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Cardiovascular
Pathophysiology 4 - Cardiovascular system
| Question | Answer |
|---|---|
| what is blood | connective tissue that circulates the body |
| what are the three functions of blood | - transport - protection - regulation |
| what does the blood transport | - gases - nutrients - wastes - hormones |
| what does the blood regulate | - temperature - pH - fluid volume |
| how does the blood protect | - protects against blood loss - protects against infection |
| there are two components of blood | plasma (liquid components) and formed elements (solid components) |
| what are the formed elements of blood | - red blood cells (erythrocytes) - white blood cells (leukocytes) - platelets |
| majority of plasma proteins are | albumin |
| name the plasma proteins | - albumin - globulins - fibrinogen |
| describe erythrocytes | - transport gases - biconcave discs - anucleic - no organelles - have hemoglobin - synthesized in bone marrow |
| what are the function of platelets | - assists in blood clotting - releases chemical messengers |
| what is homeostasis | - the stoppage of blood flow |
| list the three stages of homeostasis | 1) vascular constriction 2) formation of the platelet plug 3) Blood coagulation |
| function of aspirin/clopidogrel | - platelet aggregation inhibitors - prevent clot formation |
| list three diseases that ASA and Plavix help treat | - Peripheral artery disease - strokes - myocardial infarctions |
| a primary blood disorder | the problem starts within the blood |
| a secondary blood disorders | the cause agent is not with the blood |
| describe qualitative | cell abnormalities of plasma factor dysfunction |
| describe quantitative | increase/decreased cell production/destruction |
| define anemia | when there is a decrease in oxygen carrying capacity resulting in decreased oxygen to body tissue. it can be from insufficient erythrocytes of decreased hemoglobin |
| etiology/mechanisms of anemia | - blood loss - decreased RBC production - increased RBC destruction - deficiency anemias |
| (name at lease 5) clinical manifestations of anemia | - tiredness - weakness - pale skin - rapid/irregular heart beat - dyspnea - dizziness - lightheadedness - headaches - chest pain - cold hands/feet |
| causes of acute anemia | - surgery - cuts - trauma |
| causes of chronic anemia | - internal bleeding (ulcer) - menstrual issues - chronic infection (AIDS, Cancer, Autoimmune) - inflammation |
| cause of aplastic anemia | ~ 50% is idiopathic -when bone marrow fails to produce RBCs |
| labs that would help identify chronic anemia | - mild anemia - high ferritin - low reticulocytes - low TIBC - low transferrin |
| list a couple causes of hemolytic anemia | - infections - drugs - cancers - autoimmune |
| define normochromatic | normal color of RBCs |
| define hypochromatic | decreased color of RBCs |
| define normocytic | normal RBC size |
| define microcytic | small RBC size |
| define macrocytic | large RBC size |
| why is RBC size and shape important | it gives us information about cause of anemia |
| what is transferrin | - transports iron in blood - measured with Total Iron Binding Capacity (TIBC) |
| TIBC | Total Iron Binding Capacity |
| etiology of sickle cell anemia | - point mutation (recessive trait) - causes abnormal Hemoglobin S (HbS) |
| heterozygous sickle cell | sickle cell trait |
| homozygous sickle cell | sickle cell disease |
| mechanism of sickle cell anemia | - cells become sickled with deoxygenation - increases RBC adhesiveness and adherence |
| clinical manifestations of sickle cell anemia | - blood vessel occlusion - ulcer formation (due to lack of blood flow and ischemia) - **acute chest syndrome** - functional asplenia - hyperbilirubinemia (causing jaundice and gall stones) |
| the leading cause of hospitalization for those with sickle cell anemia | acute chest syndrome |
| symptoms and other clinical presentations related to acute chest syndrome | - atypical pneumonia - pulmonary infarction - dyspnea - chest pain - cough |
| how is sickle cell anemia diagnosed | - hemoglobin electrophoresis - all other hemoglobinopathies are done at birth |
| treatment for sickle cell anemia | - no known treatment - focused on preventing sickling episodes - goal is symptom management |
| describe the treatment for sickle cell symptoms | - immunization is key - hydroxyurea (medication) to promote synthesis of more HbF and less HbS |
| etiology for Thalassemia | - inherited - two types ------ alpha Thalassemia (mostly Asian) ------ beta Thalassemia (mostly Mediterranean European) |
