CV Flashcards
General causes of edema
Increased hydrostatic pressure (impaired venous drainage, CHF)
Decreased oncotic pressure (nephrotic syndrome, cirrhosis, and protein malnutrition)
Generalized edema is called
Anasarca
Pulmonary edema is usually caused by
LV failure or ARDS
Edema has this effect on the inflammatory process
It diminishes it, causing impaired wound healing and ability to fight infection
When blood accumulates within a tissue, it is referred to as a
hematoma
Classification of hemorrhages
1-2mm = petechiae 2-5mm = purporas 1-2cm = bruises (SQ hematoma with RBC deposition which are then phagocytosed by macrophages)
Resolution of a bruise
RBCs are phagocytosed by macrophages. The hemoglobin is metabolized into bilirubin, which is then converted to hemosiderin (golden-brown)
Examples of cardiac dysfunction that can cause thrombus formation
1) MI- irregular contraction of the myocardium and damage to endocardium cause mural thrombus formation
2) Rheumatic heart disease- mitral valve stenosis, causes atrial dilation with a-fib-> stasis of blood->mural thrombus
3) Atherosclerosis (causes EC injury and abnormal BF)
What is a mural thrombus?
A thrombus in a large vessel that will decrease blood flow through that vessel
Septic shock has a mortality rate of ______% and is associated with _______failure
25-50%
multi-organ
Layers of the BV wall and their components
Tunica intima
- Endothelium
- Basement membrane
- Internal elastic membrane
Tunica Media
- Smooth muscle cells
- Elastic fibers
Tunica adventitia
- Areolar connective tissue (thin layer of connective tissue that runs lengthwise down the vessel).
Characteristics of vascular smooth muscle cells
1) Contractile
2) Secretory (formation of matrix, growth factors, and proteases)
3) Plasticity (can hypertrophy, proliferate, and change phenotype)
Vascular tone is regulated by
Myogenic tone (intrinsic tone) and neurohormonal tone (extrinsic factors in the blood)
Vasodilators secreted by the endothelium
NO and prostacyclin (PGI2)
prostacyclin also inhibits platelet aggregation
Vasoconstrictor released by the endothelium
Endothelin
Factors released by the endothelium
Vasodilators (NO and PGI2)
Vasoconstrictors (endothelin)
Anti-aggregatory for platelets
Anti-mitogenic for vascular smooth muscle
5 Roles of the endothelium
1) Acts as a barrier
2) Secretory (vasodilators and constrictors)
3) Modulatory (on platelets and vascular smooth muscle)
4) Metabolic (ACE produces angiotensin II and breaks down bradykinin)
5) Plasticity (angiogenesis in response to injury and ischemia)
What controls blood flow into a region?
Resistance of the microcirculation. Arterioles are the main factor responsible for the SVR. Precapillary sphincters also help maintain BP and selectively regulate flow through vascular beds.
What is the equation for Poiseuille’s Law?
P = (8nLQ)/(pi r^4)
3 ways local blood flow is controlled
1) Metabolic regulation (local metabolites produce vasodilation)
2) Autoregulation (increase in transmural pressure causes vasoconstriction)
3) Shear stress (causes vasodilation). Constant “scratching” from shear stress can cause endothelial damage
What is lymph composed up?
Mostly water and some small amounts of protein (mostly albumin) that are too large to be absorbed by the capillary.
Capillary outflow exceeds venous absorption by about _____L/day
3 L/day
This is why we need our lymphatics!
Pathway of the lymphatics and how the fluid moves
Valves ensure unidirectional flow, and the lymphatic vessels are occasionally compressed by contraction of skeletal muscle, pulsatile expansion of arteries within the same sheath, and by contraction of the smooth muscle of the lymphatic vessel. Lymph returns to the circulation via the thoracic duct and the right lymphatic duct.
Oncotic pressure in the interstitium should be
0
How does fluid enter the lymphatic system?
Pressure gradients. As fluid escapes the capillary, the interstitial pressure rises and enters the lymphatic vasculature.
Five most common causes of edema
1) Increased capillary permeability
- Inflammation
2) Increased capillary hydrostatic pressure
- CHF, ascites/liver cirrhosis, venous obstruction
3) Decreased plasma oncotic pressure
- Malnutrition, protein loss via urine, liver disease
4) Lymphatic obstruction
- Node removal, neoplasm, post-irradiation
5) Sodium retention
- Excessive salt intake with renal insufficiency, increased reabsorption of Na, renal hypoperfusion, RAAS activation
Why is edema a problem?
Edema increases the distance required for nutrients, oxygen, and wastes to move between the capillaries and tissues. Increased tissue pressure may also decrease capillary blood flow.
