hemodynamics Flashcards
(112 cards)
1
Q
hemodynamics
A
movement of blood
2
Q
what signs of inflamm could indicate a disorder of hemodynaimcs
A
edema, hyperemia, hemorrhage
3
Q
Hemodynamic Disorders
A
• Edema – escape of fluid
• Congestion – Abnormal accumulation of blood in tissue/organs
• Infarction – ischemic necrosis
• Shock – tissue injury secondary to systemic hypotension
4
Q
Hemostatic Disorders
A
• Hemorrhage – escape of whole blood into tissuen
• Thrombosis – undesired clotting of blood
• Embolism – detached intravascular mass
5
Q
Distribution of Body Water
A
• Water accounts for 60% of the lean body weight
• Total body water is distributed between the intracellular and extracellular compartments
• Intracellular compartment (40%)
• Extracellular compartment- Intravascular (5%) and Interstitial (15%)
6
Q
Forces balancing Movement of Water Between the Intravascular and Interstitial Spaces
A
• Hydrostatic Pressure- Pressure exerted by volume of blood when confined
to a blood vessel
• Osmotic (Oncotic) Pressure- Proteins in blood vessels (Albumin)
7
Q
where is hydrostatic pressure higher
A
Aa, outweighs osmotic= fluid out
8
Q
where is osmotic pressure higher
A
Vv (does not change remains constant), outweighs hydrostatic= fluid in
9
Q
residual fluid left in the ISF
A
• Outflow at the arterial end is nearly balanced by inflow at the venular end
• Residual fluid left in the interstitium is drained by lymphatic vessels
10
Q
causes of edema
A
• Increased hydrostatic pressure or decreased plasma osmotic pressure will cause interstitial fluid to increase
• If the capacity for lymphatic drainage is exceeded, fluid accumulates (edema)
11
Q
edema
A
swelling of tissues that result from excessive accumulation of fluid
12
Q
locality of edema
A
• May be highly localized as occurs in a small region of skin involved with an insect bite
• May be more regionalized, involving an entire limb or a specific organ, such as the lungs (e.g., pulmonary edema)
• May be generalized, involving the whole body
13
Q
pathophyisiological categories of edema
A
inflammatory and non-inflammatory
14
Q
terminology of fluid accumulation
within tissues?
within thorax?
within pericardium?
within peritoneum?
generalized edema?
A
• Accumulation of interstitial fluid within the tissues= Edema
• Accumulation of fluid within body cavities
• Hydrothorax – pleural effusion
• Hydropericardium – pericardial effusion
• Hydroperitoneum – ascites
• Anasarca – generalized edema
15
Q
• Inflammatory causes of edema
A
• inflammatory edema is caused by increased vascular permeability is a protein-rich exudate (exudate)
16
Q
Non-inflammatory causes of edema
fluid composition?
A
- edema caused by increased hydrostatic pressure or reduced osmotic pressure is usually protein-poor fluid (transudate)
• Heart failure
• Renal failure
• Hepatic failure
• Malnutrition
17
Q
categories of edema fluid
A
transudate and exudate
18
Q
edema flow chart with heart failure, renal failure, and malnutrition/ decreased hepatic syn/ nephrotic syndrome
A
19
Q
• Exudate, leads to?
A
– high specific gravity – protein rich
• Inflammatory edema
20
Q
• Transudate edema fluid
due to?
A
– low specific gravity – protein poor
• Due to Volume/pressure overload or Reduced plasma protein
21
Q
categories of edema fluid
A
transudate and exudate
22
Q
Lymphangitis
A
Lymphatic spread of bacterial infection
• Painful red streaks and regional lymphadenopathy
23
Q
• Lymphedema
A
a term used to describe an increase in fluid in the interstitial space caused by an abnormality
in the lymphatic system
24
Q
what is in tissues in lyphadema
A
lymphatic fluid collects in tissues causing edema
25
lymphadema congenital or acquired
can be either
26
acquired lymphadema from?
• Infection such as filariasis
• Surgery, radiation therapy
27
congenital lymphadema, example
due to Aplasia
• Congenital malformation of lymphatic system
• Age 1 Week: Lymphoscintigraphy exhibits no migration of radiopharmaceutical agent from right foot to right inguinal nodes
• Diagnosis: congenital aplasiaof the lymphatic system of right leg
28
axillary lymph node dissection can lead to?
acquired lymphadema, swollen arm
29
Stewart-Treve Syndrome
• Angiosarcoma arising from chronic lymphedema
• Long-standing lymphedema secondary to surgical lymph node dissection and/or radiation therapy
30
renal dx can lead to what form of edema?
anasarca, severe generalized edema
31
What edema(s) is seen with congestive HF
Pitting edema of the extremities and acities possible
32
alcoholics may have what edema?
