Mitral Valve Prolapse, Ballooning of mitral valve into left atrium during systole., Seen in 2-3% of US adults; effect women especially., Due to myxoid degeneration (accumulation of ground substance) of the valve, making it floppy., Etiology is unknown; may be seen in Marfan syndrome or Ehlers-Danlos syndrome., Presents w/ an incidental mid-systolic click followed by a regurgitation murmur; usually asymptomatic, Click and murmur become louder with squatting (increased systemic resistance decreases left ventricular emptying)., Complications are rare, but include infectious endocarditis, arrhythmia, and severe mitral regurgitation, chest pain., Treatment, Valve replacement., Reduntant leaflet billow back in the LA during systole causing the mid-systolic click and late systolic regurgitant muramur. The timing of the click and duration of the murmur influenced by LV loading conditions change w/ dynamic auscultation., Mitral prolapse syndrome: chest pain, palpitations with an unclear cause., Note: mitral valve prolapse has so many variant murmur sounds that dynamic auscultation is a very important tool to use to distinguish MVP from other things such has Hypertrophic Cardiomyopathy (HCM)., Murmur of MVP may radiate anteriorly and is often late systolic
Mitral Regurgitation, Reflux of blood from the left ventricle into the left atrium during systole., Usually arises as a complication of mitral valve prolapse; other causes included LV dilatation (e.g., left-sided cardiac failure), infective endocarditis, acute rheumatic heart disease, and papillary muscle rupture after a myocardial infarction., Clinical Features, 1. Holosystolic "blowing" murmur; louder w/ squatting (increased systemic resistance decreases left ventricular emptying) and expiration (increased return to left atrium)., 2. Results in volume overload and left-sided heart failure., Etiology, Organic (leaflet /chordae problem) -Mitral valve prolapse -Rheumatic mitral valve disease -Mitral annular calcification -Endocarditis -Anorexigens, ergot alkaloids -Papillary muscle or chordal rupture -Congenital cleft anterior leaflet, Functional (tethered leaflets) -Ischemic (post infarct the papillary muscle is displaced causes an insufficient closure of the mitral valve leaflets leading to regurgitation. However, there is nothing wrong with the actual mitral valve itself. -Dilated cardiomyopathy, Note: If the LA Pressure is measured for MR it will have large V-waves very similar to what is seen when measuring JVP., Chronic MR, CHF, Elevated LA/PCW pressures, Pulmonary HTN, Palpitations (atrial arrhythmias), Arterial thromboembolism, Physical Exam, S1 may be soft, Laterally dissplaced, hyperdynamic PMI, S3 (increased early diastolic filling), Apical holosystolic murmur radiating to axilla, Loud P2 and elevated JVP if concurrent PulmHTN, Parasternal heave from LA enlargement or concurrent RV dilatation or hypertrophy, Diagnosing Chronic MR, Typical physical findings, Expected symptoms, Echo/Doppler, LV & LA size, LV systolic function, Pulm pressures, Presence and severity of MR, Invasive hemodynamics, Contrast ventriculography, Cardiac MRI, Complications of MR, LV systolic dysfunction, Irreversible pulm HTN, Atrial arrhythmias, Arterial Thromboembolism, Endocarditis
Mitral Stenosis, Narrowing of the mitral valve orifice, Usually due to chronic rheumatic valve disease, Clinical features, Opening snap followed by diastolic rumble, Volume overload leads to dilatation of the left atrium, resulting in 1. Pulmonary congestion w/ edema and alveolar hemorrhage, 2. Pulm HTN and eventual right-sided heart failure. 3. Atrial fibrillaton w/ associated risk for mural thrombi, No S4 when atrial fibrillation is present.
Tricuspid Regurgitation, Mild, 'physiologic' regurgitation can be seen in most normal individuals on echocardiography., Etiology, Longstanding PulmHTN leading to right ventricular and TV annular dilation, Damage from pacemakers and ICDs, Carcinoid heart disease, Rheumatic heart disease, Prolapse, Endocarditis, Pathophysiology, Volume overload of the RV; RV and RA compensatory dilatation., Physical Exam findings for TR, Elevated JVP w/ prominent V waves, Parasternal heave from RV dilatation, Loud P2 if concurrent PulmHTN, Low pitched holosytolic murmur at LSB (may be high pitched if PulmHTN), RV S3 at LSB, Pulsatile liver, possibly ascites, Peripheral edema, Presentation, Edema, Fatigue, Atrial arrhythmias, Treatment, Diuretics, Anticoagulation for atrial arrhythmias, Surgery (annuloplasty)
Tricuspid Stenosis, Eitology is usually rheumatic, Due to obstruction of RV filling during diastole leads to elevated RA pressure., Presentation, Fatigue, systemic congestion (edema, ascites, etc.), Physical Exam findings for Tricuspid Stenosis, Elevated JVP w/ prominent A waves (This is NOT cannon A waves that are seen in complete heart block!), Opening snap at left sternal border, Delayed diastolic murmur at left sternal border, Edema, hepatomegaly, ascites, Treatment, Surgery (valvuloplasty)
Aortic Stenosis, Narrowing of the aortic valve orifice. Usually due to fibrosis and calcification from "wear and tear", 1. Presents in late adulthood (>60yrs), Common in 35% of those >65y/o., 2. Bicuspid aortic valve increases risk and hastens disease onset. A normal aortic valve has three cusps; fewer cusps results in increased "wear and tear" on each cusp., May also arise as a consequence of chronic rheumatic disease from "wear and tear". More specifically from Calcification, Rheumatic Heart Disease, Congenital Bicuspid or unicuspid valve, or Radiation (Cancer Treatment)., Cardiac compensation leads to a prolonged asymptomatic stage during which a systolic ejection click followed by a crescendo-decrescendo murmur is heard., Complications, 1. Concentric left ventricular hypertrophy- may progress to cardiac failure, 2. Angina and syncope w/ exercise- Limited ability to increase blood flow across the stenotic valve leads to decreased perfusion of the myocardium and brain., 3. Microangiopathic hemolytic anemia (MAHA)- RBCs are damaged (producing schistocytes) while crossing the calcified valve., Treatment, Treatment is aortic valve replacement (AVR) after onset of complications., Aortic valve replacement Percutaneous aortic valvuloplasty of limited utility in adults Percutaneous valve replacement (TAVI), Class I Indications for AVR, Severe, symptomatic aortic stenosis, Severe, asymptomatic aortic stenosis w/ LV systolic dysfunction (EF<50%), Severe, asymptomatic aortic stenosis at the time of CABG, aorta, or mitral valve surgery., Summary, Focal thickening of valve cusps with normal excursion and no obstruction to flow Common (25% of those >65 years) Causes early peaking SEM at RUSB Pathophysiology similar to atherosclerosis Increases risk of coronary events two-fold May progress to aortic stenosis, Pathophysiology, 1. Obstruction to LV outflow leads to pressure overolad of LV 2. LV compensates with concentric hypertrophy 3. LV filling pressure increases 4. Cardiac output becomes ‘fixed’ 5. Ultimately, compensatory hypertrophy fails and LV systolic function declines, Physical Exam Findings for Aortic Stenosis, 1. Systolic ejection murmur at RUSB radiating to carotids (and apex)., timing of the peak intensity correlates w/ severity: early peaking= mild, late peaking = severe. Usually harsh grade II or higher., 2. Delayed and weak carotid upstrokes (pulsus parvus et tardus), narrow pulse pressure, 3. Sustained LV apical impulse, 4. Fourth Heart Sound (+/- S3 late in course), 5. Decreased A2 Component of S2 in severe cases., Dx of Aortic Stenosis, Typical findings on Physical exam, classic symptoms, ECG evidence of LVH, ECHO (confirms)/Doppler, and Cardiac Catherization
Aortic Regurgitation, Backflow of blood from the aorta into the left ventricle during diastole., Arises due to aortic root dilation (e.g., syphilitic aneurysm and aortic dissection) or valve damage (e.g., infectious endocarditis); most common cause is isolated root dilation., Clinical features include, 1. Early, blowing diastolic murmur, 2. Hyperdynamic circulation due to increased pulse pressure, Pulse pressure is the difference between systolic and diastolic pressures., Diastolic pressure decreases due to regurgitation, while systolic pressure increases due to increased stroke volume., Presents with bounding pulse (water-hammer pulse), pulsating nail bed (Quincke pulse), and head bobbing (deMusset's sign), 'pistol shot' sound over femoral artery (Traube's sign), systolic & diastolic bruits when femoral artery lightly compressed (Duoziez's sign), Results in LV dilation and eccentric hypertrophy (due to volume overload), Treatment, Valve replacement once LV dysfunction develops., Etiology of Aortic Regurgitation, Dilation of the aortic root & aortic annulus, Ascending aortic aneurysm (Marfan's, Ehlers Danlos, bicuspid aortic valve, familial, annuloaortic ectasia, ankylosing spondylitis, osteogenesis imperfecta)., Chronic Type A aortic dissection, Arteritis (i.e. Takayasu's, giant cell, syphilis), Abnormal Aortic valve cusps, Pathophysiology, Diastolic leaking of blood back into LV leads to LV overload. LV compensates for the volume overload by dilating (eccentric hypertrophy). Stroke volume increases to maintain forward output. Increased SV leads to systolic HTN and pressure overload of LV. LV compensates for pressure overload w/ concentric hypertrophy. Then with time eccentric hypertrophy fails and LV diastolic pressure increases. With time concentric hypertrophy fails and LV contractile function falls (EF declines)., When severe AR- U can here an Austin Flint Murmur that sounds just like Mitral Stenosis., Aortic Regurgitation: Diagnosis, Typical findings on physical exam, Expected symptoms, ECG evidence of LVH, ST-T changes, Echo/Doppler, Contrast aortography, Invasive hemodynamics, Cardiac MRI, Helps a physician to quantify a regurgitant lesion.
Bicuspid Aortic Valve, 1-2% of the population (4x more in males) Can develop stenosis, regurgitation or both Many patients will ultimately require surgery (younger age) At moderate risk for endocarditis Systolic ejection click on exam Associated with aortic disease -Ascending aortic aneurysm in 50% -Coarctation in 10% (30-50% with coarct have bicuspid valve) -Aortic dissection
Chronic Aortic Regurgitation, Chronic AR, Soft S1, Systolic ejection click if bicuspid aortic valve., PMI displaced laterally and hyperdynamic, S3 if LV systolic dysfunction has developed, High pitched, decrescendo immediate diastolic murmur., Early peaking systolic ejection murmur, Delayed diastolic, low pitched apical murmur (Austin Flint)= Severe Aortic Regurg and sounds just like Mitral Stenosis., Natural History of Chronic AR, Asymptomatic w/ normal LV, -Risk of death <0.2%/yr -Development of asymptomatic LV dysfunction 3.5%/yr - Development of symptoms +/- LV dysfunction <6%/yr, Asymptomatic w/ LV dysfunction, - Progression to symptoms >25%/yr, Symptomatic, - Mortality> 25%/yr, Treatment, AVR (+/- replacement of aortic root), Vasodilator therapy, - Patients w/ indication for surgery who are not operative candidates., This does not improve the outcome in surgical candidates; however, this is a treatment option best for persons who are not candidates for AVR surgery., Class I Indications for AVR in Chronic AR, Severe, symptomatic AR, Severe, asymptomatic AR w/ LV systolic dysfunction (EF<50%), Severe, asymptomatic AR at the time of CABG, aorta, or other valve surgery.
