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Hemodynamic Disorders Flashcards

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1
Q

What is blood hemostatis?

A
  1. Vessel Walls - balance between intravascular hydrostatic pressure and plasma colloid osmotic pressure to prevent edema
  2. Liquid blood - balance to prevent hemorrhage or thrombosis

**Body tries to keep us in hemostatic state to prevent these things from happening

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2
Q

What is edema?

A

Increased fluid in interstitial space or body cavities

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3
Q

What is hydrothorax

A

Pleural effusion (edema in lung)

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4
Q

What is hydroperitoneum

A

Ascites (edema in peritoneal cavity in abdomen)

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5
Q

What is Anasarca

A

Severe, generalized edema with profound subcutaneous swelling

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6
Q

What is Dependent edema?

A

Gravity dependent (common in congestive heart failure)

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7
Q

What is Pitting edema?

A

Finger pressure displaces interstitial fluid

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8
Q

What are the two types of edema?

A

Non-inflammatory - protein poor, transudate (getting water and electrolytes out but not cells b/c permeability has not increased)

Inflammatory - protein rich, exudate (leaky b.v. cause loss of proteins)

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9
Q

Describe the pathogenesis of edema

A

-Increased hydrostatic pressure
-Reduced plasma osmotic pressure
-Lymphatic obstruction (lymphatics normally return extra fluid back to the heart. So when these stop working, the extra fluid doesn’t get back and just pools in the interstitial space)
-Sodium retention
-Inflammation

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10
Q

Describe what normally happens in a capillary bed

A

-At the arterial end, fluid gets pushed out increasing hydrostatic pressure
-Interstitial fluid pressure is increased because of fluid coming out
-Plasma osmotic pressure in the venous end drops causing fluid to be pulled back in
-Fluid in the venous end is more dense because there is more protein component per volume of fluid than you had on the arterial end b/c some of this fluid has come out
-Fluid balance is eventually restored through lymphatics

**Problems occur when hydrostatic pressure on arterial end becomes excessive, or colloid osmotic pressure increases

(see slide 7)

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11
Q

What can cause increased hydrostatic pressure

A

Impaired venous return due to:
-Congestive Heart Failure (CHF) –> decreased blood to kidney stimulates renin/angiotensin pathway which worsens the peripheral edema
-Liver disease (ascites)
-Venous obstruction/compression: thrombosis, mass (external pressure), inactivity

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12
Q

What is the function of Renin?

A

Constricts renal b.v. and retains Na+ bringing in water

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13
Q

Describe the Renin pathway

A
  1. Any decrease in blood flow causes renin release which converts Angiotensin to Angiotensin I
  2. Angiotensin I flows through renal and stimulates ACE which converts Angiotensin I to Angiotensin II
  3. Angiotensin II causes:
    -Increased Na+ reabsorption b/c of Aldosterone secretion
    -Increased Na+ brings water with it
    -Arteriolar vasoconstriction in the kidney
    -ADH secretion from pituitary causing collection duct to absorb more water
  4. All of this leads to increased water and salt retention. Effective circulating volume increases. Perfusion of the juxtaglomerular apparatus increases.
    *The goal was to get more blood back to the kidney but if your heart is defective, then it’s not going to help.
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14
Q

What part of the heart stops functioning in someone with CHF? What does this lead to?

A

-Left ventricle
-When the left ventricle stops working, blood backs up into the lungs causing shortness of breath and tiring easily (this is the initial phase of CHF called “Left Sided Heart Failure”)
-If not treated, it will effect the R side of the heart b/c of pulmonary hypertension

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15
Q

After right sided-heart failure in CHF, what is the first place in gravity fluid will hit?

