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83 Cards in this Set
- Front
- Back
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-a continuum of disorders that eventually lead to the inability of the heart to meet the needs of the peripheral organs for blood flow or its inability to meet those needs without compensatory mechanisms
-formerly known as CHF -affects about 5 million people in the US -kills about 260,000 US citizens each year -numbers are expected to double in next 40 years -half or more pts will be dead within 5 years of diagnosis -risk factors: age, obesity (poor diet and lack of exercise), smoking, alcohol abuse, HTN, DM esp with retinopathy, dyslipidemia, high sensititvity CRP |
Heart Failure
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-stage of HF
-pts with risk factors but without structural heart disease or symptoms -just high risk factor |
Stage A
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-stage of HF
-pts with structure heart disease, but no signs or symptoms of failure -dr notices something is changing but pt has no sx |
Stage B
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-stage of HF
-pts with current or past symptoms of heart failure such as shortness of breath |
Stage C
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-stage of HF
-pts with refractory heart failure who might be eligible for specialized tx strategies |
Stage D
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Most common causes of HF - 3
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1 - Ischemia Heart Disease - 35-40%
2 - Cardiomyopathy - 30-34% 3 - HTN 15-20% |
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-progressive breathlessness
--> exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, dyspnea at rest, acute pulmonary edema: pulmonary congestion and rales, nocturnal cough that may recover bloody sputum -fatigue -nocturia -cerebal symptoms from hypoxia: confusion, anxiety, nightmares, memory loss, and even delirium -caridac edema: sign of right side failure -peripheral edema esp in lower extremities -reduced renal perfusion and increased blood volume -anorexia - unkown reason, hepatic congestion -peripheral cyanosis -tachycardia -additional heart sounds |
Signs and Symptoms of HF
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-normal heart sound
-closure of the mitral and tricuspid valves |
S1
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-normal heart sound
-closure of pulmonic and aortic vavles |
S2
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-abnormal heart sound
-early diastolic sound -rapid filling of ventricles causes sound in dilated chamber -ventricular gallop -sloshing in -lub dupa |
S3
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-abnormal heart sound
-late diastolic sound -loss of compliance of chamber walls -stiff ventricle and when atrium wants to fill it with blood and needs that extra beat to do this -assoc with hypertrophy -atrial gallop -ta lup dup -a stiff wall |
S4
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-HF syndrome
-most common causes are ischemia heart disease, HTN, aortic and mitral valve disease, cardiomyopathies -left chamber is usually dilated -LV cant keep pace with venous return from lungs- |
Left Heart Failure
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-type of HF syndrome
-most common causes are left heart failure, lung diseases that cause pulmonary vascular bed such as COPD and pulmonary emboli, and tricuspid or pulmonic valve disease -kind of a slacker |
Right heart failure
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-type of heart failure
-high CO that is unable to maintain tissue perfusion -thyrotoxicosis -pregnancy -chronic severe anemia |
High output heart failure
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-type of HF
-decreased contractility or increased afterload -MI -increased systolic pressure: HTN and aortic stenosis -cardiomyopathies: toxic (drugs, alcohol), and idiopathic (viral infection implicated) |
Systolic HF
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-type of HF
-abnormal relaxation -impaired active relaxation: impaired Ca uptake into sarcoplasmic reticulum at beginning of diastole, MI -abnormalities in passive filling: stiffness from hypertrophy or infiltration |
Diastolic HF
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-EKG: may be helpful if MI is cause of HF
-chest radiograph for enlargement and lung congestion -echocardiogram for enlargement, valvular disease -cardiac catheterization for assessing valves and exudate individual chambers of heart |
Diagnosis of HF
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-pt and family education
-correct the underlying cauase -vaccination against pneumococcal disease and influenza -dietary salt restriction -adequate rest and avoidance of exertion -some regular exercise to improve exercise capacity |
Tx for all stages of HF
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-part of HF tx for all ages
-the next Vit C -reduce inflammation and sympaathetic stimulation -correct the underlying cause of HF |
Statins
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-type of tx for HF stage B
-lower systemic vascular resistance and venous pressure -decrease level of circulating catecholamines -includes catopril, lisinopril, and enalapril -cheaper |
