Cardiovascular Flashcards
Vessel Wall Structure
o Tunica Intima – endothelium (typically first thing injured) and basement membrane
• Surveys blood and releases anti-inflammatory and anti-coagulants
Internal elastic membrane
o Tunica Media – smooth muscle and elastic fibers
o Tunica Adventitia – connective tissue
Active Role of Endothelium
o Secretory & Modulatory for vascular smooth muscle tone and growth, and platelet function
Endothelial-derived vasodilators: nitric oxide and prostacyclin
Endothelial-derived vasoconstrictors: endothelin
Anti-aggregatory for platelets
Anti-mitoenic for vascular smooth muscle
o Metabolic – processing of vasoactive factors – angiotensin-converting enzyme production of angiotensin II (vasoconstrictor) and breakdown of bradykinin (inflammation)
o Plasticity – angiogenesis (new vessel growth) in response to injury and ischemia
Vascular Smooth Muscle Cell Functions
o Contractile – contraction and relaxation
o Secretory – formation of matrix, growth factors, proteases
o Plasticity – hypertrophy, proliferation, large changes in phenotype
o Vascular tone – tone or state of contraction due to myogenic tone (intrinsic factors) or neurogenic and humoral tone (extrinsic factors)
o Vasomotion – change in caliber of a blood vessel
Control of Local Blood Flow
– flow through a region is governed mainly by the resistance of the microcirculation; Pressure = 8 (viscosity) x (length) x (flow rate) / (radius)4
o Metabolic regulation – local metabolites (vasodilation mostly)
o Autoregulation (myogenic regulation) – transmural pressure results in vasoconstriction
o Shear stress-induced vasodilation – force the fluid makes on the vascular wall
Edema
– increased fluid in interstitial spaces
o Normally – fluid entering on arterial end = fluid leaving venous; excess drained via lymphatics
o Disturbances in fluid homeostasis
Increased hydrostatic pressure – impaired venous drainage, congestive heart failure
Decreased oncotic pressure – reduced albumin (nephrotic syndrome, cirrhosis, protein malnutrition)
Increased capillary permeability
o Local disturbances result of regional insults
o Systemic disturbances result of kidneys
o Stasis of flow is major issue – toxic waste products and pathogens build up; endothelial cells overwork in area of insult and die
o Clinically Relevant: Edema indicates disease, inflammation and impairs ability to fight infection
Shock Characteristics and Mechanism
– systemic hypoperfusion due to reduced cardiac output or circulating blood volume
Results in cellular hypoxia that is initially reversible but becomes irreversible
Progressive disorder that leads to multi-organ system failure (liver, kidneys, CNS)
• Nonpregressive stage-compensatory mechanisms activated, perfusion maintained
• Progressive stage – tissue hypoperfusion (hypoxia) and onset of worsening of circulatory and metabolic imbalances
• Irreversible stage – tissue/cellular injury too severe and necrosis occurs; decreased myocardial contractility; renal shutdown due to acute tubular necrosis; ischemic bowell allow flora into circulation (superimposed endotoxic shock)
Cardiogenic Shock
– heart failure – intrinsic myocardial damage, ventricular arrhythmias, outflow obstruction
Catecholamine release – increases HR, contractility, and systemic vascular resistance
Renin aldosterone – attempts to maintain adequate BV
Hypovolemic Shock
– loss of blood or plasma – hemorrhage, severe burns, trauma
Spleen can try to compensate
Neurogenic Shock
– anesthetic or spinal cord injury – lose vascular tone, peripheral pooling of blood
Increased PNS output resulting in massive vasodilation
Anaphylactic Shock
– IgE hypersensitivity – systemic vasodilation and increased vascular permeability
• End result is hypovolemia and decreased cardiac output and tissue perfusion
Vasoconstriction of vascular smooth muscle in GI and unnecessary organs
Increased capillary permeability
Increased peripheral vasodilation
Septic Shock
– systemic microbial infection – most by gram negative endotoxins
Vasodilation (hypoperfusion), pump failure, and DIC (extracellular injury and activation of coagulation factors) will lead to multi-system organ failure
Consumptive coagulopathy – formation of spontaneous clots in unwanted areas and consume all the coagulation factors no coagulation factors to fight potential trauma
1st among deaths in ICUs
Inflammatory Response
o Local Inflammation – low quantities – involves neutrophils, macrophages, and epithelial cells
o Systemic Effects – moderate quantities – fever
o Septic Shock – high quantities – BV depleted and vessel injury resulting in stasis of blood
Hemorrhage
– extravasation of blood due to rupture in vessel wall
o Hematoma – blood accumulates within a tissue
Petechiae (1-2mm) – minute in size; into skin, mucus, or serosal membranes
Purporas (3-5mm)
Bruises (ecchymoses) (1-2cm) – subcutaneous hematomas with RBC deposition which are then phagocytosed by macrophages
