CHAPTER 28– CARDIOLOGY Flashcards
Canadian cardiovascular scale
class 1 = angina with strenuous or protracted activity Class II =occasional angina with normal daily activities EG climbing stairs Class III =marked limitation of activities and pain with everyday activities Class IV =symptoms at rest
unstable angina
= non-ST elevation myocardial infarction
–Generally due to formation of nonocclusive thrombus at site of rupture of surface or of atherosclerotic plaque
–Thrombus progresses until includes blood cell vessel or embolizes to distal vessels
–Sudden onset unrelated to precipitating event is Hallmark
acute myocardial infarction with ST segment elevation
–abrupt onset of unremittent chest pain
–Usually with dyspnea diaphoresis and sense of doom
–Usually caused by abrupt occlusion of coronary artery I thrombus at site of ruptured atherosclerotic plaque
–EKG shows ST elevation in 2 or more leads the territory of the artery
–if not treated within 6-12 hours, suffers significant myocardial damage
Prinzmetal angina
–uncommon
–coronary spasm, usually at site atherosclerotic lesion
–transient chest pain with ST elevation
–Often occurs at rest
syndrome X
patients with –Angina –Evidence of exercise-induced ischemia –Normal epicardial coronary arteries –70% female –Average age = 50 years –etiology not understood
differential diagnosis of angina
–multiple causes of similar pain
Response to nitroglycerin seen in
–Esophageal spasm
–Diastolic dysfunction
diagnoses mimicking angina or MI
–esophageal spasm –Peptic ulcer –Asthma –Aortic dissection –Mitral valve prolapse –Pulmonary embolus –Exertional hypertension –Cholecystitis –Musculoskeletal syndromes –Panic attack –pericarditis –Pleuritis –Congestive heart failure –Diastolic dysfunction –Costochondritis
diagnosing chronic stable angina
–physical exam not uses a helpful
–+/- S1 or S4.. Systolic or diastolic dysfunction
–EKG usually normal
–May have a prior myocardial infarction or ischemia with ST depression
–Exercise treadmill will show EKG changes with exercise
–post exercise echocardiogram also helpful
–64 slice CAT scan can image coronary arteries
–Coronary angiography is gold standard
acute coronary syndrome definition
–unstable angina
–Non-ST elevation myocardial infarction
–ST elevation myocardial infarction
EKG changes in various ST elevation myocardial infarction
–anterior MI = V1–V4
–Lateral MI = V1, V6, 1, aVL
–Inferior MI = II, III, aVF
CK–MB and cardiac troponins occurred when
CK–MB and cardiac troponins do not elevated for the first 8 hours after an MI
other name for statin
=HCM–CoA
= Hydroxy methyl Glutaryl coenzyme A
medications to treat angina and MI symptoms without improvement in survival
nitrates and calcium channel blockers
–Avoid amlodipine and felodipine if left ventricular dysfunction
symptoms seen in MI
–substernal chest pain –Radiation to either arm, neck, jaw, epigastrium –diaphoresis –Nausea or vomiting –Palpitations –Weakness –Lightheadedness
–Atypical symptoms often an elderly and/or diabetic
–more than 40% presented with sudden cardiac death as first symptom of MI
differential diagnosis of possible MI
AORTIC DISSECTION
– stabbing ripping chest pain radiating to the back
–different blood pressures between left and right arm
– wide mediastinum x-ray
–new diastolic murmur of aortic regurgitation
PULMONARY EMBOLUS –Dyspnea –Pleuritic chest discomfort –Hemoptysis –Low oxygen saturation
PERICARDITIS
–Sharp pleuritic pain
–Positional, better sitting up or leaning forward
–Friction rub or pulsus paradoxus
EKG evidence for reperfusion therapy
–new Left bundle-branch block
–New ST segment elevation greater than 0.1 mV in 2 or more continuous leads
–Also useful in posterior MIwith ST depression in V1–6
conditions that obscure EKG diagnosis of MI
–known left bundle branch block –Paced rhythm –Left ventricular hypertrophy with strain –Wide complex tachycardia –Wolff-Parkinson-White syndrome
biomarkers of MI onset and peak
