Hemodynamic Disorders. A16-A21 Flashcards
A/16. Pathogenesis, stages and types of shock
Types of shock
- Hypovolemic
- Cardiogenic
- Obstructive
- Distributive
A/16. Pathogenesis, stages and types of shock
Cardiogenic shock, causes.
Cardiogenic shock. Insufficient cardiac output for adequate perfusion.
- Systolic Failure
- Diastolic Failure
- Outflow Dysfunction
- Endocrine shock
- ARDS-induced shock.
Systolic failures:
- Heart failure
- Myocardial infarct
- Arrhythmias
- Aortic valve stenosis
- Septal rupture.
Diastolic failures:
- Cardiac tamponade
- Due to transmural infarct rupture
- Constrictive Pericarditis
Outflow dysfunction / obstructive shock:
- Massive pulmonary embolism causing right sided forward failure
- Tension pneumothorax
Endocrine shock:
- Hypothyroidism
- Addisonian crisis
ARDS induced shock
- Insufficient oxygenation of blood causes a type of cardiogenic shock
- Combined with strong inflammatory cytokine release from the damaged lung tissue during ARDS which creates a septic-shock/distributive shock-like effect.
A/16. Pathogenesis, stages and types of shock
Hypovolemic shock, causes
Hypovolemic shock
- Loss of blood from internal or external bleeding. - esophageal varicies
- Dehydration, loss of plasma volume.
- Severe burns - form blisters and cysts
- Severe vomiting or diarrhea
- Osmotic diuresis in DM
- Internal dehydration from ascites, acute pancreatitis.
A/16. Pathogenesis, stages and types of shock
Distributive shock, causes
Septic, Anaphylactic, and Neurogenic forms of distributive shock.
Septic shock:
- Any septic infection, but most often gram negative bacteria.
- Systemic endotoxin and exotoxin release
- Systemic large scale inflammatory cytokine release
- Widespread vasodilation and increased vascular permeability
- Massive inflammatory reaction also causes Disseminated Intravascular Coagulation,
- microthrombii simultaneously formed and lysed throughout the entire body, forming huge numbers of thromboembolisms that block many small vessels and causing diffuse multi-organ damage.
- coagulation and clotting factors are consumed also causing diffuse bleeding.
Anaphylactic shock:
- Severe allergic reaction causing widespread mast cell degranulation and massive histamine release.
- Usually to a drug or other allergen in the bloodstream.
- IgE mediated type 1 hypersensitivity reaction.
- Requires a 1st sensitization exposure, and then a second exposure will induce the reaction.
- Vasodilation and increased vascular permeability.
- Fluid shifts from vascular compartment to interstitial/cellular compartments, causing hypovolemic shock.
- Bronchospasm and respiratory distress.
Neurogenic shock: induced by Traumatic Spinal Injury
- Autonomic dysregulation causes loss of vascular tone, widespread dilation
- Aslo causes decreases sympathetic tone of the heart, decreasing CO.
A/16. Pathogenesis, stages and types of shock
Clinical signs of shock
Clinical signs:
- Low blood pressure
- Rapid heart beat
- Shock index: Heart rate / Systolic blood pressure. Normal range is about 0.5-0.7. As heart rate increases, but blood pressure drops, it gets higher. If its larger than 0.9 this indicates shock, and the patient should be treated like they are actively bleeding.
- Signs of blood centralization - Renal shut down
- Pale cool skin - hypovolemic or cardiogenic
- Pulmonary edema - obstructive shock due to embolism
- Warm, red skin - distributive shock
A/16. Pathogenesis, stages and types of shock
Stages of shock
Stages: Reversible/non-progressive, Progressive, Irreversible
Reversible stage: Compensatory neurohumoral mechanisms are activated and effectively maintaining perfusion:
- a. Renin‐angiotensin system.
- b. Secretion of catecholamines to maintain tone and contractility.
- c. ADH release
- d. General sympathetic stimulation
- Consequences:
a. Tachycardia.
b. Vasoconstriction.
c. Renal conservation of fluid.
d. Perfusion of vital organs is maintained.
- *Progressive stage**:
1. Hypoxia
2. Anaerobic glycolysis and production of lactic acid, which causes ->.
3. the Vasomotor response (arterioles dilate leading to pooling of blood on the arterial side and worsening of cardiac output).