Acute Regurgitation, Usually caused by endocarditis, type A aortic dissection, or trauma., LV has not had time to dilate, LV diastolic pressure increases dramatically. Forward cardiac output falls as a large amount of each SV is lost backward., Results in pulmonary edema and cardiogenic shock., Classic findings of wide pulse pressure are NOT seen and diastolic murmur will be short., Requires emergent AVR
Acute Rheumatic Fever is a systemic complication of pharyngitis due to group A Beta-hemolytic streptococci; affects children 2-3 weeks after an episode of stretococcal pharyngitis ("strep throat")
Caused by molecular mimicry; bacterial M protein resembles proteins in human tissue.
How to Diagnose Acute Rheumatic Fever, 1. Eveiden of prior group A beta-hemolytic streptococcal infection (e.g. elevated ASO or anti-DNase B titers) with the presence of major and minor criteria., 2. Minor criteria are non-specific and include fever and elevated ESR., 3. J.O.N.E.S. criteria (Major Criteria), Joint, Migratory polyarthritis- swelling and pain in a large joint (e.g. wrist, knees, ankles) that resolves w/ in days and "migrates" to involve another large joint., O (a heart symbol), Pancarditis- all the layers of the heart are inflammed., a. Endocarditis- Mitral Valve is involved more commonly than the aortic vlave. Characterized by small vegetations along lines of closure that lead to regurgitation., b. Myocarditis- w/ Aschoff bodies that are characterized by foci of chronic inflammation, reactive histiocytes w/ slender, way nuclei (Anitschkow cells), giant cells, and fibrinoid material; myocarditis is the most common cause of death during the acute phase., c. Pericarditis- leads to friction rub and chest pain, Nodules, Subcutaneous nodules, Erythema, Erythema marginatum- annular, nonpruritic rash w/ erythematous borders, commonly involving trunk and limbs., Sydenham chorea, Rapid, involuntary muscle movements.
The heart has four valves (tricuspid, pulmonary, mitral, and aortic) that prevent backflow.
Valvular lesions generally result in stenosis (decreased caliber of the valve orifice) or regurgitation (backflow).
Prosthetic Valve Complications, Endocarditis -Risk is highest shortly after implantation and then levels off at ~1% per year (5% per 5 years) -Bioprostheses & mechanical prostheses have same risk Structural failure (stenosis & regurgitation) Thromboembolism -Depends on prosthesis type, location, & patient risks -Without anticoagulation, risk is ~8% yearly Bleeding on anticoagulation
Types of Prosthetic Heart Valves: Bioprostheses, Xenografts (porcine, pericardial) Homografts Autografts (Ross procedure) Advantages: -Low thromboembolic risk (no need for anticoagulation) -Good hemodynamics Disadvantages: -Relatively short lifespan (10-15 years)
Prosthetic Heart Valves: Mechanical Prostheses, Ball & cage valve (Starr Edwards) Tilting disk valve (Bjork-Shiley & Medtronic Hall) Bi-leaflet valves (St. Jude & Carbomedics) Advantages: -Durability Disadvantages: -High thromboembolic risk (require anticoagulation)
Valvular Heart Disease: Goals of Surgery, Alleviate symptoms & improve functional status Prevent progressive, potentially irreversible LV dysfunction Prevent progressive, potentially irreversible pulmonary HTN Prevent death
Valvular Heart Disease: Deciding When To Operate, Risks of the patient: -Age -Comorbidities -LV function -Functional class Risks of the operation: -Concurrent CABG needed -Multi-valve disease Risks of the prosthesis, Note: if the person has poor LV function or poor functional class they tend not do as well post surgery as their counterparts who don't have any of these issues. Therefore it is important to have surgery before LV dysfunction and functional class become severe because the LV dysfunction is usually irreversible.
Valvular Heart Disease: When to Operate, Symptomatic severe valvular disease, Asymptomatic severe valvular disease with evidence of LV dysfunction, Asymptomatic severe mitral valve disease with evidence of significant pulmonary HTN, Asymptomatic moderate to severe valvular disease when performing other cardiac surgery, Asymptomatic, normal LV function but repairable valve ? (Assess all risks)
Pre-operative Coronary Angiography Prior To Valve Surgery: Class I Indications, History of CAD, chest pain, or other evidence of ischemia Patients at risk of concurrent CAD: -Men > 35 years old -Post-menopausal women -Pre-menopausal women > 35 with coronary risk factors Patients in whom an autograft (Ross procedure) will be performed
When A Patient With Stable Valvular Disease Suddenly Deteriorates, Consider…, New onset atrial arrhythmias, Endocarditis, Concurrent ischemic heart disease, Sudden progression of disease -Chordal rupture creating flail segment
Chronic Ischemic Heart Disease
STABLE ANGINA, Quick Summary:, Stable angina is chest pain that arises w/ exertion or emotional stress. Due to atherosclerosis of coronary arteries w/ >70% stenosis; decreased blood flow is not able to meet the metabolic demands of the myocardium during exertion., Represents reverible injury to myocytes (therefore no necrosis)., Presents as chest pain (lasting <20 mins) that radiates to the left arm or jaw, diaphoresis, and shortness of breath., EKG shows ST-segment depression due to subendocardial ischemia., Symptoms are relieved by rest or nitroglycerin
UNSTABLE ANGINA, Quick Summary:, Unstable angina is chest pain that occurs at rest. Usually due to rupture of an atherosclerotic plaque w/ thrombosis and incomplete occlusion of a coronary artery., Represents reversible injury to myocytes (there no necrosis) -just like in Stable Angina, EKG shows ST-segment depression due to subendocardial ischemia., Relieved by Nitroglycerin (NOT REST- b/c by definition this type of angina is one that occurs at rest)., High risk of progression to Myocardial Infarction (MI)
PRINZMETAL ANGINA, Quick Summary:, Prinzmetal angina is episodic chest pain unrelated to exertion. Due to coronary artery vasospasm., Represents reversible injury to myocytes (no necrosis) - just as in both Stable and Unstable angina., EKG shows ST-segment elevation due to transmural ischemia but this is transient. (The full thickness of the heart wall becomes ischemia with this type of angina)., Relieved by nitroglycerin or calcium channel blockers (i.e. verapamil)
A CASE, 55 yo male smoker w/ a history of HTN has had 2-3 episodes of diffuse, sub-sternal pressure-like discomfort w/ radiation to the left arm when 'hurrying' over the past few months. He has no symptoms w/ usual activities. His BP is 132/76 in both arms on medication (HCTZ). HIs exam is w/in normal limits., What is the likelihood that his chest pain is ischemic?, What further evaluation would you recommend?, What treatment would you prescribe?
What is ischemia heart disease?, A. Group of syndromes related to myocardial ischemia; IHD is the leading cause of death in the US., B. Usually due to atherosclerosis of coronary arteries, which decreases blood flow to the myocardium, Risk factors for IHD are similar to those of atherosclerosis; incidence increases w/ age., Traditional Risk Factors for Atherosclerotic Disease, Age (>45 for men & >55 for women), Family Hx (first degree relative), Male <55 & Female <65, Diabetes (impaired glucose metabolism), Important to note: Type 2 DM is a coronary artery disease EQUIVALENT! Because in a study conducted in NEJM, 1998 by Haffner et.al showed that over a 7 year period the incidences of Fatal heart attacks where no different between persons who had diagnosed coronary artery disease and persons who had type 2 Diabetes Mellitus! ****Summary: Type2 DM= Coronary Artery Disease!!!!!!!, Hypertension, Smoking, Cholesterol (elevated total & low HDL), Obesity (BMI>30), Sedentary lifestyle, Novel Risk Factors for Atherosclerotic Disease, Chronic inflammation, Elevated hsCRP in serum, ***Homocysteine, Chronic Kidney Disease, Coagulation abnormalities, ? Chronic infection, Metabolic Syndrome also increases the risk of Ischemic Heart Disease, Any 3 of the following:, Hypertension ( >/= 130/85), Abdominal Obesity (waist >40cm in men and >35cm in women), HDL <40 (<50 in women), Triglycerides >/= 150, Fasting plasma glucose >/= 100, note: Associated w/ inflammation, coagulation abnormalities, progression of type 2 DM., However, there are some Non-Athersclerotic Coronary Artery Disease causes of IHD., Coronary vasospasm, Anomalous coronary arteries (e.g. located in an area where the artery can be compressed by a surrounding structure)., Coronary arteritis (Kawasaki's and Giant-Cell arteritis) *Note- this link works. Just press it twice if necessary., Coronary dissection, Myocardial bridge, Coronary embolization.
Definitions, Coronary artery disease: abnormal narrowing, ectasia, or occlusion of coronary vessels., What exactly is ectasia?, Coronary heart disease: coronary artery disease that has become manifest as chronic stable angina, unstable angina, myocardial infarction, or heart failure., Ischemia: sub-normal myocardial blood flow.
