Hemodynamics Flashcards
Acute Vs Chronic Pulmonary Congestion
Acute:Due to left ventricular failure
Alveolar capillaries are engorged
Alveolar septal edema
Pink transudate in alveolar space
Chronic:Brown induration
Thickened fibrous septa
Heart failure cells
Acute Vs Chronic Liver Congestion
Acute: Right heart failure, Budd Chiari
syndrome
Central vein and sinusoids distended
with blood
Degeneration of central hepatocytes
Chronic: Central region of hepatic lobule is
reddish brown accentuated against
surrounding areas of uncongested tan
liver – resembles Nutmeg
What is hemorrhage?
Extravasation of blood to the exterior of the body or into non-vascular body space.Due to damage of blood vessels or defective thrombosis
* Trauma
* Atherosclerosis
* Aneurysms
* Bleeding disorders
Hematoma
Hemorrhage into soft tissues
Petechiae
Pinpoint 1-2 mm hemorrhage in skin/conjunctiva- rupture of capillary or arteriole
Purpura
Diffuse superficial hemorrhage up to 1 cm in diameter
Purpura
Diffuse superficial hemorrhage up to 1 cm in diameter
Ecchymosis
Superficial hemorrhage >1 cm in diameter
Disseminated Intravascular Coagulation
thrombo-hemorrhagic disorder seen as a complication
of many disorders
systemic activation of coagulation which
results in the formation of thrombi throughout the microcirculation→ “consumption coagulopathy” → bleeding
DIC give rise to:
-Tissue hypoxia and microinfarcts: due to formation of
microthrombi.
-Bleeding disorder: due to pathologic activation of fibrinolysis and depletion of the clotting factors required for hemostasis
Epithelial injury can cause this, after injury thromboplastic agents are in circulation activating coagulation.
**IL-1 and TNF cause upregulation of tissue factor and down regulation of thrombomodulin = excessive clotting
Lab investigations:
- increased fibrin products and D-dimers (fibrinolysis)
- decreased fibrinogen due to excessive use
- decrease clotting factors -> increase bleeding time
- consumption of platelets and aggregation -> increase bleeding time
GIVE HEPARIN TO prevent further formation
Shock
clinical state characterized by a generalized decrease in
perfusion of tissues associated with reduction in effective cardiac output or reduction in effective circulating blood volume.
Cardiogenic Shock
results from myocardial pump failure
* Intrinsic myocardial damage (infarction), ventricular arrhythmias
Hypovolemic Shock
results from loss of blood or plasma volume
* Hemorrhage
* Fluid loss from severe burns or trauma, vomiting, diarrhea
Distributive shock
results from excessive vasodilation causing abnormal
distribution of blood flow
Septic: caused by systemic microbial infection
* Gram- positive infections, gram-negative infections (endotoxic
shock), fungi
Neurogenic/ CNS injury: imbalance between compartments
* Anesthetic, spinal cord injury – loss of vascular tone, peripheral
pooling
Anaphylactic: generalized Ig-E mediated response
* Systemic vasodilation, increased permeability
* Reduced tissue perfusion
* Degranulation of mast cells and basophils- histamine, bradykinin, leukotrienes
Obstructive Shock
results from extracardiac causes leading to decreased
cardiac output
Pulmonary embolism
* Tension pneumothorax
* Cardiac tamponade
Non-progressive stage (adaptation)
Compensated by reflex mechanisms
-Baroreceptors, release of catecholamines, renin- angiotensin, antidiuretic hormone (ADH)-> increase BP
sympathetic stimulation and aldosterone release –
tachycardia, peripheral vasoconstriction, renal conservation of fluid,
relatively maintained blood pressure.
Cutaneous vasoconstriction – cool, pale skin
Progressive Stage (Reversible injury)
impaired tissue perfusion
*Imbalance between circulation and metabolic needs
*Intracellular aerobic respiration replaced by anaerobic
glycolysis -> low pH
*Sludging of RBCs (red blood cells)
*Blunting of vasomotor response
*Arterioles dilate and blood pools into microcirculation
*Reduced cardiac output, anoxic endothelial injury, DIC
* Patient confused, urine output decrease
Irriversible stage
- Severe widespread cell and tissue injury
- Leakage of lysosomal enzymes (aggravate shock)
- Failure of multiple organ systems
- Myocardial depressant factor reduces cardiac output
- Perfusion of brain and myocardium at critical level
- ATN (Acute tubular necrosis), ARF (Acute renal failure) → renal uremia
- Ischemic bowel, entry of bacteria → endotoxic shock
- Survival difficult even if hemodynamics are corrected
Systemic Inflammatory response syndrome
the body’s systemic inflammatory reaction to an infectious or non-infectious insult which is shown
clinically by changes in vital signs, such as elevations in Temperature, heart rate and respiratory rate.