ACE inhibitors
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-type of tx for HF stage B
-similar to ACEI except to do not produce a cough -can be added to ACEI therapy? -includes valsartan, cadesartan, ibersartan, and losartan |
Angiotensin II receptor antagonists/blockers
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-stage A and B therapies
-ACEI and beta blockers in all patients: carvediol, metoprolol, bisoprolol -diuretics -cardiac glycoside |
Tx for Stage C HF
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-tx for Stage C HF
-start with thiazide and move to loop if dyspnea and edema persist -spironolactone decreases mortality |
Diuretics
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-type of Stage C HF tx
-increase contractility in certain pts -includes Digoxin |
Cardiac Glycoside
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-inotropes
-biventricular pacemaker: in pts with conduction defects or those not responding to therapy -implantable cardioverter defribrillator -left ventricular assist device as bridge to transplantation -cardiac transplantation -stem cell repair - future |
Therapy for Stage D HF
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-part of Stage D HF tx
-increase strength of contraction -beta adrenergic agonists - used as a bridge to transplantation |
Inotropes
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-therapy for part of HF
-oxygen therapy when acute -diuretics: furosemide -morphine sulfate reduces pt anxiety - caution in pts with low systolic BP, respiratory depression can occur -nitroglycerine - vasodilator |
Therapy for Pulmonary Edema
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-imbalance between the cardiac need for oxygenated blood and its supply
-a leading cause of death in US -risk factors: gender susceptibility, males more than females?, HTN and DM, cig smoking, sedentary lifestyple, psychosocial well-being, advancing age, lipoprotein levels, high sensitivity CRP, diet and obesity, migraine HA with aura, work stress, lack of social support, depression, and personality |
Ischemic Heart Disease
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-prevalence of CHD in sexes is equal in older years
-less likely to survive MI -due to different pathophysiology: smaller coronary arteries, endothelial dysfunction where there is a less productionof NO -different risk factors: low estrogen levels, elevated testosterone levels and polycystic ovary syndrome -different prodromal symptoms: fatigue, sleep disturbance, and dyspnea, often there is no previous hx of chest pain -different diagnostic testing: endothelial function, stress echo and SPECT, intravascular ultrasonography |
Ischemic Heart Dx in Women
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-chest pain that results from transient Myocardial ischemia
-may also have pain in neck and jaw |
Angina Pectoris
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-fixed atherosclerotic narrowing that decrease blood supply when demand is increased
-usually provoked by exercise or emotional stress -presents over a few seconds or minutes -lasts 5 to 15 minutes -relieved with rest or sublingual NTG |
Stable or typical angina
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-vasospasm superimposed on fixed stenoses
-occurs more commonly in women -common at night or in early morning hours --> a decrease in amt of NO production in these pts -assoc with cig smoking -may exhibit other signs of arterial hypersensitivity --> migraines, Raynaud's phenomenon -usually relieved by NTG and possibly txed with Ca channel blockers |
Prinzmetal's or variant angina
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-resting and stress EKG
--> abnormal ST segment can be seen during stress because of prolonged polarization from heart injury -stress thalium -echo -cardiac catheterization with angiography |
Diagnosis of AP
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-activity guidelines and weight loss where appropriate
-warning signs that indicate need for medical attention --> discomfort not relieved with 2-3 NTG tablets given 5 min apart -control of risk factors: HTN, DM, hyperlipidemia, smoking -tx underlying conditions: anemia and thyroid disease -medical therapy includes ASA, nitrates, beta blockers, and calcium channels |
Management of AP
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-part of medical therapy of AP
-81 g qd -does not prevent first heart attack in women -less helpful in preventing first heart attack but impt in preventing stroke and second heart attack |
ASA
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-part of medical therapy of AP
-sublingual, oral, dermal, and IV are available -very rapid acting -for venodilation |
Nitrates
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-part of medical therapy of AP
-limit myocardial oxygen demand |
Beta blockers
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-medical therapy for AP
-prevent coronary spasm and for vasodilation |
Calcium channel blockers
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-type of surgical therapy for AP
-less invasive -stenting almost always performed with this -glycoprotein IIB/IIA inhibitors to inhibit platelet aggregation - block a receptor on platelet and decrease ability of platelets to aggregate |
