Cardio review

HIsto Findings pots MI -

*During the first 24 hours* (1) No gross changes are evident until 24 hours. (2) Coagulation necrosis is present within 12 to 24 hours. (3) Neutrophils begin to enter the area of infarction from the periphery. * From 1 to 3 days* (1) Pallor of the infarcted tissue is apparent. (2) Myocyte nuclei and striations disappear (see Fig. 2-15A). (3) Neutrophils are abundant and lyse dead myocardial cells. * During days 3 to 7* (1) Red granulation tissue surrounds the area of infarction. PERICARDITIS (2) Macrophages begin to remove necrotic debris. WEAKNESS (3) This period is the most dangerous time for rupture. *From 7 to 10 days* (1) Necrotic area is bright yellow (Fig. 11-6; see Fig. 2-15B). (2) Granulation tissue and collagen formation are well developed. *During the first 2 months* (1) Infarcted tissue is replaced by white, patchy, noncontractile scar tissue. (2) If the amount of scar tissue is increased, CIHD is likely to occur (see earlier).

Classic ECG patterns in AMI

*LAD coronary artery anterior wall infarction* • Q waves in leads V1-V4 *Anteroseptal infarction due to proximal LAD coronary artery occlusion* • Q waves in leads V1-V2 * Anterolateral infarction due to mid-LAD or circumflex coronary artery occlusion* • Q waves in leads V4-V6, I, aVL *Lateral wall infarction due to left circumflex coronary artery occlusion* • Q waves in leads I, aVL *Inferior wall infarction due to RCA occlusion* • Q waves in leads II, III, aVF

Causes of RV hypertrophy

*Pulmonary Hypertension (SMC apoptotic factor bmpr2 out, SMC hypertrophy)* Plexiform lesions -Emphysema -MCTD [U1 ribonucleoprotein] -L2R shunts VSD --> (Eisenmenger) -Recurrent PE's -Obstructive Sleep apnea *Pulmonary Valve Stenosis*

PV stenosis in ToF

(A)Minimal infundibular PV stenosis or PV stenosis - Leads to increased oxygenation of blood in the lungs - Less right-to-left shunting of blood through the VSD - Absence of cyanosis (Sao2 >80%; acyanotic tetralogy). (B) Severe infundibular stenosis or PV stenosis -Less oxygenation of blood in the lungs - Increased right-to-left shunting of blood through the VSD -Cyanosis is present (Sao2 <80%). A PDA shunts unoxygenated blood from the Ao to the PA for oxygenation in the lungs.

Tricuspid valve (TV) regurgitation

-MC from stretching in RHF Pansystolic murmur heard best along the left parasternal border (1) S3 and S4 heart sounds are present (2) Deep held inspiration for 3 to 5 seconds increases the intensity of the murmur and the abnormal heart sounds Retrograde blood flow into the RA during systole due to stretching of the TV ring or damage to the TV Causes RA dilatation and hypertrophy and backup of pressure into the venous system c. Eccentric RVH due to volume overload of the RV -Pulsating liver Blood backs up into the venous system and increases hepatic vein blood flow to the central venules, leading to an increase in pressure in the sinusoids and portal vein. - Dependent pitting edema from increased venous hydrostatic pressure - Ascites due to increased portal vein pressure -Giant c-v wave is present in the jugular venous pulse

Pharmacologic therapy for angina involves the use of antiischemic agents

-Nitrates (release nitric oxide) cause venodilation (reduces preload and wall tension in the ventricles) vasodilation of the coronary arteries, and vasodilation of peripheral resistance arterioles (reduces afterload). -β-Blockers decrease myocardial O2 consumption by reducing heart rate and systolic blood pressure (initial therapy for all patients with stable angina) -Calcium channel blockers cause vasodilation of the coronary arteries and peripheral resistance arterioles. They are the drug of choice for treating Prinzmetal variant angina. -Aspirin inhibits platelet aggregation, which decreases the risk for developing a platelet thrombus -Clopidogrel (inhibits platelet aggregation by irreversibly inhibiting a receptor called P2Y12, an Gi purogenic ADP chemoreceptor on platelet cell membranes.) should be used if patients are allergic to aspirin -Heparin plus aspirin is used for patients with unstable angina and reduces the risk for developing a myocardial infarction and refractory angina -Ranalozine (Na+ channel blocker, last resort for chronic angina - inhibits calcium overload) -If homocysteine levels are increased, the patient should be placed on pharmacologic doses of folic acid -prevent platelet thrombosis in these revascularization procedures, abciximab (inhibits the Gpllb-llla fibrinogen receptor in platelets

SHF treatment

-decrease afterload/ workload ACEi (ARB if bradykinin or angioedema develops) Diuretics to decrease preload B-blockers to reduce O2 consumption Digitalis may be useful because of its inotropic and vagotonic effects, particularly in those with severe heart failure or atrial arrhythmias. Direct vasodilating drugs (e.g., hydralazine) reduce systemic vascular resistance and pulmonary venous pressure.

IE pathology

-fever of unknown origin -Roth spot (irregular red area with central white do) -splinter hemorrhages -janeway lesions (painless on palms and soles) -osler node (painful nodules on pads of fingers or toes) -Heart murmurs (regurgitant types) may change in intensity because of microembolization and progressive damage to the valve (85% of cases). Splenomegaly is present if IE is subacute. Turbulent blood flow damages the valve → adherence of fibrin and platelets to the areas of damage → trapping of circulating bacteria/fungi → proliferation of the pathogens + laying down of fibrin to encase the vegetation - Viridans group of streptococci infect previously damaged valves. -. Staphylococcus aureus infects normal or previously damaged valves. a. Vegetations destroy the valve leaflet and chordae tendineae b. Valve destruction leads to regurgitation murmurs.