A

The liver causing enlargement of the liver

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16
Q

Describe what happens with Liver Disease

A

-Liver disease prevents blood from flowing through the heart normally
-Portal vein gets increased pressure (portal hypertension) and blood flows back to other organs leading to enlargement of the organs (intestine, stomach, spleen –> symptoms of abdominal swelling (ascites))
-With liver disease we see deoxygenated blood right around the central vein (called central lobular necrosis) b/c right on the central vein you have no oxygen so the cells die at that area. This area will gradually enlarge and then reach the portal triad and ongoing –> 1. Inferior Vena Cava, 2. Hepatic Vein, 3. Central Vein, 4. Portal Triad Vein, 5. Out to Spleen, Stomach, Abdomen

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17
Q

What causes reduced plasma oncotic pressure?

A

Decreased albumin (main blood protein) in the blood (the protein component of the blood is altered)
-Inadequate synthesis - liver disease
-Increased loss of albumin - nephrotic syndrome

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18
Q

What is the net result of reduced plasma oncotic pressure?

A

Net result is stimulation of renin-angiotensin-aldosterone pathway with Na+ and fluid retention
–> If you lose protein into your urine, the plasma oncotic pressure of blood decreases and water tends to go with it. So blood volume decrease and that stimulates renin, which tries to increase water retention but there’s no protein to go with it so you retain the water but lose it into the interstitial fluid

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19
Q

What causes lymphatic obstruction?

A

Due to inflammation or neoplastic growth
-parasitic infection (filariasis)
-breast cancer

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20
Q

What is Lymphadema?

A

Edema related to deficient lymphatics

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21
Q

What causes sodium and water retention?

A

-Acute renal failure
-Post-strep glomerulonephritis (autoimmune stimulating kidney not to work)

*Normal excretion and retention of Na+ gets thrown off. So instead of excreting the appropriate amount, you start not filtering at all and so you retain more Na+ and water over time leading to edema

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22
Q

What is the significance of edema in the brain

A

Herniation, compression of brainstem vessels, can cause death

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23
Q

What is the significance of edema in the lung

A

-Edema may occur here due to LV failure
-Causes breathing difficulty, infections

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24
Q

What is the significance of edema in the larynx

A

Airway obstruction (Ludwigs’ angina)