4. Ischemic injury
iii. Irreversible stage:
1. Leakage of lysosomal enzymes.
2. Worsened contractility
3. Ischemic bowel may lead to intestinal flora to enter the circulation and develop
endotoxic shock.
4. Renal failure due to tubular necrosis.
ARDS due to hyaline arteriolosclerosis
A/16. Pathogenesis, stages and types of shock
Compensatory mechanims of shock
1) the immediate neural response
- carotid sinus and aortic arch high pressure mechanoreceptors sense the drop in systolic blood pressure, activate baroreceptor response. at MAP <90
- aortic arch low pressure receptors activate at Pa O2 less than 50 mmHg
- CNS ischemic response actiavtes at PaO2 < 40 mmHg
2) Interstitial fluids Intrinsic response, fluid shit back towards the vasculature
* low pressure in the capillaries causes a net resorption from the cellular and interstitial compartments
3) Humoral/delayed response
- The RAS system is strongly activated, along with ADH, causes water and salt retention, increasing blood volume.
- Strong ACTH and cortisol release
A/17. Causes and types of edema
Basic molecular causes of edema (9)
Terminology for edema depending on its location (5)
Causes
- Increased hydrostatic pressue
- Decreased colloid osmotic pressure in the vessels
- Increased extracellular colloid pressure
- Lymphedema, from blocked lymphatics
- Venous blockage, from thrombus or from tumor mass, as in Superior Vena Cava syndrome
- Increased vessel permeability - as in inflammation or immune response.
- Cytotoxic edema, hypoxia, trauma, or other ion pump deficiency causes cell swelling, expecially in the brain.
- Vasogenic cerebral edema = Perifocal edema of the brain. Regions near a brain lesion will have edema due to the damaged BBB
- Right sided heart failure, causing edema first in the legs, then everywhere.
Types:
- Edema
- Ascites aka hydroperitoneum
- Hydrothorax aka Pleural Effusion
- Hydropericardium aka Cardiac tamponade
- Anasarca - extreme generalized edema with fluid throughout the subcutaneous tissue, especially of the face. caused by low fluid oncotic pressure.
A/17. Causes and types of edema
Specific clinical cause examples
- Venous blockage
- thrombus
- usually of the lower limbs, DVT.
- SVC syndrome, tumor mass blocking the SVC
- Neck veins distended, facial edema especially around the eyes
- Liver Cirrhosis, compressing portal veins and IVC
- Ascites, Leg egema
- thrombus
- Right sided heart failure
- Edema of the lower limbs, progressing to
- Anasarca
- Ascites
- Eventually bilateral hydrothorax and hydropericardium
- Left sided heart failure (backward)
- Bilateral Pulmonary edema, pleural effusion
- Eventual ARDS from the hyaline accumulation in the alveoli
- Lymphedema
- From surgical ablation, or irradiation
- Also from local inflammation or damage, which can compress the thin lymphatic vessels.
- Parasitic blockage as in elephantiasis.
- Inflammatory edema
- permeability and increased flow causing local edema
- Cytotoxic edema
- Vasogenic cerebral edema, perilesion edema of the brain from BBB breakdown.
- Systemic hypoproteinemia or hypoalbuminemia
- Face and eyes are the first place edema is seen
- Rh or ABO incompatibility
- causes systemic inflammatory reaction against blood cells, seen in fetus and newborns
10.
- causes systemic inflammatory reaction against blood cells, seen in fetus and newborns
A/18. Causes and types of thrombosis
The essential causes of thrombosis generation
Thrombosis. Hemostasis is the coagulation of blood in an injured vessel or injured tissue to protect against bleeding. The pathological form is thrombosis.
Virchow’s Triad of thrombosis:
- Endothelial injury
- Stasis or turbulent flow
- Increased coagulability
Endothelial injury is the most important.
- Exposing collagen, TF.
- Generates endogthelial signals which are activagte platelets and are pro-coagulative/pro-inflammatory.
- Can change local blood flow, also prothrombotic.
A/18. Causes and types of thrombosis
Examples of sources for endothelial damage
Denuding endothelial injuries: These are the most thrombogenic. Involved endothelial cell dirsuption or death, exposing the undrylying basal lamina/myocytes.
Denuding damage:
- Ulcerated or Eroded atherosclerotic plaque
- Endocarditis. Causes changes in the endothelium of the cardiac valves, causing platelet aggregation to them.