*Chronic (stable) angina pectoris* Exercise-induced substernal chest pain lasting 30 seconds to 30 minutes • Other precipitating events include sexual intercourse, climbing stairs, eating a heavy meal, emotional stress, and cold temperature. (2) Often accompanied by shortness of breath, diaphoresis, numbness, and pain in the left inner arm, shoulder, or jaw

1) Fixed, atherosclerotic coronary artery disease (most common cause) Severity of stenosis is usually >70%. 2) Aortic stenosis or HTN with concentric LVH • O2 supply is not adequate for the thickened muscle wall 3) Hypertrophic cardiomyopathy 4) Cocaine-induced coronary artery vasoconstriction Subendocardial ischemia due to decreased coronary artery blood flow or a thick muscle wall (concentric hypertrophy) -Relieved by Nitroglycerin ST Depression greater than 1mm

ToF -Tet spells (hypoxemic episode): squatting ↑PVR → reverses shunt → ↑PaO2

1- VSD 2- Infundibular (most common) or PV stenosis • Degree of PV stenosis determines whether the infant develops cyanosis or not after birth (see later). 3 -RVH 4- Dextrorotated aorta with a right-sided aortic arch (25% of cases) Onset of cyanosis usually after 3 months of age Harsh systolic crescendo/decrescendo murmur that results from RV outflow tract obstruction -Cardioprotective shunts increase oxygenation in tetralogy of Fallot. (a) Presence of an ASD steps up Sao2 in the RA; therefore the blood that is shunting into the left side of the heart has a higher Sao2.

Pulmonary valve regurgitation

1. Most often a functional murmur from stretching of the PV ring —pulmonary hypertension (called a Graham Steell murmur) -Volume overload of the RV, which leads to eccentric RVH 3. Produces a diastolic murmur heard after the second heart sound 4. S3 and S4 heart sounds are present

diastolic heart failure (DHF) treatment

ACE inhibitor and β-blocker, the latter decreasing heart rate, which prolongs diastolic filling. Diuretics must be used with caution, because excessive diuresis may produce volume depletion and decrease the cardiac output

Infective endocarditis (IE)

Acute IE: Staphylococcus aureus MCC Endocarditis in IVDAs • Staphylococcus aureus (most common), Pseudomonas aeruginosa, Candida spp., and enterococci Subacute endocarditis • Viridans group of Streptococcus (most common overall pathogens causing endocarditis), Streptococcus bovis, enterococci, Staphylococcus aureus infection of the endocardial surface of the heart, which may encompass one or more valves or a septal defect in CHD (1) Diabetes mellitus, HIV infection (2) Poor dental hygiene, CHD (3) MVP, AV stenosis (4) Hemodialysis, prosthetic hearT valve -Prosthetic valve IE early: Staphylococcus epidermidis (coagulase negative) MCC or Candida LATE after 60 days implant = S. Aureus, Group D strept Enterococci in urinary cathers, S. Aureous in venous catheters Strept Bovis in Colon Cancer, or UC Neutrophilic leukocytosis occurs in acute IE. Monocytosis occurs in subacute IE.

Antiarrythmics

Afib rate control: Ca2+ blocker, B-blocker, Digoxin Afib rythym control: 1C, 3

Dilated cardiomyopathy

Alcoholism (direct effect or thiamine) -doxorubicin, daunorubicin, and cocaine -Postpartum state • May occur in the last trimester or within 6 months postpartum Findings: -Narrow pulse pressure due to a decreased stroke volume Dilated: echocardiography—EF <40%

Consequences of ventricular hypertrophy -S4 heart sound correlating with atrial contraction in late diastole (atrial gallop) = blood entering a noncompliant ventricle

Angina pectoris with exercise (only a complication of LVH) -In the normal LV, the subendocardium receives the least amount of blood from the coronary arteries.(only during diastole) -as heart rate increases, which decreases the time for diastole and the filling of the coronary arteries.

Truncus arteriosus

Ao and the PA share a common trunk and intermix their blood.

Pulmonary valve (PV) stenosis -Carcinoid syndrome -Noonan

Associated with CHD and carcinoid heart disease 3. Systolic ejection murmur in the left second intercostal space (see Box 11-1). 4. Concentric RVH

Class 2 Antiarrythmics -control RATE through AV node but not correct problem -reduce rate of sudden death post MI -control SVT -some VT but not really

B-blockers Reduce both heart rate & myocardial contractility (β1) via slowing of phase 4 and prolonging AV node (PR) conduction Slow conduction of impulses through myocardial conducting system • Reduce rate of spontaneous depolarization in cells with pacemaker activity (block of adrenergic release) • Little effect on action potential in most myocardial cells

Aortic valve (AV) stenosis -Harsh systolic ejection murmur in the right second intercostal space with radiation into the neck • Deep held inspiration for 3 to 5 seconds does not increase the intensity of the murmur. b. Left-sided S4 heart sound, due to decreased compliance of the LV c. Decreasing preload lessens the volume the LV must eject. (standing, valsava) Murmur intensity decreases d. Increasing preload increases the volume the LV must eject. • Murmur intensity increases

