
A
- abscess
- neoplasm
- trauma
25
Q
what causes generalized cerebral edema
A
- encephalitis
- hypertensive crisis
- obstruction of venous outflow
- trauma
26
Q
describe the gross appearance of cerebral edema
A
- swollen brain has distended, flattened gyri and narrowed sulci due to compression of brain against skull
27
Q
Define Hyperemia
A
- active process in which arteriolar dilatation results in INCREASED FLOW of blood to a tissue
- -> skeletal muscle during exercise
- -> inflammation
- -> Blushing
- Tissue is erythematous (red) due to engorgement with oxygenated blood
28
Q
define congestion
A
- passive process due to IMPAIRED OUTFLOW of blood from a tissue
- caused by:
- -> systemic = CHF
- -> local venous obstruction
- blue-red coloration due to accumulation of deoxygenated hemoglobin (cyanosis)
- congestion and edema commonly occur together
29
Q
describe chronic passive congestion
A
- long term congestion producing stasis of poorly oxygenated blood can result in cellular degeneration and death
- capillary rupture at these sites may result in small foci of hemorrhage
- if there is capillary rupture, breakdown and phagocytosis of the red cell debris results in accumulation of hemosiderin-laden macrophages at the site
30
Q
describe the microscopic findings in acute pulmonary congestion
A
- alveolar capillaries engorged with blood
- alveolar septal edema
- focal intraalveolar hemorrhage
31
Q
describe the microscopic findings in chronic pulmonary congestion
A
- thickened and fibrotic septa
- heart failure cells hemosiderin-laden macrophages in alveolar spaces
- MORE SEVERE
32
Q
describe chronic hepatic congestion
A
- Nutmeg liver = central regions of hepatic lobules are grossly red/brown and depressed (due to cellular loss) surrounded by unaffected areas
- Microscopically
- -> centrilobular necrosis = hepatocelular death and accompanying hemorrhage with hemosiderin laden macrophages
- -> long standing hepatic congestion may result in hepatic fibrosis
33
Q
Describe Hemorrhage
A
- Extravasation of blood due to ruptured vessel
- hemorrhage classified as external or internal
34
Q
what does hemorrhage result from
A
- Trauma
- atherosclerosis
- aneurysm
- neoplasia or inflammation
- capillary bleeding can occur in chronic congestion
- hemorrhagic diathesis potentiates bleeding (fragility of vessels, platelet dysfunctions, coagulation defects etc)
35
Q
define hematoma
A
- collection of blood under the skin
36
Q
describe the various types of hematoma’s
A
- Petechiae = 1-2mm hemorrhage in skin, mucous membrane or serosal surfaces (pin point)
- Purpura = >3mm
- Ecchymoses = > 1-2cm (LARGE)
37
Q
describe the common causes of ecchymoses
A
- usually occur due to trauma
- can also occur as a first sign of acute myelogenous leukemia due to a low platelet count (thrombocytopenia)
38
Q
what is the clinical significance of hemorrhage
A
- RAPID loss of 0% of blood volume has an insignificant impact on healthy individual but can be lethal in the compromised patient
- sites where bleeding occurs has significant prognostic value (e.g. bleeding into the brain can be rapidly fatal)
- chronic or recurrent bleeding can result in iron deficiency
- internal blood loss may allow reuse of iron