Sepsis
this is the body’s systemic inflammatory response (SIRS) to a source of infection in the body.
Septic Shock
this is Sepsis causing severe hypotension and organ dysfunction.
- Gram positive bacteria common cause
- localized infections can cause systemic shock w/o bloodstream
-dilation leads to hypotension and hypoperfusion
- DIC susceptible
- cellular/organ dysfunction due to hypoperfusion
Metabolic Abnormalities in Septic Shock
- insulin resistance -> hyperglycemia
- increase in glucose release due to increase catecholamines
- Hyperglycemia decreases bacterial activity of neutrophils
- strong release of glucocorticoid then no production due to necrosis of adrenal glands
- decrease in glut 4 due to insulin resistance
Changes in Organs affected by hypoxic injury (septic shock)
-Platelet-fibrin thrombi -> found mostly in kidney
-acute tubular necrosis kidney
- aveolar damage in lungs
- cerebral watershed areas are susceptable
all areas can recover except for neurons and myoctes.
Septic Shock Clinical Features
-Systemic Hypotension
-Weak rapid pulse
-Warm, Flush skin in septic shock
-Hyperventilation
-Oliguria/Anuria
-Bleeding- DIC
Septic Shock Treatment
- O2
- insulin
- doses of corticosteroids
- vasopressor - maintain blood pressure
-fluid replacement
-antibiotics for infections
Thrombosis
The formation of a solid mass from circulating blood elements in the intact circulation.
Normal role for thrombus formation is to plug defects produced by everyday activities in the vessel walls.
Thrombus formation occurring within circulation at sites of no injury or relatively mild injury
Hemostasis
Hemostasis is a precisely orchestrated
physiologic process that occurs at the site of
vascular injury and culminates in the formation of
a blood clot to prevent or limit the extent of
bleeding.
-vascular wall
-platelets
-coagulation
Virchows Triad
Endothelial integrity is the most important factor.
Abnormalities of procoagulants or anticoagulants can tip the balance in favor of thrombosis.
Abnormal blood flow (stasis or turbulence) can lead to
hypercoagulability directly and indirectly through endothelial dysfunction.
Endothelial injury (Thrombosis)
Most important factor
- injury exposes VWF(platelet bindding site) -> increase tissue factor
- Inflammation -> increase plasminogen activator inhibitor (pro) -> decrease anticoagulant factors.
- platelet adhesion
- clots are rich in platelets
Abnormal Blood flow (Thrombosis)
Turbulence can cause direct injury to endothelial cells, while pockets of stasis allows platelets and leukocytes to come in contact with endothelium.
contribute to abnormal BF:
Atherosclerotic Plaques -> turbulent flow across plaque which can damage the fibrous cap covering the atheroma, causing bleeding and exposing subendothelial collagen causing platelet adhesion and therefore thrombus formation over the ulcerated atherosclerotic
plaque. This is the pathogenesis of acute myocardial infarction.
Aneurysmsv-> aortic aneurysms cause blood to settle within the dilated lumen. Loss of blood flow in the aneurysm predispose to stasis and clot formation.
Atrial or Ventricular Fibrillation -> ineffective contraction and emptying of left atrium or ventricle causing stasis of blood and clot formation within the heart chamber.
Hypercoagulability
Abnormally high tendency of activation of the clotting cascade in blood.
Very important risk factor for venous thrombosis.
Factor V Leiden
Most common cause of hereditary thrombosis and most commonly presents with
veinous thromboses such as deep vein thrombosis (DVT).
Factor V Mutation produces a factor V that is resistant to inhibition by Protein C, a natural
anticoagulant. Note: PT, PTT are normal in this condition
Prothrombin mutation
- A single-nucleotide substitution (G to A) in the 3′-untranslated region. The
result is increased transcription of prothrombin and increased levels of prothrombin in the blood.
Clinically there’s an increased risk of veinous thromboses.
Antithrombin Deficiency
Antithrombin inhibits Factors IIa (Thrombin) and factor Xa. Note: PT, PTT
are normal in this condition.
Protein C,S Deficiency
Loss of inhibition of Factor Va and Factor VIIIa. Warfarin inhibits factor II,
VII, IX, X, Protein C and Protein S. Protein C and Protein S have shorter half lives than factors II, IX
and X, therefore treatment with warfarin causes a transient procoagulant state presenting with skin
necrosis in patients with protein C and protein S deficiency.
