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coronary circ pt 2

patho exam 2

QuestionAnswer
Specific Acute Coronary Syndromes (ACS) Acute form of CAD
Specific Acute Coronary Syndrome types NSTE-ACS, NSTEMI, STEMI
NSTE-ACS non-st-segment elevation acute coronary syndrome
NSTEMI non-st-segment elevation myocardial infarction
STEMI st-segment elevation myocardial infarction
Risk factors of acute coronary syndrome CAD, other triggers still being explored
Shared pathophysiology of acute coronary syndrome CAD most commonly progresses to its acute form, atherosclerotic plaque ruptures, prompts thrombogenesis and blood flow obstruction
Pathogenesis of Acute coronary syndrome sudden imbalance of myocardial oxygen consumption and myocardial demand
stable fixed atherosclerotic plaque is seen in what? stable angina
plaque disruption and platelet aggregation is seen in what? unstable angina
complete occlusion of vessel is seen in what? STEMI
Non-ST-segment elevation acute coronary syndrome NSTEMI and unstable angina
Differences between unstable angina and NSTEMI degree of ischemia that results, whether damage causes release myocardial necrosis biomarkers
myocardial necrosis biomarkers troponin, creatine, kinase-MB, myoglobin
troponin protein on top of myocardium
myoglobin protein that carries O2 located only on inside of muscle
Non-ST-segment elevation acute coronary syndrome pathogenesis atherosclerotic plaque rupture, coronary artery vasoconstriction, myocardial oxygen demand and supply imbalance
Non-ST-segment elevation acute coronary syndrome risk factors cigarette smokin (vasospastic angina)
Non-ST-segment elevation acute coronary syndrome clinical manifestations presentation of unstable angina and NSTEMI similar, severe chest pain lasting more than 20 minutes (even after you sit patient)
Non-ST-segment elevation acute coronary syndrome- emergency medical services needed incase of: chest pain (lasting after patient is sitting), severe dyspnea (patient is sweating), syncope or pre syncope episode, palpitations
Non-ST-segment elevation acute coronary syndrome diagnosis ECG, serial cardiac troponins
Non-ST-segment elevation acute coronary syndrome treatment supplemental oxygen, short acting sublingual nitroglycerin, intravenous nitroglycerin, morphine sulfate, oral beta blockers, high-intensity statin therapy, anti platelet therapy and anticoagulation therapy, invasive strategies
What does nitroglycerin induce? vasodilation, increasing blood flow to the heart
ST-segment elevation myocardial infarction more precise definition of a heart attack, complete blockage of vessel
"STE" meaning in STEMI ECG tracing of ST-segment elevation
"MI" meaning in STEMI myocardial infarction
ST-segment elevation myocardial infarction prevention of death requires rapid: recognition, reperfusion treatment, management (avoid stress or severe exercise)
ST-segment elevation myocardial infarction pathogenesis disruption of atherosclerotic plaque leads to thrombosis and disrupts blood flow, imbalance of myocardial oxygen supply and demand results
ST-segment elevation myocardial infarction causes non-obstructive CAD, coronary artery vasospasm, contusions related to trauma, cocaine abuse, hematologic problems
non obstructive CAD thrombus that was not obstructive but becomes obstructive
coronary artery vasospasms vessels constrict
contusions related to trauma lose a lot of blood, not enough blood to supply heart
cocaine abuse restarts system and blood flow, increases blood flow to brain which is why people can complete more tasks, reduces blood flow to heart
hematologic problems changes in RBC (ex. sickle cell)
ST-segment elevation myocardial infarction risk factors same as for CAD, air pollution, prinzmetal angina, contusions related to trauma to coronary arteries, cocaine abuse, aortic insufficiencies, hematologic problems, atrial fibrillation (embolus)
prinzmetal angina type of variant, no formation of thrombus, but smooth muscle spasms reducing blood flow
ST-segment elevation myocardial infarction clinical manifestations classic chest pain and dyspnea, malaise and fatigue, radiating pain, diaphoresis, dizziness, weakness, palpitations, altered mental status, feeling of doom, tachycardia, bradycardia
ST-segment elevation myocardial infarction diagnosis ECG, cardiac troponins
