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Today’s Review Session

Today’s Review Session. 4:00-5:30 Mara will cover: Foley Aslam Docherty 5:30-7:00 Christine will cover: Etamadian Parsa Nowrangi. HTN Foley. PRIMARY HTN. HTN = high blood pressure = high MAP Remember that equation: CO x TPR = MAP

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Today’s Review Session

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  1. Today’s Review Session • 4:00-5:30 Mara will cover: • Foley • Aslam • Docherty • 5:30-7:00 Christine will cover: • Etamadian • Parsa • Nowrangi

  2. HTNFoley

  3. PRIMARY HTN • HTN = high blood pressure = high MAP • Remember that equation: CO x TPR = MAP • So anything that increases MAP (ie CO or TPR) causes HTN • Increased NE • Reset Baroreceptors • Renin-Angiotensin-Aldosterone System • Na+ and H2O Retention • Changes in Blood Vessel Wall • Nitric Oxide • Endothelin-1 • EDLS (Endogenous Digitalis-like Substance) • Other effects of Aldosterone • Insulin Resistance/Hyperinsulinemia • Obesity

  4. Anything that Increases NE • Increased release • Decreased re-uptake/degradation • Increased sensitivity of receptors (so the same amount of NE has a greater effect)

  5. Resetting Baroreceptors • Baroreceptors keep your BP in check—if it gets too high they signal the vagus nerve to increase parasympathetics (which will decrease BP) • If they are reset to a higher threshold, your BP can run high without being regulated. (It takes a higher pressure to stimulate the baroreceptors) • Results in symp/parasymp imbalance

  6. Renin-Ang-Ald System • Renin(from kidneys) converts angiotensinogen to Ang I • ACE (from lungs) converts Ang I to Ang II • ACE also breaks down bradykinin (a vasodilator) • Ang II goes to the target organs and promotes sympathetic effects which increase BP • It does all those things that increase NE (increased release, decreased re-uptake, increased receptor sensitivity) • It causes adrenal cortex to secrete aldosterone, which leads to renal Na+ and H2O retention (This causes increased BP because you have greater blood volume in the same size vessels, and you increase VR which increases CO)

  7. This system functions to increase BP. Your kidneys monitor BP by checking pressure in the afferent arteriole and Na+ delivery to the macula densa. If either of these are decreased the kidney releases renin. The kidneys will also release renin in response to sympathetic impulses. • Remember negative feedback? As BP increases, renin secretion should decrease.

  8. Na+ and H2O Retention • Blood volume (ECF volume) increases • Increased venous return and CO (remember that increased CO causes increased MAP) • Excess blood flow to tissues may result in generalized increase in peripheral vascular resistance (autoregulation) • Na+ accumulation in vascular tissue • Increase H2O content of vessel wall (increased wall thickness, decreased lumen, increased resistance to flow)

  9. Changes in Blood Vessel Wall • Vessels must adapt to increased transmural pressure • Hyperplasia (more smooth muscle cells) • Increase collagen (decrease compliance) • Increase wall thickness/decrease lumen • Increase vascular resistance (remember, decreasing the diameter of the lumen has the same effect as vasoconstriction)

  10. Nitric Oxide • Vasodilator • A deficiency of NO may contribute to HTN

  11. Endothelin-1 • Vasoconstrictor • May have local effects

  12. Aldosterone- other effects • Remember aldosterone increases renal Na+ and H2O retention (which increases blood volume, VR, and thus CO), and it acts to increase available NE • Decreases NO (remember NO is a vasodilator) • Increases endothelin (remember this is a vasoconstrictor) • Decrease compliance/ increase stiffness of blood vessels • Cause damage/fibrosis to vasculature, heart, and kidneys

  13. Insulin Resistance/Hyperinsulinemia • High insulin causes: • Increased renal Na+ reabsorption (and H2O follows the Na+) • Increased symp activity and release of catecholamines • Arterial vascular smooth muscle hypertrophy • Increases cell MB permeability and intracellular Ca++ in vascular smooth muscle

  14. Obesity • The fatter you are, the more leptin you produce • Leptin may increase symp activity

  15. SECONDARY HTN • HTN is caused by a specific lesion, so it is secondary to that lesion • Renovascular HTN • Renal Failure • Pheochromocytoma • Increased aldosterone (ie primary aldosteronism) • Increased glucocorticosteroids (ie Cushings)

  16. Renovascular HTN • Stenosis of renal artery causes decreased renal blood flow • Remember that when you have decreased renal blood flow there is less pressure in the afferent arteriole, which signals the kidney to release renin (and starts the renin-ang-ald cascade) • This leads to HTN

  17. Renal Failure • When the kidney fails it cannot excrete Na+ and H2O like it should • So you get retention of Na+ and H2O which increases the blood volume ( and the VR, and the CO….is this getting repetative?)