| what is Beta Thalassemia | the deficiency is in the Beta chain |
| what is Alpha Thalassemia | the deficiency is in the alpha chain |
| heterozygous thalassemia | thalassemia minor ---- normal hemoglobin synthesis ---- prevents severe anemia |
| the mechanisms of thalassemia | - increase in erythropoietin secretion - hypochromic and microcytic anemia - decreased synthesis of affected chain - accumulation of affected globulin chain |
| clinical manifestations of thalassemia | - severe growth retardation (if left untreated) - hyperplasia of bone marrow (impairs bone growth) - splenomegaly - osteoporosis - osteopenia - hepatomegaly |
| treatment(s) of thalassemia | - blood transfusions early in life and regularly throughout life (iron overload is a complication of this) - iron chelation therapy (reduces iron overload) |
| how do you treat chronic inflammation anemia | - underlying disease - erythropoietin therapy - iron supplements - blood transfusions |
| etiology/mechanisms of iron deficiency anemia | - loss of iron (through bleeding, chronic or acute, most common cause world wide) - increased demand (pregnancy) - iron deficient diets - chronic blood loss (most common in developed world) |
| chronic blood loss is the most common cause of iron deficiency anemia in the developed world. list at lease 3 causes of this type of anemia | - menses - GI bleed - hemorrhoids - vascular lesion - intestinal polyps - cancer |
| clinical manifestations of iron deficiency anemia | - impaired oxygen transport - fatigue - palpitations - angina - tachycardia - brittle hair/nails - sores in mouth - pica (ice/dirt) |
| how to diagnose iron deficiency anemia | - (on CBC) decrease in hemoglobin - (on CBC) decrease in Hematocrit - decrease in iron stores/serum iron/(most specifically) ferrin levels - increase in total iron binding capacity (TIBC) |
| treatment for iron deficiency anemia | - prevention is key - 0-1 year old ---- avoid cows milk ---- iron fortified diet - 1(+) years ----- iron rich foods and supplements ----- treating chronic blood loss |
| metablastic anemias | vitamin B12 and folic acid deficiencies |
| etiology of B12 deficiency | - B12 and folic acid deficiency (slowly develops, dietary deficiency is rare) - lack of interinsic factor (possibly autoimmune, neoplasms, gastrectomy/ileal resection) |
| what is pernicous anemia | anemia caused by lack of intrinsic factor (produced in stomach) |
| what is the mechanism for B12/folic acid anemia | enlarged RBCs (megaloblastic anemia) |
| what are some clinical presentations of b12/folic acid anemia | - moderate-severe anemia - mild jaundice - neurological changes (like peripheral neuropathy, confusion, dementia) - myelin breakdown |
| how is b12/folic acid anemia diagnosed | - elevated MCV, yet normal MCHC - low serum B12 - schillint test mesure |
| treatment for B12 anemia | - B12 injections for life - high doses orally |
| why is folic acid important for life | required for DNA and RBC maturation |
| how can folic acid be obtained | - found in vegetables, fruit, cereal, meat - absorbed in the intestine - also lost in cooking |
| what is the most common cause of folic acid anemia | - malnutrition - mediation and tumor cells can also block folic acid absorbtion |
| agranulocytosis is the same term as | neutropenia |
| what is neutropenia | - lack of wbc - puts a person at risk for infection |
| etiology of neutropenia | - bone marrow failure - infection/sepsis - medications (chemotherapy) - abscesses |
| list some signs and symptoms of neutropenia | - infections - malaise - chills - fever - weakness -fatigue |
| what is homeostasis | arrest of bleeding |
| 5 steps of homeostasis | 1) vascular spasm (constriction) 2) formation of platelet plug 3) coagulation (clotting) 4) clot retraction 5) clot dissolution |
| what is a thrombus (the most common type of thrombus) | a clot that develops and persists in unbroken vessel (DVT) |
| what is an embolus (the most common types) | -thrombus freely floating in blood stream (pulmonary embolus, cerebral embolism) |
| thrombocytosis | increased platelet |
| arterial thrombus is associated with atherosclerosis and results from ___________________ | - increased platelet number or restricted blood flow with platelet adhesion |
| causes of secondary hypercoagulability states | - increased pro-coagulation factors (increased platelet activity) - decreased anticoagulation factors (conditions that cause increased activity of coagulation pathways) |
