Pathophysiology Exam 3

What is in whole blood?
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What do platelets produce and release?Growth factors that can stimulate other cells to reproduceWhy can't bleeding be seen if it occurs all the time?1. Blood vessels are flexible and don't break easily in young people 2. Fix bleed quickly via physiological hemostasisSource of most plasma protein?LiverWhat is platelet aggregation dependent on?ProstaglandinProstaglandinClass of chemicals that can be inhibited upon formation by NSAIDsWhat is less effective for older people?Clotting/Hemostatic mechanisms because the organs shrink as we ageWhat happens when you don't have as many clotting factors and the vessels break easily?Start to see blood under the skinCapillaries- Fragile - Made of living cells - Single cell layerWhat happens when capillaries are worn out?There is a tendency for blood to leak out of vessels until epithelial cells are replacedNSAIDNon-steroidal anti-inflammatory drugWhat do NSAIDs do?Cut down on platelet aggregationWhat do platelets adhere to?Broken edges of blood vessels when they recognize proteins in the wall of the broken vessel that they don't normally seeWhat triggers platelet aggregation?Chemicals that get released from the broken edge of a blood vesselPlatelet plugOccurs when platelets bind togetherWhat should not be given to a person who had a stroke?AspirinWhy should aspirin not be given to those with an acute MI?Aspirin will not help because clot has lodged into blood vessel + obstructed blood flow to tissue in the heart.Steps in healing involving platelets:1. Plug capillaries 2. Repair vessels 3. Remove clotClotting factors- Soluble - Mostly plasma proteinsWhere are clotting factors made?LiverWhat kind of feedback occurs when an injury tears a blood vessel?Negative feedbackWhat happens when negative feedback occurs?Blood vessels break, blood cause vessels to constrict to reduce amount of blood leaking outCollagen- Most abundant protein - Triggers platelet adhesion and aggregationCoagulation- Activated platelets adhere to wall and plugs vessel - Cytokines released to activate intrinsic clot factorsIntrinsicFound in bloodExtrinsicFound outside of bloodCytokinesInflammation and extrinsic clot factorsWhat do damaged cells release?CytokinesWhat is the main point of clotting?Form structure made up of lots fibrinFibrin- Protein which polymerizes during clot formation - Used to tie together all the platelets and RBC forming bulk of clot - PolymerWhat is the precursor of fibrin?FibrinogenWhen clotting occurs inappropriately, what is the disease called?ThrombosisProducts of thrombosis are calledThromboses which can lead to thromboembolismsFibrinogen- Always present in case of bleed - Ready to be converted to fibrin monomersWhere is fibrinogen made?LiverThrombinEnzyme that converts fibrinogen to fibrin during coagulationWhat does a platelet plug need?FibrinWhat can occur if you don't have fibrin for a platelet plug?Bleed to death over course of few yearsExtrinsic Factor of Clotting Pathway- Forms faster and looser clot - Less fibrin - In wall/outside of blood vesselsIntrinsic Factor of Clotting Pathway- Forms a more compact clot - More fibrin - In the blood - Soluble and expressed on platelets/RBCs surface or endothelial cellsCommon Path of Clotting Pathway includes:- Factor V/Factor X plus calcium activates prothrombin - Then activates thrombin to convert fibrinogen to fibrinProthrombin TimeMeasures how fast someone clots by looking at rate of conversion from prothrombin to thrombinProthrombinGets converted into thrombin when there is an activated factor XFactor XIII (Clotting Pathway)Causes polymerization of fibrinWhat do platelet plugs result in?- Platelet gets tied together - Becomes denser structure - Making fibrin that wraps it upWhat does a clot undergo?ContractionContraction (clotting)Final step in making dense clotAs vessel walls are repaired, what must the clot be doing?DissolvingUndoing clot mechanism- Kinases activate plasminogen to become plasmin - Plasmin enzymatically breaks down fibrin and WBC come by to get rid of itPlasminNicks polymer fibrin into chunksPlasminogenPrecursor of plasmin that comes from the liverWhen does clotting help?On a smaller level, not in big vesselsBleeding DisordersBleeding too much or not clotting enoughWhen do vessel problems occur?When blood leaks to tissueVessel problems include:- Aging (ex. Loss of hepatic functions) - Genetics - Vitamin C problems - Etc.ThrombocytosisToo many plateletsWhat can thrombocytosis be a result of?Can be due to cancer in blood cell formation, stress, or exerciseWhy is cancer a cause of thrombocytosis?Ex. Leukemia can be using resources elsewhere and not getting enough resources to produce clotThrombocytopeniaToo few plateletsWhat can thrombocytopenia be a result of?Caused by meds, autoimmunity disorders, and other forms of hematopoietic diseasesWhat is a treatment option of thrombocytopenia?Platelet administrationWhat is a benefit of platelet administration?You don't have a higher concern of rejecting platelets like that in a blood transferHemophilia- Common coagulation disorder - Mutation in Factor VIII or Factor IX gene - X-linked recessiveHow does a mutation in Factor IX play a role in hemophilia?Mutation results in inability to produce polymeric fibrinWhat is the treatment requirement of hemophilia?