CK-MB –elevated in 4 hours –Peaks 12-24 hours –Duration 36-48 hours –low sensitivity and specificity
TROPONINS
–begins in 3-6 hours
–Elevated 7-14 days
–Worse prognosis than MB CK elevation
which artery involved in various MI
anterior infarct =
–left proximal anterior descending artery (LAD)
Anterolateral infarct=
– left circumflex, or diagonal branch of left anterior descending artery
Diaphragmatic =
–inferior infarct = right coronary artery
True posterior infarct =
–distal circumflex artery posterior descending artery
–Distal right coronary artery
percent reduction in early MI mortality with aspirin
24%
direction of P wave in various leads
–positive in lead 1, 2, V5, V6
–negative in aVR
–Up, down, or biphasic in V1
Ectopic foci may be normal if close to the sinus node
direction of P wave in PR interval
–includes P wave and PR segment
–Encompasses atrial repolarization and depolarization AV node and His-Purkinje system
–Prolonged by slow AV node conduction
––Decreased sympathetic tone
––Increased vagal tone
––Drugs e.g. digitalis and beta adrenergic blocking agents
PR interval shortened one pulses Risa ventricles to AV node bypass tract as in Wolff-Parkinson-White
direction of QRS wave
–ventricles depolarized simultaneously
–Left ventricle is 3 times larger than the right therefore overshadows electrically
–Upright in lead 1, V5, V6, left side, posterior leads
–Negative in aVR and V1, right-sided and more anterior leads
–Abnormal in bundle branch blocks, fascicular blocks
–
factors affecting amplitude of QRS complex
–thickness of ventricular wall
–Presence of pleural or pericardial fluid
–Affected by age, sex, race
–Younger patients have greater QRS voltages
–Men have greater QRS voltages
ST segment and T-wave
–represent ventricular repolarization
–T wave results of sequential repolarization of ventricular cells
–Abnormalities and repolarization shown by elevation or depression of ST segments and changes in polarity of T wave
–T-wave amplitude should be at least 10% of QRS complex
–Inverted T waves in lead 1 her always abnormal
–Flat or inverted T waves often occur with rapid ventricular rates. Her nonspecific
–Most common cause of ST segment elevation includes
––Acute transmural ischemia
––Pericarditis
––High potassium
––Acute myocarditis
U-wave
–precise etiology not clear
–May increase with hypokalemia
QT abnormalities
–QT = onset of Q-wave to end of T-wave
––Includes QRS, ST segment, T-wave
–Interval is rate-dependent
–Affected by ––Temperature ––Drugs ––Electrolyte abnormalities ––Genetic factors ––Neurogenic factors ––Ischemia
–Low potassium,or low calcium prolonged QT
–high potassium or high calcium lengthens QT
significant of peaked or tented T-wave
high potassium
acute ischemia and infarction on EKG
characterized by changes in ST segment, QRS complex, T-wave
–
sequence of EKG changes with ischemia and infarction
- Peaking of the T-wave
- ST segment elevation or depression
- Development of abnormal Q waves
- T-wave inversion
incidence of peripheral artery disease
10-30% of adults over age 50
–Marker for coronary and cerebrovascular disease
–60% of patients with PAD have CAD cerebrovascular disease or both
–Patient with PAD 3 times greater risk for CVA and MI
etiology of PAD
–starts early in life
–Plavix start in endothelial tissue
–Expanded increments on to subclinical episodes of plaque rupture
–TriCor is surrounded by complex fibrotic Composed of calcium, connective tissue and smooth muscle cells
–Plaque rupture exposes highly thrombogenic core to circulating blood elements resulting in platelet activation and aggregation along with activation fibrinogen
–Strongest risk factor the cigarettes
main symptoms of claudication
–cramping pain and lower extremities were by Dr.,
–Reliably produced by threshold level of exercise
–Relieved by a few minutes of rest
–Elevation of limb worsening claudication
–Classic symptoms occur in only one third of patients
–Symptoms may be mild
PAD symptoms and location of stenosis
calf claudication = femoral artery stenosis