| list some causes of bleeding disorders | - platelet coagulation factors - blood vessel structure |
| list three types of thrombocytopenia | - drug-induced thrombocytopenia (DITP) - Heparin Induced Thrombocytopenia (HIT) - Immune Thrombocytopenic Purpura (ITP) |
| DIC stands for | Disseminated Intravascular Coagulation |
| what is DIC | -clots form and simultaneously hemorrhage at the same time |
| etiology of Hemophilia | - X-linked recessive trait - leads to defective clotting factors. |
| clinical presentations of hemophilia | - spontaneous and prolonged bleeding - hematuria - epistaxis - hemarthrosis |
| how is hemophilia treated | - replacing clotting factors - use of drugs to proliferate vW factor or antifibgolytic |
| risk factors for secondary hypercoagulation (atherosclerotic plaque) | - increased cholesterol levels - diabetes - smoking |
| two major characteristics of thrombocytosis | - platelet count > 450k/microL - regulated by a *negative* feedback loop |
| what is erythromelalgia | painful throbbing in fingers caused by occlusion in arterioles |
| secondary thrombocytosis usually occurs because of | a diseased state |
| primary hypercoagulability condition is caused by | - it is inherited - factor V gene (prothrombin gene/factor V Leiden mutation) is the most common |
| the mechanism of the factor V gene in a primary hypercoagulability state | it cannot be activated by protein C |
| what is antiphospholipid syndrome | autoantibodies (mostly IgG) acting against protein -binding phospholipids |
| what are the clinical manifestations of the antiphospholipid syndrome | - arterial thrombin - recurrent miscarriages - thrombocytopenia |
| Hemophilia A | - factor VIII deficiency - X-linked recessive disorder - while it does run in families it can be spontaneous. |
| Hemophilia B | - factor IX deficiency |
| 4 parameters of Cardiac Function | - contractility - preload - After load - heart rate |
| what is contractility | the ability of a heart to change rate of force of contraction without a change in diastolic length |
| what do positive intropic effects do | increase heart contractile force |
| list some things that have a positive intropic effect on the heart (name 3) | - Sympthaetic Nervouse system - afterload - catecholamines - increased heart rate - drugs - intracellular calcium levels |
| what do negative intropic effects do | decrease contractility |
| list 4 things that have a negative intropic effect on the heart | - parasympathetic nervous system - heart failure - hypoxia - drugs |
| what is the frank-starling principle | as end diastolic volume increases then the force of contraction also increases |
| the frank-starling principle fits into which parameter of cardiac function | preload |
| what is preload | the amount of blood volume has to pump with each beat |
| larger preload means | a higher end diastolic volume |
| two major factors effecting preload | - venous return - filling time |
| venous return is affected by | - blood volume - muscular activity and rate |
| filling time is affected by | heart rate |
| what is afterload | - the pressure in the aorta that the ventricles must overcome to eject blood |
| what increases afterload | any factor that restricts blood flow through the arterial system -- vasoconstriction -- hypertension |
| what decreases afterload | vasodilation |
| an increased afterload also increases what | end systolic volume |
| what is ESV | end systolic volume (blood left in ventricles after systole) |
| ejection fraction | end diastolic volume/end systolic volume (should be around 60%) |
| average cardiac output (what is the number and unit) | 4-6 L/minute |
| what does cardiac output measure | volume of blood pumped out of heart per minute |
| how is cardiac output measured | stroke volume (SV) X heart rate (HR) |
| what is stroke volume | the volume of blood expelled by ventricles with each beat |
| how is stroke volume measured | end diastolic volume - end systolic volume |
| what is pericardium | though, thick sac surrounding the heart |
| what is the purpose of the pericardium | - holds heart in place - acts as a barrier to infection |
| what is the septum | the wall that separates the chambers of the heart into right side and left side |
| mitral valve is located | between left atrium and left ventricle |
| mitral valve is also called | bicuspid valve |
| where is the tricuspid valve located | right side (between atrium and ventricle) |
| route of the electrical signal that creates a heart beat | - Sinoatrial (SA) node - atrioventricular (AV) node - Bundle of His - Perkinje fibers |