Percutaneous coronary intervention
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-type of surgical therapy for AP
-transplanted vessels bypass blockage -internal mammary arteries -saphenous veins -repeat procedure in 5 years for 5-10% -more for severe or advanced disease |
Coronary artery bypass grafting
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-it includes unstable angina, non ST elevation myocardial infarction, ST-elevation myocardial infarction
-common mechanisms include: rupture or erosion of fibrous cap of coronary artery cap, platelet aggregation and adhesion, thrombus formation and vasoconstriction, and embolization |
Acute Coronary Syndromes
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-change in status of angina - progressive nature is concerning
-basis is usually multifactorial: cornoary AS with progressive luminal narrowing, and fibrous cap erosion with thrombosis of coronary branches -rest pain -intermediate between stable angina and MI -unpredictable onset of rest pain -preinfarction angina |
Unstable or crescendo angina
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-less severe form of MI
-partially occluded coronary artery -no elevation of the ST segment -differentiate from unstable angina --> positive cardiac enzymes in this: troponin I and T, CK, and CK-MB -doesnt expect us to know how to read an EKG -this shows less damage -only partial occlusion of coronary artery in this one |
Non-ST elevation MI
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-more severe type of MI
-ECG changes shows large amt of heart muscle damage -total occlusion of coronary artery -Myocardial necrosis occurs within 15 to 30 min |
ST elevation MI
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-1.5 million with 500,000 deaths each year in US
-many pts dies before reaching hospital -sudden onset of pericardial pain that may radiate to left arm and jaw -pain lasts more than 30 minutes and not relieved with NTG -nausea, diaphoresis, and dyspnea common -about 20% AMI are mild or silent - spells that grandparents have -not relieved with rest or nitroglycerine -weak often thready pulse |
MI
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-physical exam: pt in pain and apprehensive, hypotension and tachycardia may be present
-ECG abnormalities: deep Q waves from loss of ventricular muscle mass, ST segment abnormalities -cardiac enzymes |
Diagnosis of MI
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-morphine sulfate for pain relief
-oxygen -nitroglycerine -ASA - chew -antiarrhthmic therapy if necessary -GP IIB/IIIA inhibitors and PCI if possible or thrombolysis with tissue-type plasminogen activator - given within 3 hours of onset of pain -low molecular weight heparins - enhance the effect of t-PA -induced hypothermia - cool the body to 91.4 degrees for 12 to 24 hours |
Immediate therapy of MI
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-beta blockers reduce arrhthmias and risk of reinfarction
-ACE inhibitors reduce post-infarction remodeling -statins help stabilize plaques -anticoagulants may be necessary -ASA in both men and women to prevent second attack -clopidogrel added to ASA decreases risks for second MI |
Adjunctive therapy of MI
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-part of future therapy of MI
-prevents cell death and limits scar formation -applied to damaged skin and helps skin regenerate |
Thymosin beta-4
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-acute arrythmias and conduction defects - can be fatal
-HF when greater than 30% of myocardium is infarcted -chamber wall defects: ventricular septal defect, ventricular aneurysm, and cardiac rupture |
Complications with MI
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-within 6 hours of sx
-majority are due to coronary heart disease -other causes include valvular diseases, cardiomyopathies, and congenital/developmental disorders |
Sudden cardiac death
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-type of valvular disease
-constriction or narrowing of an orifice |
Stenosis
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-type of valvular dysfunction
-return of blood through heart valve |
Regurgitation
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-type of valvular dysfunction
-a sinking down or protrusion of a tissue - floppy valve |
Prolapse
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-cause: congenital stenosis in men, senile calcific is most common, bicuspid aortic valve (congenital defect that leads to premature calcification by 4th or 5th decades), or rheumatic heart disease
-pathophysiology: pressure overload on left entricle and leads to left ventricular hypertrophy -systolic ejection murmur -soft S2 sound because the aoritc component is absent leaving only the pulmonic component -development of S4 from hypertrophy -no hyperplasia -bulking up of heart muslce leads to a back up in the system -angina occurs in 35 to 50% of pts and 50% die within 5 years if valve is not replaced -syncope with exercise - survival is 2 to 3 years if valve is not replaced -heart failure - 50% die within 1 to 2 years if not corrected |
Aortic stenosis
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-almost all cases are secondary to rheumatic heart disease