Ascites in Hepatic Alcoholic Cirrhosis
33
edema danger zones
• Lungs - Pulmonary edema
• Brain - Cerebral edema (central nervous system)
34
cerebral edemas
Cerebellar Tonsil Herniation
• Increased intra-cranial pressure may result in herniation through the foramen magnum
• Compression of the medulla results in depression of the centers for respiration and cardiac rhythm control
35
what inflammatory edema can we see with dentistry
cellulitis secondary to dental infection
36
angioedema
Inflammatory Edema - Angioedema – Due to Type I Hypersensitivity Reaction
37
Localized Edema vs. Generalized Edema
causes?
• Localized edema is usually caused by: Increased vascular permeability (injury-inflammation)
or Obstruction of venous or lymphatic outflow
• Generalized edema is generally caused by decreased plasma osmotic pressure
38
• Increased hydrostatic pressure
leads to?
due to?
• Increased hydrostatic pressure = impaired venous return
• due to Congestive heart failure or Venous obstruction or compression
39
• Decreased plasma osmotic pressure (hypoproteinemia) due to?
• Protein-losing glomerulopathies (nephrotic syndrome)
• Liver cirrhosis (ascites)
• Protein malnutrition
40
types of lymphatic obstruction
• Inflammatory
• Neoplastic
• Postsurgical
• Postirradiation
41
how can sodium retention cause edema
• Excessive salt intake with renal insufficiency
• Increased tubular reabsorption of sodium- Renal hypoperfusion and Increased renin-angiotensin-aldosterone secretion
42
how does inflamm cause edema
increased permiabilty
43
Hyperemia
active or passive?
where can this occur?
color of tissues? why?
An active process in which arteriolar dilation leads to increased blood flow
• Sites of inflammation
• Skeletal muscle during exercise
• Affected tissues turn red (erythema) because of engorgement of vessels with oxygenated blood
44
Deep Venous Thrombosis
type of issue? passive or active?
results from?
systemic or local?
tisses appearance? why?
congestion issue
• A passive process resulting from reduced outflow of blood from a tissue (stasis)
• May be systemic (heart failure) or local (isolated venous obstruction)
• Congested tissues take on a dusky, reddish-blue color (cyanosis) due to red cell stasis and accumulation of deoxygenated hemoglobin
45
chronic passive congestion of liver appearence
nutmeg liver
46
Superior Vena Cava Syndrome
•Compression of superior vena cava by neoplasm obstructing venous return (congestive)
47
Factors Favoring Thrombosis (Virchow’s Triad)
• Endothelial injury
• Stasis or turbulent blood flow
• Hypercoagulability of the blood
48
what determines thrombi outcome
• Balance between antithrombotic and prothrombotic properties of endothelium determines whether thrombus formation, propagation or dissolution occurs
49
NORMALLY, endothelial cells exhibit what properties regarding thrombi
• Normally, endothelial cells exhibit antiplatelet, anticoagulant and antifibrinolytic properties
50
how can endothelial cells be activated?
activated endothelial cells exhibit what properties?
• Endothelial cells may be activated by trauma, infectious agents, hemodynamic forces, plasma mediators and cytokines
• After activation, endothelial cells acquire procoagulant activities
51
• Mural thrombi
• Mural thrombi
• Occur in heart chambers or aortic lumen
52
• Arterial thrombi
• Frequently?
•most common locations
• Superimposed?
i
• Frequently occlusive
• Coronary, cerebral, femoral arteries, most commonly
• Superimposed on ruptured, ulcerated atherosclerotic plaque
53
• Venous thrombi
• Usually?
• common location?
• Usually occlusive – thrombus forms a long cast of the lumen
• Veins of lower extremities
54
• Vegetations
• Vegetations – thrombi on heart valves
55
Morphology of Thrombi
attached to?
propogation?
embolization?
• Thrombi are focally
attached to the underlying
vascular surface
• Thrombi propagate from
the point of attachment in
the direction of blood flow
• The propagating portion
of a thrombus is often
poorly attached and is
prone to fragmentation
and embolization
56
• Arterial or cardiac thrombi begin where and propogate in what direction?
• Begin at sites of turbulence or endothelial injury
• Propagate away from the heart
57
• Venous thrombi occur at and propogate in what direction?
• Occur at site of stasis
• Propagate toward the heart
58
Lines of Zahn
present with?
appearence/histo?
signifies?
distinguishing from post-mortem clots?