| what is cardiac reserves | max % of cardiac output that can be achieved above normal resting level (300-400%) |
| what is ejection fraction | the amount of blood pumped out of the heart with head ventricular contraction |
| what are the two parts of the circulatory system | - pulmonary circulation - systemic circulation |
| what are hemodynamics | principles that regulate blood flow |
| what are the three factors of hemodynamics | - pressure - resistance (opposition to blood flow) - flow |
| two factors that affect blood flow | - radius of the blood vessel - blood viscosity (fluid thickness) |
| define compliance | - total quantity of blood that can be stored in a given portion of the circulation for each millimeter of mercury (mmHg) rise in pressure |
| the mathematical relationship between compliance and volume and pressure | - there is a direct relationship between an increase volume and compliance - there is an indirect relationship between increased pressure and compliance |
| what is compliance REALLY measuring | - the ability of a vessel to distend and increase volume with increasing pressure |
| (arteries/veins) are most compliant vessels | veins (they can handle increased volume with minor pressure changes) |
| what is wall tension | the force in the vessel wall that opposes the distending pressure inside the vessel |
| why is blood pressure important | it helps keep a constant flow to the body's vital organs |
| why is hypotension dangerous | it can prevent adequate blood flow to tissue and other organs |
| why is hypertension dangerous | it can be fatal |
| what is pulse pressure | the difference between SBP and DBP |
| what is typical pulse pressure | 40 mmHg |
| what are the two factors that affect blood pressure | - stroke volume - total distensibility of the atrial tree |
| what is mean atrial pressure | - average pressure in the arterial system during a cardiac cycle (~90-100 mmHg) |
| mean atrial pressure is a good indicator of | tissue perfusion |
| how is mean arterial pressure measured | cardiac output (HR x SV) x Perpheral vascular resistance (PVR) |
| neural mechanisms for BP control | autonomic nervous system and barioreceptors (found in the walls of the great vessels and heart, pressure sensitive) |
| list three humoral mechanisms of BP control | - renin-angiotensin-aldostrone system - vasopressin (ADH) - epinephrine/norepinephrine |
| baroreceptors measure | - changes in heart rate - rate of contraction - vascular smooth muscle tone |
| the humoral mechanism that has a *major* role in BP control | renin-angiotensin-aldostrone system |
| process of the renin-angiotensin-aldostrone system | - renin released by kidneys - renin converted to angiotension I in blood stream - angiotension I converted to angiotension II in lungs - angiotension II vasoconstricts and stimulates adrenal cortex - adrenal cortex releases aldostrone - Na+ retention |
| what is the trigger for renin release | - changes in extracellular fluid - changes in sodium levels - decrease in BP - increase in sympathetic activity |
| what converts angiotension I to angiotesin II | angiotensin converting enzyme |
| target organ(s) of angiotension II | -smooth muscles of vessels - adrenal cortex |
| function of aldostrone | increase salt and water retention by the kidneys (increasing BP as a secondary effect) |
| great long term regulation of BP | renin-angiotensin-aldostrone system |
| what is vasopressin | antidiuretic hormone |
| what is the trigger for ADH release | decrease in BP |
| what is ADH released from | posterior pituitary |
| what is the function of vasopressin | vasoconstriction |
| what is the target organ of vasopressin | - tubules of kidneys - smooth muscle of arterioles |
| epinephrine an norepinephrine come from | the adrenal medulla (when stimulated by the sympathetic nervous system) |
| what is the function of the catecholamines | - vasoconstriction - increase heart rate - increase contractility - increased BP is a secondary effect to the above functions |
| many blood pressure meds focus on what | increased sodium and water elimination by the kidneys |
| what is the etiology of hyperlipidemia | (multifactoral in nature) bottom line: excess LDL and cholesterol levels in the blood |
| what is(are) the mechanisms of the hyperlipidemia | - excess lipids in blood - genetic defects in apoprotiens - low ldl receptor availability - low hdl levels |
| why is excess lipids in blood stream (hyperlipidemia) a problem | it is a major contributor to atherosclerosis and risk factor for heart attack and stroke |