-most cases occur in women -back up in pressure in atrium -largely pulmonary problems -things back up in to the right side and then causes failure of right side followed by ventricular failure -impedes left ventricular filling -elevated left atrial pressure is referred to the lungs and results in pulmonary congestion -increased effort required by the right ventricle to propel blood can result in failure -dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea from reduced left ventricular output -edema, ascites, anorexia, and fatigue with right side dysfunction -hemoptysis from rupture of small bronchial veins -embolism as result of stagnant blood in enlarged atrium -hoarseness if large left atrium impinges on laryngeal nerve -diastolic murmur -commissurotomy and balloon valvuloplasty |
Mitral stenosis
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-idiopathic aortic root dilation is the most common cause - possible in HTN but usually with advancing age
-rheumatic heart disease and collagen vascular disease are also causes -regurgitation of part of ventricular volume during diastole --> requires greater stroke volume to compensate for regurgiated amt --> leads to increased pulse pressure and systolic pressure --> can lead to left ventricular dysfunction -left ventricular failure - dyspnea, orthopnea, paroxysmal nocturnal dyspnea -syncope -angina from reduced coronary flow -increased left ventricular size |
Aortic Regurgitation
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-part of AR
-capillary pulsation in nail beds |
Quincke's Sign
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-part of AR
-head bobbing with each heartbeat |
De Musset's sign
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-mitral valve prolapse is a cause - redundant chordae tendinae, usually benign syndrome
-cornary artery disease, rheumatic heart disease, and ruptured chordae tendinae are also causes -increased left atrial pressure -decreased forward Cardiac output -palpitations -left ventricular failure - dyspnea, orthopnea, paroxysmal nocturnal dyspnea -systemic embolization |
Mitral Regurgitation
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-EKG for hypertrophy or arrhythmias
-Echo of suspected valves -catheterization to assess valves and chamber pressures -chest radiography for enlargement |
Diagnosis of Valvular Dysfunction
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-type of surgical therapy for valvular dysfunction
-homograft or allograft -heterograft - durability is limited -mechanical valve -autograft - pulmonic to aorta and homograft for pulmonic |
Valve replacement
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-diuretics to decrease volume overload
-digitalis for contraction and arrhythmias -anticoagulants if risk for embolism -vasodilators to reduce outflow resistance |
Medical therapy of Valvular dysfunction
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-infection of endocardial surface and the valves
-many possible sources --> bacterial: STAPH AUREUS is most common --> fungi: Candida albicans is most common -acute: fever and a new or changed heart murmur -subacute: often very insidious - malaise, murmurs, cardiac failure, splinter hemorrhages of the conj, and Roth Spots -high morbidity and mortality if tx is delayed -blood culture for infection - multiple times separated by 12 hours -echo showing valve dysfunction or abscess -supporting evidence: fever, elevated CRP, history of event that would lead to IE, emboli, hemorrhage, Janeway lesions -tx: IV antibiotics and multidisciplinary hospital care - can take as long as 6 weeks, and surgery might be necessary if extensive valvular damage |
Infective Endocarditis
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-part of infective endocarditis
-historically found -white dot with hemorrhages around it -seen also with diabetes and leukemia |
Roth Spots
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-often down prior to invasive procedures in pts with a hx of valvular disease
-amoxicillin 2-3 po 1 hour before procedure -clindamicin 600mg po 1 hour before procedure if pt is sensitive to PCN |
Prophylaxis tx of Infetive Endocarditis
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-impaired contraction in absence of pressure overload or CAD
-previous viral myocarditis -EtOH abuse -pregnancy related -genetic basis -clinical manifestations related to HF -course is usualy progressive deterioration - 35% die within 5 years, 70% die within 10 years -remove any known contributing offending agent -supportive therapy: salt restriction -digitalis, diuretics, vasodilators, and beta blockers -surgical ventricular restoration: piece of cow heart to strengthen dilated ventricle -cardiac transplantation |
Dilated Cardiomyopathy
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-inappropriate hypertrophy
-decreased ventricular volume and hypercontracting heart -contributory history: most often young adults, strong family hx in more than 50% -exertional dyspnea -angina at rest with exercise -syncope after exercise -SCD possible -medical therapy: beta blockers, digitalis only in end stage of disease when dialtion has occurred -pacemaker and defibrillator implantation -intentional septal infarction to reduce obstruction -myomectomy to reduce thickness of septum |
Hypertrophic Cardiomyopathy
