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FPP: pre-midterm > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

What needs to be maintained in normal fluid homeostasis? Give examples of when these fail.

A
  • vascular wall integrity (trauma causes focal defects in vessel wall)
  • intravascular hydrostatic pressure (CHF causes alveolar capillary congestion and eventually pulmonary edema)
  • osmolarity (cirrhosis causes low intravascular protein levels, leading to edema)
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2
Q

Define edema (what is the normal fluid balance?)

A

Accumulation of interstital fluid in subcutaneous tissues or body cavities (e.g. pleural cavity)

**Normally 2/3 intracellular and 1/3 extracellular body fluid

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3
Q

What is anasarca?

A

Very severe generalized edema

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4
Q

What causes edema?

A

Either increased hydrostatic pressure or decreased osmotic pressure (leads to net accumulation of fluid in interstitium)

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5
Q

What are some causes of increased hydrostatic pressure?

A
  • Venous obstruction (e.g. DVT)
  • Impaired venous return (e.g. CHF -> increased alveolar capillary pressure -> pulmonary edema)
  • Arteriolar dilation (e.g. from heat or CNS dysfunction)
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6
Q

What are some causes of reduced osmotic pressure?

A
  • Excessive loss of albumin from…
    • nephrotic syndrome
    • enteropathy (IBD, infections, etc)
    • malnutrition
    • liver disease (reduced synthesis of albumin)
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7
Q

What are three causes of lymphedema?

A
  1. Inflammation (e.g. lymphatic fibrosis from parasitic infection)
  2. Neoplastic
  3. Post-surgical/post radiation (most common)
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8
Q

What are three common locations edema is observed?

A
  1. Subcutaneous (from CHF/renal failure)
  2. Pulmonary (most commonly from left ventricular failure)
  3. Edema of the brain (focally from tumors or diffusely from viral infections)
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9
Q

Define hyperemia

A

Increase in blood volume within a tissue (due to increase blood flow and arteriolar dilation… an ACTIVE process)

e.g. conjunctivitis inflammation or in exercising skeletal muscles

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10
Q

Define congestion

A

Increase in blood volume within a tissue (due to decreased outflow of venous blood… a PASSIVE process)

e.g. systemically (liver/lung congestion due to CHF), or locally (obstruction of superior sagittal sinus of dura)

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11
Q

Define hemorrhage. What are some common causes?

A

Extravasation of blood from vessels and its accumulation within a space

Common causes:

  • ruptured vessel (trauma, aneurysm)
  • peptic ulcer
  • chronic congestion (liver, lungs)
  • predisposition to hemorrhage (decreased ability to clot)
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12
Q

Define hematoma

A

Accumulation of blood within a tissue (e.g. epidural/subdural, intracerebral, subcutaneous)

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13
Q

What are petechial hemorrhages?

A

Hemorrhages into skin, mucous membranes, or serosal surfaces (1-2 mm)

**associated with low platelet counts, platelet dysfunction, loss of vascular wall support, or local pressure

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14
Q

Define purpura

A

>3 mm hemorrhages associated with same disorders as petechiae

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15
Q

Define ecchymoses

A

>1-2 cm subcutaneous hematomas (bruises) associated with trauma

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16
Q

What are some main players in inhibiting thrombosis?

A
  1. Protein C (along with protein S) causes the proteolysis of factors Va and VIIIa -> shuts down clotting cascade
  2. Antithrombin III inactivates thrombin -> prevents fibrin formation (from fibrinogen)
17
Q

Contrast primary and secondary hemostasis factors

A
  • Primary (platelets adhere to wall)
    • vasculature
    • blood flow
    • platelet count/function
    • extracellular matrix proteins
  • Secondary (clot formation)
    • platelet plug
    • coagulation factors (thrombin, fibrin)
18
Q

What are the laboratory screening tests for primary and secondary hemostasis?

A
  • primary hemostasis
    • platelet count and function (PFA-100, aggregation studies)
    • vWillebrand studies (antigen and activity)
  • secondary hemostasis
    • prothrombin time (PT -> extrinsic and common pathways)
    • activated partial thromboplastin time (aPTT -> intrinsic and common pathways)
    • fibrinogen activity
19
Q

What is factor 5 leiden?

A

The most common inherited predisposition to thrombosis (a single point mutation in the cleavage site for protein C)

**mutation means protein C doesn’t work correctly and cannot break down factors Va and VIIIa -> increased clotting results

20
Q

What is Virchow’s triad?