• Thrombi often have groosly and microscopically apparent laminations called lines of Zahn
• Pale platelet and fibrin deposits alternating with darker red cell-rich layers
• Laminations signify that a thrombus has formed in flowing blood
• Their presence can therefore distinguish antemortem thrombosis from the bland, non-laminated clots that occur postmortem
59
lines of zahn
60
venous seepage may cause
liver clot
61
Fates of a Thrombus
• Dissolution – fibrinolysis (plasmin)
• Propagation – accumulate additional platelets and fibrin
• Embolization – dislodge and travel to other sites in the vasculature
• Organization and recannalization
62
• Organization and recannalization of thrombus
• Ingrowth of endothelial cells, smooth muscle cells and fibroblasts
• Capillary channels eventually form that re-establish the continuity of the original lumen to a variable degree
63
clinical problems of thrombi
obstruct vv and aa
embolize
64
venous thrombi clinical issues
• Congestion and edema in vascular beds distal to the obstruction
• Embolize to lungs and cause death
65
arterial thrombi clinical issues
• Thrombotic occlusions at critical sites (stroke, myocardial infarct) or can embolize and cause downstream infarctions
66
where do most venous thrmbi occur
superficial or deep veins of the legs
67
outcomes of superficial venous thrombi
cause local congestion, swelling, pain and tenderness
rarely embolize
68
outcomes of DVT
offset of symptoms?
often go where?
symptomiatic? when realized?
• Cause local pain and edema – rapidly offset by collateral channels
• More often embolize to lungs
• Half are asymptomatic, recognized in retrospect after embolization
69
risk factors of venous thrombi
coagulation?
endothelium?
bedrest?
heart?
traumas?
pregnancy?
tumors?
• Hypercoagulable states
• Endothelial injury
• Bedrest, immobilization
• Congestive heart failure
• Trauma, surgery, burns
• Thrombotic diathesis of pregnancy
• Neoplasia
70
Risk Factors for Arterial and Cardiac Thrombi
can they embolize? where could they cause infarcts?
major cause of arterial thrombi?
Predisposition to cardiac thrombi associated with?
• Cardiac and aortic mural thrombi may embolize
peripherally and cause infarcts of brain, kidney and spleen
• Major cause of arterial thrombi is atherosclerosis
• Predisposition to cardiac thrombi associated with: MI, Rheumatic heart disease, and Atrial fibrillation
71
Disseminated Intravascular
Coagulation (DIC)
formation of?
visable?
may cause circulatory insufficiency where?
results in decreases of?
mechanisms activated?
may evolve into?
primary dx? associated with?
• Formation of widespread fibrin thrombi in the microcirculation
• Thrombi not grossly visible – can be seen microscopically
• May cause diffuse circulatory insufficiency, especially in brain, heart, lungs and kidneys
• Widespread microvascular thrombosis results in platelet and coagulation protein consumption (consumptive coagulopathy)
• Fibrinolytic mechanisms are activated
• The initially thrombotic disorder may evolve into a bleeding disorder
• Not a primary disease but a potential complication of any condition associated with widespread activation of thrombin: Obstetric complication and Advanced malignancy
72
embolus
• A detached intravascular solid, liquid or gaseous
mass that is carried by the blood to a site distant
from its point of origin
• Lodge in vessels too small to permit further passage and cause partial or complete occlusion
73
embolus major consequence
ischemic necrosis of downstream tissue (infarction)
74
• Thromboembolus
• Thromboembolus – almost all emboli represent
some detached part of a thrombus
75
Venous and Arterial Emboli vessels sizes
Aa move towards decreasing sizes and Vv move towards increasing sizes
76
failure on one side of the circulatory system
leads to increased stress on the other
(aa or vv)
77
venous emboli tend to?
tend to lodge in one vascular bed (lung)
78
Arterial emboli can travel to?
wide variety of sites
79
arterial emboli point of arrest depends on?
• Point of arrest depends on source and relative amount of blood flow
80
major site of arterial emboli arrest
lower extremities and brain
81
consequences of arterial emboli arrest depend on?
vulnerability of tissue to ischemia, caliber of occluded vessel and collateral blood supply
82
sources of arterial emboli
mainly athersclerosis of arteries and mural thrombi, endocarditis may contribute as well
83
pulmonary embolus
saddle embolus- will saddle to bifurcation of the pul Aa
of greater than 60% blood flow cut off pt will die
84
Paradoxical Embolus
• An embolus that originates on the right side venous circulation and lodges in the left side systemic arterial circulation, bypassing pul circulation
85
Types of Emboli
most originate from?
bone?
air?
nitrogen?
atherosclerosis?
tumors?
amniotic fluid?
foreign bodies?