Calcific AV stenosis is the most common cause of stenosis in persons >60 years old (if under 45 look for biscupid av) -The cardiac output decreases with exercise, leading to syncope with exercise and angina -Reduction in the AV orifice area produces concentric LVH and poststenotic dilatation of the aorta, due to the jet stream of blood impacting on the wall of the vessel. -Hemolytic anemia (microangiopathic) with schistocytes • Indication for AV replacement. Diminished pulse pressure (difference between SBP and DBP) with severe stenosis

Right-sided heart failure (RHF) -RV cannot effectively pump venous blood into the lungs

Caused by Increase in RV afterload (increased resistance to blood flow out of the RV) from LHF (most common cause RHF), PH, PV stenosis, saddle embolus Signs: 1) Prominence of internal jugular veins, stretch TV --> regurg, 2) Painful hepatomegaly due to centrilobular hemorrhagic necrosis 3) Increased Venous HS -> pitting edema 4) Cyanosis of mucous membranes - backup of venous blood allows for time to deO2 blood decreasing O2 saturation

Mitral valve prolapse (MVP) -Bulging of the anterior and/or posterior leaflets into the LA occurs during systole -Heart murmur of MVP is present. (1) Midsystolic click • Click is due to sudden restraint by the chordae tendineae of the prolapsed MV. (2) Mid to late systolic, MV regurgitant murmur follows the click

Commonly associated with Marfan, Ehlers-Danlos, and Klinefelter syndromes d. Caused by defective embryogenesis in cells of mesenchymal origin -->Redundancy of MV tissue • Excess of dermatan sulfate in the MV leaflet (called myxomatous degeneration) -Decreased preload causes the click and murmur to move closer to the S1 heart sound (length of systole is decreased); [Standing, Valsava, Anxiety increasing HR decreasing diastolic filling time] -Increased preload causes the click and murmur to move closer to the S2 heart sound (the length of systole is increased) [Reclining, squatting, sustained hand grip - increased hand grip] Tx if symptomatic: B-blocker decreases HR and ionotropy leading to less stretch on leaflets

Direct Vasodilators -decrease preload (more blood on arterial side of body) -decrease afterload (reduce PVR)

Concurrent use of two oral vasodilators: hydralazine & isosorbide dinitrate can produce sustained improvement in LVEF Hydralizine AE: tachycardia, peripheral neuritis, lupus-like syndrome

Restrictive cardiomyopathy -Pompe glycogenosis, hemochromatosis -Endocardial fibroelastosis in a child (under 2 you think this disease!) • Thick fibroelastic tissue in the endocardium Sarcoidosis + Systemic sclerosis

Decreased ventricular compliance Diastolic dysfunction type of LHF (problem filling) Restrictive: ↓ventricular compliance; biventricular heart failure -low voltage ECG

1C antiarryhtmics Propafenone, Flecainide -use Severe symptomatic ventricular arrhythmias (lifethreateningvonly), premature ventricular contraction or ventricular tachycardia resistant to other therapy

Decreases rate of rise of Phase 0 depolarization without affecting duration of action potential -• Prolongs conduction & refractoriness in all areas of the myocardium

*Ventricular septal defect * (1) Most common CHD L--->R -ToF -Cri du Chat (Ch5p) -FAS -Alpert's Syndrome -Down's Syndrome -trisomy 13/18 pansystolic-holosystolic, harsh, vibratory, murmur at the left lower sternal border (LLSB) loud, pulmonic S2 -During a squatting (or hand grip) maneuver, total peripheral resistance is increased, forcing more blood through the defect and causing a louder murmur

Defect in the membranous part of the IVS (75%-80% of the cases), the muscular or trabecular part of the septum (5%-20% of cases), or in less common sites - Equal frequency in males and females -(8) Acquired in an AMI with rupture of the IVS (9) Harsh pansystolic murmur is present along the lower left sternal border. (10) Increased Sao2 in the RV and pulmonary artery (PA)

Complete transposition of the great arteries

Definition—embryologic defect results from abnormal formation of the truncal and aortopulmonary septa (2) Defects in complete transposition (a) Aorta arises from the RV. (b) PulmArt arises from the LV. (c) Left and right atria (LA, RA) are normal (the vena cava empties into the RA and the pulmonary vein empties into the LA). * Cardioprotective shunts* (a) ASD steps up Sao2 in the RA. • Increases Sao2 in the RV for delivery to tissue via the transposed Ao (b) VSD shunts blood into the LV for oxygenation in the lungs via the transposed PA. (c) PDA shunts blood into the transposed PA for oxygenation in the lungs

A 28-year-old woman with a history of treated Hodgkin's lymphoma presents to her physician complaining of dizziness and fatigue. Physical examination reveals hypertension, narrow pulse pressure, and jugular venous distention, accompanied by an S4 heart sound. In addition, pulmonary auscultation demonstrates bilateral crackles at the bases. X-ray of the chest shows four-chamber dilation of the heart and a slight pleural effusion. What is the cause?