–Foot claudication suggests popliteal or proximal tibial peroneal stenosis
–Thigh and buttock pain suggests aortoiliac involvement
–Critical limb ischemia usually requires multiple sites of severe obstruction
physical findings in PAD at rest
–cool skin –Pallor –Dependent rubor –Atrophic skin and nails Delayed capillary refill Ischemic ulcers
–Ischemic ulcers tend to be painful and occur at the lateral malleolus, tips of the toes, metatarsal heads, bunion area
In contrast venous stasis ulcers are usually painless and occur over medial malleolus
Lack of bruits reduce his likelihood of significant PAD
differential diagnosis of PAD like–symptoms
pseudo-claudication (symptom of spinal stenosis)
–Less reproducible on specific effort level
–Not relieved by rest
–Only relief with sitting or lumbar flexion
Claudication pain improves when standing still, but not was pseudo-claudication
interpreting ABI
ratio of brachial blood pressure to dorsalis pedis and posterior tibial artery pressure
–ABI of 0.9 has 95% sensitivity and 100% specificity
–ABI <0.4 consistent with severe PAD
–Extremities with ischemia at rest generally associated with a ABI <0.20
treatment of PAD
–risk factor reduction –Glycemic control –ACE inhibitor's –Diuretics –Beta blockers –Antiplatelet the agents, aspirin –Statins –clopidogrel slightly superior to aspirin but minimal difference –Exercise
guidelines for prevention of infective endocarditis in the presence of vvalvular or congenital heart disease
–optimal oral health and hygiene
–Antibiotic prophylaxis only for those at highest risk
––History of previous infective endocarditis
Test test prosthetic heart valves
––Cardiac transplant recipient’s with valvulopathy
––Unrepaired cyanotic congenital heart disease
–Completely repaired congenital heart disease with prosthetic materials are devices during the first 6 months of after the procedure
–Those with residual defects at or adjacent to site of a prosthetic patch should be treated indefinitely
some things for which antibiotic prophylaxis 4 infective endocarditisis not recommended
–respiratory procedures
–genitourinary procedures
–Gastrointestinal procedures
procedures for which antibiotic prophylaxis for infective endocarditis is recommended
–all dental procedures involving manipulation and gingival tissue or periapical region and teeth –Perforation of the oral mucosa –Respiratory tract –Infected skin or skin structures –Musculoskeletal tissue
etiology of congenital aortic stenosis
–usually defect in aortic valve
–Bicuspid aortic valve present in 2% of population and undergo accelerated degenerative change
nonvalvular congenital lesions
–can be discrete subaortic membrane
–Or supravalvular aortic stenosis
Hypertrophic cardiomyopathy
pathology of aortic stenosis
–results in fixed outflow obstruction and left ventricular pressure overload
–compensatory left ventricular hypertrophy increase his myocardial oxygen demand causing ischemia even in the absence of coronary disease
––Hypertrophic can cause abnormal myocardial relaxation, decreased chamber compliance and diastolic left ventricular dysfunction
clinical presentation of mild aortic stenosis
–midsystolic murmur
–Loudest in the second right intercostal space
–Transmitted to the neck
May have diminished slowly rising arterial pulse
May have systolic thrill in second right intercostal space or suprasternal notch
May have aortic ejection sound
clinical presentation of moderate to severe aortic stenosis
–angina
–Syncope
–Left heart failure
–Prognosis is worse with left heart failure
–can cause atrial fibrillation
differential diagnosis aortic stenosis
–hypertrophic cardiomyopathy causes dynamic left heart ventricular outflow obstruction
––Murmur loudest at left sternal edge
–midsystolic murmur frequently normal in childhood and adolescence
diagnosis of aortic stenosis
echocardiogram possibly followed by cardiac catheterization
management of aortic stenosis
–if asymptomatic, annual evaluation and education.
