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69 Cards in this Set
- Front
- Back
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Acute Cornary Syndromes
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Include Unstable angina, STEMI, and Non-STEMI.
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Location of Myocardial Infarction and Mortality
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An anterior wall infarction (V2-V4) has a moratlity rate greater than 30 to 40% with in the first year if untreated. An inferior wall myocaridal infarction (II,III, and AVF) has moratliry rate of less than 5% if left untreated.
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Lower Morality and Acute Cornary Syndrome
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Administration of asprin is shown to lower mortality the most. Morphine, oxygen, and nitroglycerine are also given, however, decrease in mortality is not shown with these drugs.
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Managment of Acute Cornary Syndrome and Prioritzation of Treatment
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Which decreases mortality the most and which must be done first.
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Diagnostic Tests and Acute Coronary Syndrome
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EKG must be given at onset of pain, if positive will show elevated ST segment or q wave if older. Myoglobin elevation occurs 1 to 4 hours after chest pain. CK-MB 4-6 hrs after onset of pain, and Troponin I 4 to 6 hrs after onset of pain.
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Troponin Limitations
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Troponin levels will be falsely elevated in the case of kidney failure. Also troponin can not tell the difference between infarction an reinfarction due to being elevated 10 to 14 days after initial event.
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Diagnostic for Reinfarction
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If patient presents with onset of chest pain a few days following intial Acute cornary syndrome check EKG for new ST segment elevations and CK-MB elevation, as CK-MB will have already decreased from initial event. New onset pulmonary edema.
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ICU Monitoring and Acute Conary Syndromes
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The greatest cause of mortality in the days following acute conary syndrome is ventricular tachycardia, therefore, continous monitoring of EKG should be done.
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Treatment of STEMI
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Patient is given chewable asprin. If intolerant to asprin give clopedigrel or pastrugel. Angioplasty should then be performed with in 90 minutes of patient arriving to hospital. Thrombolytics are only to be performed if noth catherization lab is not present at hostpital and nearest one is hours away.
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Complications of PCI
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Rupture upon inflation of balloon. Restenosis. Hematoma at site of entry of into artery (femoral
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CI to Thrombolytics
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Major GI bleed. CNS bleed. Surgery in past 2 weeks. Severe Hypertension. Nonhemorrhagic stroke in the past 6 months.
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Acute Coronary Syndromes and Indications of Heparin Use
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Heparin is used in longterm care anticoagulation therpay following PCI and thrombolytics in STEMI. Used as initial therapy in Non-STEMI and ST-depression.
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Acute Coronary Syndrome and Beta BLockers
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Proven to lower all cause mortality, but not time dependent in causing its maximal effect.
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ST-segment Depression and Treatment
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Heparin is given as initial therapy along with GPIIB/IIIa inhibitors. If patient is not improving, persistent chest pain, S3 gallop or CHF developing, worse EKG changes, and rising troponin levels, then urgen angiorpahy and possibly angioplasty should be done.
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GPIIB/IIIa Inhibtors and Indication of Use
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STEMI that is treated with PCI. Non-STEMI.
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LMWH vs. Heparin in ACS Mortality
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LMWH decreases mortality in non-STEMI more than heparin.
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Wafarin and CCB in ACS
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Wafarin and calcium channel blockers have not shown a decrease in mortality in acute cornary syndromes.
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Bradycardia and AMI
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Bradycardia can form from an acute myocardial infarction due to infarction of SA node. This can lead to Sinus bradycardia or third degree heart block. If cannon A waves are present, indication of of third degree heart block. Form due to atria contracting against closed tricuspid valve.
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Right Ventricular Infarction Presenation and Treatment
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Patient will present with new inferior MI and lungs clear to ausculation due to no blood getting to the lungs. Right ventricle infarction will occur 40% of the time of inferior wall MI. Do not treat with nitroglycerin as it decreases right ventricular filling.
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Beck's Triad
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Decreased arterial pressure. Distant heart sounds. Distended neck veins.
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Valve or Septal Rupture Following MI
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During repair of damaged myocardium 4-7 days after infarct scar tissue is its weakest and may result in damage to the valve or septum. Will result in new onset murmur and pulmonary congestion. Mitral regurge will be heard systollic and radiate to the axilla. Septal damage will result in holosystollic murmur in the tricuspid region. Also increase in oxygen saturation from right atrium to right ventricle.
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Diagnostic Test for Valve or Septal Rupture
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Echocardiogram.