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25
What is the significance of edema in the subcutaneous
May indicate RV failure, kidney dysfunction
26
What is the significance of edema in the tooth
Can lead to pulpal necrosis
27
What is Hyperemia
-"Active" -Arteriolar dilation -Red tissue (ex. pulpitis) Active increase of oxygenated blood coming into a space due to arterial dilation (increased influx of blood)
28
What is Congestion
-"Passive" -Decreased venous return -Hypoxia and cyanosis --> shunting or cell death Normal amount of fluid coming in but we're not taking it out of the capillary bed (decreased flow on venous side) and now starts to swell with deoxygenated blood
29
List the two types of Congestion
Acute and Chronic
30
Describe Acute Congestion
-Pulmonary (lungs) - blood-filled alveoli -Hepatic (liver) - vessel distension (enlarged) *Build-up w/in a space preventing normal flow
31
Describe Chronic Congestion
-Pulmonary - hemosiderin-laden macs (by-product of RBC breaking down) and fibrosis (scar tissue). Often due to LV failure -Hepatic - "nutmeg" liver, often due to RV failure -Splenic - caused by liver disease
32
Describe the Chronic Congestion pathogenesis
-Decreased venous drainage --> increased pressure --> blood slowing OR capillaries dilate, cell survival -Blood slowing --> hypoxia and RBCs destroyed by Macrophages -RBCs destroyed by macrophages --> hemosiderin -Hypoxia --> cell damage and necrosis --> fibrosis
33
What is the cause, pathogenesis, and pathology of chronic passive congestion in the lung
Cause: LV failure Pathogenesis: Increased vascular pressure --> pulmonary edema Pathology: Thickened septa, hemosiderin-laden macrophages
34
What is the cause, pathogenesis, and pathology of chronic passive congestion in the Liver
Cause: RV failure Pathogenesis: Backflow from interior vena cava, stasis in liver Pathology: Nutmeg liver, centrilobular necrosis
35
What is the cause, pathogenesis, and pathology of chronic passive congestion in the Spleen
Cause: Liver disease or heart failure Pathogenesis: Backflow into spleen Pathology: Splenomegaly, deep purple or blue; firm
36
What is a Hemorrhage?
Extravasation of blood from vessels into extracellular space
37
What is the pathogenesis of a hemorrhage?
-Trauma -Atherosclerosis -Inflammatory or neoplastic erosion of vessel wall -Blood disorders (uncommon)
38
List the types of Hemorrhage
Hematoma (general term) -Petechiae (1-2mm) -Purpura (3-5mm) -Ecchymoses (1-2cm) "bruise" or contusion -In body cavities: hemothorax, hemoperitoneum, hemopericardium
39
Describe the pathophysiology of an internal hemorrhage
-RBC breakdown --> Iron saved as hemosiderin in macrophages --> Heme porphrin ring --> biliverdin (green) --> bilirubin (yellow) --> Globin returns to protein pool -Additional fluid reabsorbed -Gross: red --> purple --> green --> yellow brown --> fades -Can be fatal in brain or pericardium
40
Describe the pathophysiology of external hemorrhage
(Outside the body - mouth --> anus) -If rapid, can cause hypovolemic shock -Chronic (peptic ulcer, menstrual bleeding) leads to iron deficiency
41
What is hemostasis?
-Maintenance of blood in a fluid state with rapid formation of hemostatic plug at site of vascular injury -Tightly regulated
42
What is Thrombosis
Pathologic form of hemostasis occurring in a non-traumatized vessel or where there is excessive clot formation
43
Thrombosis and Hemostasis both involve what?
vascular wall, platelets, and coagulation cascade
44
Describe the pathogenesis of thrombosis
-Endothelial cell injury or dysfunction (main factor) -Altered blood flow (stasis and turbulence) -Hypercoagulable blood *May act independently or in concert
45
What does endothelial injury lead to?
Thrombus formation -Direct trauma -Ulcerated atherosclerotic plaques -Inflammatory process (vascculitis)
46
T/F: Direct epithelium loss is not required, only change in balance of pro/anti-coagulant production for thrombosis formation
TRUE The epithelium can look fine but is dysfunctional. Is caused by: -Hypertension Scarred heart valves -Bacterial endotoxin
47
What does turbulent blood flow cause?
-The turbulent area is static blood -Can have increased concentration of coagulation factors that pre-dispose you to forming a clot
48
Disruption of blood flow leads to irregular flow or _____ which can injure endothelial cells
Turbulence
49
Turbulence forms countercurrents or pockets of ______
Stasis
50
List the consequences of stasis
-Promotes endothelial cell activation and leukocyte adhesion -Prevents dilution of clotting factors and inflow of anticlotting factors -Major factor in venous thrombi formation
51