Coronary Artery Anatomy, Coronary Blood Flow: Supply and Demand, Manifestations of Coronary Artery Disease, Chronic Stable Angina, Unstable Angina, Myocardial Infarction, Ischemic Cardiomyopathy (CHF), Sudden Cardiac Death, Silent Ischemia
Myocardial Ischemia Secondary Causes (Remember to consider these when forming your differential dx.), Severe anemia, Hypoxemia, Uncontrolled hypertension, Severe LVH, Uncontrolled Tachycardia, Thyrotoxicosis
Defining Angina Pectoris (sign of Ischemic Heart Disease), Symptoms, Visceral discomfort, Diffuse & sub-sternal pain, Accompanied by dyspnea, diaphoreses, nausea, light-headedness, Provoked by physical exertion, emotional upset, heavy meals, working in cold temperatures., Onset usually over several minutes, Relieved by rest and/or Nitroglyerin (NTG), Types of Angina, Typical Angina, Sub-sternal, Brought on by exertion, Relieved by rest or NTG, Atypical Angina, Missing one or more of the typical angina features., Non-anginal, Canadian Cardiovascular Society Classification of ANGINA (Note: very similar to the New York Heart Association classification of Dyspnea), Class 1: No angina, Class 2: Angina on more than usual activity, Class 3: Angina on less than usual activity, Class 4: Angina at rest or on any activity, HIGH YEILD!!!!!!!!!: There are Angina "Equivalents" (seen more in women), Dyspnea, Arm, jaw, or back pain
Abnormality of heart or great vessels present at birth (although may be discovered as an adult) • Usually refers to structural abnormalities such as abnormal chamber and vessel relationships, abnormal connections (holes), obstructions, absence or maldevelopment of structures, and other anatomic abnormalities • By convention, usually does not include congenital tumors, infections, cardiomyopathies • Ranges from trivial (bicuspid aortic valve) to lethal (absent left ventricle) • If severe, causes delayed development, failure to thrive, increased susceptibility to infectious diseases in childhood, cardiac failure, and rarely sudden cardiac death • Increased risk for endocarditis (generally true for any structural abnormality, congenital or acquired; i.e. prosthetic valve) • Increased risk during pregnancy for women with CHD • Hyperviscosity due to polycythemia • Nearly twice as many children die from CHD in the U.S. as from all forms of childhood cancer combined (Am. Heart Association, 2005)
Causes of Congenital Heart Defects (CHD), Usually unknown - probably multifactorial (may see discordance of CHD in identical twins!), Around 5% chromosomal (Trisomies, Turner’s), Some (? 3%) associated with non-chromosomal single gene defects (Noonans, DiGeorge, numerous others), May be seen in many malformation associations (VATER, polysplenia), Rare infectious cause (rubella)
How to categorize CHDs, Can be categorized into 3 Categories, Cyanotic - when blood from the right side of the heart (deoxygenated blood) enters the left side without going through the lungs (right to left shunt), Right to Left Shunts • Cause cyanosis from early infancy (blue baby) • May be complicated by paradoxical emboli, CHD with Right to Left Shunt (Cyanotic), Tricuspid Atresia, TAPVR (TAPVC), TOGV, Truncus Arteriosus, Tetralogy of Fallot (if sufficient pulmonary outflow restriction), Hypoplastic left heart syndrome probably should be considered as cyanotic, Note: All the cyanotic types start with a T except the last one., Eisenmenger’s Syndrome • Is a switch from noncyanotic to cyanotic CHD due to reversal of shunt flow • Due to right ventricular hypertrophy and pulmonary vascular changes after prolonged pulmonary HTN • Too late to surgically repair since pulmonary vascular changes become irreversible • Not the same as Eisenmenger’s complex, Noncyanotic - when blood from the left side of the heart enters the right side (left to right shunt), Left to Right Shunts • No (initial) cyanosis (pink baby) • Causes pressure (or volume) overload of the pulmonary circulation • Eventually can reverse shunt direction and become cyanotic (see below), CHD with Left to Right Shunt (Noncyanotic), ASD (increased pulmonary blood volume more than pressure), VSD, AV septal Defect (AV canal), PDA, Note: All the noncyanotic types have a D., “Other” (i.e. no shunts, example - obstructions)
Quick Summary:, A VSD is a defect in the septum that divides right and left ventricles. The most common congenital heart defect!, Associated w/ Fetal Alcohol Syndrome (FAS)!!!, VSDs result in left to right shunts in blood circulation; size of the defect determines extent of shunting and age at presentation., Small shunts are often asymptomatic; however, large shunts can lead to Eisenmenger Syndrome (denoted by RV hypertrophy, Polycythemia, and clubbing of the fingers).
Quick Summary:, A ASD is a defect in the septum that divides right and left artria; most common type is ostium secundum (90% of cases)., Ostium primum type is associated with Down Syndrome (trisomy 21)., Results in left-to-right shunt and split S2 sound on auscultation (increased blood in right heart delays closure of pulmonary valve)., FIXED S2 SPLIT, Paradoxical emboli are an important complication., Pulmonic Outflow Ejection Murmur
Quick Summary:, PDA is a failure of the ductus arteriosus to close; associated w/ congenital RUBELLA!, Results in left-to-right shunt between the aorta and the pulmonary artery, During development, the ductus arteriosus normally shunts blood from the pulmonary artery to the aorta, bypassing the lungs., Asymptomatic at birth with holosystolic 'machine-like' murmur; may lead to Eisenmenger syndrome, resulting in lower extremity cyanosis., Treatment involves indomethacin, which decreases PGE, resulting in PDA closure (PGE maintains patency of the ductus arteriosus).
Characterized by 1. Stenosis of the right ventricular outflow tract, 2. right ventricular hypertophy, 3. VSD, and 4. an aorta that overrides the VSD.
Right-to-left shunt leads to early cyanosis; degree of stenosis determines the extent of shunting and cyanosis.
Patients learn to squat in response to a cyanotic spell; increased arterial resistance decreases shunting and allows more blood to reach the lungs.
"Boot-shaped" heart on X-ray.
Characterized by pulmonary artery arising from the left ventricle and aorta arising from the right ventricle.
Associated w/ maternal diabetes
Presents w/ early cyanosis; pulmonary and systemic circuits do not mix., Creation of shunt (allowing blood to mix) after birth is required for survival., PGE can be administered to maintain a PDA until definitive surgical repair is performed.
Results in hypertrophy of the right ventricle and atrophy of the left ventricle.
Quick Summary:, • Term for lesions that cause under-development (hypoplasia) of the left ventricle and ascending aorta • Significant aortic valvular stenosis or atresia are the usual causes (but not known what causes valve stenoses) • HLHS is surgically treatable by the Norwood procedure, but HLHS is a common indication for cardiac transplants in infants • The heart grossly appears to be “all right ventricle” with the left ventricle very small, sometimes slit-like or undetectable • The left ventricle may show thick endocardial fibroelastosis (EFE) due to high intraventricular pressure • Infants are dependent on the ductus after birth, and also need an “ASD” to shunt left atrial blood to the right
Characterized by a single large vessel arising from both ventricles., Truncus fails to divide.
Presents with early cyanosis; deoxygenated blood from right ventricle mixes with oxygenated blood from left ventricle before pulmonary and aortic circulations separate.
Tricuspid valve orifice fails to develop; right ventricle is hypoplastic.
Often associated with ASD, resulting in a right-to-left shunt; presents with early cyanosis.
Narrowing of the aorta; classically divided into infantile and adult forms.
Infantile, Infantile form is associated with a PDA; coarctation lies after (distal to) the aortic arch, but before (proximal to) the PDA., 1. Presents as lower extremity cyanosis in infants, often at birth. 2. Associated w/ Turner Syndrome
Adult, Adult form is not associated w/ a PDA; coarctation lies after (disto) the aortic arch., 1. Presents as hypertension in the upper extremities and hypotension with weak pulses in the lower extremities; classically discovered in adulthood. 2. Collateral circulation develops across the intercostal arteries; engorged arteries caused 'notching' of ribs on x-ray. 3. Associated w/ bicuspid aortic valve.
Benign mesenchymal tumor w/ a gelatinous appearance and abundant ground substance on histology
Most common primary cardiac tumor in adults. 90% occur in the atria (most commonly left atrium). Myxomas are usually described as "ball valve" obstruction in the left atrium (associated w/ multiple syncopal episodes).
Usually forms a pedunculated mass in the left atrium that causes syncope due to obstruction of the mitral valve.
Benign hamartoma of cardiac muscle
Most common primary cardiac tumor in children; associated with TUBEROUS SCLEROSIS!!!!!
Usually arises in the ventricle.
Metastatic tumors are more common in the heart than primary tumors. Common metastases to the heart are BREAST, LUNG, MELANOMA, and LYMPHOMA.
Most commonly involves the pericardium, resulting in a pericardial effusion. Be mindful that breast and lung are thoracic neighbors to the heart and can more readily metastasize to the heart.
Aortic Dissection, Intimal tear w/ dissection of blood through media of aortic wall. Occuris in proximal 10cm of the aorta (high stress region) w/ preexisting weakness of the media., Most common cause is HTN (older adults); also associated w/ inherited defects of connective tissue (younger individuals)., HTN results in hyaline arteriosclerosis of the vasa vasorum; decreased flow causes atrophy of the media., Marfan Syndrome and Ehler-Danlos
Abdominal Aortic Aneurysm
Large-Vessel Vasculitis, Temporal (Giant cell) Arteritis, Granulomatous vasculitis that classically involves branches of the carotid artery, Most common form of vasculitis in older adults (middle age; >50 y/o); usually affects females., Presentation, Headache (temporal artery involvement), visual disturbances (opthalmic artery involvemnet), and jaw claudication. Flu-like symptoms with joint and muscle pain (polymyalgia rhematica) are often present. ESR is elevated., Biopsy of the superficial temporal artery required (5cm section is need- cannot always confirm Dx because the disease can be "patchy"); reveals inflammed vessel w/ giant cells and intimal fibrosis., Lesions are segmental; diagnosis requires a long segment of vessel, and remeber a negative biopsy does NOT exclude disease., Treatment, Corticosteroids; high risk of blindness without treatment!, Takayasu Arteritis, Granulomatous vasculitis that classically involves the aortic arch at branch points., Presents in adults <50 y/o (classically, young ASIAN FEMALES) as visual and neurologic symptoms w/ a weak or absent pulse in the upper extremity. (Takayasu has been called the Pulseless Disease) Elevated ESR!, Treatment w/ corticosteroids
Medium-Vessel Vasculitis, Polyarteritis Nodosa, Necrotizing vasculitis involving multiple organs, lungs are spared!, Presentation, Classically presents in young adults as hypertension (renal artery involvement), abdominal pain with melena (mesenteric artery involvement), neurologic disturbances, and skin lessions. Associated with serum Hepatitis B Surface Antigen (HBsAg), Lesions of varying stages are present. Early lesion consists of transmural inflammation with fibrinoid necrosis; eventually heals with fibrosis, producing a 'string-of-pearls' appearance on imaging., Treatment, Corticosteroids and cyclophosphamide; fatal if not treated!, Kawasaki Disease, Classically affects Asian Children <4 y/o, Presentation, Presents w/ nonspecific signs including fever, conjunctivitis, erythematous rash of palms and soles, and enlarged cervical lymph nodes., In addition to conjunctival injection children get changes in lips/oral mucosa- Classic STRAWBERRY TONGUE, and a desquamating rash., Cornonary artery involvement is common and leads to risk for 1. thrombosis w/ myocardial infarction, 2. aneurysm w/ rupture., Treatment, Aspirin and IVIG (Intravenous Immunoglobulin); disease is self-limited, Note: Normally, one would NOT prescribe Aspirin to a child due to implications of Reye's Disease (Encephalopathy); however, in this case the benefit of preventing an acute MI outweighs the risk of causing Reye's syndrome in this patient., Summary, Kawasaki disease (mucocutaneous lymph node syndrome): vasculitis affecting small- and medium-size arteries of infants and children → acute, often self-limited disease characterized by the mnemonic, “CRASH and Burn”:, Conjunctivitis — bilateral, non-purulent (e.g., nonexudative conjunctival injection) Rash — polymorphic, usually on the trunk but can involve the palms and soles Adenopathy — cervical lymphadenopathy > 1.5cm, most commonly unilateral Strawberry tongue and other mucocutaneous findings (e.g., erythema oral cavity; dry, cracked lips) Hand and foot edema and/or erythema, often with desquamation of fingers/toes Burn — fever (T ≥101.4F) lasting at least 5 days, Other common S/Sx include “STEAM”: - STERILE PYURIA!!!! - Thrombocytosis - ↑ ESR and/or ↑ CRP - Aseptic Meningitis, Buerger Disease, Necrotizing vasculitis involving the digits; Intermittent claudication may lead to gangrene, ulcerations autoamputation of digits (fingers and toes), superficial nodular phlebitis (vein inflammation forming chords on the skin)., Also Segmental Thrombosing Vasculitis, Note: Usually Raynaud phenomenon is often present!, Highly associated w/ heavy smoking; Males <40y/o, Treatment, smoking CESSATION!