| what are some clinical manifestations of hyperlipidemia | - high ldl levels - xanthomas - appearance of atherosclerosis |
| what are xanthomas | cholesterol deposits (around tendons) |
| list the 5 types of lipoprotiens | - chylomicrons - very-low-density lipoprotien (VLDL) - intermediate-density lipoprotien (IDL) - low-density lipoprotein (LDL) - high-density lipoprotein (HDL) |
| which lipoprotein is good and which one is bad cholesterol | HDL is good, LDL is bad |
| what are the function of apoprotiens | play a role in mediating removal of lipids from blood stream |
| function of VLDL | carry triglycerides in blood stream |
| where are lipoproteins synthesized | small intestine and liver |
| what is the function of HDL | carries cholesterol away from peripheral tissue and back to the liver for excretion. this helps atherosclerosis and lowers risk |
| what is primary hyperlipidemia | - elevated cholesterol that develops independently of other health problems (ie skinny lifestyle blogger/influencer with 5 stents) |
| what is secondary hyperlipidemia | assosicated with other problems and behaviors (ie morbid obesity, decreased thyroid function) |
| familial hyperlipidemia | - autosomal dominant disorders - deficiency/defective LDL receptors |
| heterozygous familial hyperlipidemia | LDL will be roughly 250-500 mg/dL |
| homozygous familial hyperlipidemia | LDL will be roughly 1000 mg/dL |
| what are three medication classes that can elevate lipids | - beta blockers - estrogens - protease inhibitors (HIV medication) |
| how is hyperlipidemia diagnosed | lipid panel labs |
| how is hyperlipidemia treated | - dietary and lifestyle changes (1st) - pharmaceutical therapy (2nd) |
| list 4 risk factors for hyperlipidemia | - smoking - HTN - family history - HDL < 40 mg/dL |
| list the 5 classes of hyperlipidemia drugs | - HMG CoA reductase inhibitors (statins) - bile acid-binding resins - cholesterol absorption inhibitor agents - niacin - fibrates |
| how do HMG CoA reductase inhibitors (statins) work to lower cholesterol | - reduce/block hepatic synthesis of cholesterol |
| how do bile acid-binding resins work to lower cholesterol | - bind and sequester cholesterol-containing bile acids - usually used in adjunct to statin therapy |
| what drugs are part of the HMG CoA reductase inhibitors | all the statins |
| what drugs are in the class bile-acid-based resins | - cholestyramine - colestipol (petal) - colesevelam (welchol) |
| vitamin B3 | niacin (nicotinic acid) |
| how does niacin work to lower cholesterol | - block synthesis and release of VLDL by liver |
| what medications are part of the fibrate class | - fenofibrates - gemfibrozil |
| what is the function of fenofibrates | lower VLDL |
| what is the etiology of atherosclerosis | - hardening of the arteries - multifactoral causes |
| what is the mechanism of atherosclerosis | - fibrofatty lesions in lining of arteries (macrophages play a large role in this) |
| what are clinical manifestations of atherosclerosis | - usually many are not aware they have it until after a medical emergency presents itself - is arterial stenosis - production of ischemia - sudden vessel obstruction (due to plaque hemorrhage or rupture) (many others) |
| the most common arteries affected by atheroscerosis feed which organs | - brain - heart - kidneys - legs - small intestine |
| name at least 5 risk factors for atherosclerosis | - hyperlipidemia - obesity - smoking - visceral fat - DM I/II - HTN - increased age - family history - gender - elevated CRP - elevated serum lipoproteins |
| three lesion types of atherosclerosis | - fatty streak (mostly in children) - fibrous atheromatous plaques - complicated lesions |
| describe the fatty streaks | - thin, flat, yellow lines - present in childhood - asymptomatic |
| describe fibrous atheromatous plaques | the basic lesion of clinical atherosclerosis --- increased size = increased occlusion |
| describe complicated lesions | - lesions that break open (hemorrhage, ulcer, or scar) - thrombus formation (causes turbulence, occulsions, weakened arteries, and aneurysm developments) |
| Hypertension stage 1 definition | 130-139 OR 80-89 |
| hypertension stage 2 definition | >= 140 OR >= 90 |
| hypertensive urgency definition | >180 and or >120 |
| hypertensive emergency definition | > 180 + organ damage and or >120 + organ damage |
| non-modifiable risk factors for HTN | -family history - age related - race - some diseases (renal disease, renal artery stenosis, endocrine disorders (aldosteronism)) |