List the factors that alter blood flow ("the rocks in the river")
1. Atherosclerotic plaque - narrowing of lumen with turbulence 2. Aneurysms (dilated vessel due to weakened wall) - lead to stasis (b/c the fluid slows down and at the edges it will stop) 3. Atrial dilation (due to mitral valve stenosis) - leads to stasis 4. Site of previous infarct - damaged vessels 5. Hyperviscosity syndromes (polycythemia vera, sickle cell anemia) - prmotes coagulation
52
Alteration of coagulation pathways (incresases/decreases) risk of thrombosis
Increases
53
Describe primary (genetic) hypercoagulability
1. Factor V mutation (Leiden) -prevents Va cleavage by Protein C (anti-thrombotic)(common pathway is staying on) -common in recurrent deep vein thrombosis pts 2. Prothrombin gene mutation - increased prothrombin 3. Protein C or S deficiency
54
Describe secondary (acquired) hypercoagulability - high risk
Immobilization, cardiac failure, prosthetic heart valves, cancer
55
Describe Antemortem thrombus
-Clot formed before the person died -Firm, red (RBCs) with white (fibrin/platelet) laminations called lines of Zahn -Focally attached to vessel wall
56
Describe Postmortem thrombus (2 parts)
-Clot formed after death -Dark red, soft and gelatinous portion (RBCs) -Fat and plasma "chicken fat" portion -Not attached to vessel wall
57
What is thrombus dissolution
Fibrinolysis and/or retraction of the clot that can occur for recently developed thrombi
58
What is thrombus organization
Granulation tissue formation --> remodeling into scar tissue --> incorporates into the vessel wall to reestablish blood flow (recanalization)
59
What is thrombus propagation
Growth can lead to vessel obstruction
60
What is thrombus embolization
Dislodging of thrombus and travel to distant site where they lodge at smallest passageway
61
In both ______ and ______, blood flow is re-established w/o serous compromise
Dissolution and Organization/Recanalization
62
What is an Embolus?
Detached intravascular solid, liquid or gaseous mass, carried to a distant site from its point of origin
63
What can cause an embolization?
Can occur from fat, air/nitrogen, atherosclerotic debris (cholesterol emboli)
64
What can embolization lead to?
Ischemic necrosis (infarction) of downstream tissue
65
99% of embolization are a _______
detached thrombus (thromboembolus)
66
Describe air emboli
-Gas bubbles in circulation -During childbirth, chest wall injury or "decompression sickness"
67
Describe amniotic fluid emboli
Torn veins during parturition
68
What is venous thrombi (phlebothrombosis)?
-Also known as red or stasis thrombi - a lot of RBCs -Occlusive - obstructs the vessel -Grow downstream, in the direction of blood flow, conforming to the vessel shape -Soft and friable, parts can break off -90% effect leg veins
69
Describe venous thrombi propagation
-Can lead to vessel occlusion -May affect the superficial leg veins - swelling, pain, varicose ulcers (increase risk of infection). Superficial venous thrombi rarely embolize -Collateral circulation typically prevents infarction in the extremities
70
Describe venous thrombi embolization
-Arise in deep leg veins - at or above knee may embolize -Typically travel to the lungs (pulmonary embolus) -Can be caused by stasis induced by a hypercoagulable state (surgery, trauma, burns, cardiac failure, late pregnancy and postpartum, disseminated cancers)
71
Where do most pulmonary thromboembolisms start?
Most from venous thrombi in the deep leg veins --> right heart --> lodge in pulmonary arteries
72
Small, solitary pulmonary thrombus may....
dissolve or recanalize
73
What can small multiple/chronic pulmonary thrombi cause?
Pulmonary hypertension --> dyspnea, RV failure
74
What can medium pulmonary thrombi cuase?
- hemorrhage --> hemoptysis - infarction
75
What can large pulmonary thrombi cause?
Cardiogenic shock --> cyanosis and sudden death
76
Describe arterial thrombi
-Occlusive, gray/white, often on top of atherosclerotic plaque, retrograde growth -Affects the coronary, cerebral, and femoral arteries
77
Describe mural thrombi
-Adheres to the wall of the heart, form due to abnormal contraction, trauma etc. -Adhere to aortic wall due to aneurysm or atherosclerotic plaque
78
What is the most important outcome (sequella) with Arterial/Mural thrombi?
Occlusion of vessels at critical sites (coronary and cerebral vessels) -May also embolize to extremities, brain, kidneys and spleen
79
Describe systemic thromboemboli
-Occur within the arterial circulation and usually cause infarction -Most are from intracardiac mural thrombi (2/3 from LV infarcts, 1/4 from dilated left atria (mitral valve disease)) -Most go to the legs but can travel anywhere