––echocardiography every 3-5 years
–Moderate aortic stenosis, ––echocardiogram every year
–Severe aortic stenosis evaluate semiannually for possible valve replacement
–Physical activities need not be limited in mild stenosis
–Moderate to severe stenosis should avoid contact sports
–Do not use diuretics or vasodilating drugs
aortic insufficiency
= aortic regurgitation
–Multiple causes including valvular, rheumatic,, infective, congenital
–Chronic aortic regurgitation causes compensatory left ventricular dilatation enhance chamber compliance resulting in increasing end-diastolic volume without arise and filling pressure
–Ultimately results in left heart failure
Acute aortic regurgitation, especially by infective endocarditis close pulmonary edema and shock
clinical presentation of aortic regurgitation
–usually have high-pitched, early diastolic decrescendo murmur at left sternal edge
Moderate-to-severe agitation causes
–Systolic hypertension
–Widened pulse biferiens (“double tap”) carotid pulse
–Displaced apical impulse
–Usually midsystolic murmur from the outflow tract (Austin Flint) murmur
–Can cause heart failure
Acute aortic regurgitation failure developed rapidly
therapy of aortic regurgitation
if mild, repeat evaluation
If symptoms of left heart failure, need aortic valve replacement
Treatment vasodilators and beta blockers
most common cause of mitral stenosis
rheumatic heart disease
etiology of mitral stenosis
–left ventricular inflow obstruction causes increase in left atrial pressure, which can initially maintain left ventricular filling.
Over time excess pressure results and left atrial dilatation, pulmonary vascular congestion, and secondary pulmonary artery hypertension
–Long term produces irreversible pulmonary vascular disease
presentation of mitral stenosis
–earliest signs –Increase amplitude of first heart sound –Opening snap –Mid diastolic murmur at the mitral area –Half have history of rheumatic fever
–Symptoms frequently developed during pregnancy
Often with atrial fibrillation
–High risk of systemic thromboembolism
treatment of mitral stenosis
–mild treated with diuretics and beta blockers
–Anticoagulation and antirrhythmic if atrial fibrillation
Later, treatment with percutaneous balloon valvuloplasty or surgical valve replacement
etiology of mitral regurgitation
–congenital mitral regurgitation rare
–Acquired mitral regurgitation causes are ––Papillary muscle dysfunction ––myxomatous disease ––Mitral prolapse ––Rheumatic heart disease ––Spontaneous rupture chordae tendon a
complications of mitral regurgitation
–left atrial dilatation
–Usually asymptomatic and mild
With moderate to severe regurgitation, progressive left ventricular dilatation leads to exercise intolerance
–Acute mitral regurgitation does not allow for left atrial dilatation and consequently pulmonary venous pressure rises producing a reversal pulmonary edema
clinical presentation of mitral regurgitation
–holosystolic murmur loudest at mitral area
––, Transmitted to the axilla or left sternal edge
Moderate to severe regurgitation can cause
–lateral displacement of the oral impulse, –third heart sound,= S3
–wide splitting of S1
management of mitral regurgitation
echocardiographic when change in functional status
–repair surgically when practical
most common cause of heart failure
cardiomyopathy
what are cardiomyopathies
broad category of myocardial pathology with either systolic or diastolic ventricular dysfunction
3 types of cardiomyopathy
–dilated cardiomyopathy
–Hypertrophic cardiomyopathy
–Restrictive cardiomyopathy
also
–arrhythmogenic right ventricular dysplasia=Arrhythmogenic right ventricular cardiomyopathy
etiology of dilated cardiomyopathy
–characterized by dilatation and appeared contraction of the ventricle, primarily left ventricle
–Is most common type of chronic cardiomyopathy
–Gradual compensation leads to cardiac remodeling first with hypertrophy and later with dilatation
––Increased ventricular size give short-term compensatory relief by starling effect
most common cause of dilated cardiomyopathy
ischemic cardiomyopathy produces to centers of all heart failure
–After MI, infarct scar can become area of nonfunctioning myocardium and over months become dilated and poorly contractile ventricle
–idiopathic cardiomyopathy is usually genetic
various causes of dilated cardiomyopathy
–ischemic heart disease –Hypertension –Valvular heart disease –Infectious –Cardio toxins ––Alcohol ––Catecholamines ––Heavy metals –Hypothyroidism –Hyperthyroidism –Diabetes –Adrenal insufficiency –Lupus –Scleroderma –dermatomyositis –Rheumatoid arthritis –Wilson's disease –Amyloidosis –Sarcoidosis –Kwashiorkor Anemia –Peripartum cardiomyopathy –Muscular dystrophies –Familial X-linked
various causes of hypertrophic cardiomyopathy
–hypertension –Asymmetric septal hypertrophy with obstruction –Genetic mutations –glycogen-storage disease –HIV –trypanosomiasis –Lyme disease
various causes of restrictive cardiomyopathy
–amyloidosis –Sarcoidosis –Hemochromatosis –Endomyocardial fibrosis –Radiation fibrosis –Scleroderma –Carcinoid heart disease –Noonan syndrome –Idiopathic
discussed hypertrophic cardiomyopathy
HCM characterized by left or right ventricular hypertrophy caused by hypertrophied cardiomyopathy, which impair normal relaxation or compliance of the ventricle resulting in diastolic dysfunction
–Markedly thickened ventricular walls, but normal or even small ventricular chamber
–Ventricular systolic function preserved
–May progress to dilated cardiomyopathy
–Most common cause in elderly his severe hypertension
Second most common cause is genetic mutations of the myocardial Sarka we’re
––Is causing unexpected sudden cardiac death in young athletes
––Usually asymptomatic as young and found on electrocardiogram
define restrictive cardiomyopathy
=diastolic dysfunction with impaired relaxation of the ventricle
–Is not caused by ventricular hypertrophy, rather, caused by intrinsic disease process affecting the myocardium.