| modifiable risk factors for HTN (name at least 5) | - high salt intake - obesity - excessive calorie intake - alcohol abuse - low potassium intake - insulin resistance - DMII - hyperlipidemia - Sleep apnea - some drugs |
| tips for preventing HTN | - avoid processed foods - drop 10 lb (if obesity is a factor) - decrease alcohol abuse - increase potassium (found in many fruits and veggies) |
| how potassium helps with HTN | - helps secrete sodium in kidneys - suppresses the renin-angiotension- aldostrone system |
| prolonged HTN can lead to | - LVH - nephrosclerosis (hypofunctions of glomerulous) - worsened DMII neuropathy - can also effect eyes, blood vessels, and kidneys and lead to target organ damage |
| how is htn diagnosed | - repeated BP measurements - lab tests (to rule out possible primary causes) |
| how is HTN treated | - lifestyle changes (modifiable risk factors...1st) - DASH diet (lost of fruits and veggies, whole grains, low dietary fats) - weight loss - increased physical activity - medications |
| list the classes of HTN drugs | - diuretics - ACE inhibitors - ARBs - calcium channel receptor blockers |
| what drugs are in the diuretics | thiazides |
| function of diuretics | - decreased CO, renal reabsorption of sodium (water follows sodium), peripheral vascular resistance |
| name the ACE inhibitors | the -prils (ramipril, lisinopril, |
| function of ACE inhibitors | prevent conversion of angiotensin I to angiotensin II |
| name the ARBs | the -sartans (losartan, valsartan, olmesartan) |
| function of the ARBs | prevent angiotensin II from binding to angiotension II receptors |
| function of the calcium channel receptor blockers | inhibit movement of calcium into the cardiac and vascular muscles |
| effects of the ACE inhibitors | - reduces vasoconstriction, aldosterone release, intrarenal blood flow, GFR |
| effects of ARBs | decreases peripheral resistance |
| effects of calcium channel receptor blockers | - decreased vasoconstriction, cardiac contractility, heart rate, cardiac output, venous return |
| what is the etiology of coronary artery disease | impaired cardiac blood flow |
| what are the mechanisms of coronary artery disease | - atherosclerosis - myocardial ischemia |
| how is CAD diagnosed | - EKG changes - stress testing - cardiac cath - angiography - echo - dopplers - mri - ct |
| risk factors for CAD | - smoking - chronic htn - diabetes - obesity - decreased physical activity - increased LDL - decreased HDL |
| main arteries of the heart | - left coronary artery (becomes the circumflex and left anterior descending) - righte coronary arteries (posterior descending) |
| what are the determinants of myocardial oxygen demand (MVO) | - heart rate (mist important factor) - left ventricular contractility - systolic pressure/myocardial tension |
| what happens to cardiac oxygen demand with increase cardiac contractility | oxygen demand is increased |
| what does an EKG measure | - electrical potential of a cardiac cycle |
| what does a 12 lead EKG help diagnose | - conduction defects - arrhythmias - electrolyte imbalances - drug effects - genetic electrical or structural abnormalities |
| what is the function of stress testing | - determine how the heart functions under stress |
| what is the function of an echocardiogram | - structure and function of the heart - mechanics of a heart beat |
| what is the function of a cardiac cath | an invasive procedure |
| name the two types of CAD | - acute coronary syndrome (ACS) - chronic ischemic heart disease |
| this type of CAD covers a wide range of acute ischemic disease (from unstable angina to MI( | acute coronary syndrome (ACS) |
| what is chronic ischemic heart disease | - recurrent/transient episodes of myocardial ischemia and stable angina |
| what causes chronic ischemic heart disease | narrowing of coronary artery lumen through - atherosclerosis - vasospasms |
| types of atherosclerotic lesions | - fixed/stable plaque - unstable/vulnerable plaque (high risk plaque) |
| what type of atherosclerotic lesion will produced stable angina | fixed/stable plaque |
| problems with unstable/vulnerable plaque | - can rupture - can cause platelet adhesion - thrombus formation |
| cardiac function is determined by | how the supply (oxygenated blood) meets the demand (myocardial demand for Oxygen) |
| what is stable angina | - chest pain/tightness/discomfort and or shortness of breath with exertion and relieves with rest or nitro |
| what does stable angina mean | > 70% stenosis of a coronary artery |