Arterial thrombi
Paler than venous thrombi
seen in heart and aorta
seen in other smaller arteries coronaries, carotids, femoral, mesenteric
Venous Thrombi
Takes shape of the vessel
redder than arterial thrombus
superficial veins rarely embolize
deep veins -> embolize
Clinical manifestations of Thrombus
- pain, tenderness, features of necrosis such as blue/black discoloration.
- Venous thrombi: swelling, pain, tenderness, pitting edema, warm and discolored due to
congestion (limb). - aterial thrombi: Infarct (e.g. Myocardial infarct) Slow – ischemia, atrophy, fibrosis,
collateral vessel formation (e.g. Stable angina, limb claudication); pale and cold (
Venous embolize to lung usually
arterial embolize to organs/tissue or lower extremeity
Embolism
detached mass that is carried in the blood from point of orgin to a distant site, can cause infarction or dysfunction.
most common emboli come from the heart then to the lower extremities or brain
Most emboli were part of a dislodged thrombus
Pulmonary Thromboembolism
Common origin is from the deep leg veins to the lungs
major contributor to death in hospital, when they first get out of bed.
Massive -> sudden obstruction of 60%/sudden death
Major -> medium occlusion dyspnea, pain/ infarction of 10%
minor -> small vessels obstructed/ asymptomatic
Systemic Thromboembolism
arterial circulation emboli
originates from the heart (80%)
aorta from plaques
venous circulation from atrial septal defect (paradoxical)
Can lead to infarction due to embolization brain lower extremities and bowel
Fat Embolism
Trauma to bone, subcutaneous tissue, burns → fat globules enter the circulation by rupture of the marrow vascular sinusoids or rupture of venules
Mechanical blockage - Globules enlarge in circulation, platelets adhere
Biochemical injury – Free fatty acids are released from adipose tissue in the circulation and are toxic to endothelial cells – DIC, clogged pulmonary and
systemic capillaries.
Pulmonary insufficiency, neurologic symptoms, anemia, thrombocytopenia
* Symptoms appear 1-3 days after injury – sudden onset of tachypnea, dyspnea, tachycardia, petechiae
* Neurologic symptoms- irritability, restlessness, progression to delirium, coma
Air Embolism
Air embolisms usually form via venous circulation due to lower pressure.
Arterial circulation has more pressure and is less likely to get air.
150L can cause death -> obstructive shock -> prevents outflow of blood from RV.
Tx with placing them on the left lateral decubitus so air embolism will rise to right lateral wall
Caisson disease/ Bends? Nitrogen embolism
Deep diving without Caissons chamber deeper than 10m.
02 and N2 dissolve in high amount in tissue due to pressure -> sudden resurface -> releases 02 and N2 -> 02 is reabsorbed but N2 bubbles out rupturing tissue and forming embolism. -> Platelets adhere to N2-> aggravate ischemia-
Treat with slow decompression chamber
Amniotic Fluid Embolism
rare sudden event after labor-> Squames, hair, meconium in mother’s pulmonary vessels
Usually fatal due to DIC or diffuse alveolar injury
Atherosclerotic Embolism
autopsy finding
small dislodged fragments of plaques that obstruct end of arteries
rarely clinical symptoms
Bone Marrow Embolism
Found in small pulmonary vessels are cardiac resuscitation
autopsy finding
not the cause of death
Infarctions
Ischemic necrosis caused by occlusion of arterial supply or venous drainage in tissue
99% of infarcts are from embolism or thrombosis
can be caused by anything that occludes the artery or vein
White infarcts
little bleeding
solid organs like kidney, spleen, heart
arterial occlusions
Red infarcts
large amount of bleeding into organ
tissues with dual supply (lungs)
venous occlusion
5 factors influencing infarcts
- nature of vascular supply. single or dual?
- rate of development. Sudden or slow?
- Tissue vulnerability. brain or muscle?
- Oxygen carrying capacity. anemia increases chances
Nature of blood supply prevention
Dual blood supply will lessen chances of infarct
Collateral circulation -> more anastomoses the lessly likely risk of infarction.
Pulmonary Infarction (nature of blood supply)
Pulmonary emboli with compromised bronchial circulation -> infarction
Pulmonary emboli with healthy circulation -> no infarction.
Cerebral Infarction
Embolism is most common cause from mural thrombi
Thrombotic occlusions found in areas of carotid or middle cerebral artery.
Myocardial Infarction
Coronary atherosclerosis with superimposed thrombosis
left anterior descending most common; coagulation necrosis
pale scar
increase cardiac enzymes
severe chest pain