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Aneurysms and Mural Thrombus Diagnostic and Treatment
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Aneurysms and Mural thrombus are complications of infarcts. Diagnostic test include echocardiogram and heparin anticoagulant treatment to prevent mural thrombus formation.
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Detection of Persistant Ischemia and Discharge
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All patients get stress test done prior to discharge, including post-MI. This will determine the need for angiography. However, do not doe a stress test if patient is symptomatic (constant chest pain).
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Medication Post Infarction for Discharge
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Patient should be started on asprin, metoprolol, ACE inhibitors (particularly anterior wall MI), and statins. DO NOT give phrophylatic antiarrythmic.
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Sexual Issues and Post Myocardial Infarction
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Person can participate in sexual activity immediately following MI. Erectile dysfunction typically occurs due to anxiety, however, adverse effect of beta blockers is erectile dysfunction. If post MI stress test is normal can perform any excersie.
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Cardiomyopathy
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Is a patholgy that results in abnormally contracting or relaxing myocardium. Can be caused by dilated, hypertrophic, or restrictive cardiomyopathy that leads to vavular and ascultory dysfunctions.
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Hypertrophic Cardiomyopathy Synomyns
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Diastolic dysfunction. Cardiac failure with perserved ejection fraction.
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Dilated Cardiomyopathy Synonyms
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Low ejection fraction. Systollic Dysfunction.
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General Presenation of Cardiomyopathy
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All present with shortness of breath. Also the presence of distened JVP, rales, and peripheral edema maybe present.
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Diagnostic Test for Cardiomyopathy
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The best is echocardiogram.
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Treatment for Cardiomyopathy
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Generally all cardiomyopathies are treated with diuretics. Each type of cardiomyopathy has its own form of treatment.
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Causes of Dilated Cardiomyopathy
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Alcohol. Infarction. Doxorubicin. Viral myocarditis. Chagas Disease.
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Presentation of Diastolic Heart Failure
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Shortness of breath will be present along with distended JVP, rales, and peripheral edema. Also S3 heart sound may be present and dyspnea.
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Diagnostic of Dilated Cardiomyopathy
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Echocardiogram. Chest X-ray. EKG for old infarcts.
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Treatment of Dilated Cardiomyopathy
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Treated with ACE. Beta Blockers (metoprolol and carvedilol). Diuretics. In acute decompensation digoxin is used.
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QRS >120ms and Dilated Cardiomyopathy Treatment
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Must use biventricular pacemaker.
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HCM
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Is hypertrophic cardiomyopathy that is caused by the myocardium thickening in response to stress such as increased blood pressure. The thickening of the myocardium causes decrease in relaxation, therefore, smaller chamber size. Diastolic dysfunction occurs.
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HOCM
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Is hypertrophic cardiomyopathy that occurs due to a genetic disorer that results in thickening of myocardium.
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Presentation of Hypertrophic Cardiomyopathy
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Shortness of breath will be present as will distened JVP, rales, and peripheral edema. However, these symptoms will be much less and there will be an S4 heart gallop heard.
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Hypertrophic Obstructive Cardiomyopathy Presentation
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Dyspnea will be present like other forms of cardiomyopathy, however, syncope and sudden death occur more frequently. Obstruction worsens with anything that increases heart rate like exercise and dehydation. Worsened by drugs that decrease chamber such as ACE, hydralizine, and valsalva.
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Treatment of HCM or HOCM
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Beta blockers are good intial treatment. Negative inotropic effects such as verampril or disopyrmide will help. Diuretics may help in HCM, but not in hypertrophic obstructive cardiomyopathy. ACE unclear benifit in HCM, BUT DOESN NOT WORK IN HOCM. HOCM also should be treated with implanted defibilator in patients with syncope. Myomectomy.
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Systolic Anterior Motion of Mitral Valve
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Symptomatic of HOCM.
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EKG and HOCM
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Left ventricular hypertrophy findings, but can be nomral in 25% of patients.
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Causes of Restrictive Cardiomyopathy
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Sarcoidosis. Amyloidosis. Endomyocardial fibrosis. Hemochromatosis.
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Presentation of Restrictive Cardiomyopathy
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Dyspnea and signs of right sided heart failure: Ascites. Kussmal Sign. Distended JVP. Peripheral edema.
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Kussmal Sign
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Is distended JVP upon inhalation.
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Diagnostic Test of Restrictive Cardiomyopathy
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Echocardiogram is the best diagnostic, which may show normal or elevated ejection fraction. EKG will show low amplitude. Biopsy will be done elsewhere in body for amyloidosis or hemachromatosis.