  18. Pheochromocytoma • What is it? An adrenal medullary tumor which secretes epi and NE • Epi and NE have symp effects on heart and vasculature (so vasoconstriction which increases TPR, and increased contractility and CO)….all lead to increased MAP

  19. Hypersecretion of Aldosterone or Glucocorticosteroids • Primary Aldosteronism: Na+ retention, K+ depletion, inhibits uptake of catecholamines • Glucocorticosteroids (Cushings): similar effects

  20. CARDIAC CONSEQUENCES OF HTN • Pressure Overload • Increased myocardial O2 consumption (from increased work) • Cardiac hypertrophy (due to increased work load) • Changes in contractility (initially elevated, diminished as hypertrophy develops) • Relative Ischemia • Vascular supply cannot keep up with muscle hypertrophy • Angina pectoris

  21. VASCULAR CONSEQUENCES OF HTN • Atherosclerosis and PVD: • Mechanical stress leads to endothelial damage • Form plaques which narrows lumen (which leads to more HTN) • Weakens vessel walls (predisposing you to hemorrhage) • Cerebral : hemorrhage, embolism (stroke) • Renal : damage vessels, hemorrhage, embolism (eventually lead to kidney failure)

  22. CHF Dr. Foley

  23. Quick Review of pp1-2 Backward failure: ventricles don’t empty completely so increase EDV, pressure backs up into veins and capillaries and causes filtration of fluid from blood into surrounding tissues (venous congestion, edema), this results in decreased plasma volume so the kidney holds on to Na+ and H2O which increases the blood volume (and thus pressure), which exacerbates the venous congestion and edema, and the vicious cycle goes on and on…. Forward failure: decreased CO leads to decreased renal perfusion, the kidneys aren’t getting as much blood flow as they expected so they retain Na+ and H2O to increase blood volume, which contributes to venous congestion and edema… Left ventricular failure: when the left ventricle fails, blood backs up into pulmonary circulation causing pulmonary congestion and edema Right ventricular failure: when the right ventricle fails, blood backs up into the systemic circulation causing systemic congestion and edema (ie hepatic, lower extremities)(Note: left failure is #1 cause of right failure)

  24. Compensatory Mechanisms • Decreased cardiac contractility • Be able to recognize/read/picture these curves • Length tension curve: • Systolic dysfunction: neg. inotropic (less contractility), curve shifts down and right • Diastolic dysfunction: negative lusitropic (less relaxation), curve shifts up and left • In CHF your heart sucks, so it doesn’t contract or relax as well as it should • Force Velocity Curve • Decreased contractility (curve shifts down and left) • Decreased Vmax • Decreased ejection fraction

  25. Cellular changes: all lead to inadequate energy supply to heart • Decreased mitochondria # and fxn (so less ATP) • Decreased ATPase activities of myosin and actomyosin • Inhibited Ca++ pumps and channels in myocardial SR (neg inotropic = can’t contract) • Abnormal phospholamban- stimulates Ca++ uptake when phosphorylated (neg lusitropic = can’t relax)

  26. Fluid Balance: this is the same thing we talked about in forward failure • Decreased CO leads to decreased renal blood flow • Activates renin-ang-ald system which retains Na+ and H2O • This increases blood volume, boosts CO • Increases interstitial fluid and total body Na+….causes edema

  27. Initial compensation may have unfavorable effects • Frank Starling mechanism: • High EDV causes high EDP • high EDV causes decreased ventricular compliance • high EDPcausesvenous congestion • Increased sympathetics • Positive inotropic effect eventually depletes myocardial NE stores, so this effect is limited • Ventricular remodeling (dilation and hypertrophy) • Starts with high EDV (which dilates the ventricle, increasing wall tension), wall hypertrophies(wall thickness increases) to offset tension produced by dilation, increased muscle mass results in high MVo2, contractility and efficiency gradually decline

  28. Peripheral Circulation: distribution of LV CO changes to meet needs • Decrease renal and cutaneous flow by increasing sympathetic vasoconstriction • Decrease heat dissipation • Increase cerebral and coronary flow • More vasoconstriction than normal, so O2 delivery to tissues is decreased, lactic acid accumulates

  29. Endothelin-1 • Released from endothelial cells • Release is stimulated by hypoxia, NE, epi, angII • Effects: • Cardiac hypertrophy • General vasoconstriction: increases TPR/decreases CO • Aldosterone secretion: Na+/H2O retention in kidneys leading to edema • Renal vasoconstriction: renal Na+/H2O retention leading to edema

  30. ANP and BNP • Vasodilate and inhibit renin-ang-ald system • Fxn is to decrease Na+ and H2O retention • CHF pts have elevated levels in plasma, Na+ and H2O retention persist (kidneys are less responsive to the peptides) • Plasma BNP is used clinically as an index of the severity of CHF

  31. NON CARDIOGENIC SHOCK Dr. Foley

  32. Types • Hypovolemic: decreased blood volume • Causes: hemorrhage, trauma, dehydration • Neurogenic: increased volume capacity (aka relative hypovolemia—massive vaso/venodilation) • Causes: damage/blockade of symp NS (ie spinal anesthesia or spinal cord damage) • Other: drug OD (ie barbs), hypoglycemia

  33. Pathophysiology • Decreased blood volume…decreased VR and CO…decreased SP/DP/MAP/PP …increased HR • Usually hypovolemia due to hemorrhage

  34. Compensatory Responses • Baroreceptor reflex: symp vaso/venoconstriction • Chemoreceptor reflex: responds to hypoxemia, hypercapnia, and acidemia • Autoinfusion: capillaries absorb interstitial fluid • Renal Na+ and H2O retention by decreased filtration, increased R-A-A, increased ADH (increase collecting duct H2O reabsorption) • Vasoconstriction in response to catecholamines, ang II, vasopressin • Cerebral ischemic response: if MAP<50 get massive symp discharge to increase TPR

  35. Uncompensated Shock (irreversible) • Lysozome breakdown • Formation of vasoactive substances • Histamine from damaged cells • Anaerobic glycolysis • Accumulation of vasodilating metabolites • Acidemia • Decreased organ fxn • Increased capillary permeability (from endothelial damage) • Na/K pump fails • Intravascular coagulation

  36. That’s It For Foley!

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