- Treatment should begin early in life - Administration of Factors which are deficient - Blood transfusionsWhat did hemophiliacs get in the 1980s?Most had HIVvon Willebrand's Disease- Most common inherited coagulation disorder - Most are autosomal dominant - Occurs when von Willebrand's factors are deficientWhat occurs in von Willebrand's disease?Platelets don't adhere to collagen in damaged vessel wallsvon Willebrand FactorBinds to Factor VIII and shields it from being degraded by an enzyme that is always present in the blood for degradation of Factor VIIIWhy could estrogen be used as a treatment for von Willebrand's diseases?- Proliferative property - Causes things to grow and compensate for clotting factors - Help women control loss of blood during mensesTreatment of von Willebrand disease includes:- Factor VIII - Plasma - EstrogenDisseminated Intravascular Clotting (DIC)- Vessel damage, meds, etc. can lead to many small clots - Ischemic problems as many small vessels are pluggedIschemiaRestriction of blood flowSepsis- Infection in blood - Immune system can react severlyPlacental abruption- Common cause of DIC and septicemia - Placenta tears away from the wall of uterus prematurelyConsequences of DIC in injury/surgeryClotting factors/resources are all used up and are not present to stop bleedingTreatment of DIC- Heparin - Administration of factorsHeparin- Anticoagulant - Soaks up clotting factors reducing clottingElectrolyte- Charged - Carries ions as they move - Requires movement of water from one part to another - Salt must be moved first to ensure water goes where it needs to goTwo main compartments for fluids in the body:Extracellular and IntracellularHow much total fluid is inside the cell?In all, except for infants, 2/3 of total fluid is inside cellsHow much total fluid is inside the cells of newborns?50/50Where is the majority of the extracellular compartment found?Interstitium (Space)What is the extracellular compartment made up of?- Blood - Interstitial fluid - Lymph - Everything elseSalt WaterIntracellularWhat happens when plasma volume is lost?- There is a reduction in the volume of the blood - If bad enough, then not enough blood will pump throughout the bodyIntracellular fluid contains- Potassium - Magnesium - Phosphates - ProteinsExtracellular fluid contains- Lots of sodium - Chloride - Bicarbonate - Soluble proteins (can be found outside of cells, just in the blood)In adults, what percentage of our body weight is water?50-60%Plasma Membrane- Ensures things can get though and out of cells - Is in charge of what inside cell looks likeMost proteins in the interstitium are...- Not soluble - Forms structureHow much urine must adults make daily?300-400mLWhy is urine made?Urine is made to get rid of wasteHow can fluids be obtained?- Ingested orally - Made during metabolismHow are fluids distributed among the compartments?By forces Ex. PerfusionWhat is the distribution between the vascular and interstitial compartments a result of?Filtration through capillary endothelialHydrostatic Pressure/Interstitial Osmotic PressureDrive/pull fluid out of capillariesCapillary Osmotic/Interstitial Hydrostatic PressueDrive/pull fluid from interstitium into the capillaries and lymphExcretionLoss of fluids from the body via skin, bowels, lungs, and urineWhat hormones control the amount of fluid loss via urine?1. Antidiuretic Hormone (ADH) 2. AldosteroneAntidiuretic Hormone (ADH)Neural hormoneWhere is ADH made?HypothalamusWhere is ADH stored and released?Stored/released from posterior lobe/pituitary glandWhat happens when ADH is release?Reabsorb water from distal tubules and collecting ducts in the kidneysWhat happens when ADH release increase?- Increased osmolarity of extracellular fluid, decreased blood volume and some other thingsWhere is aldosterone made and released?Adrenal cortexAldosteroneSteroidWhy is aldosterone release?- In response to increased angiotensin II activity which increases with decreased blood volume and/or increased potassium concentration in bloodAldosterone causes renal tubes to...Increase their reabsorption of sodium (with water following)How does the body know it is volume overloaded?- As you absorb volume, it fills up the plasma volume - More blood in cardiovascular system - More blood back in heart from veinsWhat happens when there is more blood in cardiovascular system?Blood fills up the right atrium more than it did before causing walls of the right atrium to stretch moreWhat does the stretching of the wall in the right atrium trigger?- Triggers stretch receptors in muscle that cause the release of atrial natriuretic peptides that swim though blood - Hits kidneys to pee out more salt water and bring the volume back down over time.If you lose volume and not becoming concentrated, what happens?Aldosterone gets release to pull salt solution back into the body from the urineAtrial natriuretic and brain natriuretic hormones are released by:Ventricles in humanAtrial Natriuretic HormoneCause you to pee out more salt water; volume unloaderADH means there is...Less but more concentrated urineAldosterone means there is...Less urineWhere are natriuretics produced?In the heart when muscles are stretched because sodium is lost in the kidneysExtracellular fluid imbalancesAbnormality in amounts and not concentration.Volume deficit- Release aldosterone - Loss of sodium-containing fluid - Concentration of ECF doesn't change - Usually occurs in whole body, but could also be a separate compartmentAscitesThe accumulation of fluid in the peritoneal cavity, causing abdominal swellingWhat is a sensitive measure of ECF volume deficit?