ST-segment elevation myocardial infarction treatment very invasive, PCI, CABG, anitplatelet therapies, anticoagulation agents, morphine for pain
PCI precutaneous coronary intervention, catheter is placed in the artery to compress the plaque and widen the artery, in most cases a stent is then placed to keep the artery widened
CABG coronary artery bypass grafting, uses vein or artery from another part of the body as a graft providing a new pathway for blood to reach the heart
What usually comes after MI? chronic heart failure
Chronic heart failure treatment palliative care, complete organ transplant, mechanical assist device
palliative care patient rests and monitor heart, cardiac rehabilitation- patient observed while exercising
What happens in chronic heart failure? stroke volume decreases because left ventricular contraction fraction decreases, sometimes can reduce oxygen to other tissues depending on extent of damage to heart
Complications of acute coronary syndrome inflammatory complications, embolic events, mechanical complications
Inflammatory complications of acute coronary syndrome pericarditis, dressler syndrome
embolic events caused by acute coronary syndrome thromboembolism
mechanical complications of acute coronary syndrome mitral regurgitation, ventricular aneurysm and rupture, heart failure, cardiogenic shock
Main complication that causes sudden cardiac death cardiac arrest
cardiac arrest abrupt loss of cardiac function- due to electrical issue SA node can stop functioning stopping electrical impulse generation
dysryhthmias and sudden cardiac death- Cardiac arrest causes acute MI when plaque ruptures, thrombosis completely occludes coronary artery, dysfunction of autonomic nervous system
dysfunction of autonomic nervous system that can cause cardiac arrest development of dysrhythmias, automaticity, absolute refractory period, electrolytes
dysryhthmias and sudden cardiac death- Cardiac arrest clinical manifestations prodromal symptoms angina, dyspnea, weakness , fatigue, palpitations related to dysrhythmias, syncope
dysryhthmias and sudden cardiac death- cardiac arrest clinical manifestations specific to heart disease that occur within hours or minutes of cardiac arrest related to dysrhythmias, ischemia, heart failure, heart skips a beat or is beating hard and fast
main difference in clinical manifestations of cardiac arrest and CAD manifestations of cardiac arrest occur a lot faster
dysryhthmias and sudden cardiac death- Cardiac arrest diagnosis ECG, continual heart monitoring, exercise and stress testing, long-term ECG recording, invasive electrophysiologic studies
long term ECG recording for diagnosis of dysrhythmias and sudden cardiac death most frequently used, holter monitor (most often used), event recorders, implantable loop recorders
dysryhthmias and sudden cardiac death treatment antiarrythmics, anticoagulants, integrated approach using nurse-based, physician supervised care, pacemakers and implantable cardioverter-defibrillators (ICDs), acute situation- assessment and basic life support
pacemakers and implantable cardioverter-defibrillators avoid cardiac arrest, any problems with SA nose and electrical aspects of heart can be resolved with pacemaker
Myocardial rupture related to ischemia of acute MI includes rupture of free walls of left or right ventricle, ventricular septum, left ventricle papillary muscle (includes mitral valve)
ventricular septum very common with newborns, problems with oxygenation
other causes of ventricular rupture blunt or penetrating trauma, abscesses related to infective endocarditis
ventricular aneurysm and rupture complications acute mitral regurgitation, cardiac tamponade
cardiac tamponade increase in fluid in the pericardium cavities
ventricular aneurysm occurs from a defect where? in left or right ventricle wall
ventricular aneurysm due to defect in ventricle wall, it bulges outward during both systole and diastole
what is ventricular aneurysm a result of? MI
Ventricular aneurysm diagnosis systolic murmur, ECG is characterized by ST elevation
ventricular aneurysm treatment aneurysmectomy, management of complications
ventricular septal rupture abnormal opening between left and right ventricles, left-to-right shunting
What does ventricular septal rupture result from? complete coronary artery occlusion with little collateral circulation
What does any problem with the septum result in? mixture of oxygenated and deoxygenated blood