A

Three primary abnormalities lead to thrombus formation:

  1. endothelial injury
  2. abnormal blood flow
  3. hypercoagulability
21
Q

Define thrombosis

A

Formation of a blood clot within intact vessels

*may fragment and create emboli

22
Q

What are lines of Zahn?

A

Laminations apparent grossly and/or microscopically produced by alternating layers of platelets, fibrin, and RBCs

23
Q

What are some characteristics of a venous thrombosis?

A
  • No associated inflammation
  • 50% are asymptomatic
  • Thrombi in superficial veins (saphenous) of legs rarely embolize -> cause loval swelling/pain/skin ulceration
24
Q

What are the possible fates of a deep vein thrombus?

A
  • Resolution (only if given thrombolytic agent)
  • Embolization to lungs
  • Organization and recanalization
  • Propagation towards heart (rare)
25
Q

Define embolus

A

A detached intravascular mass carried by blood to site distant from origin

26
Q

What are some types of emboli?

A
  • Thromboembolism (most common)
  • Fat (long bone fractures, soft tissue damage/burns)
  • Air (obstetric procedure, divers)
  • Amniotic fluid
  • Tumor (metastasis through blood)
27
Q

What is the most common type of embolism?

A

A pulmonary embolism (usually from a DVT)

*Most are asymptomatic but can cause serious consequences with “saddle” emboli at bifurcation of pulmonary arteries or multiple emboli

**Cause sudden death and pulmonary hemorrhage/infarction

28
Q

Define infarction

A

Area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage of affected tissue

29
Q

Contrast a red infarct and a white infarct

A
  • Red
    • hemorrhagic
    • classic example= lung infarct secondary to embolus
    • occurs in loose tissues (allows blood to collect)
    • occurs in dual circulation tissues
    • occurs when flow is re-established and in venous occlusions
  • White
    • anemic (no blood)
    • occurs in solid organs with end-arterial circulation (e.g. spleen, kidney)
30
Q

Give examples of dual blood supply organs and end arterial circulation organs

A

dual blood supply organs

  • lung (bronchial and pulmonary arteries)
  • liver (hepatic arter, portal vein)
  • forearm/hand (ulnar and radial arteries)

end arterial circulation organs

  • kidney
  • spleen
31
Q

What is the difference between a hematoma and a hemorrhagic infarct?

A

A hemorrhagic infarct has blood intermixed with necrotic tissue

In a hematoma, blood is collected and forms a solid mass

32
Q

What is disseminated intravascular coagulation (DIC)?

A
  • Characterized by initial clotting (microangiopathy), resulting in organ ischemia, followed by bleeding tendencies
  • “Consumption coagulopathy” (widespread clotting leads to consumption of factors/platelets
  • Associated with severe illness (sepsis, trauma, cancer, burns, ischemia)
33
Q

Define shock (cardiovascular collapse)

A

Systemic hypoperfusion caused by:

  • reduced cardiac output (pump failure from infarct, embolism, arrhythmia)
  • decrease in effective circulating blood volume (from hemorrhage, fluid loss, septic/neurogenic/anaphylactic shock)

**hypotension -> impaired perfusion/cellular hypoxia -> tissue injury -> death

34
Q

What are the major types of shock?

A
  1. Cardiogenic (failure of myocardial pump)
  2. Hypovolemic (inadequate blood/plasma volume)
  3. Septic (many mechanisms including DIC)
  4. Neurogenic shock (interruption of sympathetic vasomotor input with spinal cord injury)
  5. Anaphylactic shock (IgE mediated hypersensitivity)
35
Q

What are the stages of shock?

A
  • Nonprogressive phase (initial)
    • tachycardia, peripheral vasoconstriction, renal fluid conservation (via sympathetic stimulation)
    • perfusion of organs maintained
  • Progressive phase
    • tissue hypoxia/lactic acidosis
    • lowering of tissue pH and blunting of vasomotor response
    • tissue hypoperfusion present
  • Irreversible phase
    • cellular/organ injury preventing survival
    • excessive production of lactic acid (anaerobic glycolysis)
36
Q

What are some clinical manifestations of shock?

A
  • hypovolemic and cardiogenic:
    • hypotension, tachycardia, tachypnea
    • cool, clammy, and cyanotic skin
  • septic shock:
    • hypotension, tachycardia, tachypnea
    • peripheral vasodilation initially leads to warm and flushed skin
37
Q

What is the common cause of septic shock?

A

Most often gram POS bacterial followed by gram NEG bacteria and fungi

FPP: pre-midterm (19 decks)

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