80
What are thrombi on heart valves also known as? What are the two types?
"Vegetations" Septic and Sterile
81
What are Septic thrombi?
Thrombotic masses filled with infectious organisms (i.e. infective endocarditis)
82
What are Sterile thrombi?
Thrombotic mass without organisms -Non-bacterial endocarditis in hypercoagulable state -Verrucous endocarditis in SLE (Libman-Sack's endocarditis)
83
What is an infarction?
An area of ischemic necrosis
84
What causes infarction?
1. Arterial occlusion 2. Venous obstruction -Venous thrombosis usually --> obstruction and congestion --> bypass channels open so no infarction -Only causes infarction in single venous outflow organs (i.e. testis, ovary) 3. Other causes: vasospasms, swelling of an atheroma 2 degree to hemorrhage, vessel compression by tumor
85
What are the types of infarcts based on?
Color (amount of hemorrhage) and Presence/Absence of infarction
86
Describe the types of infarcts based on color
1. Red (hemorrhagic) infarcts occur -with venous occlusion -in loose tissues (lung) where blood can pool -in tissues with dual circulation (lung, small intestine) 2. White (anemic) infarcts occur -with arterial occlusion -in solid organs (heart, spleen and kidney)
87
Describe infarcts based on presence/absence of infection
1. Septic - bacterial vegetations embolize and cause an infarct that turns into an abscess 2. Bland - without organisms
88
Describe the gross infarct characteristics
Wedge-shaped, occluded vessel at the apex
89
Describe the micro infarct characteristics
Ischemic coagulative necrosis with inflammatory border (liquefactive necrosis in the brain)
90
Describe the aging infarct characteristics
Hours to days to show up. Resolves with scarring
91
What are the determinants of infarction severity?
1. Blood supply - most important -Dual circulation - Lungs (pulmonary, bronchial); Liver (hepatic artery, portal vein) or collateral circulation (legs) help prevent damage -End organ (Kidney, Spleen) - worse outcome 2. Rate of development 3. Tissue sensitivity to hypoxia - neurons are fragile (3-4 min) 4. Oxygen content of blood - anemia, cardiovascular and pulmonary disease
92
Describe Shock
Cardiovascular collapse (reduced cardiac output or reduced circulating blood volume) resulting in: -hypotension -decreased perfusion and hypoxia of tissues
93
List the types of shock
1. Cardiogenic 2. Hypovolemic 3. Neurogenic 4. Anaphylactic 5. Septic
94
What is Cardiogenic Shock?
Arrhythmias, compression, pulmonary embolism
95
What is Hypovolemic shock?
Hemorrhage, fluid loss
96
What is Neurogenic shock?
Loss of vascular tone, sudden vasodilation and decreased BP
97
What is Anaphylactic shock?
Type I hypersensitivity
98
What is Septic shock?
Systemic immune response to microbial infection *Septic shock leads to multi-organ failure!!
99
What is the cause of septic shock?
Gram + and gram-negative bacteria and fungi *20-30% fatal, most common cause of mortality in ICUs
100
Describe the pathogenesis of septic shock
Pathogen-associated molecular patterns (PAMPS) are bound to cells of innate immunity (remember TLR) and are activated --> IL-1 and TNF released --> activation of endothelial cells, complement and Factor XII --> 1. thrombosis -ischemia and reduced organ perfusion 2. increased vascular permeability - edema 3. vasodilation (decreased blood pressure) - reduced organ perfusion
101
List the stages of shock
Nonprogressive Progressive Irreversible
102
Describe the nonprogressive stage of shock
Reflex mechanisms protect
103
Describe the progressive stage of shock
Hypoperfusion --> hypoxia --> lactic acidosis. Circulatory and metabolic imbalance worsens --> DIC
104
Describe the irreversible stage of shock
Cell survival not possible
105
Organ failure with necrosis occurs in the _______
kidney, adrenals, liver
106
Ulcers and hemorrhage occur in the ______
stomach
107
__________ endothelial damage leaks protein out into alveoli
Lung - actue respiratory distress syndrome (ARDS)
108
What are the physical signs/symptoms of hypovolemic, cardiogenic?
-Hypotension -Weak and rapid pulse (compensating for lack of blood) -Increased respiratory rate (b/c there'es not enough blood to carry it) -Cool/clammy and cyanotic skin
109
What is the physical signs/symptoms of septic?
Warm and flushed skin (b/c vasodilation systemically)
110
You must discover and and control underlying causes of hemodynamic disorders to avoid _______
renal shutdown, GI bleed, respiratory failure
111
What is the prognosis for Hypovolemic? Septic and cardiogenic?
Hypovolemic - 90% survival Septic and Cardiogenic - 25% survival

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