- Vasculitis. Immune complex precipitation or direct Ig reaction against endothelium.
- Smoking
- Sepsis
Non-denuding damage: not as thrombogenic as denuding damage, but still promotes thrombosis
- Hypercholesterinemia, causes general changes to endothelial cell function that are thrombogenic
- Stable atherosclerotic plaques
- Irradiation
- Hyperhomocysteinemia
A/18. Causes and types of thrombosis
Causes of hypercoagulability states
Primary hypercoagulable states: Congenital genetic mutations altering hemostasis pathways
- Leiden factor V mutation: Mutated factor V is resistant to degradation by Activated Protein C. Thus, pro-coagulative. This is the most common primary hypercoagulability in Europeans/Americans
- Prothrombin activating mutation.
- Protein C deficiency. APC cleaves factors V and VIIIa, inactivating them
- Protein S deficiency, a cofactor for APCs anticoagulant reactions.
Secondary hypercoagulability:
- Oral contraceptives. The most important and common one. They cause excess coagulation factor expression by the liver, causing hypercoagulability in 1-2% of people
- Old age
- Obesity
- Smoking
- Disseminated cancer. Cancers may secrete coagulation factors, cytokines, or mucin.
- Acute promeylitic leukemia. Excessive granulocyte production and pro-coagulant factor expression
A/18. Causes and types of thrombosis
How does stasis or turbulence promote thrombosis?
Causes of stasis or turbulence
Effects of stasis/turbulence:
- Directly promotes thrombus formation
- Promotes endothelial damage
Laminar flow generates a stratified flow in the vessel, with cells and platelets in the center, and a plasma rich, cell free layer near the vessel walls. Disrupting this with stasis or turbulence directly promotes thrombosis.
Causes of altered blood flow:
- Stenotic atherosclerotic plaque.
- Aneurysm, dilation of the vessel.
- causes both turbulence and stasis
- Mitral stenosis. - causes atrial/auricle stasis
- Atrial fibrillation
- Hyperviscocity of the blood
- from polycytemia, leukemia,
- slows the blood flow, increasing thrombocity
6.
A/18. Causes and types of thrombosis
Types of thrombi:
1) by composition
2) by location
- White thrombus: Platelets and Fibrin. Will adhere tightly to the vessel wall. Are harder and rougher surface
- Red thrombus: Mostly RBCs, red. Also called a Sedimentation or Stangation Thrombus. Indicates blood stasis and coagulation of the whole blood content. Often postmortem, and not adherent to the wall. Will crumble easily and have a smooth, gelatinous texture.
- Composite thrombus: Head is white, and tail is red. Initial platelet clot caused stasis and RBC coagulation behind it.
- Laminated thrombus: alternating lines of white and red. Indicates that it formed at a site of rapid blood flow, while the patient was alive.
- Dessiminated Intravascular Coagulation: Systemic intraluminal coagulation causes capillary emoblii throughout the body, widespread multi-organ damage and micro-hemorrhages.
By location
-
Mural thrombus. Within the heart, or aorta lumen.
- Atrial thrombi: from valve stenosis, backward heart failure, or atrial fibrillation.
- Ventricular thrombi: from the scar of an old myocardial infarct, develop in the resulting aneurysm of scarred cardiac tissue.
- Valvular: Originating on diseased valves or in endocarditis.
- Aortic: from ulcerated plaques or aortic aneursym.
- Arterial thrombus. From ulcerated plaques or aneurysms. Typically white thrombi, or composite thrombi.
- Venous thrombus, aka Phlebothrombosis. Usually red/stasis thrombi.
A/18. Causes and types of thrombosis
Fates of thrombii
Propagation: As in a composite thrombus, with a white head, and the thrombus propagates behind itself, from the obstructed, static blood
Embolization: The thrombus loses its attachment to the vessel and moves downstream, where it obstructs a smaller vessel.
Dissolution: The fibrinolytic pathway successfully lyses and dissolves the thrombus. This is only effective in young thrombi, within a few hours. If the thrombus remains for a long time, it becomes resistant to most fibrinloytic agents.
Organization and Recanalization:
- Endothelial cells grow back over the top of the thrombus, fibroblasts, smooth muscles, and macrophages cells invade the thrombus, creating new fibrous/cellular tissue. Organizaiton
- New capillaries grow into and through the thrombus, providing new routes of blood flowreferred to as re-canalization.,