• Hemoglobin metabolized bilirubin hemosiderin (golden brown)
Thrombosis
– formation of a clot inside of a blood vessel
o Result of dysregulation of hemostasis described by Virchow triad (endothelial injury, abnormal blood flow, hypercoagulability)
Propagation (accumulation of platelets/fibrin) embolization (dislodged) dissolution (fibrinolytic activity) organization (inflammation,fibrosis, EC smooth muscle cell ingrowth) & recanalization results in thickened vascular wall & re-established blood flow
Virchow’s Triad
– endothelial injury, abnormal blood flow, and hypercoagulability
o Hypercoagulability – tends to be more genetic factors
o Abnormal blood flow – result of either stasis or turbulence
o Endothelial injury – compromises the ability to regulate both in front and behind
Often due to lipid deposition causing abnormal vasoconstriction or inflammation that leads to progressive vessel damage
Or due to the endothelium stop making normal antithrombic and vasodilatory substance like prostaglandins and nitric oxide
Cardiac/Arterial Thrombi
– cardiac dysfunction often origin of thrombi; thrombus formation begins at site of injury (plaque) or turbulence (bifurcation); associated with retrograde growth
o Myocardial infarction mural thrombus (clot in heart)
o Rheumatic heart disease mitral valve stenosis left atrial dilation with atrial fibrillation augments blood stasis mural thrombus
o Atherosclerosis
Venous Thrombi
– commonly occur at sites of stasis; either superficial varicosities or deep veins of leg
o Local congestion, pain, swelling, tenderness rarely embolize
Edema and impaired venous drainage predispose skin to infection from slight trauma and can develop varicose ulcers
o Deep thrombi (larger veins above knee) embolize, and are often asymptomatic
o Bypass channels commonly open to facilitate proper venous drainage
o Clinical Relevance – result of detached intravascular solid, liquid or gaseous mass, almost always a thrombus
Atherosclerosis
– can start as early as age of 13
o Intimal Thickening – healing response to vascular injury; process by which smooth muscle cells migrate, proliferate, and deposit extracellular matrix can lead to stenosis or occlusion
New layer of vessel wall contains smooth muscle cells that lose the ability to contract
o Atheroma/plaque Formation – endothelial dysfunction oxidized LDL foam cell formation atheroma formation (intimal lesion from fatty streak; lipid core covered by fibrous cap)
o Preclinical phase (begins age 10) – formation of fatty streak and fibrous cap that advance
o Clinical phase – aneurysm and rupture; occlusion by thrombus; critical stenosis
o Factors that decrease coronary blood supply (coronal plaque) or increase myocardial oxygen demand (increased HR/preload/afterload/contractility) can lead to ischemia and anginal pain
Pulmonary Thromboembolism
– can start as early as age of 13
o Intimal Thickening – healing response to vascular injury; process by which smooth muscle cells migrate, proliferate, and deposit extracellular matrix can lead to stenosis or occlusion
New layer of vessel wall contains smooth muscle cells that lose the ability to contract
o Atheroma/plaque Formation – endothelial dysfunction oxidized LDL foam cell formation atheroma formation (intimal lesion from fatty streak; lipid core covered by fibrous cap)
o Preclinical phase (begins age 10) – formation of fatty streak and fibrous cap that advance
o Clinical phase – aneurysm and rupture; occlusion by thrombus; critical stenosis
o Factors that decrease coronary blood supply (coronal plaque) or increase myocardial oxygen demand (increased HR/preload/afterload/contractility) can lead to ischemia and anginal pain
Systemic Thromboembolism
– emboli that migrate through arterial circulation – forward failure
• Can cause complications within lower limbs, brain, intestines, kidneys and spleen dependent on origin and relative blood flow
• Consequences dependent on collateral blood supply & caliber of vessels occluded
Intracardiac thrombi – left ventricular wall infarcts; dilated left atrium
Ulcerated atherosclerotic plaques
Aortic aneurysms
Hypertension
– contributes to several conditions of cardio- and cerebrovascular disease
o BP = cardiac output x peripheral resistance; cardiac output = HR x SV
Peripheral constrictors = alpha-adrenergics
Peripheral vasodilators = beta-adrenergics
Humoral constrictors = angII, catecholamines, thromboxane, leukotrienes, endothelin
Humoral vasodilators = prostaglandins, kinins, NO
Local factors – autoregulation and ionic (pH, hypoxia)
o Genetics and environmental factors play a role – cause defects in renal sodium homeostasis, functional vasoconstriction, and defects in vascular smooth muscle growth and structure
o 95% of cases idiopathic (unknown); essential (benign) hypertension secondary to renal disease
o 5% can have rapidly increasing BP if not treated & can result in death = malignant hypertension
Presents with BP >120mmHg, renal failure, and retinal damage
