Haemodynamic Disorders Flashcards
What is a thrombus?
Intravascular mass formed in life consisting of red blood cells, platelets and fibrins
Virchow’s triad
Endothelial injury, stasis, hypercoagulabiliy
Common clinical states leading to thrombus
Venous stasis
Contact activation
Paraneoplastic syndrome
Estrogen (pro-coagulator)
Endothelial injury
Causes of venous stasis
Prolonged bed rest, immobilisation, atrial fibrilation
Causes of contact activation
Prosthetic heart valve (anti-coagulants are needed for life)
Causes of paraneoplastic syndrome
Cancer cells secreting clotting factors (lung/pancreas)
Causes of high estrogen levels
Oral contraceptives, late pregnancy
Causes of endothelial injury
Post-surgery, post-birth
Fates of thrombi
Dissolution by fibrinolysis - for new thrombi, old thrombi are more cross-linked
Propagation - accumulation of more platelets
Organisation and recanalisation - ingrowth of new capillaries to restore flow
Embolisation - detachment and lodging in a distant site, may become infected (septic emboli)
Causes of edema
Increased capillary hydrostatic pressure
Decreased capillary oncotic pressure
Sodium and water retention
Increased vascular permeability and active hyperaemia - AKA local inflammation giving exudate
Obstruction of lymphatic drainage
Causes of increased capillary hydrostatic pressure
Local - impaired venous drainage (e.g. DVT)
General - congestive heart failure, portal hypertension
Causes of decreased capillary oncotic pressure
Nephrotic syndrome (loss of proteins in urine)
Hypoalbuminemia (liver damage causing decreased albumin synthesis)
Malnutrition
Causes of sodium & water retention
Low renal perfusion leading to activation of RAAS system
Low renal perfusion could be due to two reasons:
Low blood volume (as a result of high capillary hydrostatic pressure and low capillary oncotic pressure, increased transudate and hence decreased blood volume)
Low blood pressure (left heart failure)
Causes of obstruction of lymphatic drainage
Filariasis (elephantiasis)
Neoplasm - Lymphoma
Post-surgical/radiation damage
Cardiac causes of edema
RHF leading to backpressure effects on systemic circulation, increased venous pressure and increased capillary hydrostatic pressure > transudate and edema
Decreased cardiac output causing low renal perfusion and hence RAAS activation and ADH secretion > increased sodium and water retention, increased plasma volume and increased capillary hydrostatic pressure > transudate and edema
What is an embolus?
Detached intravascular solid, liquid or gaseous mass carried by the blood to a site distant its point of origin
Types of embolism
Pulmonary embolism
Systemic thromboembolism
Air embolism
Fat embolism
Amniotic fluid embolism
Pulmonary embolism
Typically venous in origin (e.g. DVT)
May cause:
Sudden death - saddle embolism is lodged in the bifurcation of the pulmonary trunk
Pulmonary hypertension > strain right heart
Pulmonary infarction is uncommon because lungs have dual blood supply
Systemic thromboembolism
Typically arterial in origin:
Intramural emboli due to LV infarction and LA fibrillation
Aortic aneurysm and atherosclerotic plaques
Results in vascular occlusion anywhere in the systemic circulation
Fat embolism & effects
Typically caused by fracture of long bones which contain fatty marrow
May cause:
Vascular occlusion and pulmonary insufficiency
Neurologic disturbances
Thrombocytopenia and anemia as RBCs and platelets adhere and aggregate to fat globules, leading to increased splenic sequestration
Petechiae can be a diagnostic feature
Air embolism
Iatrogenic injury (surgery or laparoscopic procedures)
Chest wall injury
Decompression sickness - gas dissolved in tissues, esp. N2, bubbles out quickly with rapid ascent after deep sea diving
Decompression sickness can present with:
Joint pain (bubbling out in joints)
Respiratory distress
Ischemic necrosis
Treated with hyperbaric chambers
Amniotic embolism
Rare obstetric complication where amniotic fluid and fetal tissue infuses into maternal circulation due to tear in placental membrane or uterine rupture
Can cause pulmonary circulation obstruction
Circulating fetal tissues can cause disseminated intravascular coagulation
What is an infarct?
Necrosis due to ischemia due to occlusion in either arterial supply or venous drainage
**Venous occlusion only leads to infarct when the tissue is drained by a single efferent vein (e.g. testis, ovaries) - if not, bypass channels can open up and the result is merely congestion
Causes of infarction
Thrombotic/embolic occlusion - most common cause
Extrinsic vessel compression - tumour, herniated sac, edema in a limited space (e.g. anterior compartment syndrome - anterior tibialis muscle swells too big for sheath)
Torsion of vessles - spermatic cord, bowel volvulus (red)
Morphology of infarcts (how to classify?)