• Thromboemboli – most emboli are thromboembolic in origin
• Fat - bone fractures
• Bone marrow - bone fractures
• Air
• Nitrogen bubbles – decompression sickness in divers caisson disease
• Atherosclerotic debris (cholesterol emboli) -
• Tumor fragments -
• Amniotic fluid – obstetric complication
• Foreign bodies – catheters,
86
Bone Marrow Embolus in the Pulmonary Circulation histo
embolism possesses heamtopoetic SC and marrow fat globules
87
Amniotic Fluid Embolism in the
Pulmonary Circulation histo
fetal squamous cells
88
• Infarct -
• Infarct - an area of ischemic necrosis caused by occlusion the
vasculature
89
• Most infarcts occur from?
• Most infarcts occur from thrombotic or embolic arterial
occlusions
90
• Venous thrombosis may cause ________, but usually just _________
• Venous thrombosis may cause infarction, but usually just congestion
91
• Atherosclerotic vascular disease causes___% of all deaths in the United States – mostly?
• Atherosclerotic vascular disease causes 40% of all deaths in the
United States – mostly myocardial infarction or cerebral
infarction
92
• Ischemia
• Restriction in blood supply, usually due to factors in
the blood vessels
• Oxygen, glucose and other blood-borne materials fail to arrive
93
• Infarct
An area of ischemic necrosis
--Complete loss of blood supply, resulting in necrosis
94
• Hypoxia
• More general term denoting a shortage of oxygen
• Usually a result of lack of oxygen in the air being
breathed
95
Acute Transmural Myocardial Infarction results in?
coagulative necrosis of myocardium
96
cerebral infarctions lead to? whaat form of necrosis could be seen?
lead to stroke and liquifactive necrosis
97
remote kidney infarcts healing?
replacement of infarct with fibrous scar
98
red infarcts
occurs in lung/ loose tissue with dual blood supply
vv occlusion, causes blood to collect
99
Factors that Influence Development of an Infarct
• Nature of the vascular supply
• Rate of occlusion development
• Vulnerability of individual tissue to hypoxia
• Amount of oxygen in the blood
100
white infarct
Aa occluded in organs with single blood supply
101
Nature of the vascular supply – single vs double and development of an infarct
what tissues have single what have double?
dual supply tissues are less susceptible to infarcts
• Lungs – dual pulmonary artery and bronchial artery blood supply
• Liver – dual hepatic artery and portal vein circulation
• Kidney and spleen circulations are end-arterial, single supply
102
• Rate of occlusion development, slowly developing allow?
• Slowly-developing occlusions provide time to develop
alternate perfusion pathways – collateral circulation
103
Vulnerability of individual tissue to hypoxia
nn?
cardiac myocytes?
fibroblasts?
• Neurons – 3 to 4 minutes
• Cardiac myocytes – 20 to 30 minutes
• Fibroblasts - hours
104
• Amount of oxygen in the blood and development of infarcts affected by?
– anemia or cyanosis
105
Gangrene in Peripheral Vascular Disease
most common cause gangrene?
types of gangrene?
often associated with?
• Insufficient blood supply is the most common cause of gangrene
• Ischemic gangrene (dry gangrene)
• Infectious gangrene (wet gangrene)
• Often associated with peripheral vascular disease secondary to diabetes and long-term smoking
106
Thrombophlebitis -
Phlebothrombosis can form where?
• Superficial veins
• Deep leg veins – high risk
of pulmonary embolus
107
Trousseau Syndrome
due to?
considered?
leads to?
seen with?
• Due to Migratory thrombophlebitis (vv swelling due to thrombus)
• considered a Paraneoplastic syndrome
• Leads to: Hypercoagulability seen in pts with Adenocarcinomas (Pancreas, Colon, Lung)
108
Shock
leads to?
inital damage?
prolonged?
• Systemic hypotension due to either reduced cardiac output or to reduced effective circulating blood volume
• Leads to impaired tissue perfusion and cellular hypoxia
• Initially reversible cellular injury
• Prolonged shock leads to irreversible cellular injury
109
• Cardiogenic shock
seen in?
– low cardiac output due to pump failure
seen in:
• Myocardial infarct
• Ventricular arrythmias
• Extrinsic compression (cardiac tamponade)
• Outflow obstruction (pulmonary embolism)
110
• Hypovolemic shock
– low cardiac output due to loss of blood or plasma volume
seen in:
• Massive hemorrhage
• Fluid loss from severe burns
111
• Septic shock
– vasodilation and peripheral pooling of blood as part of a systemic immune reaction to a bacterial or fungal infection
112
types of shock
cardiogenic
septic
hypovolemic