Small-Vessel Vasculitis, Wegener "We'C'ener" Granulomatosis, Necrotizing granulomatous vasculitis involving Nasopharynx, Lungs, and Kidneys. (NLK) Associated with "Saddle-Nose Deformity", Presentation, Classic TRIAD (More Detailed Below), 1. Focal Necrotizing Vasculitis, 2. Necrotizing granulomas in the lung and upper airway (nose, etc), 3. Necrotizing glomerulonephritis, 1. Middle-aged male w/ UPPER RESPIRATORY TRACT perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis, or nasopharyngeal ulceration, 2. Also LOWER RESPIRATORY TRACT hemoptysis w/ bilateral nodular lung infiltrates as well as cough and dyspnea., 3. RENAL issues may been seen such as hematuria due to rapidly progressive glomerulonephritis., Note: Serum c-ANCA levels correlated w/ disease acitvity! Biopsy reveals large necrotizing granulomas w/ adjacent necrotizing vasculitis. (mnemonic: We'C'ener is for C-ANCA), Also note that urinalysis may show hematuria, red cell casts., Treatment, Corticosteroids and cyclophosphamide; relapses are common., Microscopic Polyangiitis, Necrotizing vasculitis involving multiple organs, especially LUNG and KIDNEY. There is skin involvement, pauci-immune glomerulonephritis and PALPABLE PURPURA!, Definition of Pacui-immune glomerulonephritis: Pauci-immune (pauci- Latin: few, little) is a general term used to refer to a form of vasculitis that is associated with minimal evidence of hypersensitivity upon immunofluorescence and a lack of Anti-glomerular basement membrane antibody., Presentation, Similar to Wegener Granulomatosis, but Upper Respiratory Tract (nasopharyngeal) involvement and granulomas are absent., Note: Serum p-ANCA levels correlate w/ disease activity!(Mneumonic: "P"olyangiitis is for P-ANCA), Treatment, Cyclophosphamide and glucocorticoids; relapses are common., Churg-Strauss Syndrome, Nectozing granulomatous inflammation w/ EOSINOPHILS involving multiple organs, especially lungs and heart., Asthma and peripheral eosinophilia are often present., Serum p-ANCA levels correlate w/ disease activity also IgE levels are elevated!!!!!, Asthma, sinusitis, PALPABLE PURPURA (like in microscopic polyangiitis), peripheral neuropathy (e.g., wrist/foot drop). Can involve GI and Kidneys (pauci immune glomerulonephritis- just like microscopic polyangiitis) in addition to lungs and heart., Henoch-Scholein Purpura, Vasculitis due to IgA immune complex deposition; most common vasculitis in children, Presentation, Presents w/ PALPABLE PURPURA on buttocks and legs, GI pain and bleeding, and hematuria (IgA nephropathy); usually occurs following an upper respiratory tract infection. (Note: in the kidney IgA complexes are getting deposited in the mesangium. Also, the previous respiratory tract infection usually is the factor that produces the excess IgA.), Classic TRIAD, 1. Skin: palpable purpura on buttocks/legs, 2. Arthalgia, 3. GI: abdominal pain, melena, multiple lesions of same age., Treatment, The disease is self-limited, but may recur; treated also w/ steroids if severe.
Primary HTN, HTN of unknown eitology (95% of cases), Risk factors include age, race (increased risk in African Americans, decreased risk in Asians), obesity, stress, lack of physical activity, and high-salt diet.
Secondary HTN, HTN due to an identifiable eithology (5% of cases), Pathophysiology, 1. Stenosis decreases blood flow to glomerulus., 2. Juxtaglomerular apparatus (JGA) responds by secreting renin, which converts angiotensinogen to angiotensin I., 3. Angiotensin I is coverted to angiotensin II (ATII) by angiotensin converting enzyme (ACE)., 4.ATII raises blood pressure by 1. contracting arteriolar smooth muscle, increasing TPR and 2. promoting adrenal gland release of aldosterone, which increases resorption of sodium in the distal convoluted tubule (expanding plasma volume)., 5. Leads to HTN w/ increased plasma renin and unilateral atrophy (due to low blood flow) of the affected kidney; neither feature is seen in primary hypertension., http://www.youtube.com/watch?v=PEVE4ZR66V0&list=PLqTetbgey0ad6pWRVGoRIoj--pneouZQh Renin-ATII-Aldosterone System, Renal artery stenosis is a common cause of (renovascular HTN)., Important causes of stenosis include atherosclerosis (elderly males) and fibromuscular dysplasia (young females)., Fibromuscular Dysplasia, Fibromuscular Dysplasia • The Wall Street Journal says many medical schools do not address this! • Refers to focal/segmental thickening of the walls of medium to large muscular arteries (usually medial, arteries may have a “string of beads” appearance) • Can affect renal, splanchnic, carotid, vertebral arteries • F > M, typical age 20 to 50 years • Can be asymptomatic or cause hypertension, headaches, dizziness, tinnitus (depending on the artery involved), even with aneurysm formation or rupture or stroke if severe • Condition is developmental and familial in some cases • Treatment may be antihypertensive and antithrombotic meds or angioplasty if necessary
Benign HTN, HTN is a mild or moderate elevation in blood pressure; most cases of HTN are benign., Clinically silent; vessels and organs are damaged slowly over time.
Malignant HTN, Severe elevation in blood pressure (>200/120 mm Hg); comprises <5% of cases., May arise from preexisting benign HTN or de novo., Presentation, Presents w/ acute end-organ damage (e.g., acute renal failure, headache, and papilledema) and is a medical emergency.
General Info, Increased blood pressure; may involve pulmonary or systemic circulation. Systemic HTN is defined as pressure >/= 140/90mm Hg (normal </= 120/80 mm Hg); divided into primary or secondary types based on eitology.
Atherosclerosis, • This is the most significant type of arteriosclerosis, and is responsible for approximately half of deaths in the Western world • It primarily affects the aorta and the larger elastic and muscular arteries (the arteries that have names that you know), Involved Arteries in Atherosclerosis • Aorta, abdominal > thoracic; worse around major ostia • Popliteals, internal carotids, Circle of Willis • Coronaries • Usually spared are the upper extremity arteries, mesenteric & renals except at ostia • Pulmonary arteries not involved except with severe pulmonary hypertension; veins not involved, Note: If the ascending thoracic aorta is severely involved, the causes include diabetes mellitus, hyperlipidemia type II, and syphilis., Basic Lesion: The Atherosclerotic Plaque, • Start out as small intimal plaques -> get larger -> more numerous -> coalesce • Plaques are typically patchy and eccentric • Plaques secondarily compress and thin the media • Plaques consist of varying amounts of lipid and fibrous tissue • Some compensatory dilatation of the vessel may occur (up to a point), Notes: The three principle components of the plaque are:, Cells: Modified smooth muscle cells, macrophages recruited from blood, monocytes, and T lymphocytes, Lipid: Intra- and extracellular. Mostly cholesterol and cholesterol esters, Other extracellular content: Collagen and elastin, proteoglycans, calcium, Complicated Atherosclerotic Plaques, • Calcification – may be extensive • Focal rupture or ulceration – may be accompanied by: o Hemorrhage into plaque o Thrombus formation on plaque o Escape of lipid from plaque --> cholesterol emboli (atheroemboli) • Weakening of media --> aneurysm formation, Note: Thrombus may occlude the lumen --> infarct, or may cause thromboemboli. Hemorrhage into a plaque may also cause occlusion of lumen & hematoma formation in vessel wall., Note: There is initially some outward remodeling of the affected vessel in order to preserve the lumen (allowing blood flow). However, the remodeling fails after some time and the plaque begins to grow into the lumen obstructing blood flow., The Fatty Streak, • Yellow, minimally raised intimal lesions seen in children & young adults • Microscopically see lipid-laden macrophages in the intima – streaks go away as AS takes over • Location of streaks is similar (not identical) to later AS plaques • Relationship to later AS is complex and unclear, Note: Both fatty streaks and atherosclerotic plaques are related to increased blood lipids and smoking. Fatty streaks may be seen in populations where atherosclerosis is not prevalent., Epidemiology, Age: Starts in childhood & progresses over decades. Early AS is a common autopsy finding in teens & 20s, but not clinically significant until middle age or later when AS causes symptoms/organ injury., Sex: M>F, Uncommon in women of child bearing age (unless other strong risk factors are present). The difference equals out by about age 60 – 70. Estrogen replacement offers some protection., Genetics: There is a well-established genetic predisposition to atherosclerosis, probably polygenic & related to the genetics of the other risk factors; i.e. diabetes, hyperlipidemia, hypertension., RISK FACTORS, Hyperlipemia (increased LDL and decreased HDL cholesterol), Hypertension (blood pressure >130/80 mm Hg or on antihypertensive medication), Cigarette smoking, Family history of premature AS (coronary heart disease in 1st degree male relative <55 years old or 1st degree female relative <65 years old), Diabetes mellitus
Ateriolosclerosis, Narrowing of small aterioles; divided into hyaline and hyperplastic types., Hyperplastic arteriolosclerosis involves thickening of vessel wall by hyperplasia of smooth muscle ('onion-skin' appearance)., 1. Consequence of malignant HTN, 2. Results in reduced vessel caliber w/ endo-organ ischemia, 3. May lead to fibrinoid necrosis of the vessel wall w/ hemorrhage; classically causes acute renal failure w/ a characteristic 'flea-bitten' appearance (in the kidney- pinpoint hemorrhages)., Hyaline Ateriolosclerosis, Hyaline ateriolosclerosis is caused by proteins leaking into the vessel wall, producing vascular thickening; proteins are seen as pink hyaline on microscopy., 1. Consequence of long-standing benign HTN or diabetes, 2. Results in reduced vessel caliber w/ endo-organ ischemia; classically produces glomerular scarring (arteriolonephrosclerosis) that slowly progresses to chronic renal failure.