| what is unstable angina | chest pain/tightness/discomfort without exertion and does NOT relieve with nitro or rest |
| what does unstable angina mean | total occlusion of at least one coronary artery |
| layman's term for myocardial infarction | heart attack |
| (physiologically) what is a myocardial infarction | portion of myocardial death |
| clinical manifestations of acute MI | - unstable angina (sometimes present in jaw, left arm, or neck) - dyspnea - nausea/vomiting - sweating - EKG changes - elevated troponin - elevated creatine kinase MB (CKMB) - other visible signs of distress |
| in an MI situation, what is the goal of a medical provider | reprofuse the myocardium |
| the goal for medical personnel is to reprofuse the myocardium after an MI, how is this accomplished | - thrombolytic drugs - surgical procedures - other treatments |
| thrombolytic drugs used for MI | -streptokinase - tissue plasminogen activator (tPA) |
| some invasive procedures to treat an MI | - Cardiac stenting - angioplasty - CABG |
| list some treatments used to help treat an MI | - Oxygen - ASA - nitrates - pain meds - antiplatelet therapy - anticoagulant therapy - betablockers |
| death after an MI | - within 1 hour after 1st symptom - caused by fatal arrhythmias |
| treatment approaches for CAD | - decrease heart demand for oxygen - increase vasodilation of coronary vessels |
| function of beta blockers with CAD | decreased heart demands for Oxygen |
| function of calcium channel blockers with CAD | - mostly decrease heart demand for Oxygen - also helps with decreasing vasospasms |
| function of nitrates with CAD | - vasodilate coronary arteries - decreases both preload and afterload |
| describe hypertrophic cardiomyopathies | _ LVH with disproportionate thickening of interventricular septum - most common cause of death of young athletes |
| describe dilated cardiomyopathies (DCM) | - common cause of heart failure - leading indication for heart transplant - dilation of ALL chambers - decreased wall thickness - decreased systolic function |
| describe restrictive cardiomyopathy | - infiltrative processes within myocardium - caused by ----- amyloidosis ----- sarcoidosis - can be right or left |
| describe myocarditis (inflammatory cardiomyopathy) | - viral causes (coxsackie B virus) |
| signs and symptoms of | - fever - myalgias - dyspnea on exertion - hemodynamic collapse - sudden death |
| what are arrhythmias | - abnormal heart rhythms - uncoordinated electrical conduction = uncontrolled contraction |
| normal sinus rhythm | 60-100 bpm |
| bradycardia | < 60 bpm |
| tachycardia | > 100 bpm |
| list some atrial arrhythmias | - PAC's - multifocal and focal atrial tachycardia - a flutter - a fib |
| list some ventrical arrhythmias | - PVC - V. Tach - V. fib |
| what is multifocal atrial tachycardia | - irregular p wave intervals - seen in pulmonary disease |
| describe paroxysmal atrial tachycardia | - focal atrial tachycardia - starts and ends suddenly |
| describe a flutter | - reentrant circuit that is on a loop - atrial rate 200-400 bpm |
| describe a fib | - reentrant circuits spinning around - no discernible P waves - most common chronic arrhythmia |
| describe pvc | - ectopic ventricular pacemaker - compensatory pause ----- after pvc and prior to the normal sinus rhythm |
| describe vtach | - reentrant circuit - seen with ----- MI - rate 70-250 bpm - dangerous rhythms |
| describe v fib | - multiple reentrant circuit - more uncoordinated than Vtach - (without intervention) results in sudden death |
| etiology of heart failure | - functional/structural impairment of ventricular filling/ejection - low cardiac input/output |
| diseases that can cause heart failure | - CAD - HTN - Dilated cardiomyopathy - valvular diseases |
| mechanisms of systolic heart failure | - impaired ejection during systole - inability to contract efficiently - produce volume overload |
| mechanism of diastolic heart failure | - impaired filling capacity during diastole - impeded expansion of ventricle - |
| mechanism of right sided heart failure | - decreased ability of right ventricle - peripheral edema - measured through daily weight checks - most commonly caused by left ventricular failure |
| mechanism of left sided heart failure | - decreased ability for blood to be ejected from left ventricle - decreased cardiac output - blood accumulates in heart and lungs |
| what are the most common causes for left sided heart failure | -MI - HTN - valve stenosis or regurgitation ------ aortic valve ------ mitral valve |