- Sudden weight loss - Water is heavyVolume Excess- Opposite of deficit - [ECF] is normal - Can occur as a result of improper ADH production/secretionWhat is involved in concentration problems?Intracellular compartmentConcentration ProblemVolume is fine, but concentration is wrongWhat indicates concentration problems?Sodium concentration in the blood is an indicatorWhat is the normal concentration of sodium in the blood140 mEq/LHyponatremiaToo little sodium per volume in bloodWhat can lead to hyponatremia?- Increased ADH release - Losing too much salt compared to water - Drinking too much waterWhy does an increased ADH release lead to hyponatremia?- Water gets pulled back in from kidneys without pulling back sodium - Something could be telling brain/pituitary to produce/release too much ADH or form an ADH-producing tumorHypernatremiaToo much sodium, concentration wiseWhen does hypernatremia occur?Occurs from too much salt vs. water coming in or too much water loss vs. saltEdema- Imbalance - Too much fluid in the interstitiumWhat can lead to edema?- Too much hydrostatic pressure - Too little capillary osmotic pressure - Too much interstitial osmotic pressure - Blockage of movement of fluid into the lymph (normally driven by interstitial hydrostatic force)Electrolytes must do what after ingestion?Must be absorbedHow are electrolytes absorbed?- Concentration gradient - Brought in via binding proteinsHypokalemia- Low potassium concentrations in the blood - Below 3.5 mEq/LWhat is the normal extracellular [K]?Around 5 mEq/LWhat does a low serum K mean?- May not indicate low total body potassium - Could be movement of K into cells, increased loss via kidneys, not enough K in dietHow does a too high/low concentration of potassium affect the body?Heart can stopWhat does [K] play a role in?Cells are very sensitive to extracellular [K] due to its role in membrane potential regulationWhat does a lower K mean?More polarization of resting membrane potentialWhat happens when there is more polarization of resting membrane potential?1. Leads to less likelihood of cellular activation. 2. Slower/less repolarization in excitable cellsWhat part of the body shows an effect of hypokalemia?Muscles become weak and slowWhat happens to cardiac cells in very low [K]?Hyperpolarize and become incapable of firing, leading to dysrhythmiasHyperkalemia[K] above 5 mEq/LWhat part of the body is affected by hyperkalemia?- Muscles show the effects first/most -Affects the heart via dysrhythmias, can cause cardiac arrestFlaccid Paralysis (Hyperkalemia)Reduced polarization leads to contraction in smooth and skeletal muscle but no resetting of membrane potentialHypomagnesia- At least 1.5 mEq/L in serum - Can lead to hypokalemia and must be fixed before hypokalemiaWhat is the role of magnesium under normal conditions?Keeps acetylcholine release under control in the neuromuscular junction.What happens when there is low magnesium?- More acetylcholine is released - Contract too much - Neuromuscular excitabilityWhat happens when magnesium is high?- Can lead to flaccid paralysis due to too little release of acetylcholine - Won't be able to use muscles very muchHypermagnesiaCan occur with increased intake due to laxatives/antacids and decreased lossHypermagnesia occurs often in who?GER pt due to antacid useChanges in acid/base production does NOT necessarily mean.Blood pH is going to changeStrong BuffersPrevent acids and bases from altering the pH in our blood and tissues since we can't tolerate drastic changes in pHWhy do we become alkaline?Most of the time it is due to lack of acid productionNormal pH7.4What can easily pass through capillary walls?ProtonsHow can pH be measured?Taking the pH in the blood because it is the same as pH in interstitial fluid due to highly permeable capillary wallsWhy do small changes in the pH mean big problems?pH is a log functionHow big of a pH change can we handle before we die?+/- 0.4 pH unitsWhat are the acids that metabolism produces?CO2, carbonic acid, etc.List the three main systems in the body that regulates acid-base balance.- Buffers - Respiratory systems - KidneysWhat needs to happen in order for you to get rid of acid from the body?Breathe fasterWhat is the relationship between acid and respiratory rate?If acid increase, respiratory rate increaseList the two main buffers.- Bicarbonate - PhosphatesWhat substance in the body can vary so that our pH doesn't vary?UrineHow low can the pH of urine drop?Can drop to 4.5Bicarb BufferCO2 + H20 <--> H2CO3 <--> H+ +HCO3- H2CO3: Carbonic acid HCO3-: Conjugate badeCarbonic AnhydraseCan convert carbon dioxide to carbonic acid and vice versaHow does the dissociation of carbonic to bicarb and hydrogen ions occur?