Dialated Cardiomyopathy

*Digoxin in HF (mainly with aFIB)* increase PR interval, decrease QT interval Slightly decrease refraction in purkinje but increases refractory period in AV node and decreases conduction velocity -decreases rate of SA node and atrial contraction DO NOT USE IN DIASTOLIC HF or Bradycardia -large Vd accumulates in muscle, small theraputic window AE: arrythmias (bradycardia), ventricular arrythmias from speeding up refractory perkinje (give lidocaine), headache, fatigue, confusion, blurred vision, alteration of color perception, halos on dark objects toxicity when hypokalemic, hypomagnesium, hypercalcemia

Digoxin can decrease the symptoms of heart failure, increase exercise tolerance and decrease rate of hospitalization, but does not increase survival + inotrope (increase Ca2+ in cells) - chronotrope (decreased inward Na+ at SA node) • Reduced sympathetic activity • Reduced peripheral resistance decreased HR • Enhanced vagal tone decreased myocardial O2 demand, opens K+ hyperpolarizing SA node, increase AV node refractoriness

Ductus arteriosus

Ductus arteriosus is kept open by prostaglandin E2, a vasodilator synthesized by the placenta. (closed by indomethacin) -Fetal pulmonary arteries (1) Hypertrophied from chronic vasoconstriction due to decreased Po2 (2) Prevents blood from entering the pulmonary capillaries and left atrium

Tricuspid Atresia LV hypertrophy (left ventricular axis) [compare to ToF with right ventricle hypertrphy]

EKG: tall P-waves (due to right atrial enlargement), left-axis deviation (due to hypertrophy of the left ventricle), and small/absent R-waves in precordial leads V1-V3 (due to a hypoplastic right ventricle) In individuals with TVA, there is vital right-to-left flow of the entire systemic venous return across the foramen ovale because there is no direct communication between the right atrium and right ventricle. As a result, the left ventricle, which receives all the systemic venous return, becomes the dominant ventricle. There has to be a source of pulmonary blood flow, commonly a ventricular septal defect (95%), which results in a systolic murmur at the LLSB. Blood flow through the VSD is left-to-right. If there is no VSD, a patent ductus arteriosus is usually the source of pulmonary blood flow.

Congenital Heart Disease Maternal risk factors

Examples of maternal risk factors (1) Increased age (>45 years old) (2) Previous child with CHD (1 : 50 chance of having second child with CHD) (3) Poorly controlled DM during pregnancy -Left-ventricular outflow obstruction (e.g., AV stenosis, hypertrophied IVS) -Transposition of the great arteries, ventricular septal defect (VSD) (4) Alcohol intake during pregnancy • PV stenosis, VSD (5) Congenital infection (e.g., rubella) during pregnancy • PDA, PV stenosis (6) Aspirin intake • Persistent PH syndrome (7) Diphenylhydantoin intake • AV stenosis, PV stenosis (8) Systemic lupus erythematosus (SLE) • Heart block, pericarditis, endomyocardial fibrosis

Rheumatic fever (RF) -Type 2 HS

First attack of RF usually occurs between 5 and 15 years of age, 1-5 weeks (20days) after Pyogenes pharygitis -migratory polyarthritis (not permanent) -Pericarditis, Myocarditis (Aschoff bodies: Lesions have a central area of fibrinoid necrosis surrounded by Anitschkow cells [reactive histiocytes], Endocarditis (MV> AV> TV Regurg w/ Sterile, verrucous vegetations develop along the line of closure of the valve) -Erythemia Migrans (circular rings, c shaped) -Subcutaneous Nodules (Fibrinoid necrosis just like RA) -Sydenham chorea is characterized by reversible rapid, involuntary movements affecting all the muscles -increased ESR, increased CRP, neutrophilia, ASO, DnaseB -

Decreasing venous return increases what murmurs? -Vaslva manuer -Standing quickly -taking a nitrate

HOCM MVP

Congestive Heart Failure (CHF)

In LHF, blood backs up in the lungs (pulmonary congestion). In RHF, blood builds up in the systemic venous system.

PDE 3 inhibitors

Inamrinone, Milrinone • Inhibit myocardial cAMP PDE activity--> increased cAMP levels (+ve inotropic effect and increased cardiac output) • Possess systemic & pulmonary vasodilator effects (reduce both preload and afterload) • Shown to increase AV conduction slightly • Used for short-term therapy in patients with intractable heart failure

Coarctation of the aorta

Infantile (preductal) coarctation 70% -Constriction in the Ao is between the subclavian artery and the ductus arteriosus. [Turner syndrome] infants will dev CHF *Adult (Constriction of the Ao distal to the ligamentum arteriosum) *- systolic ejection murmur posteriorly in the midthorax. Look for biscupid aorta -increased risk aortic dissection, cerebral aneursyms -Pulse Deficit + 10mmHg diff in lower limbs, leg claudication (hypotrophy), HTN from renal ischemia -collaterals develop between intercostals -Anterior ICAs arise from the internal thoracic artery, Posterior ICAs arise from the Ao. Collaterals develop between the superior epigastric artery and the inferior epigastric artery. (a) Internal thoracic artery becomes the superior epigastric artery. (b) Superior epigastric artery forms collaterals with the inferior epigastric artery, which is a branch of the external iliac artery. (c) Reversal of blood flow in the inferior epigastric artery forces blood into the external iliac artery. (3) Chest radiograph shows rib notching on the undersurface of the ribs. • Increased blood flow through the enlarged, pulsating ICA in the neurovascular bundle in the costal groove of the rib wears the bone away, producing rib notching.

Prinzmetal variant angina -Stress test shows ST-segment elevation (transmural ischemia).