| what are the clinical manifestations of right sided heart failure | - peripheral edema - hepatomegaly - ascites - enlarged spleen |
| what are the clinical manifestations of left sided heart failure | - blood accumulation in the heart - blood accumulation in the lungs |
| what are some clinical manifestations of heart failure (in general) | - SOB - fatigue - weakness - orthopnea (SOB while lying flat) - paroxysmal nocturnal dyspnea (SOB/cough at night) - limited activity tolerance - fluid retention - increased jugular venous pressure - ascites - cyanosis |
| list some mechanisms for heart preservation during heart failure | - Frank-starling mechanism - activation of the SNS - renin-angiotensin-aldosterone mechanism (vasoconstriction) - natriuretic peptides - endothelins - myocardial hypertrophy + remodeling |
| how does the frank-starling mechanism help preserve the heart | - increases muscle stretch (intropy) |
| how does activation of the SNS help preserve the heart | - more immediate - increases heart rate - increases cardiac output |
| how doe the renin-angiotensin-aldosterone mechanism help preserve the heart | - decreases cardiac output - decreases renal blood flow - increases sodium and water retention |
| name the two natriuretic peptides | - atrial natriuretic peptide (ANP) - brain natriuretic peptide (BNP) |
| how do the natriuretic peptides preserve the heart | - both are diuretics (release sodium) - both (ANP and BNP) are elevated in heart failure patients |
| how do endothelins help preserve the heart | - vasoconstrictor peptides - from the endothelial cells |
| how is heart failure diagnosed | - H+ P - lab studies - ekg studies - CXR studies (shows enlarged heart) - echo studies |
| how do lab tests show heart failure | they can show - anemia - electrolyte imbalances - chronic liver congestion |
| how doe echos diagnose heart failure | - assess left ventricle wall ------ motion ------ thickness ------ chamber size - valve function - heart defects - ejection fraction - pericardial disease |
| how does a physical help diagnose heart failure | - heart sounds - bp level - jugular vein congestion - lung congestion - BLE edema |
| how does a CXR help diagnose heart failure | - measures heart size - measures heart shape - pulmonary vasculature |
| what are the goals of heart failure treatment | - relieve symptoms - improve quality of life - reduce/eliminate risk factors |
| how is heart failure treated | - exercise training - sodium and fluid restriction - weight management - pharmacological assistance |
| list the pharmacological classes used to help treat heart failure | - diuretics - ACE inhibitors - angiotensin II receptor blockers - beta blockers - digoxin - vasodilators |
| function of diuretics with heart failure treatment | - fluid excretion - decreased preload |
| the function of both ACE inhibitors and angiotensin II receptor blockers in heart failure treatment | - prevent angiotensin from being converted to angiotensin II - decrease vasoconstriction - decrease aldosterone production - Na and water retention in kidneys - dilates arteries - decreases afterload |
| the function of beta blockers in treating heart failure | - decrease left ventricular dysfunction - prevents actuation of SNS - decrease ventricular rate |
| the function of digoxin in treating heart failure | - increase force and strength of ventricular contraction - decreased heart rate - increased diastolic filling time |
| etiology of cardiogenic shock | - the heart fails to pump properly - most common cause is an MI |
| what are the mechanisms of cardiogenic shock | - decreased CO - hypotension - hypoperfusion (low oxygen perfusion) - tissue hypoxia - decreased SV - increased vascular resistance - increased fluid retention (renin-angiotensin-aldosterone sys) |
| clinical presentations of cardiogenic shock | - hypoperfusion (decreased O2 levels) - hypotension - cyanosis - decreased urine output - neurological changes (poor cerebral perfusion) |
| treatment of cardiogenic shock | - improve CO - decrease workload of myocardium - increased coronary perfusion - maintain fluid load - correct/prevent arrhythmias and pulmonary edemas - increase vasodilation - increase BP - decrease ventricular wall tension |
| medication used for cardiogenic shock | - vasodilators ----- nitroprusside ----- nitroglycerin |
| function of vasodilator medications in cardiogenic shock patients | - increased O2 delivery to myocardium - decreased venous return |
Created by:
kandriot
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