- On its own - Essentially instant depending on concentrationLe Chatlier's Principle (Bicarb Buffer)- Appearance of acid will drive reaction to the left - Appearance of bases (other than bicarb) will soak up hydrogen ions on the right and pull the reaction rightward - If less on the left, then reaction will go towards the leftWhat do the lungs excrete?CO2 and water which make up carbonic acidCarbonic acid- Is volatile making it the only acid that is able to be lost from the lungsHow is CO2 released?Through exhalationHow are other acids released from the body?Little bit can be lost through sweat/feces, but majority of other acids are excreted from the urine dealt with in the kidneysCompensationWhen the lungs are not working fast enough, then the urine must work harder to remove more acid (everything but CO2) and vice versaWhat is the acceptable pH range?7.35-7.45What will happen when non-carbonic acids builds up in the body?Hyperventilation will occurWhy does hyper ventilation occur when there is a build up of non-carbonic acid?It will not get rid of the non-carbonic acid, just the carbonic acid to help keep control over pH (AKA compensation)What happens when there is a pH change in someone?- The buffers are exhausted - Patient is no longer accommodating pH changesCompensation does not ...Guarantee a control in the pHWhat can kidneys get rid of?Any acid except for carbonicHow are acids removed by the kidneys?- Bicarb get put into the urine - Hydrogen ions follow - Bicarbs get reabsorbed into blood - Hydrogen ions lost in urineWhat do hydrogen ions in the urine combine with?Phosphate, Creatinine, AmmoniaWhy do we acidify the kidneys?To pullout alkaline/basic substances in the blood fasterWhat are bicarb concentrations in the blood an indicator of?Renal regulations of metabolic acidsWhat happens to the bicarb concentration when there is an increase in metabolic concentration in the blood?DecreaseHow do we tell when pH changes w/o measuring pH?Watching bicarbWhat does a lower concentration of bicarb mean?There is more acidWhat does a higher concentration of bicarb mean?More bicarbs can interact with protons to make less acidWhat does it mean when a patient makes more acid?- There are more protons flowing around freely - Protons will combine with bicarb, making carbonic acid - There are less bicarbHow do the kidneys compensate for an increase in carbonic acid?By losing more metabolic acidsAcidosisMaking more acid now than beforeAlkolosisMaking less acid now than beforeAcidemiaDrop in pH in the bloodAlkalemiaRise in blood pHMetabolic acidosis- Kidneys aren't doing their job well enough - Hyperventilation will act to compensate - This will reduce CO2 concentration in the blood - Arterial blood will show low bicarb concentrationsRespiratory Acidosis- There is low respiratory rate - Too much carbonic acidWhat causes respiratory acidosis?- Problems with the lungs and getting rid of CO2 - Arterial blood will have high concentration of CO2In Respiratory acidosis, compensation occurs via ...Renal excretion of acid to increase the amount of bicarb which increases the bicarb to carbonic acid ratio and pHMetabolic alkalosisLoss of lots of non-carbonic acid due to increase in bicarb, decrease in non-carbonic acid or bothWhat can lead to metabolic alkalosis?- Bicarb ingestion via antacids - Loss of stomach acid by vomitingAntacidsNeutralized acids in stomach and small intestinesExample of metabolic alkalosisBulimic patient vomits and loses acid in the body and cannot keep up resulting in becoming quite alkalineHow does metabolic alkalosis occur?Reduction in ECF volume (contraction) will increase bicarb ion concentrationHow does hypokalemia cause alkalosis?H/K exchange rates in the kidneyHow does compensation occur with metabolic alkalosis?Hypoventilation will produce an increase in arterial CO2 concentrationRespiratory alkalosisLow CO2 in arterial bloodWhat causes respiratory alkalosis?Voluntary hyperventilationWhat does compensation do in respiratory alkalosis?Reduces bicarbonate concentrationPanic attacksNon-life threatening hyperventilation that occurs despite the fact that there is not an increase in amount of acid in bloodWhy do people lose consciousness when they have panic attacks?Brain communicates that it is too alkaline and causes the body to lose consciousnessWhy does a paper bag help with panic attacks?It helps get enough oxygen in and recirculates itWhat organ do you need one of to function?KidneyDialysis- Tubes to vessels to arm and clean blood to put back - Very invasive procedures that can put fistula - Buys you time for kidney to arrive and postpone deathWhen may dialysis be necessary?When there is too much acid in the body and you can't excrete it fast enough through the lungs and the kidneysWhat do the majority of people with coronary artery have?Advanced atherosclerotic disease within coronary arteriesWhat do myocardial cells need?They need oxygen at just the right amount because they have little tolerance for too little or too much temporally and concentration wiseCoronary vessels adjust themselves to meet ...Changing demands of myocardiumWhat can chest pain be due to?Ischemia in myocardium (not getting enough blood)What are the clinical syndromes of coronary disease?