Monckeberg Medial Calcific Sclerosis, Calcification of the media of musclar (medium-sized) arteries; non-obstructive. Not clinically significant; seen as an incidental finding on X-ray or Mammography.
General Info, • Simply means hardening (sclerosis) of arteries • May affect small arteries/arterioles (arteriolosclerosis) • A rare type is fibromuscular dysplasia • The big one is atherosclerosis, Clinical Consequences of Arteriosclerosis • Ischemia of distal organs/tissues: o Myocardial infarct o Brain infarct (stroke) o Small bowel and kidney infarcts o Gangrene of lower extremities • Abdominal aortic aneurysm, Note: Ischemia in general is worse than hypoxia. With ischemia, tissues are hypoxic and cellular waste products are not removed. Some degree of adjustment to pure hypoxia is possible, e.g. accommodation to high altitude.
Hemangioma (p.278 FA2013), General Info, Benign tumor comprised of blood vessels. Commonly present at birth; often regress during childhood. Most often involves skin and liver., Strawberry Hemangioma, Benign capillary hemangioma of infancy. Appears in first few weeks of life (1/200 births); frows rapidly and regresses spontaneously at 5-8yrs of age., Cherry Hemangioma, Benign capillary hemangioma of the elderly. Does not regress. Frequency increases w/ age., Pyogenic granuloma, Polypoid capillary hemangioma that can ulcerate and bleed. Associated w/ TRAUMA and PREGNANCY!!
Angiosarcoma, Rare blood vessel malignancy typically occuring in the head, neck, and breast areas. Associated w/ patients receiving RADIATION THERAPY, especially for breast cancer and Hodgkin's lymphoma. Very agressive and difficult to resect due to delay in diagnosis., General Info, Malignant proliferation of endothelial cells; highly aggressive. Common sites include skin, breast, and liver., Liver angiosarcoma is aocciated w/ exposure to POLYVINYL chloride (PVC Pipes), arsenic and Thorotrast.
Kaposi Sarcoma, Endothelial malignancy most commonly of the skin, but also mouth, GI tract, and respiratory tract. Associated w/ HHV-8 and HIV. Frequently mistaken for bacillary angiomatosis., General Info, Low-grade malignant proliferation of endothelial cells; associated by HHV-8., Presentation, Presents as purple patches, plaques, and nodules on the skin; may also involve the visceral organs., Classically are seen in 1. Older Eastern European males- tumor remains localized to skin; treatment is surgical, 2. AIDS- tumor spreads early; treatment is antiretroviral agens (to boost immune system, and 3. Transplant recipients- tumor spreads early; treatment involves decreasing immunosuppression.
Bacillary angiomatosis, Benign capillary skin papules found in AIDS patients. Caused by Bartonella henselae infections. Frequently mistaken for Kaposi's Sarcoma.
Lymphatic tumors, Lymphangiosarcoma, Lymphatic malignancy associated w/ persisten lymphedema (e.g., post-radical mastectomy)., Cystic hygroma, Carvernous lymphangioma of the neck. Associated w/ TURNER Syndrome!!!!!!!
Globus Tumor, Benign, PAINFUL, reb-blue tumor under fingernails. Arises form modified smooth muscle cells of glomus body.
What causes the sound of a murmur?, The sound of a murmur can be caused by turbulent flow through chambers of the hear or open orifices in the heart. There for some murmurs may be the sound of a natural occurrence and ensue no pathology (i.e. Pregnancy due to blood volume expansion). However, some murmurs are pathological and are more directly caused by: flow into dilated chambers, flow across abnormal connections between chambers (i.e. VSD, fistula)
Murmurs have different Intensities that are graded 1-6 (2 & 3 are the most commonly evaluated.), Grade 1: Not immediate audible (takes a lot of experience to hear this grade of murmur), Grade 2: Heard w/ each cardiac cycle but not loud., Grade 3: Loud murmur w/o a thrill, Grade 4: Loud murmur W/ a THRILL!!!! (the thrill denotes a grade 4 murmur-key concept), Grade 5: A very loud murmur (thrill still included), Grade 6: May be heard w/ stethoscope off the chest (thrill still included)
Murmurs are classified based on the timing in which they occur during the cardiac cycle., Systolic Murmurs, Systolic Ejection Murmurs (Most common type of murmur!), Description: Originates from Ventricular outflow tracts (either LV or RV). This makes sense because the blood flows OUT the ventricles during systole---consistent w/ this being a systolic murmur. Begins after the S1 and terminates before S2! This murmur has a diamond shaped patter or crescendo-decrescendo pattern (non music people it gets loud to a maximum volume and then gets softer- all of this happening between the S1 and S2 sounds). Duration and timing of peak intensity vary with severity of OBSTRUCTION., Causes, Increased flow through normal structures (i.e. anemia, fever, pregnancy, thyrotoxicosis, etc.), Increased flow through abnormal structures (i.e. subvavular (Hypertrophic Cardiomyopathy), valvular (aortic stenosis, or pulmonic stenosis), or supravalvular (usually problems in the left ventricle/ LV)., Note: the duration and timing of the peak intensity (the maximum volume) is prognostic and helpful with diagnosis. (i.e. early peaks are not as severe- usually pregnancy or some other non threatening state. late peaks are usually severe- aortic stenosis.), Holosystolic Murmurs (throughout systole), Description: This murmur is ALWAYS ABNORMAL!!! The murmur has a plateau configuration that starts with S1 and ends with S2. (Plateau means that the volume of the murmur is constant throughout systole. The loudness of the murmur does not increase or decrease when observed.), Causes, Reflects abnormal flow between two chambers that have different pressures throughout systole. (i.e. Mitral Regurgitation, Tricuspid Regurgitation, or a VSD), Late Systolic Murmurs (Immediately think Mitral Valve Prolapse!!!), Description: This murmur occurs late in systole (delay after S1- unlike holosytolic murmurs), crescendos until S2, and is usually preceded by a midsystolic click (from the mitral valve leaflets "popping back on each other like a parachute in to the left atrium")., Causes, Mitral Valve Prolapse, Persons are born with increased tissue in the mitral valve leaflets. This tissue consists of extra glycoprotein that absorbs more water causing the floppy mitral leaflets. This causes the billowing effect into the LA during systole. Note: the heart's Cardiac Output with MVP is actually better initially due to the decreased afterload (systemic pressure's effect on outflow of blood from the aorta) because the afterload pressure is relieved by the Mitral valve prolapsing into the left atrium during ventricular contraction (when normally the mitral valve would be shut tight not able to alleviate the afterload pressure)., Diastolic Murmurs, Immediate ('early') diastolic murmurs, Description: This murmur begins with S2 and has a decrescendo pattern (gets softer in sounds as diastole progresses). This sound is produced when a semilunar valve has regurgitation! i.e. Aortic Regurgitation, Delayed ('mid') diastolic murmurs, Description: This murmur begins after S2 and this is a low pitched sound.The sound is augmented w/ atrial contraction., Causes, (Most Common) Mitral or Tricuspid Valve Stenosis, Severe Aortic Regurgitation/ Austin Flint murmur (an interesting Exception), Regurgitant flow pushes the mitral valve shut prematurely., Continuous Murmurs (throughout Systole and Diastole), Description: This murmurs begins with S1 and sounds throughout sytole and diastole. THINK PATENT DUCTUS ARTERIOSUS (PDA)! The sound of the murmur is due to flow form high pressure to low pressure through the cardiac cycle. It sounds like a "high pitched" 'Machinery' type murmur., Causes, (Most Common) PDA- Patent Ductus Arteriosus; fistula, Normal Variants, Mammary Souffle (Rare)- The sound of blood flowing through the left internal mammary artery can be appreciated. Also the thoracic artery., Cervical Venous Hum- sound of the SVC and IVC in children., Radiation of Murmurs (most common), Aortic valve murmurs are located at the RUSB and radiated to the carotids or apex., Pulmonic valve murmurs are located at the LUSB and radiate to the back., Mitral valve murmurs are located at the APEX and radiate to the axilla., Tricuspid valve murmurs are located at the LLSB (no radiations), Note: Mitral Valve Prolapse (MVP) can radiate anteriorly.
Dynamic Auscultation, Dynamic auscultation is a tool that we use to augment murmurs to better distinguish between similar sounding murmurs. This method is used mostly to distinguish Mitral Valve Prolapse (MVP) from Hypertrophic Cardiomyopathy! (For ICM purposes this is all that well will evaluated the difference between.)
