Hemodynamics and Shock Flashcards
Thombus vs thrombosis vs embolus
Thrombus: Wanted blood clot
Thrombosis: Unwanted clot
Embolus/thromboembolism: Moving clot/dislodged in veins or arteries
Most common location of thrombosis
*Atherosclerotic bifurcation
Thrombosis causes
*Endothelial damage
Blood flow irregularity
Hyper coagulability
Result of thromosis
Ischemia or infarction
Virchow’s Triad- three categories that can increase the risk of thrombosis
Stasis (blood flow irregularity)
Vessel wall injury to endothelium
Hypercoaguability
*maybe inflammation (chronic and acute)
How does endothelial damage lead to thrombosis formation? Risk factors?
Endothelial breakdown/damage= exposed collagen where pro-clotting factors can bind= thrombosis formation
Risk factor: Atherosclerosis* (DM, HTN, hyperlipidemia)
Anything that damages endothelium
How does circulatory stasis lead to thrombosis formation? Risk factors?
Slow, irreg, turbulent, or stationary blood flow causes local accumulation of pro-clotting factors= thrombosis
Risk: Immobility or paralysis*, arrhythmia, heart failure, aneurysm.
How does hypercoagulability lead to thrombosis formation? Risk factors?
Predisposition towards clotting (congenital or acquired) alters blood chemistry and causes increased risk of thrombosis.
Congenital: Sickle cell
Acquired: Dehydration, pregnancy, malignancies, thombophilia, sepsis.
Risk factors: Any that promote thrombus formation. Smoking, age, obesity
Arterial thrombosis Cause Effect Risk factors Tx
Cause: *atherosclerosis, atrial fib, valvular disease
Effects: *MI, *Stroke, peripheral artery disease
Risk factors: *Smoking, *HTN, *high cholesterol, *Diabetes
Tx: Lifestyle changes, medications, surgery (angioplasty, graft)
Venous thrombosis Associations: Location: effects: Treatment: Risk factors:
Associations: *Venous stasis, *hypercoagulability
Location: *deep vein. Big veins= slow flow
effects: Local pain and swelling or pulmonary edema
Treatment: Anticoagulants
Risk factors: *Immobilization, orthopedic surgery, oral contraceptives.
Deep veins in legs
Saphenous, popliteal, femoral
Deep vein thrombosis labs/tests
Elevated d dimer
ultrasound angiography
3 possible outcomes to venous thrombosis
Resolution
Embolism to lungs
Organized and recanalized–> organized and incorporated into wall.
Venous thrombosis can lead to-
Thromboembolism (dislodged thrombus) Can be fatal. Coronary or pulmonary embolism or stroke.
Pulmonary embolism is associated with
Deep vein thrombosis
Pulmonary embolism symptoms and tx
*Shortness of breath
Hemoptysis- coughing up blood
Sharp chest pain
Tx: Anticoagulation meds
Hemoptysis
Coughing up blood. Happens in pulmonary embolism
Venous thrombosis ocular manifestations
Papilledema: Venous sinus thrombosis. Bilateral swollen ON due to CSF not being able to drain.
BRVO, CRVO
3 types of aneurysms
Saccular- berry (most common)
Fusiform- spindle like
Dissecting (Inner wall of blood vessel tears and forms false channel. = turbulent blood flow. Could also occur inside fusiform)
Risk factor for aneurysm
*Tobacco use Connective tissue disorders (marfans, ehlers danlos- lots of elastic tissue= weak arteries) Trauma HTN M>F Age Atherosclerosis
Aneurysm. What is it?
Localized thinning of arterial wall- high pressure vessels.
Location of aneurysms
*cerebral arteries
*Brain stem
Aortic arch
Thoracic artery
Abdominal arteries
High pressure arteries. Not so much veins
3 complications to aneuryssms
Rupture –> Hemorrhagic (bleeding) stroke
Dissection (tear/false valve in vessel) –> ischemic stroke
Thrombus –> secondary turbulent blood flow–> Clotting –> ishchemic stroke
Tx of aneursysm
Stent
Clip- stops bleeding.
Coiling-fill out pouching so blood can’t enter. Promotes clotting that seals off.
Liquid embolic agents- fill out pouching with “glue” so blood can’t enter.
Blood thinner
HTN meds
aneurysms are more likely to form where?
In high pressure vessels. Usually arteries over veins.
Ocular manifestations of aneurysms
Aneurysmal 3rd nerve palsy. Could lead to hemorrhagic stroke and death. Life threatening. Posterior communicating artery has 20% of aneurysm that compresses CN III.
VF changes
3 required functioning organ systems for life
Cardiovascular
Respiratory
Renal
Primary circulatory system component
Heart pump, fluid volume, closed circulatory system. Ideally no addition or removal.
Shared feature of all shock
inadequate tissue perfusion (not enough O2 to necessary organs) Causes homeostasis to become compromised
Result: Body wide shift to anaerobic metabolism.
Fatal if untreated.
Inadequate cell o2 –> anaerobic metabolism. What other two paths?
- Inadequate energy production –> Metabolic failure of pumps –> Cell death
- Lactic acid production –> Metabolic acidosis –> cell death.
shock MOA (3)
- Inadequate oxygen deliver*
- respiratory failure
- Anemia or hemorrhage
- Fluid loss: vomit, diarrhea, dehydration
- Cardiac pump failure - Impaired oxygen uptake due to biochem poisoning
- Inadequate nutrient delivery
- Malnutrition
- GI absorption disorder
- Lack of insulin (diabetes mellitus)
Final common pathway of shock
Metabolic acidosis and cell death
5 main types of shock
What do they all have in common
Hypovolemic shock * Cardiogenic shock Septic shock Hypotonic/anaphylactic Neurogenic
All involve reduced blood oxygen
Hypovolemic shock *
Decreased blood volume due to trauma, child birth, dehydration.
Cardiogenic shock
Ineffective cardiac pumping
MI, pulmonary embolus, cardiac tamponade
Septic shock
Blood infection- systemic inflam response to secondary infection.
Exo or endo toxin mediated
**Fever and peripheral thrombosis
Ex: Candidia
May lead to cariogenic or hypovolemic shock
Hypotonic shock/ anaphylactic
Decreased peripheral vascular tone = Vasodilation = blood pools in peripheral tissues
Due to type 1 hypersensitivity reaction
Neurogenic shock
Brain and or spinal cord damage
Two main signs of septic shock
Fever and peripheral thrombosis
3 stages of shock
compensatory
Progressive
Refractory
Stage 1 of shock: Compensatory. What happens?
Mechanisms to fix? Presents as what?
Normal BP
Adequate tissue person
No permanent damage
Mechanisms to fix: vasoconstriction. Increase blood flow to major organs. Increase CO. Decrease urine.
Presents as decreased skin perfusion, tachycardia.
Stage 2 of shock: Progressive. What happens?
Body's mechanism starts to fail Failing BP, hypotension --> Tachycardia and tachypnea Acidosis reduced tissue perfusion Tissue damage
Stage 3 of shock: Refractory period. What happens?
Very low BP
Inadequate tissue perfusion
Widespread organ failure
Death occurs even with homeostasis restoration.
Septic shock may lead to what other forms of shock?
May lead to cariogenic (loss of pumping power) or hypovolemic shock (Decreased blood vol and vasodilation)