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-broken heart syndrome, stress cardiomyopathy
-non-ischemia cardiomyopathy triggered by emotional stress -occurs primarily in women with no previous heart disease -symtpoms mimic an MI but diagnostic testing is equivocal --> insignificant cardiac enzyme elevation --> normal coronary arteries --> LV ballooning -believed to be result catecholamine effect on microvascular arteries] -may require aggressive therapy upon presentation to ED -completely resolves within several days to weeks --> no residual heart damage -recurrences not reported |
Takotsubo Cardiomyopathy
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-cause is MI, viral infection, SLE, infectious endocarditis, malignancy, radiation, and drugs (INH, procainamide)
-inspiratory chest pain on left side -friction rub during systole and diastole -tx underlying disorder -NSAIDs, steroids or colchicine to try and relieve the inflammation |
Acute Pericarditis
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-cause is inflammation in acute pericarditis
-usually no symptoms, but heart sounds become soft -tx pericarditis -may involve aspiration of fluid |
Pericardial effusion
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-cause is rapid accumulation of fluid from pericarditis that compresses heart and inhibits cardiac filling
-life threatening condition -decreased systolic pressure during inspiration -shock -emergency pericadiocentesis |
Cardiac tamponade
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-cause is thickened pericardium in response to previous inflammation
-dyspnea on exertion and orthopnea -edema, ascites, and hepatic tenderness with jaundice -pericardiectomy - relief of symptoms may not be appreciated for up to 6 weeks |
Constrictive pericarditis
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-atherosclerosis is leading cause
-lumen must be lower than 50-90% before distal flow affected -Bruits are helpful signs but absence doesnt exclude this -one of the most shocking symptoms is loss of vision |
Carotid artery disease
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-part of carotid artery disease
-have increased risk for major stroke and early death -risk of mortality 3 to 5 times greater -risk of stroke is 2 to 3% per year -hollenhorst plaques -amaurosis fugax, or homonymous hemianopsia -hemiparesis, monoparesis, or clumsiness of one limb - numbness, loss of sensation, or paresthesia involving one or both limbs -ataxia - irregularity of voluntary muscle coordination -aphasia -dysarthria -diplopia -vertigo -smoking should be discontinued -alcohol consumption should be limited -dietary changes for obesity and high serum cholesterol -control of blood pressure |
Carotid TIA
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-impairment of ability to speak
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Aphasia
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-difficulty in speech secondary to impairment of the tongue or other muscles essential to speech
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Dysarthria
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-tx option for Carotid artery disease
-carotid artery exposed and plaque is excised -generally reserved for pts with more than 75% occlusion but not 100% -not if permanent neurological defects or total occlusion |
Endarterectomy
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-tx for carotid artery disease
-investigation of combined filter to catch embolic debris |
Carotid artery stent
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-usually the result of atherosclerosis, but also due to thrombosis or embolism
-presenting symptoms are pain and limping while walking, pallor, paralysis, pulselessness, and hair loss -type of peripheral arterial disease -avoid trauma -carefool foot and toe hygiene -cessation of smoking |
Lower limb ischemia
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-part of peripheral arterial disease
-distal neuropathy caused by vascular insufficiency -50 to 75% nontraumatic lower extremity amputations -insensate, poorly perfused foot at risk for ulcers -adequate foot care can help prevent -intensive antibiotics -crutches, wheelchair or bed rest |
Diabetic foot
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-part of peripheral arterial disease
-vasospasm and structural disease of blood vessels - varies from min to hours -prevalens estimated to be 5 to 10% in nonsmokers and up to 22% in premenopausal females -pallor of digits, ears, nose or tongue -cyanosis -erythema from subsequent vasodilation |
Raynaud disease and phenomenon
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-part of peripheral venous disease
-dilated, tortuous superficial veins in the lower extremities -pain usually with periods of standing -can be primary or secondary to vein obstruction -inherited defect - defective valves or vein wall weakness -increase in venous pressure from prolonged standing or lifting -nonsurgical tx: support stockings up to knee, leg elevation, and limit activities involving long periods of standing -surgical tx: sclerotherapy and compression, removal of the varicosity, endovenous laser therapy, radiofreq ablation |
Varicose veins
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