Intermittent coronary artery vasospasm at rest with or without superimposed coronary artery atherosclerotic disease. -Vasoconstriction, in some cases, may be due to:increase in platelet thromboxane A2 originating from thrombus material overlying an atherosclerotic plaque or, in 10% of cases, a thrombus not overlying an atherosclerotic plaque or an increase in endothelin (vasoconstriction), can be inhibited by bo*sentan*, sitaxentan or ambrisentan. The latter drug selectively blocks endothelin A receptors, decreasing the vasoconstrictive actions and allowing for increased beneficial effects of endothelin B stimulation, such as nitric oxide production

juxtacapillary (J)-receptors aka Pulmonary C receptors

Interstitial fluid stimulates them innervated by vagus nerve, inhibiting the patient from taking a full inspiration -Cheyne Stokes star

R-dom heart -posterior wall domination

L: LAD - Anterior wall, interventricular septum, apex LCX- lateral free wall (aVL, L1, V5, V6) R: Marginal RCA = anterior RV Posterior interventricular: inferior wall (diaphramatic), posterior wall LV, posterior RV, posterior septum. The sinuatrial nodal artery (or sinoatrial nodal artery) is an artery of the heart which supplies the sinoatrial node, and arises from the right coronary artery in around 60% of people. In about 40% of cases, the sinoatrial artery is a branch of the left coronary artery or one of its branches. [1] The origin of the sinoatrial node artery is not related to coronary artery dominance. In contrast, the atrioventricular nodal branch is dependent on coronary artery dominance

L-dom Heart

LAD- anterior free wall LV, anterior interventricular septum LCX - inferior wall, posterior LV, Apex

Left-sided heart failure (LHF)

LV cannot efficiently eject blood into the aorta Causes an increase in the LV-EDV and LV end-diastolic pressure (LVEDP) Systolic Failure (MC) = impaired contraction like Ischemia, Myocarditis, Dilated Cardiomyopathy Diastolic Failure = non-compliant ventricle, impaired filling due to Concentric LVH (essential HTN is the most common cause of DHF) -AV stenosis, HOCM, restrictive cardiomyopathy (amyloidosis or glycogenosis).

Carcinoid heart disease

Liver metastasis from a primary carcinoid tumor of the small intestine (refer to Chapter 18) is the most common cause. -Serotonin is produced by the metastatic foci in the liver and gains access to the hepatic vein → inferior vena cava → right side of the heart. - In the right side of the heart, serotonin increases fibrosis of the TV and PV, producing TV regurgitation and PV stenosis

Dopamine

Lower doses = mainly dopaminergic stimulating (produce renal and mesenteric vasodilation) • Higher doses = both dopaminergic & β1 stimulating (produce cardiac stimulation & renal vasodilation) • Large doses = stimulate α receptors (vasoconstriction) • Used in the treatment of shock (eg, MI, open heart surgery, renal failure, cardiac decompensation) which persists after adequate fluid volume replacement. Dopamine also promotes diuresis.

*Aortic valve regurgitation* Incompetent closure of AV leading to retrograde blood flow into the LV in diastole -ACUTE: markedly increased LVEDP, a normal left ventricular size, decreased SBP (decreased stroke volume), normal to decreased pulse pressure, and decreased cardiac output -CHRONIC: Chronic AV regurgitation: normal LVEDP, ↑SBP, ↓DBP, ↑pulse pressure, normal cardiac output -AV regurgitation: eccentric LVH

MC = aortic root dilatation. Infective endocarditis • Most common infectious cause of acute AV regurgitation Chronic RF = Most common cause of AV regurgitation in developing countries Dilated AV ring, syphilitic aortitis, aortitis in ankylosing spondylitis and Takayasu arteritis *Early diastolic murmur, due to blood dripping back into the LV right after the second heart sound* (1) S3 and S4 heart sounds are present (2) Deep held inspiration does not increase sound b. In chronic AV regurgitation, signs of a hyperdynamic circulation are caused by a widened pulse pressure (1) Bounding pulses (Corrigan water-hammer pulse) (2) Head nodding with systole (de Musset sign) (3) Pulsating nail bed with elevation of the nail (Quincke pulse) + Pulsating uvula c. Austin Flint murmur (1) Regurgitant stream from the incompetent AV hits the anterior MV leaflet, producing a diastolic murmur. (2) Presence of this murmur is an indication for AV replacement.

Pericarditis -Precordial chest pain (1) Pain is relieved when leaning forward. (2) Pain increases when leaning back. d. Pericardial friction rub (1) Scratchy, three-component rub (systole, early, and late diastole) (a) Best heard with the patient leaning forward (b) All three components are heard in ~50% of cases. (2) Does not disappear when the person holds their breath, which distinguishes it from a pleural friction rub

Most cases are idiopathic (>40% of cases). (2) Infectious (similar to the pathogens producing myocarditis) • Examples—adenovirus, coxsackievirus, and HIV (3) Drugs (doxorubicin, cocaine, zidovudine, and sulfonamides) (4) SLE (pericarditis with effusion is a common presentation), acute RF, post-MI pericarditis, autoimmune pericarditis post-MI, systemic sclerosis, uremia, metastasis (e.g., breast, lung, leukemia) -Cardiac output is decreased, because less blood is entering the right heart. (3) Neck vein distention occurs on inspiration (a) Blood cannot easily enter the RA on inspiration, because of fluid surrounding the heart. (if effusion) (b) Some blood refluxes back into the jugular vein on inspiration, causing distention (this is called Kussmaul sign). -Effusion: chest X-ray shows water bottle configuration of heart silhouette -Pericardial knock is heard due to the ventricles hitting the thickened parietal pericardium. - Chest radiograph usually shows dystrophic calcification in the parietal pericardium.