- Angina pectoris - Acute coronary syndrome (MI and unstable angina) - Chronic ischemic heart disease - Sudden cardiac deathAngina pectorisChest painAnginaA form of chest pain due to insufficient blood delivery to part of myocardium that can lead to cardiac arrest where the heart stopsNitroglycerinMakes coronary artery vasodilateWhat happens when coronary vessels break?It becomes blocked and simply cannot dilate enough to meet and increase demand for oxygen flowWhat can result from a coronary vessel break?Infarction (Ischemic death)What is the most susceptible vessel?Left ventricleWhy is the left ventricle the most susceptible?It is the thickest part of the heart and does the most workAtherosclerosisA form of arteriosclerosis characterized by fat and fibrous stuff building up in local regions starting from the inner most lining of the vesselAtheromaThrombogenic meaning the blood forms clots that become a thrombusCoronary Atherosclerosis- Fatty and tough blob grows and obstruct blood flow and also causes changes in the walls of the vessels which become stiff - Can also let go and become an embolus launching downstream somewhere causing ischemia or infarctionWhat is atherosclerosis dependent on?Age, smoking, etc.What seems to be positively correlated with risk of atherosclerosis?High lipid concentration in the bloodSmoking increases the rate of what?At which atherosclerotic plaques formHyperlipidemiaMore lipid in blood than you are supposed toWhat causes hyperlipidemia?Genetic defects and lifestyleStatinsLower blood lipid concentrationExample of genetic hyperlipidemiaFamilial hypercholesterolemia - Autosomal dominate defect in the gene for a receptor for low density lipoprotein which as a result does not get cleared from the bloodPathogenesis of atherosclerosis1. Injury to vessel wall 2. Lipid accumulates in vascular wall 3. Macrophages infiltrate wall and oxidize lipids 4. Inflammation and release of local growth factors (angiotensin II) 5. Plaque formation on intimal wall 6. Mini thrombi incorporated into plaque rupturesHypertensionHigh blood pressure even when at restWhat can hypertension harm?KidneysKidney disease can lead to what?HypertensionWhat is considered hypertensive?Above 120 / 80What is hypertension dependent on?- BP increases with age - Races - ObesityWhy does the blood pressure rise?Due to rigid tubesWhat happens when one kidney thinks that bp is too low?You will have bp that is too high leading to HTPrimary HT- Idiopathic - 95% of hypertensivesSecondary HTAssociated with diseases like renal problems or neurological disorders that result in excessive resistance to blood flow in systemic circulationWhat is the leading cause of secondary HT in children and adults?Renal diseaseWhy is renal disease the leading cause of secondary HT?Blockage in kidneys can lead to HTGestational HTDevelops as a result of pregnancy because some lose control of pressure during pregnancy and is not transferred to babyWhat happens to the maternal BP?It normally drops transiently during second trimester of gestation, then should come back to about normal in the last 1/3Anti-hypertensive drugsShould not be given during pregnancy because placenta must be maintained and drugs get passed placenta and go to babyWhat is HT in pregnancy associated with?Edema and proteinuriaWhat happens with HT in pregnancy with edema?Hydrostatic pressure increases and less protein in plasma can contribute to edemaWhat happens if a pregnant mother has edema in blood pushes protein through glomerulus?Can lead to preeclampsia where protein is detected in urineWhat does runaway HT in pregnancy lead to?EclampsiaEclampsiaSeizures and/or coma can occurSeizuresRandom firing of nerves in the brainWhat happens when pressure rises and continues to rise during pregnancy?Mom can reach a point where she may start to seizeWhat is the treatment for preeclampsia/eclampsia?MagnesiumMalignant HT (hypertensive crisis)- Systolic 180 - Mortality about 90% - Organs can't take pressure - Damage occurs in kidneys first, eyes, brains, vessels may swell and popEffects of HT- Left side of heart gets bigger (Hypertrophy) - Lumen of ventricles get reducedWhy does the lumen of the heart get reduced in HT?Less volume for blood to get pushed out which makes heart work harderEnd diastolic volumeVolume in chamber of heart at the end of diastole (heart relaxes)What occurs with left ventricle hypertrophy?- Heart will have to pump out same amount of blood as before - Wall thicken and reduce the volume in chamber - Something has to change in order to maintain cardiac output - Rate changes and heart beats fasterRemodeling- Occurs with LV hypertrophy - Will reach an end point where performance is lost in myocardiumWhat happens to the blood vessels through the body as a result of hypertension?Become less compliant and makes the heart work harderWhat happens to the wall of blood vessels as a result of hypertension?- Changes in the wall make blood work harder in tissues - Harder to get blood in and out of capillariesWhat does the hardening of arteries contribute to?Slow elevation in b.p. as you ageHow do people respond to HT medicine?Some races respond to HT medicine better than othersWhat does treatment do for HT patients?- Treatment can reduce morbidity/mortality - Small improvement can have large effects on life since it is a chronic diseaseWhat type of treatments can be used for HT?Lifestyle changes and medicineAngiotensin Converting Enzyme (ACE)Results in rise of b.p.Angiotensin Converting Enzyme (ACE) InhibitorInhibiting enzyme can drop b.p.Valves- Prevent backward flow of blood - Can interfere with blood flow to an extent, but cannot interfere more than necessaryCirculatory systemClosed systemWhat is the pressure of blood coming out of left ventricle in healthy adults at rest?120 mmHgWhere does the blood empty into if it is coming from the LV?Aorta where the blood inside is ready to be replacedWhat is the pressure of the blood that is resting in the aorta?80 mmHgWhat happens in the LV when blood is moving?