Hemodynamics Flashcards
1
Q
What are considered fluid flow?
A
- edema
- hyperemia & congestion
- hemostasis
- thrombosis
- embolism
2
Q
What are considered vascular disorders?
A
- hypertension
- arteriosclerosis
- aneurysms
- ischemic heart disease
- anomalies of heart
3
Q
What is edema?
A
increased hydrostatic pressure or decreased colloidal osmotic pressure increases fluid movement into tissues
4
Q
What are the causes of edema?
A
- increased hydrostatic pressure
- reduced plasma osmotic pressure
- lymphatic obstruction
5
Q
What are the types of edema?
A
- exudate: high protein content
- transudate: low protein content
- subcutaneous: below heart where hydrostatic pressure is high
- pulmonary: renal failure, CAD, inflammation
- brain: increased intracranial pressure causes abnormal herniation of brain tissue
6
Q
What is hyperemia & congestion?
A
- both: increased blood volume in tissue
- hyperemia: active increase is blood volume
- congestion: passive increase blood volume; have cyanosis
7
Q
What is hemostasis?
A
- maintaining blood; clot free state
- vasoconstriction & release endothelin
- glycoprotein 1B to adhere to ECM vWF
- promotes platelet aggregation=primary hemostasis
8
Q
What occurs in platelet adhesion?
A
mediated by Gp1b platelet surface receptor to collagen bound vWF
9
Q
What occurs in platelet activation & aggregation?
A
- confromational change
- secrete thromboxane A2
- platelet plug stability with fiubrin clot=secondary hemostasis
10
Q
What occurs duing secondary hemostasis?
A
- release of tissue factor 3
- thrombin production
- fibrin clot
11
Q
What occurs during antithrombotic counterregulaiton?
A
- counter regulatory mechanisms
- plasminogen activator & thrombomodulin
12
Q
What are the key players in the endothelium pro-thrombotic process?
A
- tPAI
- vWF
- tissue factor 3 thromboplastin
13
Q
What are the key players in the endothelium anti-thrombotic process?
A
- NO
- prostaglandin I2
- tPA
- thrombomodulin
- tissue factor inhibitor, heparin
14
Q
What is the coagulation cascade?
A
- product is thrombin to drive fibrin clot
- co-factor: Ca++
- intrinsic & extrinsic pathways activate factor X
15
Q
What is the fibrinolytic system?
A
- coagulation inhibited by activation of fibrinolytic apthway
- remodeling of fibrin clot
- driven by tPA
- serum plasmin inactivated by alpha 2-anti-plasmin
16
Q
What are the roles of thrombin in hemostasis?
A
- platelet aggregation
- endothelial activation
- leukocyte activation
17
Q
What are the chracteristics of hemorrhage?
A
- characterized by gross morphologic appearance
- can be internal or external
- bleeds into cavities-> hemothorax, hemopericardium, hemoperitoneum, hemathrosis (joints)
- petechiae= 1-2 mm
- purpura= 3-5 mm
18
Q
What are ecchymoses and hematomas in hemorrhages?
A
- eccy: bruises >10mm caused by trauma
- hema: solid collections of coagulated blood
19
Q
What are the 4 types of shock?
A
- cardiogenic: low cardiac output d/t myocardial pump failure
- hypovolemic: loss of blood or plasma reducing cardiac output
- anaphylactic: loss of blood/plasma reducing cardiac output d/t vasodilation
- septic: excessive vasodilation
20
Q
What are the 3 abnormalities that contribute to thrombosis?
A
Virchow’s triad
* endothelial injury
* genetic/acquired conditions
* turbulent blood flow/stasis
21
Q
What are thrombi?
A
- anywhere in vascular system
- arterial & cardiac -> endothelial injury
- mural: heart chambers & aorta
- arterial: grow in retrograde (opposite of flow)
- venous: develop at stasis; anti-retrograde (direction of flow)
22
Q
What are the significances of thrombi?
A
- superficial venous thrombi: rarely embolize, painful, swelling
- deep vein thromboses: in larger leg veins, embolize to lungs
23
Q
What are the types of systemic embolism?