–Results and stiff ventricle with restrictive diastolic filling pattern
Described heart in restrictive cardiomyopathy
’s–stiff ventricle
–Restrictive diastolic filling.
Ventricular systolic function usually preserved or mildly reduced
–Ventricular chamber size is normal
–Ventricular wall thickness using normal or mildly increased
–Hallmark of restrictive cardiomyopathy = marked biatrial enlargement compared to ventricle
most common causes of restrictive cardiomyopathy
infiltrative diseases e.g. amyloidosis and sarcoidosis
9 infiltrative diseases e.g. idiopathic fibrosis
–Endomyocardial diseases e.g. fibrosis, radiation fibrosis anthracycline toxicity
treatment of hypertrophic cardiomyopathy
–prevent progression
–Blood pressure control
––Beta blockers and calcium channel blockers
––disopyramide may improve exercise tolerance by reducing outflow gradient
––pacemakers were formerly used but not effective
–Arrhythmias or poorly tolerated potentially fatal
–Defibrillator implantation for patient’s at high risk for sudden death
––Prior cardiac arrest
––Sustained ventricular tachycardia
––Frequent nonsustained ventricular tachycardia on serial Holter monitors
––Positive family history of premature HCM related death
––History of syncope
–Abnormal (hypotensive) blood pressure response to exercise
Severe increased left ventricular wall thickness
define heart failure
= constellation syndromes previously referred to his CHF Caused by cardiac dysfunction.
–Results for myocardial muscle dysfunction with accompanied dilatation or hypertrophy of the left ventricle and neurohormonal activation
define systolic heart failure
systolic heart failure his inability of the ventricle to empty normally with reduced ejection fraction <40%, usually accompanied by ventricular dilatation.
define diastolic heart failure
diastolic heart failure has preserved systolic function.
His inability of the ventricle to relax or fill normally
–Usually normal ventricular size and systolic function, but left ventricular end-diastolic pressure is elevated
prevalence of heart failure
–effects 5 million Americans –Half million cases per year –Increases with age –Most common cause of hospitalization for patient's >65 years –Mortality rate = 50%/5 years
risk factors for heart failure
–history of hypertension –Atherosclerosis –Hyperlipidemia –Diabetes –Valvular disease –Obesity –Physical inactivity –Excessive alcohol intake –Exposure to cardiotoxin –Family history of cardiomyopathy –Sleep-disordered breathing –Smoking
etiology of heart failure
–coronary artery disease accounts for 50% of heart failure worldwide
–Caused by scar tissue, decrease systolic and diastolic performance
–Hypertension very common cause of heart failure,, especially in African-Americans in older women
–Familial cardiomyopathies account for up to one third of cardiomyopathies thought to be idiopathic
–Thyroid disease
–Chemotherapy
––Doxorubicin
––Herceptin
–Myocarditis
–HIV infection
–Diabetes
–Alcohol
–Cocaine
Connective tissue disease
–Peripartum cardiomyopathy and arrhythmias
mechanism of systolic heart failure
= ejection fraction <40%
–There is a reduction in cardiac output that is perceived as “hypovolemia” by the kidneys and triggers activation of the renin -angiotensin system
–activation of RAS causes salt and water retention which translates and slightly increase his preload improving cardiac output.