- Undergoes diastole and squeezes blood out - Then sucks in blood from LA while aorta is squeezing simultaneouslyTwo ways valves can cause problems:- Regurgitation - StenosisRegurgitationBlood flows backwardsStenosisBlood flow is impededWhat do problems with valves lead to?Lead to more work for the heartMost problems with valves stem from:Valves are slamming shut and wear out as we ageMany valve problems occur as a result of what disease?Rheumatic feverWhat is rheumatic fever a result of?Streptococcus infections of head and throatWhere is the damage done in pt with rheumatic fever?Inner lining of the cardiovascular systemWhy is damage done to the inner lining of the cardiovascular system?Vascular endothelium is continuous throughout cardiovascular sys and covers surface of the heart and the valvesRheumatic fever may be caused by:- Hyper-immune response to strep - Direct damage caused by strep on tissuesWhat happens after first exposure to rheumatic fever?Risk of subsequent attacks become greater.What do subsequent attacks of rheumatic fever lead to?- Deformation of valves and functional problems - Valves become calcified and sclerotic, which affects performanceWhat is a problem with rheumatic fever?Symptoms take years to developWhere do most valve disease hit?AortaWhy do valvular diseases hit the aorta?Could be due to higher pressure on left side of heartWhat are some non-rheumatic causes of valvular disease?- Congenital defects - Infections of the heart - AtherosclerosisMitral Stenosis- Problem with getting blood from LA to LV during ventricular diastole - Pressure thing - Can't get oxygen into body due to lungs filling with fluidWhat occurs in mitral stenosis?- Atrium hypertrophies to get blood through mitral - Pressure backs up into pulmonary circulation - Gets to RV causing hypertrophy in RVWhat occurs as a result of mitral stenosis?Pulmonary congestion and hypertensionIn normal heart, what is the pressure between the LA and LVNo real pressure difference develops between the LA and the LVHow does blood move through AV valve?Ventricle expands it lumen and sucks the blood from the atriumWhat pressure does the pulmonary circuit operate under?Pulmonary circuit operates under a pressure that is 1/7 of systemic and has 1/7 of a resistanceWhat does it mean when the pulmonary circuit operates under 1/7 of systemic pressure and has 1/7 of resistance?It is easy to push blood through pulmonary circuitWhat happens when the pulmonary circuit is pressurized more than it should be?It cannot tolerate itWhat happens when the systemic circuit is pressurized more than it should be?It can tolerate it to a significant extentPulmonary HTPressure used to squeeze blood through stenotic valve is capable of back flowing into pulmonary circuit and pressurizing pulmonary veins and capillariesWhat is a hallmark of mitral stenosis?Dyspnea (sensation of being out of breath)Concentric hypertrophyThickening of myocardiumEccentric hypertrophy- Thinning/elongation - Not stretching, but is elongation of fiber muscle - Walls are not thicker, but are longerWhere does remodeling NOT occur in mitral stenosis?LVMitral Regurgitation- Progressive disease where remodeling cannot occur forever - Volume thing - Certain percentage of blood does not get pushed into the aortaRegurgitation is also calledIncompetenceIn mitral regurgitation, what happens as the LV undergoes systole and contracts?- LA diastole - Blood travels back into LAIn mitral regurgitation, what happens initially during the compensated phase?Ventricle/Atrium undergo eccentric hypertrophy to accommodate the need to push more volume of blood outIn mitral regurgitation, what happens when the LV and LA lose their ability to compensate?- They dilate - Pressure feeds back on pulmonary circulationWhat is the normal end diastolic volume in LV in resting adults?70mLWhat happens when 10mL of volume does not injected into the aorta from the LV?- Goes back into LA - Every beat from now on will require 80mL end diastolic volume in LVAortic Stenosis- Fights flow of blood from LV to aorta during systole - Pressure gradient b/w LV and aortaWhat happens in response of aortic stenosis?Ventricular concentric hypertrophyIn aortic stenosis, what eventually happens when LV gives up?- Disease progresses quickly - Develop angina, syncope, LV failure and sudden deathAortic RegurgitationIncompetent aortic valve leads to dilation of LV to account for the blood that was missed on previous beatIn aortic regurgitation, what helps deal with the problem for a long time?Dilation of LV/hypertrophyWhy does dilation of LV give up?Disease gets to the point where protein in muscle fiber starts to lose connection with each otherWhat happens when muscles stop working?Cardiac arrestTricuspid Valve Disease- Accompanies disease of mitral, aortic valves - Valves on left side tend to make person symptomatic of valvular disease due to higher pressureWhat is the hallmark of tricuspid valvular disease?- Increase in venous pressure - Swelling of veins - Edema in the periphery - AscitesIn tricuspid valvular disease, why is edema in the periphery a serious issue?