Classification by colour:
- Red infarct has a superimposed hemorrhage, in organs with loose tissue and dual blood supply (e.g. lung, liver)
- White infarct in organs with firm tissue and end blood supply (e.g. heart, spleen, kidney)
Classification by infection
- Bland infarct - no infection
- Septic infarct - infection, and potential to become abscess
Changes in morphology over time
Ischaemia results in
- Remains viable because of compensation
- Ischemic atrophy and reduced function (e.g. renal artery stenosis causing kidney atrophy)
- Establish collateral blood flow (e.g. heart w R & L circumflex arteries) - Healing by fibrosis, replace infarcted area with fibrous tissue (e.g. can happen in heart, but more susceptible to heart failure)
- Infarct
Typical bleeding patterns of abnormal vasculature
Petechiae and purpura on skin and mucous membranes
Significant haemorrhage into joints, GIT, urinary tract, etc
Normal PT, PTT, bleeding time, platelet count
Causes of abnormal vasculature
Infections such as meningococcus and rickettsioses that cause disseminated intravascular coagulation & vasculitis
Drug reactions - deposition of drug induced immune complexes on blood vessel walls causing vasculitis (type III hypersensitivity)
Weakened vasculature: Scurvy - vitamin C deficiency causes low collagen synthesis; Cushing’s syndrome - high cortisol, catabolism of protein
Hereditary hemorrhagic telangiectasia - AD disorder causing formation of dilated, torturous, thin-walled blood vessels that bleed easily
Perivascular amyloidosis - weakened vessel walls
Causes of hemorrhage
Traumatic
Abnormal vasculature
Platelet defects (qualitative/quantitative)
Coagulation factor deficiency
Patterns of hemorrhage
Mucous/subcutaneous hemorrhage: petechiae, purpura, ecchymosis
Hemorrhage into a bodily cavity: hemothorax, hemopericardium, hemoperitoneum, hemathrosis
Hemorrhage contained within tissue: hematoma
Reactions to hemorrhage
Initial: SNS, increase blood volume
Compensate for volume loss: RAAS activation, sodium and water retention, redistribution of blood flow
Long-term: Replace RBC via bone marrow
Clinical consequences of hemorrhage
Hypovolemic shock: If more than 20% of blood volume lost rapidly
Compression by hematoma - extradural hematoma increases intracranial pressure
Iron deficient anemia: Chronic bleed externally (e.g. GIT) - will not be iron deficient if bleed is into bodily cavity because iron will be recycled
What is shock?
Inadequate perfusion of all cells and tissues leading to hypoxia and reversible cellular injury, and if severe, irreversible cellular injury and death
Types of shock
Hypovolemic shock
Cardiogenic shock
Distributive shock
Obstructive shock
Hypovolemic shock
Low blood volume due to hemorrhage, severe burns, diarrhea, vomiting
Cardiogenic shock
Pump failure due to MI, cardiac tamponade, ventricular arrhythmias/fibrillation
Distributive shock
Widespread vasodilation.
Neurogenic shock
Anaphylactic shock
Septic shock
Obstructive shock
Pulmonary embolism, pericardial embolism
Stages of shock
- Initial non-progressive stage
- Progressive stage
- Late irreversible stage
Initial non-progressive stage of shock
Neurohumoral responses kick in to maintain BP
- Baroreceptor reflex - increased sympathetic stimulation
- Catecholamine (NE, E, dopa) release
- RAAS, ADH activation and release
Redistribution of cardiac output:
- Peripheral vasoconstriction
- Autoregulation of cerebral and cardiovascular blood flow to maintain perfusion
Progressive phase (stages of shock)
Persistent hypoxia - increased anaerobic glycolysis, widespread tissue injury and death
Metabolic imbalances - lowered blood pH (lactic acidosis) which blunts vasomotor response
Increased risk of disseminated intravascular coagulation due to the cell injury and death everywhere
Late irreversible phase
Widespread cell injury and death > release of lysosomal contents into circulation, aggravating shock
Irreversible loss of vital functions
- Acute tubular necrosis - shutdown of kidneys
- Myocardial ischemia and infarction
Vicious cycles of shock
Heart (myocardial damage, infarction) + Gut (fluid loss, bacterial liberation) + Lung (alveolar damage, decreased perfusion) + Kidney (tubular damage, acidosis) + Liver (decreased lactate catabolism, acidosis)
Metabolic acidosis: depresses cardiac function and decreases the response of vasopressors
[basically, all contribute to metabolic acidosis, and metabolic acidosis aggravates the organ damage]
Clinical presentations of shock
Hypovolemic shock, cardiogenic shock: weak and rapid pulse, tachypnea, cold, clammy and cyanotic skin
Anaphylactic shock, septic shock: weak and rapid pulse, tachypnea, warm, flushed skin
Pathophysiology of septic shock
Endotoxin (lipopolysaccharides) on gram negative bacteria cell wall bind to endotoxin receptors on macrophages, activating them and causing cytokine release:
- Widespread vasodilation causes decreased tissue perfusion, causing hypoxic injury and decrease in plasma pH
- Decreased cardiac contractility
- Increased risk of disseminated intravascular coagulation: endothelial injury and endothelial activation by cytokines cause formation of microthrombi and organ damage > depletion of coagulation factors increases bleeding tendency
- Hyperglycemia: stress hormones (cortisol, catecholamines) promote insulin resistance