Mitral valve stenosis -a. Most commonly caused by recurrent attacks of RF b. Twice as common in women than men -Murmur of MV stenosis is an opening snap followed by an early to mid diastolic rumble -Deep held inspiration for 3 to 5 seconds does not alter the intensity of the opening snap or middiastolic rumble

Narrowing of the MV orifice (<2.5 cm2 [normal 4-6 cm2]; -LA becomes dilated and hypertrophied because of increased work imposed on the LA in filling the LV during diastole. -> Atrial fibrillation (irregularly irregular pulse) is a complication of LA dilation and hypertrophy. -HF cells (rusty sputum) + PH -Dysphagia for solids (LA is the most posteriorly located chamber in the heart and can compress esophagous)

STEMI (ST segment elevation myocardial infarction) (1) Full thickness of the myocardium is involved. (2) New Q waves develop in an ECG.

Non-STEMI (NSTEMI) (1) Inner third of the myocardium (subendocardium) is involved. (2) Q waves are absent. -increased risk for sudden cardiac death

Libman-Sacks endocarditis

Occurs in 30% to 50% of patients with SLE 3. Sterile vegetations are located over the MV surface and chordae. • Produces valve deformity and MV regurgitation

Pulmonary Edema -Peribronchiolar edema narrows the airway and produces expiratory wheezing (called cardiac asthma). -Bibasilar inspiratory crackles (rales) • Inspiratory crackles are due to air expanding alveoli filled with fluid.

Once pulmonary capillary HP overrides oncotic pressure (OP), a transudate enters the interstitial space and then the alveoli, producing pulmonary edema A, Pulmonary edema showing pink fluid (transudate) completely filling the alveoli. B, Chest frontal radiograph showing pulmonary edema. Note the fluffy alveolar infiltrates ("bat-wing" or "angel wing" configuration) throughout both lung fields

Nonbacterial thrombotic endocarditis (NBTE; marantic endocarditis)

Paraneoplastic syndrome of Adenocarcinomas -Sterile, nondestructive vegetations present on the MV • Most often due to the procoagulant effect of circulating mucin from mucin-producing tumors of the colon/pancreas a. Embolization of vegetation material to distant sites b. Vegetations may be secondarily infected.

High-output heart failure (HOF)

Pathogenesis * Increase in stroke volume*(hyperthyroidism), *decrease in blood viscosity* (which decreases PVR leading to increased venous return - anemia), vasodilation of PVR arterioles (thiamine deficiency, EARLY endotoxic shock (increase NO synthesis), AV FISTULA [Trauma from a knife wound, Surgical shunt for hemodialysis, Mosaic bone in Paget disease]

Valsalva maneuver (holding breath with epiglottis closed)

Produces an increase in positive intrathoracic pressure, which decreases venous return to the heart (compression of the vena cava and right side of the heart)

Left anterior descending (LAD) coronary artery a. Distribution includes: (1) Anterior portion of the LV (2) Anterior two thirds of the interventricular septum (IVS) (3) Apex of the heart b. Site for 40% to 50% of coronary artery thromboses

Right coronary artery (RCA) a. Distribution includes: (1) Posterobasal wall of the LV (2) Posterior one third of IVS • Sometimes perfused by the left circumflex artery (3) Right ventricle (80% of individuals) (4) Posteromedial papillary muscle in LV (5) Atrioventricular and sinoatrial (SA) nodes b. Site for 30% to 40% of coronary artery thromboses 4. Left circumflex coronary artery (see Fig. 11-3C) a. Supplies the lateral wall of the LV (80% of individuals) b. Site for 15% to 20% of coronary artery thromboses 5. Collateral circulation may develop over time is there is slow occlusion of the vessels by atherosclerosis. • Protective effect on preventing an acute myocardial infarction (AMI)

Chest radiograph findings of LVF include:

S3 first sign then stretching by increased LVEDV leads to regurg (a) Congestion in the upper lobes (early finding) (b) Perihilar congestion ("bat-wing configuration" or "angel-wing configuration") (c) Fluffy alveolar infiltrates (see Fig. 11-2B) (d) Kerley lines (septal edema) (e) Air bronchograms (air visible in the bronchus or small airways because fluid surrounds the airways

Unstable angina

Severe, fixed, multivessel atherosclerotic disease - Disrupted plaques, with or without platelet nonocclusive thrombi, invariably present -Clinical findings (1) Frequent bouts of chest pain occur at rest or with minimal exertion. (2) It may progress to an AMI

AMI -shock occurs in 7% of cases from STEMI -heart block from inferior or anterior mi in 4% of cases -rupture 3-7 PostMI -anterior = cardiac tamponade -Posterior medial papillary rupture from inferior AMI (RCA) -> MV regurg -IV septum rupture -> LAD coronary leads to L->R shunt [finding increased RV O2 saturation and pressure]