–Over longer period of time chronic activation of RAS results in volume overload and symptoms of heart failure.
how does decline in blood pressure trigger heart failure?
declining blood pressure due to decreased cardiac output can trigger activation the sympathetic nervous system.
–In concert with RAS activation, and elevated levels of endothelin and vasopressin, results and systemic vasoconstriction. Short-term benefit of vasoconstriction is increased perfusion of critical organs
–But is followed by worsening heart failure due to chronically increased left ventricular afterload that worsens heart failure
most common immediate cause of death in heart failure
arrhythmias
heart remodeling in heart failure
page 243
left ventricular remodeling is a maladaptive process in heart failure.
–Changes cardiac size shape and function
–Myocyte length may be increased with resulting increase in chamber volume which preserved stroke volume
–Myocyte hypertrophy also occurs as well as loss of myelocytes
Remodeled heart becomes more elliptical and more spherical, hence more dilated
–Mitral valve annulus may become dilated resulting in mitral regurgitation and further wall stress
define systolic dysfunction
ejection fraction less than 40%
–Body interprets this as hypovolemia and consequent vasoconstriction
heart failure with preserved ejection fraction
about half of the cases
–Treatment similar to heart failure with systolic dysfunction
–Affects older people, especially women
–Ischemic disease and hypertension most common causes
–Ventricular size usually normal but can be enlarged
presenting complaints with heart failure
–signs and symptomsa pulmonary congestion
–Systemic fluid retention
–Exercise intolerance
–Inadequate organ perfusion
Dyspnea on exertion –Exercise intolerance –Orthopnea –Proximal nocturnal dyspnea –Cough –Chest pain –Weakness –Fatigue –Nausea –Abdominal pain –Nocturia –Oligoria –Confusion –Insomnia –Depression –Weight loss
physical exam findings and congestive heart failure
–engorged neck veins –Rales –Pleural effusion –Displaced point of maximal intensity Right ventricular heave –S3, S4 murmurs –Hepatomegaly –Low-volume pulse –Peripheral edema
differences in presentation between
–Heart failure
–Heart failure with preserved systolic function
very little difference, if any
–Enlarged cardiac silhouette
–Assessment of left ventricular function is essential
where his cholesterol found?
primarily in the cell membranes
where his cholesterol synthesized and excreted
cholesterol is synthesized primarily in the liver and excreted as bile salts
what determines blood levels of cholesterol
–dietary intake of cholesterol
–Inheritance
–Physical activity
–Intake of dietary fats, especially saturated fats
how his cholesterol transported in the blood
cholesterol is transported as medical molecules of lipoproteins with non-polar lipid core surrounded bipolar monolayer of phospholipids
what are triglycerides?
triglycerides are esters of glyceryl and longchain saturated and desaturated fatty acids
where her triglycerides found?
triglycerides found in all plasmic lipoproteins
–Are major constituents of chylomicrons, VLDL, IDL
relationship between triglycerides and HDL
high triglycerides is associated with a low HDL
elevation of triglycerides >1000 mg/deciliter are associated with what?
–pancreatitis
–Eruptive xanthoma
discuss HDL cholesterol
–is a family of lipoproteins constituting 20%-30% of total cholesterol
–Strong inverse association with coronary heart disease risk
–Decreased by diets of polyunsaturated fats, obesity, smoking, diabetes, drugs including diuretics
–Physical activity and alcohol increase HDL
–High variation therefore must to more than 1 evaluation
discuss LDL cholesterol
–one half–two thirds of total cholesterol
–Major determinant of total cholesterol
–a subpopulation of particles of similar chemical and physical properties
–strongly associated with coronary heart disease
familial hypercholesterolemia
–1 in 500 persons are heterozygous
––2–fourfold increase in CHD
–1 in 1,000,000 = homozygous
––much greater increase in CHD
secondary causes of hypercholesterolemia
–poorly controlled diabetes
–Hypothyroidism
–Nephrotic syndrome
–Estrogen replacement therapy may elevate triglycerides
–progestins and anabolic steroids may dramatically lower HDL