Left Sided Heart Failure
Right Sided Heart Failure
Acute Pericarditis, Etiology, Most (~70%) are idiopathic-- presumed to be viral, TB/ histoplasmosis, Purulent (bacterial), Neoplastic, Radiation, Connective tissue disease, Post-myocardial infarction (Dressler’s), Uremia, Viral -coxsackie, echovirus, adenovirus, influenza -HIV, Presentation, ‘Pleuritic’ chest pain -Sharp, stabbing -Worse on deep inspiration and laying flat, better forward -Radiates to left trapezius ridge, Fever, malaise, dyspnea, URI symptoms, What on the differential Dx when considering acute pericarditis?, Acute coronary syndrome Pulmonary embolism Pneumothorax Pneumonia Pleurisy Musculoskeletal Myocarditis Esophageal, Physical Exam Findings, Sinus tachycardia, Fever, Pericardial friction rub, Phonogram of Friction Rub (Three sounds from left to right- 1. Ventricular systole, 2. Ventricular Diastole, 3. Atrial Systole), Lab Findings, ECG, Sinus tachycardia, Diffuse concave ST elevations, PR segment depression (PR elevation in aVR), How do we evaluate if a patient has acute pericarditis? What are we looking for?, Typical history, exam, ECG findings, ESR, CBC, chemistries, CXR usually normal, Echo if suspected concurrent effusion, Viral studies usually not performed, Autoimmune serologies (ANA, RF, etc.), Pericardiocentesis if suspect purulent pericarditis, malignancy, or large effusion, Treatment, High dose aspirin (2-6 grams/day), NSAIDS, Colchicine (normally treats gout- Anti-inflammatory drug), Corticosteroids, Pericardiocentesis for tamponade or suspected purulent pericarditis, Intensified hemodialysis for uremic pericarditis, Complications of Acute Pericarditis, Pericardial effusion & tamponade, Constricitve pericarditis (seen later post-percarditis episode), Relapse
Pericardial Effusion, Causes of Pericardial Effusion, **Acute pericarditis, **Radiation, **Malignancy, Cardiac perforation, Hypothyroidism, Connective tissue disease, Post-myocardial infarction/ heart surgery, Chronic renal failure, Aortic dissection
Pericardial Tamponade, Pathophysiology, 1. Pericardial fluid increases intrapericardial pressure, 2. Increased intrapericardial pressure impedes diastolic filling of LV and RV, 3. RV and LV diastolic pressure rises, 4. Stroke volume and cardiac output decrease, 5. Systemic BP drops, pulse pressure narrows, and heart rate increases, Gradual Tamponade (blue) vs. Acute Tamponade (red), When the tamponade formed gradually the pericardium had time to stretch to accommodate the increased volume; however, in an acute tamponade the volume increases faster than the pericardium can accommodate. Acute tamponade leads to very massive increase in pressure with small effusion volumes amounts that can cause severe acute diastolic dysfunction., Presentation, Depends on chronicity of the process, ‘CHF’ symptoms with clear lungs, Unexplained signs of right heart failure (edema, increased JVP), New ‘cardiomegaly’ on CXR, Sinus tachycardia, low voltage, electrical alternans on ECG, Hemodynamics in Developing Tamponade, Intrapulmonic pressure gradually rises., Heart Rate gradually rises., Stroke Volume gradually decreases., Cardiac Output gradually decreases., Mean Arterial Pressure stays constant for a while and then suddenly declines., Physical Exam findings, Sinus tachycardia, Tachypnea, Hypotension (late) with narrow pulse pressure, Elevated JVP with ****loss of Y descent, Remember, the Y descent in JVP is due to opening of the tricuspid valve which allows for blood to flow away from the Right Atrium (RA) into the Right Ventricle (RV). The blood flowing away from RA causes the decrease in JVP. However, in the case of pericardial tamponade- the right heart is compressed by fluid volume preventing diastolic filling of the ventricles. So, during diastole the tricuspid valve is open; but there is not much blood volume filling the RV due to the tamponade leading to loss of the Y descent., Edema, ****Pulsus paradoxus, Mechanism in Tamponade #1, Mechanism in Tamponade #2, Radial Artery Reading, In short the Radial Artery pulses diminish or obliterate completely on inspiration., How do we evaluate patient who we suspect have Pericardial Tamponade?, History & physical exam, ECG, CXR, Emergent echocardiogram with Doppler, Right heart catheterization (equalization of pressures), Treatment, Tamponade is a Medical emergency!!!!, IVF (temporizing), AVOID diuretics, vasodilators, etc., The tamponade causes the patient to have diastolic filling dysfunction, and giving a diuretic will cause the filling dysfunction to get worse. Why? -Because the fluid volume of the blood will decrease as a direct result of the diuretic. This will decrease the preload adding to the diastolic dysfunction., Vasopressors as needed, Prompt pericardiocentesis, Pericardial window
Constrictive Pericarditis, Pathophysiology, Chronic thickening/scarring of pericardium leads to encasement of heart and impaired diastolic filling of LV & RV, Early diastolic filling unimpaired, Chambers expand and collide with unyielding pericardium which halts further diastolic filling, ‘Dip and Plateau’ or ‘Square Root’ sign, Etiology, Idiopathic or viral 42 to 49% Post cardiac surgery 11 to 37% Radiation therapy 9 to 31% Connective tissue 3 to 7% disease Post TB, bacterial 3 to 6% Miscellaneous 1 to 10%, Presentation, Slow, indolent process, Unexplained right heart failure, systemic congestion (edema, ascites, hepatomegaly., Fatigue, Dyspnea, Often misdiagnosed as cirrhosis!, Physical Exam Findings, Elevated JVP w/ prominent X&Y descents, Kussmaul's sign, abnormal rise or unchanged pressure in JVP. Normally JVP falls with inspiration a small amount., Pericardial Knock, Systemic Congestion (hepatomegaly, ascites, edema), How do we evaluate patients we think may have Constrictive Pericarditis?, History & physical exam, ECG (low voltage, ST & T wave changes), CXR (pericardial calcification), Chest CT (pericardial thickening), Cardiac MRI, Echocardiogram, Simultaneous right and left heart hemodynamics (***equalization of LV & RV diastolic pressures), Treatment, Diuretics, Pericardial Stripping (surgical procedure)
Normal Pericardium, Sack that surrounds all cardiac chambers and reflects around great vessels., Two layers, Parietal is fibrous external sack, Visceral is adjacent to the epicardium (internal sack)., Normally, about 15cc of serous fluid is present between the two layers to increase lubrication and decrease friction.
Bradyarrhythmias and Conduction Disturbance
Dilated Cardiomyopathy, Describing Size, Function, and Thickness of the LV, Enlarged, depressed, normal respectively, Presentation of Dilated Cardiomyopathy (DCM), Symptoms, Fatigue Exertional dyspnea Orthopnea Paroxysmal nocturnal dyspnea (PND) Edema Palpitations/syncope Embolic events, Physical Exam, Low systolic BP Elevated JVP Pulmonary crackles (rales) Laterally displaced PMI S3 Parasternal heave Murmurs of functional mitral/tricuspid regurgitation Hepatomegaly Edema, Diagnosis of Dilated Cardiomyopathy (DCM), Compatible history, Typical physical findings, ECG (bundle branch block, ST-T changes), Chest film (cardiomegaly, congestion), Echocardiogram -LV dilatation and systolic dysfunction -RV dilatation and systolic dysfunction -LA/RA enlargement - ’Functional’ mitral and tricuspid regurgitation -Intracardiac thrombi, Cardiac MRI, Causes of Dilated Cardiomyopathy (Non-ischemic; excludes CAD, HTN, and valvular disorder), ****Myocarditis Toxins (alcohol, cocaine, amphetamines) Drugs (anthracyclines, Herceptin, Cytoxan) Familial- (genetic 2-30% of cases; mostly autosomal dominant inheritance of defective "CYTOSKELETAL" protein as in Duchenne & Becker Muscular Dystrophy.) Tachyarrhythmias Stress (Takotsubo) Peripartum Metabolic (thyroid, nutritional deficiencies, pheo) Muscular dystrophies Left ventricular non-compaction Idiopathic, FYI, Notes: The progression from viral myocarditis to dilated cardiomyopathy has been demonstrated by serial myocardial biopsies. However, in most cases of DCM, the heart shows little or no residual inflammation. Toxic causes of DCM are hard to prove – no good way to tell apart from other DCM. The etiology of peripartum CM may be multifactorial, including factors such as hypertension, volume overload, poor nutrition, possible metabolic abnormalities or autoimmune phenomena., ****Myocarditis most common cause of Dilated Cardiomyopathy. - Inflammatory Disease of myocardium Note: The cardiomyopathy develops years later post myocarditits event., Causes of Myocarditis, ****Viral (parvovirus B19, HSV 6, coxsackie, echo, HIV) Most common cause is Viral!!!! Other infectious (Lyme, Chagas disease, rheumatic fever) Autoimmune (lupus, RA ) Hypersensitivity reactions (drugs) Sarcoidosis Giant cell myocarditis, heart transplant rejection, Presentation of Myocarditis, Many cases are asymptomatic, Non-specific ‘viral illness’ (fevers, myalgias), Chest pain and troponin elevation mimicking MI, Pleuritic chest pain and ECG changes (myopericarditis), Fulminant course with fever, hemodynamic instability, ventricular arrhythmias or heart block, Chronic CHF with dilated cardiomyopathy, Sudden death, How to Diagnose Myocarditis, Non-specific markers of inflammation (ESR, leukocytosis) in most, Troponin elevation in 30-50%, ECG usually abnormal but non-specific, Viral titers mostly unhelpful, Echo will show global or regional LV dysfunction, Cardiac MRI showing Myocarditis, Endomyocardial biopsy (limited sensitivity due to sampling error), Indication for a Biopsy, New onset CHF of <2 weeks duration with hemodynamic compromise, New onset CHF of 2 weeks to 3 months duration with ventricular arrhythmias, heart block, or failure to respond to treatment within 2 weeks, CHF and LV dilatation in setting of suspected allergic reaction, ***Looking for evidence of giant cell myocarditis (DON'T Miss This Diagnosis!), How to Treat Myocarditis, Largely supportive, Standard treatment for LV systolic dysfunction and CHF, Immunosuppressive and anti-viral therapy generally of no use, Exceptions: Giant cell myocarditis and sarcoidosis because use of corticosteroids is permitted and has benefit for the patients with this subset of cardiomyopathy., Microscopic, Notes: Grossly, hearts with active myocarditis are described as soft and flabby. The myocardium may be mottled and the heart may be dilated. Microscopically, viral myocarditis is characterized by a (nonspecific) lymphocytic infiltrate with myocyte necrosis., Flavors of Myocarditis, Viral Myocarditis, Clinical, • May be asymptomatic or minimally symptomatic • May rapidly develop heart failure, arrhythmias, or may cause sudden death • There may be a murmur due to cardiac dilatation causing mitral regurgitation • May heal completely, or may progress to dilated cardiomyopathy years later, General Information, • The most common cause of myocarditis in the US is viral, usually due to coxsackieviruses A and B and other enteroviruses • These are very difficult to isolate by viral culture of a myocardial biopsy; PCR may help • The inflammatory injury in viral myocarditis may be secondary to an immune cross reaction with myocytes and not by direct viral cytopathic injury, Chagasic Myocarditis, • Chagas disease – the protozoan bug is Trypanosoma cruzi • Important in South America – 80% with heart involvement – may be lethal or may go into chronic phase • Transmitted by insects such as reduvid bug • Microscopically see parasites within myocytes and mixed inflammation, Note: T. Cruzi may also cause destruction of the myenteric plexus of the esophagus, duodenum, colon and ureter with subsequent dilatation of these viscera (megacolon)., Giant Cell Myocarditis, • Has a rapid onset with a poor prognosis • Microscopically see myocardial necrosis with lymphocytes, plasma cells, eosinophils and giant cells • Has some overlap with sarcoidosis, but sarcoidosis has a more insidious onset • Some patients may recover completely or with some myocardial fibrosis • Etiology is unknown, Eiology of DCM that need evaluation, (Coronary angiography), in ( )'s because this is not a usual cause of DCM; however, 10% of patients with DCM have it due to an coronary ischemic event., Family history, Other family members have died from sudden death due to DCM predisposes the patient in question to higher risk of DCM., Genetic testing, helps other family members who may possibly have DCM and are currently asymptomatic., Laboratory evaluations (thyroid, iron studies, HIV, etc.), Cardiac MRI with gadolinium, Endomyocardial biopsy, Treating DCM, (Revascularization) Correct modifiable causes Beta blockers Ace-inhibitors Spironolactone Hydralazine/isosorbide dinitrate Diuretics Device therapies (ICD, resynchronization) Advanced therapies (inotropic support, LVAD, transplant)