Sudden onset of severe, crushing retrosternal pain (1) Usually lasts >30 minutes. (2) Not relieved by nitroglycerin (3) Usually radiates down the inner left (most common) or right arm (less common), into the shoulders, or into the jaw or epigastrium (a) Nerves to the heart are T1 to T5. (b) Radiation to the inner arm and shoulder is in the T1 distribution. (c) Radiation to the epigastrium is in the T4 to T5 distribution

centrilobular hemorrhagic necrosis

Systemic venous blood backs up into the hepatic veins and then into the central venules, which expand with blood and cause *hepatic cell necrosis in zone III hepatocytes * • Serum transaminases (aspartate aminotransferase [AST] and alanine aminotransferase [ALT] are markedly increased; (can lead to B6 deficiency) (b) Increase in pressure is transmitted into the sinusoids of the liver and eventually the portal vein. • An increase in portal vein pressure produces ascites

Heart Failure -Chronic activation of SNS & renin-angiotensin-aldosterone pathway is associated with cardiac tissue remodeling. -NSAIDS, alcohol, Ca2+-channel blockers should be avoided if possible (may exacerbate HF) -Loop diuretics : more effective diuretics than thiazides -Sprinolactone + ACEi decrease morbidity and mortality (but causes hyperkalemia)

Tachycardia, decreased exercise tolerance, dyspnea, peripheral & pulmonary edema, cardiomegaly *Use of ACE-inhibitors, diuretics, & inotropic agents* *Systolic failure* Mechanical pumping action (contractility) and the ejection fraction of the heart are reduced *Diastolic failure* Stiffening and loss of adequate relaxation .. abnormal ventricular filling, resulting in a reduction -use ACEi (decrease preload and afterload but increase CO) as default, add B-blocker, or digoxin, nitrates, diuretics

Fetal Blood flow

The umbilical veins have the highest oxygen content. The ductus venosus shunts most of the blood past the liver, and the foramen ovale and the ductus arteriosus act as shunts to bypass the pulmonary circulation. All of these shunts normally close at or shortly after birth, as do the umbilical vein and distal part of umbilical arteries

apnea leading to increased CO2 which causes excessive compensatory hyperventilation, in turn causing decreased CO2 which causes apnea, restarting the cycle.

These phenomena can occur during wakefulness or during sleep, where they are called the central sleep apnea syndrome (CSAS) It may be caused by damage to respiratory centers, or by physiological abnormalities in chronic heart failure

American trypanosomiasis (Chagas disease)

Trypanosoma cruzi, a protozoan (hemoflagellate). It is transmitted by a bite around the eye or mouth that is contaminated with the feces of a reduviid bug (Triatoma, or kissing bug). Facial edema occurs near the bite site (called Romaña sign). The flagellated trypomastigotes circulate in the blood and the amastigotes (lack flagella) invade tissue. Common clinical findings are myocarditis causing chronic heart failure (most common cause of death) and arrhythmias; acquired achalasia, a motility disorder due to destruction of ganglion cells in the lower esophageal sphincter; and acquired Hirschsprung disease (large bowel motility disorder), due to destruction of ganglion cells in the rectosigmoid. The diagnosis is secured by finding trypomastigotes in the peripheral blood and/or amastigotes in tissue. Xenodiagnosis is used in some cases. An uninfected reduviid bug is allowed to feed on a patient and after a short period of time, the intestine of the bug is examined for the parasite. Serologic tests are also available. Nifurtimox is the treatment of choice.

Drugs to use in CHF

Very Ambitious Queen (verapamil, quinidine, amiodarone increase digoxin levels) Diuretics also increase levels of toxicity by causing hypokalemia

Myocarditis -Global enlargement of the heart and dilation of all chambers b. Lymphocytic inflitrates -major cause of sudden death in adults under 40 -Global enlargement of the heart and dilation of all chambers -Lymphocytic infiltrate with focal areas of necrosis is highly predictive of a viral myocarditis

Viruses • Adenovirus (most common), group B coxsackieviruses, HIV, parvovirus B19, human herpesvirus 6 Parasites • Trypanosoma cruzi (Chagas disease), Trichinella spiralis, and Toxoplasma gondii Bacteria • Borrelia burgdorferi, Mycoplasma, and Rickettsia rickettsii Fungi • Candida, Mucor, and Aspergillus Toxins -diphtheria, carbon monoxide, and venom from black widows and scorpions Drugs -- doxorubicin, cocaine, zidovudine, and sulfonamides Sarcoidosis

L--->R Shunts

Volume overload occurs in the right side of the heart -Pulmonary hypertension (PH) -concentric hypertrophy of the RV. -LVH, due to more blood returning to the left heart than normal. -Reversal of the shunt, because the pressure in the right side of the heart is greater than the pressure in the left side (a) Signs of reversal of the shunt include cyanosis (called Eisenmenger syndrome) and clubbing of the fingers (Fig. 11-12). (b) Another term is tardive cyanosis (late-onset cyanosis)

Correlation of ECG changes with pathologic changes

a. Inverted T waves • Correlates with areas of ischemia at the periphery of the infarct b. Elevated ST segments • Correlates with injured myocardial cells surrounding the area of necrosis c. New Q waves • Correlates with the area of coagulation necrosis

Patent ductus arteriosus -Treatment (a) Intravenous indomethacin (inhibits prostaglandin E2, a vasodilator) (b) Surgical closure (e.g., banding)

asocciated with: Congenital rubella, Respiratory distress syndrome (due to persistence of a decreased Pao2), Complete transposition of the great vessels, Tetralogy of Fallot -In a reversal of the shunt, unoxygenated blood enters the aorta below the subclavian artery. Child has a pink upper body and a cyanotic lower body, which is called differential cyanosis.