A
- fat: from bone fracture
- amniotic fluid: during labor
- air: in some surgeries, nitrogen into bloodstream
- septic: live bacteria; in bacterial endocarditis
- athero: disruption of atherosclerotic plaque
24
Q
What do infarction and ischemia lead to?
A
- infarction & ischemia -> coagulative necrosis
- iscehmic infarcts in CNS -> liquefactive necrosis
- restored by reperfusion
25
What are red & white infarcts?
* red: venous congestion, loose tissue with space for blood
* white: arterial in solid organs with end-arterial circulation; wedge shaped
26
What are the clinical impacts of infarction?
1. anatomy of vascular supply
2. hypoxemia
3. rate of occlusion
4. tissue susceptibility to ischemia
27
What is blood pressure?
* cardiac output & vascular resistance
* renal Na+ excretion/resorption
* caused by reduced renal Na or increased vascular resistance
28
What is arteriosclerosis?
* small arteries & arterioles in pts with hypertension or diabetes
* Monckeberg's: dystrophic calcification of media; does not result in significant luminal narrowing
29
What is hyaline arteriosclerosis?
* diabetes
* thickened arterial walls by protein deposit
30
What is hyperplastic arteriosclerosis?
* SM cells in media of small arteries (onion like)
* fibrinoid necrosis
31
What are the constitutional & modifiable risk factors of atherosclerosis?
* constitutional: family genetics, age, male, obesity
* modifiable: lyperlipidemia, hypertension, smoking, obesity
32
What is the pathogensis of atherosclerosis?
* thick intimal layer depends on endothelial cell injury hemodynamic disturbance, lipids
* SM cells -> foam cells
* fatty streak -> early atherosclerotic deposition
* plaques enlarge -> obstruction to vascular flow
* hypoxia occurs
33
What are aneurysms?
* true: involve all 3 layers of vessel
* false: blood leaks completely out of artery or vein
34
What is an abdominal aortic aneurysm?
* b/w renal arteries & aortic bifurcation
* associated with atherosclerosis
* vascular occlusions, embolism, rupture, impingement
35
What is a thoracic aortic aneurysm?
* associated with hypertension & Marfan syndrome
* result fo compression of mediastinal structures
36
What are aortic aneurysms?
* intimal tear
* results in masive hemorrhage or cardiac tamponade
* double-barreled aorta
* end-organ infarction
37
What are the types of aortic dissections?
* type A: ascending aorta (brian damage)
* type B: descending aorta (brain function is ok)
38
What are the abnormalities of the heart?
1. failure of heart pump -> ischemic heart disease
2. shunted flow -> patent foramen ovale
3. regurgitation/obstructed valve flow -> calcific aortic stenosis
4. disorder of cardiac conduction -> arrythmias
39
What is ischemic heart disease?
* myocardial ischemia
* results from coronary artery blood flow
* common clincal syndromes: angina, heart attack, chronic ischemic heart disease
40
What is angina?
* recurrent, reversible myocardial ischemia
* stable: CP & SOB precipitated by exertion or nitroglycerin
* unstable: CP & SOB at rest; plaque change; can progress ot transmural heart attack
* PRinzmetal's: uncommon; pain at rest d/t coronary vasospasm
41
What are the types of MI tissure injury?
* transmural (full wall thickness)
* subendocardial more susceptible to damage
42
What are the biomarkers of MI?
* creatin kinase-MB
* cardiac troponin
43
What is the patent foramen ovale?
* persistent right to left atrial flow
* hypoxemia
* increase risk of DVT
44
What is valvar heart disease?
* heart valves lack vasculature
* bacterial infection
45
What is calcific aortic valve stenosis?
* on older pts
* calcification
* left ventricular hypertrophy
46
What does a cardiac conduction require?
atrioventricular node, bundle of his, right & left branches
47
What are the stages of a basic ECG?
* P wave: polarization
* PR interval: conduction is normal
* QRS: depolarization
* ST: flat plateau
* T: repolarization