- Volume comes from plasma - When juice comes out of blood vessels and accumulate in interstitial spaces, then volume is being removed from bloodWhat happens when there is enough edema?You can lose volume in plasma that can impact hemodynamics/ability to push blood through bodyWhere does a lot of blood get pushed through under low pressure?LiverCompound Vascular Disease- Mixed lesions - Combined lesionsMixed lesionsRegurgitation and stenosis occursCombined Lesions- Involvement of multiple valves - Often in rheumatic feverProlapsed- Tissue pushed into wrong direction - Not an all or nothing situationWhat prevents rheumatic fever?Recognizing strep infection quickly and treatment with antibioticsRheumatic fever can be treated acutely by ...- Antibiotics - Anti-inflammatories - AnalgesicRheumatic fever can be treated chronically by ...Prophylactic antibioticsTreatment of mitral valvular disease consist of- Diuretics - Digoxin - ValvotomyDigoxin- Makes muscles of the heart beat and contract more forcefully - Has a very small margin of safetyWhat happens if digoxin is taken due to heart failure?- You will need it for the rest of the life - Heart becomes dependent on it because it needs it to help it contractDiureticsLower the volume of extracellular compartments so that there is less volume of blood that has to go through mitralValvotomyRun tiny tools into veins and arteries to observe insideTreatment of aortic valve disease- No medical treatment available for stenosis in this valve - Repair of valve by surgical meansTreatment of mitral valve disease- Valvotomy - Replacement when regurgitation and/or stenosis get too badWhat happens when aortic valves misbehaves?It leads to problems getting blood to lungs, heart, brain, kidneysTwo types of valve replacements1. Mechanical 2. TissueMechanical valves- Synthetic, durable and thrombogenic - Requires anti-coagulative therapy for lifetime - Young patients can tolerate anticoagulants wellTissue valves- Doesn't last as long as mechanicals - Don't provoke clots - Can be obtained from pigs, cows and peopleValves from pigs and cowsLots available, good for older folks and those who can't take anticoagulantsValves from people- Cryopreserved from those who don't need them anymore - Scarce, last longerWhat are mechanical events in the heart dependent on?Electrical eventDysrhythmiasAbnormal cardiac rhythm that occurs due to coordination or conduction of electrical eventsDysrhythmias occur because of1. Abnormal automaticity 2. Triggered activity due to problems w/ refractory phase 3. Re-entry (circus) pathways of electrical conductionWhere do electrical events typically originate?Within the heart in a shallow depression in right atrium called the sinal atrial nodeWhat is asked to work first and is followed by electrical events?The atriaWhere are electrical events transferred to?Down the base of ventricles so that it sweeps up the wallSA nodePacemaker because initiation of beats occur in SA nodePacemakerPart of the heart that sets the rhythmRefractorinessA resistance/reluctance or inability to respond to somethingRefractory period for cellsA short period of time that occurs after all cells have fired where cells can't be restimulatedWhy is the refractory period important?Permits the excitation of the heart followed by the period where everything has to stopWhat happens if there is no refractory period?Then there would be sparking going on all over the heart (fibrillation)How do we ensure electrical events get transmitted to the heart?Through conducting pathways (Pathway of least resistance)What part of the heart works first?The top part of the heart works first then bottom part to eject blood out to the lungs and systemic circulationWhat is the average resting heart rate?70-75 bpmTachycardiasHeart beating fastWhat usually causes tachycardias?- Increase body temp - Cardiac toxicity - Increased sympathetic discharge on myocardiumWhat are two ways to increase heart beat by caffeine?1. Interact with the heart muscles cells and tell them to fire quicker 2. Caffeine stimulates the brain to tell the heart to beat fasterHow does cocaine differ from caffeine?- Cocaine can stimulate the brain to tell the heart to beat faster but is also kills heart cells by blocking sodium channels that could put you in cardiac arrest - Has inhibitory effect on the heartWhat happens when the heart beats too fast?There is difficulty filling up ventricles and no blood will come outBradycardiasHeart beats too slowWhat does bradycardias occur as a result of?Excessive vagal stimulationVagus nerve- 10th cranial nerve - ParasympatheticSyncopeDizziness due to change in position or postureWhere does the vagus nerve carry parasympathetic stuff to?Thoracic cavity/abdomenWhat is one of the targets of the vagus nerve?The heartAcetylcholine does what to the heart rate?Slows downWhat watches the pressure going to the brain?CarotidsWhat happens when the carotids senses that the pressure is too high?