Hypertrophic Cardiomyopathy, Describing Size, Function, and Thickness of the LV, Small, hyperdynamic, increased respectively, What is Hypertrophic Cardiomyopathy (HCM)?, Unexplained left ventricular hypertrophy associated with a non-dilated ventricle in the absence of another cardiac or systemic condition that could cause the observed degree of hypertrophy, FYI, Sudden death may be due to blockage of the left ventricular outflow by the anterior leaflet of the mitral valve. The leaflet may be sucked into the LVOT by “venturi” action of the blood flowing through the narrowed passage. HCM can be managed medically better than DCM., • Features a heart that is normal in shape, but with marked wall thickening due to hypertrophy (esp LV) often with asymmetric thickening of the septum and narrowing of the LV cavity • The heart is hypercontractile without LV cavity dilatation • The problem is diastolic filling and LVOT obstruction • Has a better prognosis than DCM, but may cause angina, CHF, A-fib, mural thrombus, infective endocarditis of MV • Can affect children or adults • HCM is one of the most common causes of sudden death in young athletes, Diagnosis of HCM, Note: To diagnose HCM, it is necessary to rule out other causes of myocardial hypertrophy such as hypertension and aortic stenosis. Also, distinguish based on clinical/family history, degree and pattern of hypertrophy, genetic testing, etc. in order to diagnose the patient., Differential Dx, Hypertensive heart disease, Aortic valve disease, Physiologic hypertrophy (athlete’s heart), Infiltrative/storage diseases, Physical Exam for HCM, Bisferiens carotid upstroke (‘spike and dome’), Sustained PMI, Sign of Left Ventricular Hypertrophy, S4, Sign of Left Ventricular Hypertrophy (atrial contraction volume on a stiff ventricle)., Systolic ejection murmur, Maneuvers to decrease LV size (murmur LOUDER) - Standing -Valsalva maneuver -Amyl nitrate Maneuvers to increase LV size (murmur SOFTER) -Squatting -Isometric handgrip exercise -Phenylephrine, Holosystolic murmur of mitral regurgitation, Evaluation of HCM, Clinical exam Family history ECG Echocardiography/Doppler Treadmill exercise testing with echo/Doppler Cardiac MRI (with gadolinium)- assess high risk groups. Genetic testing Arrhythmic risk stratification, High Risk Stratification for Sudden Cardiac Death (SCD), Personal history of resuscitated SCD, Family history of SCD, Unexplained syncope, Severe hypertrophy (>3cm), Abnormal blood pressure response to exercise, Ambient ventricular arrhythmias on ambulatory monitoring, Extensive myocardial fibrosis on MRI (?), ICD therapy, Pathophysiology of HCM, Notes: The septum may bulge into the left ventricular outflow tract. This acts in concert with the adjacent anterior leaflet of the mitral valve to produce left ventricular outflow tract obstruction. A harsh systolic ejection murmur may be present. Late cardiac dilatation in the course of HCM may actually relieve the LVOT obstruction., LV diastolic dysfunction Dynamic LV outflow obstruction -Present in ~25% at rest -Provokable in up to 75% Systolic anterior motion of mitral valve (SAM) Mitral regurgitation, Treatment of HCM, Management, Family screening, Restricted from competitive athletics, ICD for those a high arrhythmic risk, Manage the obstruction due to HCM, Medicinal, Beta blockers Calcium channel blockers Disopyramide Diuretics (cautious), note: BE VERY CAREFUL W/ DIURECTICS b/c they decrease the preload which in this case can decrease LV further, leading to MORE obstruction!, Surgical (Septal Reduction therapy), Surgical Myectomy, Alcohol septal ablation, CASE, 24 yo previously healthy man is referred for evaluation of a heart murmur. He reports mild dyspnea with heavier activity but is otherwise asymptomatic. He states a brother died suddenly at a young age of unclear cause. On exam, his BP is normal as is his JVP. Lungs are clear. Cardiac exam reveals a regular rhythm with normal heart sounds and an S4. The PMI is sustained but nondisplaced. There is a harsh III/VI systolic ejection murmur heard throughout. The remainder of his exam is normal. His ECG is abnormal, suggestive of LVH., This patient has a family history, physical findings, and ECG consistent with HCM Murmur is due to dynamic LV outflow tract obstruction resulting from septal hypertrophy and SAM Family history of sudden death indicates high risk of ventricular arrhythmia and sudden death in this patient (ICD is warranted)
Restrictive Cardiomyopathy (above are large atria due to poor diastolic funciton), Describing Size, Function, and Thickness of the LV, normal, normal, normal respectively, May; however, have signs of Heart Failure, Causes of RCM, • Things that infiltrate and stiffen the myocardium: o Amyloidosis o Sarcoidosis o Metastatic tumor o Some storage diseases (hemochromatosis) o Endomyocardial fibrosis (a tropical disease of unknown cause), Infiltrative disorders (amyloid, sarcoid) Storage diseases (hemachromatosis) Radiation Endomyocardial disorders (hypereosinophilic) Idiopathic Restrictive filling can be seen in advanced stages of ischemic CMP, dilated CMP, HCM, • Things that thicken and stiffen the myocardium and endocardium: o Endocardial fibroelastosis (in children - occurs with some types of congenital heart disease and rarely occurs alone) o Loeffler endomyocarditis (assoc. with eosinophilia or eosinophilic leukemia) o Endomyocardial fibrosis (a tropical disease of unknown cause) • Idiopathic restrictive CM – myocardium shows patchy or diffuse fibrosis, Pathophysiology of RCM, Severe impairment of ventricular filling High atrial pressures Pulmonary and systemic venous congestion Normal LV size ‘Normal’ LV systolic function Wall thickness may be normal or increased in infiltrative disorders, Presentation of Cardiomyopathy, Fatigue Exertional dyspnea Orthopnea Paroxysmal nocturnal dyspnea (PND) Edema Ascites, note: RCM must be differentiated from constrictive pericarditis. The way to distinguish the two is to use dynamic auscultation., How to treat RCM, Treat underlying disorder (if possible), Diuretics, Maintain sinus rhythm, Transplantation
Information about Cardiomyopathy, Disorders of the myocardium, often genetic, leading to left ventricular dysfunction Not the result of hypertension, ischemic heart disease, valvular or congenital heart disease May be primary or part of a systemic illness. There are three types of cardiomyopathies: Dilated (DCM), Hpertorphic (HCM), and Restrictive (RCM). Note: Dilated is the most common and Restrictive is the least common cardiomyopathy., Note: the term "cardiomyopathy" is used VERY loosely in the clinical setting to mean LV dysfunction. And because LV dysfunction can be due to ischemic and non-ischemic causes we categories cardiomyopathy into two categories., Ischemic Cardiomyopathy (due to CAD), Non-Ischemic Cardiomyopathy
Infectious Endocarditis, Pathophysiology, Most patients (~75%) have underlying structural heart disease or IVDU Most common underlying cardiac disorder in recent series is mitral valve prolapse Congenital heart disease (VSD, Tetralogy of Fallot, PDA, bicuspid aortic valve, etc.) Acquired valvular disease (rheumatic fever, degenerative, prosthetic valves, etc.) Other risk factors: diabetes, hemodialysis, HIV, poor dental hygiene, indwelling catheters, Common Pathogens, ~75% caused by Staph, Strep, and Enterococcal species, S. Aureus now most frequent agent accounting for ~35% of all cases, Viridans group strep (oral flora) and Strep bovis (associated with ulcerative colon lesions) account for ~30%, Enterococcal infections account for 10-15%, Enteric GNR and Pseudomonas aeruginosa (5%), Coagulase negative Staph species (~10%), Fungi (<5%), Culture negative (5-10%) due to prior antibiotic exposure, difficult to culture organisms (Coxiella burnetti, Legionella species, Bartonella species, Chlamydia species, fungi), Presentation, Constitutional symptoms: fever, chills, weight loss, night sweats, etc., Cardiac symptoms: predominantly those of CHF, conduction abnormalities, murmurs, Symptoms of peripheral embolism, Musculoskeletal complaints in up to 40%, Classic Signs, Subacute Infective Endocarditis: insidious-onset infection of a damaged valve by a less virulent organism (most commonly Viridans Strep, e.g., S. sanguis, S. mutans) → smaller vegetations; antibiotics are often curative., Bacteria FROM JANE:, Fever (most common symptom), Roth’s spots (retinal hemorrhages around white spots), Roth Spots, Retinal hemorrhages with central clearing Immunologic phenomena 4-10% of cases, Osler’s nodes (tender raised lesions on toes and fingers), Osler Nodes, Painful, palpable nodules often in finger pulp Immunologic phenomenon 7-10%, Murmur, Mitral (most frequently involved), Janeway lesions (nontender erythematous lesions on sole and palm), Janeway Lesions, Painless, non-blanching macular lesions often on palms and soles Embolic phenomenon 5-10% of cases, Anemia (usually anemia of chronic disease), Nailbed hemorrhage (split hemorrhage), Splinter Hemorrhage, Linear streaks within nail beds 5-15% of cases, Emboli (infarcts in different tissues), Laboratory Findings, Normocytic anemia: 50-80%, Abormal urinalysis (microscopic hematuria, casts, pyuria), Elevated ESR, CRP in vast majority, Rheumatoid factor in 50%, Elevated BUN and Cr, Symptoms, Fever: 80-85% Chills: 42-75% Sweats: 25% Anorexia 25-55% Weight loss: 25-35% Malaise: 25-40% Myalgia/arthralgia: 30% Back pain: 7-10% Dyspnea: 20-40%, Most important to consider, Fever: 80-90% Murmur: 80-85% New murmur: 10-40% Clubbing: 10-20% Splenomegaly: 15-50% Emolic event: 20-40% Neurologic abn.: 30-40%, How to Dx Endocarditis, Bacteremia with a characteristic organism, Evidence of endocardial involvement New regurgitant mumur Echocardiographic findings, Echocardiography, Transthoracic echo (TTE) has sensitivity of 50-60% and is insensitive for detecting complications, Transesophageal echocardiography (TEE) has sensistivity >95% and is much better at detecting complications, Initial TEE recommended if clinical suspicion moderate to high or difficulties with TTE expected, DUKE Criteria, Table 1A., Table 1B., Minor Criteria, Complications of Endocarditis, CHF, Mechanism is usually acute or progressive valvular regurgitation (leaflet perforations, ruptured chordae, flail leaflets), Occasionally bulky vegetations can obstruct inflow and fistulas can lead to intacardiac shunts, Aortic valve involvement more common than mitral or tricuspid and acute regurgitation worse than chronic, Strongest predictor of prognosis and strongest surgical indication (morality 50% without surgery), Emboli, Occurs in 25-50% of cases, Mitral valve higher risk than aortic valve (25% vs 10%), especially anterior leaflet involvement, Large (>1cm) and mobile vegetations higher risk, 65% occur in CNS (90% in middle cerebral artery territory), Risk of embolism highest early in course and drops dramatically with therapy, Spread of Infection, Intracardiac abscess AV conduction disturbance Prolonged fever or bacteremia Prosthetic heart valve, Mycotic aneurysm, Splenic abscess, Treatment, Antibiotics, Parenteral agents, Bactericidal agents, often in combination, Prolonged (4-6 weeks) courses of therapy, Surgery, CHF (class III-IV) due to valvular regurgitation or intracardiac shunting Paravalvular extension of infection (abscess, fistula, pseudoaneurysm) Presistent active infection (fever, bacteremia) despite 7-10 days of appropriate therapy Difficult to eradicate organisms (fungus, GNRs) Recurrent emboli despite therapy Prosthetic valve endocarditis, Prophylaxis, Endocarditis Prophylaxis, Small risk of endocarditis arising from bacteremias resulting from invasive procedures, Transient bacteremias from daily activities (tooth brushing) likely much higher risk, Maintain good oral hygeine, Highest Risk Conditions, Prosthetic cardiac valves, including bioprosthetic and homograft valves, Previous bacterial endocarditis, Complex cyanotic congenital heart disease (eg, single ventricle states, transposition of the great arteries, tetralogy of Fallot), Cardiac transplant recipients with valvular disease, Procedures, Dental procedures, Procedures on respiratory tract involving incision or biopsy, Cutaneous procedures involving infected skin, GI/GU procedures NO LONGER require routine prophylaxis, What is endocarditis, Infectious endocarditis refers to infection on any part of the endocardial surface, Acute endocarditis describes a rapid course with usually marked toxicity developing over days to weeks (usually S. Aureus), Subacute endocarditis describes a slower course with often modest toxicity over weeks to months, Native valve vs. prosthetic valve, Epidemiology, Incidence of ~6 cases per 100,000 patient years Changing epidemiology: Median age of those affected increasing S. Aureus now most common agent Antibiotic resistance Increased IVDU Increased nosocomial acquisition In-hospital mortality ~25%, Endocarditis in IVDU, Risk of endocarditis ~2%/year in IVDU, S. Aureus most common organism, Predilection for tricuspid valve (75% of cases) and can affect previously structurally normal valves, Septic pulmonary emboli common (pleuritic chest pain, hemoptysis, dyspnea, abormal CXR in 70%), Frequent association with HIV
Cardinal Symptoms of Cardiovascular Disease, Dyspnea, Orthopnea, Paroxysmal Nocturnal Dyspnea, Edema, Chest Pain, Palpitations, and Syncope
New York Heart Assoc. Classification for Dyspnea, ClassI: no dyspnea, ClassII: Dyspnea on more than usual activities (able to climb 2 flights/ walk 2 blocks), ClassIII: Dyspnea on less than usual activities (unable to climb 2 flights/ 2blocks), ClassIV: Dyspnea at rest or with any activity.