Both of these factors make it difficult to heal wounds and fight infections, and can result in the development of ulcerations.
Treatment of edema
Compression stockings, salt restriction, diuretics, reduce standing for long periods of time
What is the basic definition of shock?
Failure of the cardiovascular system to adequately perfuse tissues, resulting in widespread impairment in cellular metabolism. Untreated, it will lead to organ failure and death.
Cardiogenic shock
Results from the inability of the heart to pump enough blood to the tissues. Most commonly due to an acute MI or severe myocardial ischemia. Three general causes of this type of shock:
1) Reduced contractility (MI, cardiomyopathy, papillary muscle rupture)
2) Impaired diastolic filling (ventricular dysrhythmias & cardiac tamponade)
3) Outflow obstruction (PE & valvular disorders)
Hypovolemic shock
Caused by a loss of body fluids:
1) Bood (hemorrhage)
2) Plasma (burns)
3) Other: sweat, emesis, diarrhea, diabetes insipidus, etc
Shock develops once intravascular volume has decreased by about 15%
Body will increase SVR in an attempt to maintain BP
Neurogenic shock
MASSIVE vasodilation due to imbalance between SNS and PSNS activity. Decreased SNS activity causes vasodilation, and because of this, there is not enough pressure to drive nutrients across capillary membranes, and delivery to cells is diminished.
Causes: Trauma to spinal cord or medulla
Hallmarks: decreased SVR and HR (due to unimpeded PSNS activity)
Anaphylactic shock
Due to a widespread allergic (IgE mediated) reaction. This causes systemic vasodilation and capillary leakiness, causing venous pooling, edema, and decreased nutrient delivery.
This type of shock is first among deaths in the ICU
Septic shock
Septic shock
The spread of a localized infection into the bloodstream. Release of endotoxins (LPS) from gram (-) bacteria upon their death.
These endotoxins trigger the release of inflammatory mediators such as TNF, IL-1, and IL-6/8, causing a systemic inflammatory response.
This inflammatory response causes low SVR, low BP, tachycardia, and temperature instability. Also causes endothelial damage, activating the coagulation cascade and possibly set of DIC.
Nonprogressive stage of shock
Compensatory mechanisms activated*, perfusion maintained, primarily affecting cardiac, cerebral, pulmonary (whatever that means).
- = Baroreceptor reflex, CAs, activation of RAAS, ADH, and SNS
Progressive stage of chock
Damage is occurring, but it is reversible.
Worsening O2 supply/demand (causes anaerobic metabolism and acidosis, pH induced vasodilation, and decreased venous return), endothelial cell injury and DIC. At this stage, vital organs are affected–patient may be confused and have low UO.
Irreversible stage of shock
Irreversible damage has occurred (cell death)
Necrosis, lysosomal leakage (which is damaging to the heart), and decreased myocardial contractility. Bowel becomes ischemic and leaks flora into the circulation. Kidneys fail due to acute tubular necrosis.
Characteristics of central venous thrombi in superficial veins
Cause local congestion, pain, swelling, and rarely embolize.
Swelling and impaired venous drainage predispose the skin to infection and development of venous stasis ulcers.
Characteristics of deep thrombi
Tend to be in large veins above the knee and are asymptomatic. These tend to embolize.
A PE can cause these complications if >60% of pulmonary circulation is obstructed
Sudden death, cor pulmonale, or CV collapse
Effect of small, medium, and multiple PEs
Small- infarct usually occurs
Medium- no infarct due to collateral flow, but can cause LV failure
Multiple- pulm HTN and RV failure
Virchow’s Triad
Hypercoagulability
Abnormal blood flow
Endothelial injury
Patho of atherosclerosis
Starts with endothelial Injury! May be due to smoking, autoimmune, virus, HTN, DM, high LDL, low HDL, etc).
1) Endothelial injury
2) Damaged endothelial cells become inflamed and unable to produce normal antithrombotic, vasodilatory, and anti-mitogenic substances
3) Macrophages adhere to the damaged endothelium
4) Macrophages then release ROS that oxidize LDL and further damage the vessel wall
5) Oxidized LDL enters the intima and is engulfed by resident macrophages (turning them into foam cells). Once enough of these foam cells accumulate, the lesion is called a fatty streak.
6) Once formed, the fatty streak continues to release more ROS, causing further vessel damage
7) Due to loss of anti-mitogenic effects of the endothelium, smooth muscle cells (SMCs) proliferate and migrate into the intima over the fatty streak. The SMCs also change their phenotype to a secretory cell, and what they secrete is extracellular matrix and other growth factors. Release collagen and form a fibrous plaque.
8) This fibrous plaque may calcify and protrude into the vessel, obstructing flow into distal tissues.