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Valsva/Standing and Murmurs
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Valsava increase intrathoracic pressure and standing increases leg vein capacitence, therefore, both decreasing the venous return to the heart. This is similar to the action of diuretics. Therefore, less blood pressure in the heart will decrease all stenotic and regurgetant murmurs. HCM and MVP will be increased by these manuvers and diuretics
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Handgrip and Murmurs
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When hand grip occurs there is an increase in total peripheral resistance, therefore, the afterload increases on the heart. In the case reguratation murmus the murmur will increase. In the case of stenosis, particularly aortic, the increased afterload will decrease the murmur as less blood leaves the left ventricle. Amyl nitrate and ACE inhibitors work in the opposite to the hand grip by decreasing afterload, thefore, stenosis increases as more blood enteres the aorta. Mitral stenosis is less effected. Hand grip decreases MVP and HOCM, while amyl nitrate increases.
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Causes of Pericarditis
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Infection. Inflammatory. Connective Tissue Disorder. Trauma. Cancer.
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Causes of Infective Percarditis
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Viral is the most common, but Staphylcoccus and streptococcus, and fungi can also cause.
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Connective Tissue Disorder and Pericarditis
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SLE. Wegners Granulamtosis. Rheumatoid Arthritis. Good Pasture Syndrome. Polyarteritis nodosa.
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Clinical Presentation of Pericarditis
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Patient presents with chest pain that changes with intesity on inspiration and worsens upon laying down and becomes better upon sitting up. EKG will show PR interval depression and ST segment elevation in all leads. However, echocardiogram is the most appropriate as it will show tamponde with greatest sensitivity.
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Diagnostic Tests of Pericarditis
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EKG in tamponade will show electrical alternans. Chest x-ray will show increased cardiac shadow in both directions resulting in globular heart. Echocardiogram will show right atrial and ventricular diastolic collapse.
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Treatment of Pericardial Tamponde
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Pericadialcentisis. Intravenous fluids. Window in pericadrium for reccurent cases.
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Presenation of Constrictive Pericarditis
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Constrictive pericaditis can result in calficiation and firbrosis due to any cause of pericarditis. As the right side of the heart is affected first patient will present with right sided heart failure symptoms such as distended JVP, kussmauls sign, edema, ascites, and enlarged liver and spleen. Heart "knock" may be heard on ausculation.
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Diagnostics and Constrictive Pericarditis
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Chest X-ray will show calcification and fibrosis. CT and MRI are better, but are done after chest x-ray. Echocardiogram can tell the difference between right sided heart failure and constrictive pericarditis as heart wall will move normally in constrictive pericarditis.
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Risk Factors for Peripheral Arterial Disease
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Smoking. Diabetes. Hypertension. Hyperlipidemia.
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Clinical Presentation of Peripheral Arterial Disease
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Patient will complain of pain in calfs upon exertion. Also tropic changes will occur that will result in shiny smooth legs as hair follicles, sebceous glands, and sweat glands are lost.
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Diagnostic Test of Peripheral Arterial Disease
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Ankle brachial index.
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Treatment of Peripheral Arterial Disease
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Asprin. Cessation of Smoking. Cilostazol.
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Treatment of Idopathic Pericarditis
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Typically idopathic pericarditis is diagnosed as viral, typically coxackie virus B, and treated with NSAIDS.
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Pericardial Tamponade
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Almost all causes of pericarditis can lead to fluid in the pericardial sac. As little as 50mL can cause compression on the right side of the heart chambers, however, if slow accumlation as much as 2L can accumlate in the pericardium. Blood can also accumlate due to trauma, this requires emergent thoracotomy.
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Clinical Presenation of Aortic Disection
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Pain between shoulder blades and difference in pressure between arms. May have a history of high blood pressure or smoking. Associated with marfan syndrome.
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Diagnostic Test and Aortic Disection
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Best initial test is the chest x-ray as it may show widening of the mediastinum. The most accurate test in the angiogram, however, may cause allergic reaction and kidney failure.
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Treatment of Aortic Dissection
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Beta blockers given first to decrease shearing forces on the heart. Nitroprusside is then given to decrease venous return to the heart. Surgical intervention.
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Screening Test for Aortic Aneurysm
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Ultrasound for men over 65 who have ever smoked. Although patients above 65 with new onset back pain should be screen with ultrasound to rule out abdominal aortic aneurysm.
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Peripartum Cardiomyopathy
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Is when the pregnant woman produces antibodies against the myocardium. This leads to left ventricular dysfunction. Treat with ACE inhibitors, Beta Blockers, Spirinolactone, and diuretics.
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