Cardiovascular Physical Exam, When checking blood pressure in upper and lower extremities, the systolic pressure difference should NOT exceed 20mmHg higher than upper ext., Pulse Pressure (Systolic pressure- Diastolic pressure), When feeling the patient's pulse the pulse pressure will given an idea of what underlying pathology may be present., i.e. a Wide pulse pressure will give a very strong and bounding pulse. This happens with anything that increases circulation (Aortic Regurgitation, Anemia, Thyrotoxicosis, pregnancy)., i.e. a Narrow pulse pressure will give a very weak pulse. This happens with any situation that decreases cardiovascular circulation (Aortic Stenosis, Severe LV dysfunction, Severe volume delpletion, Mitral Stenosis, and shock of any cause)., Blood PRESSURE, Normal: <120/80, PreHTN: 120-139/ 80-89, Stage I HTN: 140-159/90-99, Stage II HTN: >/= 160/100, note: 140/90 is the general diagnostic pressure for hypertension (HTN) if assessed on multiple occasions., P.E. findings/signs, Pulsus Parvus et Tardus, Slow carotid upstroke, low amplitude, small pulse pressure- usually due to severe Aortic Stenosis!, Corrigan's (Waterhammer) Pulse, Rapid carotid upstroke, high amplitude, Wide pulse pressure- usually due to Severe Aortic Regurgitation. The pulse can be so large at times that the patient will get a "bobble head"., Pulsus Paradoxus, This is a normal exaggeration of normal inspiratory fall in systolic blood pressure (note: <10mmHg fall in blood pressure during inspiration is normal). Therefore major falls in systolic BP during inspiration (>10mmHg) can be appreciated at the beside (if severe radial pulses may dissipate completely with inspiration). The major cause of Pulsus Paradoxus is PERICARDIAL TAMPONADE!!!!!! (Can also be caused by pericardial constriction, obstructive lung disease, massive Pulmonary Embolism (PE), or RV infarction., High Jugular Venous Pressure (JVP), Large 'V' waves JVP, Caused by Tricuspid Regurgitation! Blood is pumped from the RV during systole into the RA and the blood displaces up the SVC into the JV causing a subsequent rise in JVP! This can be massive depending on the severity of the regurgitation., 'Cannon' A waves JVP, Caused by Complete Heart Block (AV dissociation)! When the atria are not communicating the electrical signal to the ventricles to initiate synchronous contraction the ventricles periodically the ventricles contract while the tricuspid and mitral valves are open and this causes a MAJOR and SUDDEN increase in JVP! This increase is so large in fact that it can be appreciated at the beside by looking at the JV on the patient's right side., Hepatojugular Reflex when checking JVP, This reflex can be appreciated in a volume overloaded patient (CHF pts) by applying gentle sustained pressure over the liver to cause a transient increase in JVP. This increase is fairly large in patients with abnormal central JVP., Kussmaul Sign, Explaining what happens normally (when a Kussmaul sign is NOT present:, Normally, JVP decreases with inspiration due to increased negative intrathoracic pressure allowing blood to flow toward the heart and into the ventricles away from the JV and Atria., A Kussmaul Sign is appreciated when JVP increases during inspiration (ABNORMAL!!!)- also you will see this sign defined as a 'failure of JVP to decrease during inspiration'. The main cause of this is PERICARDIAL CONSTRICTION!!! (also RV infarct and severe RV failure)., Palpation of the Heart and great vessels, Palpable pulmonary artery in the 2nd left intercostal space suggest pulmonary HTN., If the ascending aorta is seen THINK Syphilis!!, Palpable P2 also suggest pulm HTN., PMI placement, normal, Point of Maximum Impulse (PMI) is normally located in the 4th-5th intercostal space in the mid clavicular line., Sustained, A sustained PMI is indicative of ventricular hypertrophy (RV or LV). (concentric hypertrophy- compensatory mechanism), Displaced, A displaced PMI is indicative of Left Ventricular Dilation due to volume overload. (eccentric hypertrophy- compensatory mechanism), Parasternal Heave, can be felt at the left sternal edge suggesting RV dilation/hypertrophy!, Thrills, Vibratory sensations felt on the precordium. This is used to determine/denote Grade 4 heart murmurs! This vibration is caused by abnormal flow across a heart structure particularly a valve., Tests, Jugular Venous Pressure, The jugular venous pressure (JVP) is measured by the right JV because it is a great estimate of RA pressure (note: there are no valves in the SVC or JV making the pressure in the RA translatable to the JV without interruption)., Why do we use it?, We use JVP to estimate Right Atrial Pressure (RA Pressure) when gauging volume status and intracardiac filling pressures in patients, and we use the JVP waveform to get clues on underlying cardiac disease states., JVP Wave Pattern, A Wave, The a wave is formed from atrial contraction., X descent, C wave, The C wave interrupts the X descent when the tricuspid valve closes. This cannot be appreciated at the bedside., The X descent is initiated by atrial relaxation., V Wave, The V wave is created from passive filling of the atria via SVC, IVC, and coronary sinus (RA) and (pulmonary veins for the LA)., Y descent, The Y descent is formed from opening of the tricuspid valve., Measuring Jugular Venous Pressure, Place the patient at a 45 degree angle. Measure the vertical height of the jugular venous pulsations above the sternal angle. Meaning- look along the JV for the point of maximum pulsation and mark that height level using a ruler over the sternal angle. When the number is obtained then add "5" to that number! Remember the measurement is in terms of cmH20 and not mmHg!!!!! You must convert this cmH20 to mmHg by using the specific gravity of mercury (1.36cm H20 = 1mm Hg). Note: normal JVP should be less than 7 cmH20., Blood Pressure, Heart Sounds, S1, The first heart sound is due to the closure of the Mitral Valve (and tricuspid valve). This may be split but it happens RARELY. S1 is LOUD in MITRAL STENOSIS and is soft in aortic regurgitation. (Note: S1 denotes the start of systole.) This sound is heard best at the APEX of the heart., S2, The second heart sound is due to the closure of the Aortic Valve and Pulmonic Valve. This sound is split very often- most commonly (non-pathological) is a split with inspiration. This split is due to changes in intrathoracic pressures during inspiration causes a delay in pulmonic valve closure giving the split S2 sound. The sound is heard best at the BASE of the heart. Loud P2 means pulm HTN., Abnormal S2 Splits, S2 Fixed Split, Due to an Atrial Septal Defect, S2 Paradoxic Split, Due to a Left Bundle Branch block that delays the closure of the aortic valve (closes after the pulmonic valve => paradoxical)., S2 Persistent Split, Due to a Right Bundle Branch block that causes a widened split between the aortic and pulmonic valves closing; however, this split is dynamic increasing and decreasing in split size with inspiration. The pulmonic valve is delayed and it takes long for it to close. This delay is increased further when the patient inspires, and unlike normal S2 splitting the A2/P2 Split persists during expiration., S3, Originates from rapid ventricular filling in the early diastole. This may be normal in children and young adults. This is pathologic in CHF patients. May originate in LV (apex) and RV (LSB). The sound can be augmented (made louder) by passive raising the leg and isotonic exercise., S4 (Always Abnormal), Originates in from atrial contraction into a stiff ventricle (LVH, ischemia, HTN). Therefore atrial contraction must be present in order to have the sound. Atrial fibrillation eradicates the S4 heart sound. The sound may originated from the LV and RV as well. May be augmented at bedside with isometric exercise., Early diastolic sounds (T.O.P.S.), Tumor 'plop' (atrial myxoma), Opening Snap (mitral stenosis), Pericardial knock (constrictive pericarditis), S3 (normal or pathologic), Systolic sounds, Systolic ejection click after S1 (bicuspid aortic valve), Mid-systolic click (mitral valve prolapse), Abdominal exam, Organomegaly, Pusatile Mass (abdominal aortic aneurysm), Bruits (renal artery stenosis), Ascites, Extremity exam, Clubbing (cyanotic congenital heart disease), Cyanosis, Edema, Skin exam, Splinter hemorrhages, Janeway Lesions, Osler Nodes