Ventricular septal rupture diagnosis echocardiography with doppler imaging, cardiac catheterization
ventricular septal rupture treatment surgery- closing septum
pericarditis and Dressler syndrome swelling and inflammation of pericarditis
What does pericarditis and dressler syndrome result from? injury
another name for Dressler syndrome post-MI syndrome
dressler syndrome late pericarditis, after an MI there can be a leak of fluid into pericardial cavity that can induce infection
When can dressler syndrome occur? occurs after 2-3 weeks after MI with unknown pathogenesis; autoimmune
pericarditis and dressler syndrome clinical manifestations pleuritic chest pain, pain worse with deep inspiration, coughing, swallowing, or lying in supine position
pleuritic chest pain occurs when the pleura become inflamed
pericarditis swelling and inflammation of the pericardium
pericarditis and dressler syndrome diagnosis ST-segment elevation in all or most of leads with upright or inverted T waves, pericardial effusion on echocardiography or CT scan
Pericarditis and Dressler syndrome treatment hospitalization for management and observation of possible cardiac tamponade, aspirin
cardiac tamponade increased pericardial pressure- blood or fluid buildup between myocardium and pericardium, life threatening
cardiac tamponade causes pericardial effusion related to MI, trauma, infection, cancer, medication side effects, heart failure, radiation, pericarditis, inflammatory disease, PCI, recent cardiac surgery
What does cardiac tamponade affect? diastolis of the heart due to increasing pressure
Cardiac tamponade clinical manifestations systemic and pulmonary hypoperfusion, rapid accumulation of pericardial fluid, slow accumulation of pericardial fluid, pulsus paradoxus
cardiac tamponade clinical manifestations- systemic and pulmonary hyoperfusion dyspnea, edema, oliguria, jugular venous distention, tachypnea, tachycardia
oliguria decrease in amount of urine because patient is losing fluid due to accumulation of fluid in pericardial cavity
What does rapid accumulation of pericardial fluid cause? hypotension- systolic pressure drops, systolic and diastolic pressure will be very close
What does slow accumulation of pericardial fluid cause? edema
cardiac tamponade diagnosis history (chemo/radiotherapy can induce damage), imaging such as echocardiography, CT scan, or MRI
pulsus paradoxus systolic blood pressure drops significantly during inspiration
cardiac tamponade treatment pericardiocentesis, surgical pericardiostomy
pericardiocentesis procedure where they drain the fluid from pericardial cavity and pressure around pericardium decreases so heart can function normally
surgical pericardiostomy stop the leakage into pericardial cavity
what do valvular disorders disrupt? blood flow through atria and ventricles
valvular disorders stenosis, regurgitation, prolapse
stenosis valves can not open properly
regurgitation valve can not close properly, backflow of blood either from ventricular to atrial or coronary artery
prolapse valves become enlarged and do not close properly, increase in backflow of blood
valvular disorders causes CAD and ACS, rheumatic fever
mitral regurgitation as a complication of MI common complication of acute MI, abnormalities of any part of mitral valve apparatus
valvular disorders-mitral regurgitation risk factors older age, female sex, large infarct size, heart failure, history of ACS and/or CAD
valvular disorders-mitral regurgitation clinical manifestations mild to moderate no apparent symptoms
valvular disorders-mitral regurgitation clinical manifestations acute severe shortness of breath, fatigue, new holosystolic murmur, flash pulmonary edema, shock
valvular disorders-mitral regurgitation treatment diuretics, vasodilators, surgical intervention- valve replacement
hardest valve to replace mitral
valvular disorders- mitral regurgitation diagnosis x-ray, auscultation (listen for valve closing), TTE, TEE
TTE transthoracis echocardiogram- ultrasound that creates detailed images of the heart
TEE transesophogeal echocardigram- ultrasound probe inserted into esophagus to create images of the heart
valvular disorders-mitral regurgitation treatment surgical intervention, treatment of coexisting diseases
Created by: camrynfoster
 

 



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