- They will fire - The brain will talk to the heart through the vagus nerve to slow downSinus (SA) node blockIf conducting pathways do not work, then SA node will be blocked - The SA node is fine but cannot transmit impulse quickly to rest of muscles in atriaWhat causes AV node blockade?Ischemic damage & infectionTwo functions of the AV node1. Picks up on atria firing, takes impulse & shoot it down to bottom of ventricle 2. Delays delivery of impulse to bottom of ventriclePerkinje fibersLow resistance pathway that distribute impulse to muscle cell of ventricles which contract so that blood gets squeezed out into aorta & pulmonary arteryIncomplete AV node blockageTransmission through the AV node is delayed or occasionally blockedFirst degree AV node blockadeTransmission is delayed longer than it should beSecond degree AV node blockadeTransmission is delayed and sometime blockedComplete (third degree) AV node blockade- Transmission through the AV node is completely blocked - Timing of atria is completely dissociated from timing of ventriclesPremature contractionsSomething firing before its supposed toWhat can premature contraction involve?Ectopic pacemakers, atria, AV node and ventriclesEctopic pacemakersPiece of tissue in heart that firing quicker than SA nodeWhat is premature contraction due to?- Ischemia - Atherosclerotic disease - Toxicity associated with drugs, nicotine, caffeineWhere do premature contraction frequently occur?In the atria of normal peopleWhy is premature contraction more serious in ventricles?Can lead to ventricular fibrillationParoxysmal Tachycardias- Usually due to ectopic pacemaker - Heart undergoes burst of activity of varying lengths - Can be halted (supraventricular) by vagal stimulation producing AV node blockVentricular Fibrillation- The most serious dysrhythmia - Uncoordinated contraction of bits and pieces of muscles - Restricted to ventricle or atriumWhat is ventricular fibrillation typically due to?Ischemic disease, Electric shockWhat does ventricular fibrillation often involve?Re-entryRe-entry of impulse in the heart- Starts in SA node - Sweeps through atria - Impulse gets picked up by AV node then shot down to base of ventricle - Impulse sweeps up walls then contracts - Everything stopsWhat happens to tissues surrounding damaged tissues?- Fires then resets and is ready for next impulse from the SA node, but damaged tissue is still firing so tissues see next impulse from damaged tissue - Tissue reignited at wrong time and placeFlatline EKGNo ventricles are firingAtria fibrillationBlood passively leaks into ventricles, especially as the atria tend to quiver and squeeze a little blood down into the ventriclesWhat is the main concern with atria fibrillation?- Not cardiac output b/c ventricles still suck blood out - StrokeWhy is stroke a concern of atrial fibrillation?- Chambers off of atria can form thrombi - Most concerning is formation in left chamber that can break free thrown into aorta and up carotids and into brain causing strokeHeart failure- Heart cannot meet its obligation in terms of tissue perfusion - Reduced cardiac output - Reduced pressureCongestive heart failure- More blood wants to come into heart than can be pumped out - Venous blood cant get through fast enough and starts accumulating in systemic veins which could lead to venous HT - Increase hydrostatic pressure - No change in oncotic pressure - Decrease in return of volumePreload- How much stretch is being placed in muscle cells - Related to end diastolic volumeStarling's LawThe more preload, the greater the EDV, the better the contraction in myocardial cells, and the higher the cardiac outputWhat happens after a certain point of preload?It produces no increase in cardiac output and the high pressure that lead to the increase in preload produce pulmonary or systemic congestion and/or edemaInotropic drugIncreasing force of contraction ex. DigoxinConotropic drugAlters heart rateAfterload- Amount of work heart has to do to pump blood to destination - Vasodilation decreases resistanceMyocardial failureProblems specifically with the muscles of the heartCirculatory failureProblems with the system as a wholeWhat causes heart failure over a long period of time?- Increased preload - Increased afterload - Reduced myocardial contractibilityTreatment for congestive heart failure- Restriction of salt to lower fluid retention/CV volume (lower preload) - Diuretics - Enhance contraction with inotropic drug (digoxin) - Reduce afterload by reducing resistance in the periphery (ACE inhibitors)Shock- Tissues are not being adequately perfused - Less oxygen delivery - Less clearance of waste - Shift tissue metabolism to anaerobic and produces lactic acidStage I Shock- Compensated - Compensatory mechanisms put the system in a state of (temporary) non-progressionStage II Shock- Progressive - Things get worse as a result of hypo perfusion and organ damage/dysfunctionStage III Shock- Irreversible - Cells have been damaged to the point where nothing can be done to prevent deathHow do most shocks occur?- Reduction in CO and high peripheral resistance - Rapid loss of CO/pressureWhat can shock result from?- Obstruction in the blood supply - Heart problem (not enough volume/pressure) - Circulatory volume problems (bleeding, vomiting, dehydration due to diarrhea) - Blood distribution problems (weird peripheral vasoconstriction)What is cardiogenic shock characterized by?LV dysfunctionWhat are some mechanical defects that could lead to shock?- Acute mitral regurgitation - Septal defectsTreatment for shock- Drugs will not work because it takes too long for the effect of the drug to kick in - Balloon insertion into the atria (inflation/deflation impacts systemic pressure and flow) - Bypass heart and lungs (machine oxygenates blood and pumps it through body)