ASD

associated with ->Fetal Alcohol Syndrome, ->down syndrome Soft midsystolic murmur ->along the upper sternal border ->associated with increased PA blood flow. • Characteristic *wide and fixed split of the S2 heart sound* -Increase in Sao2 in ->right atrium (RA), ->RV ->PA star

HOCM -Harsh systolic ejection murmur • Best heard along the left sternal border b. Palpable double apical impulse Murmur intensity increases (obstruction worsens) with decreased preload (note that these changes are the opposite of those that occur with AV stenosis). • Examples—standing up, Valsalva maneuver (increases positive intrathoracic pressure), and use of inotropic drugs (e.g., digitalis) d. Murmur intensity decreases (obstruction lessens) with increased preload (note that these changes are the opposite of those that occur with AV stenosis). (1) Examples—reclining, drugs decreasing cardiac contractility (e.g., β-blockers), sustained clenching of hands, and squatting (2) Increasing preload opens the outflow track

autosomal dominant (AD) with nearly complete penetrance ( B-MYOSIN heavy chain gene --> (2) Young individuals are affected. (3) Genes involved are mapped to chromosomes 11 (most common) and 14q. (4) A missense mutation occurs in multiple genes, causing a single amino acid substitution in one of the contractile proteins of the cardiac sarcomere. -helter skelter hypertrophy of septum (Proportionately greater hypertrophy of the IVS than the free LV wall) (2) IVS hypertrophy may obstruct blood flow through the LV outflow tract. -Sudden death is due to ventricular tachycardia/fibrillation

Class 3 antiarrthymics SVT and VT low doses help maintain normal sinus rythym in afib

block K+ repolarizing channels -prolong action potential and QT interval w/o altering Phase 0 *Amiodarone* blocks inactivated Na channels, decreases AV node conudction and sinus node fx, effects take weeks -AE pulmonary fibrosis, thyroid issues, blue skin *Sotalol* Potent non-selective β-blocker • Inhibits rapid outward K+ current • Prolongs repolarization & duration of action potential • Lengthens refractory period *Dofetilide*

Increased serum brain natriuretic peptide (BNP)

cardiac neurohormone secreted from the ventricles when they are volume overloaded (2) BNP is useful in: (a) Diagnosing LHF (increased) (b) Excluding LHF (normal) (c) Predicting survival (remains high; bad prognostic sign) (3) Serum atrial natriuretic peptide (ANP) is also increased in LHF because of left atrial dilatation

Pericardial effusion

clinical features: elevated JVP most common finding. Venous waveforms-*Prominent x descent with absent y descent*** Narrowed pulse pressure (due to decreased stroke volume)

Tertiary Heart Block

congenital -usually occurs at level of AVN -often associated with SS-A (Ro) and SS-B (La) -note: SS = Sjogren's syndrome acquired medications antiarrhythmics, b-blockers, Ca+ blockers digoxin -Lymes' disease -rheumatic diseases -infiltrative processes -neuromuscular disorders -ischemia/infarct -metabolic causes - toxins

Aliskrinin

direct renin inhibitor

Do not use ACEi if -same with ARBs (angiotensin 1 recptor competitive antagonist) except they do not causeincrease in bradykinin

dry cough / angioedema Hypotensive Pregnany Bilateral Renal Artery Stenosis (good drug if unilateral renal artery stenosis) Hyperkalemic

Woman 27 years dies suddenly while lifting something heavy....

early lesions = mitral regurg late lesions = mitral stensosis

Papillary Fibroelastoma

fibroelastomas have branching avascular papillae, composed of collagen, that are covered by endothelium.

Syphilus

hits the vaso vasrum causing obstructive arteritis this leads to cystic medial degeneration and aortic dilation + cor bovinum (giant LV)

Presence of hemosiderin

implies that the pulmonary capillaries have ruptured under pressure, and RBCs entered the alveoli and were phagocytosed by alveolar macrophages. --Excess iron in the macrophage binds to ferritin, which degrades into hemosiderin (rust-colored granules with H&E stain or blue with Prussian blue stain), producing a rust-colored sputum star

Mitral valve regurgitation -> volume overload eccentric LVH (added in series) Pansystolic murmur with S3 and S4 heart sounds • Deep held inspiration for 3 to 5 seconds does not alter the intensity of the murmur or the abnormal heart sounds

incompetent closure of MV causes retrograde blood flow into the LA during systole Causes (1) Mitral valve prolapse (MVP; most common cause) (2) Rupture/dysfunction of the posteromedial papillary muscle (e.g., posterior AMI; second most common cause) (3) Functional MV regurgitation (stretching of MV ring) • Example—LHF (4) Infective endocarditis (5) Other causes—acute RF, dilated cardiomyopathy, myocarditis, Libman-Sacks endocarditis in SLE, and nonbacterial thrombotic endocarditis

B1 on heart

increase PKA --> increase iCa and phosphorlyates phospholamab (regulates Ca Sarco pump) leading to increased reuptake of Ca - increasing rate of relaxation and increasing stored Ca which will increased SV and EJ -increased SA node activity via increased cAMP

+Dromotropic

increase in conduction velocity of AV node due to increased inward Ca2+ current

Increased Preload -volume of blood in the ventricle that must be expelled during systole -Correlates with the left and right ventricle end-diastolic volumes (LV-EDV, RV-EDV).

increased preload increases SV via Starlings -causes dilation and ECCENTRIC hypertrophy with duplication in series causing fibers to increase in length and width Causes: Left Ventricle = Mitral or AV regurg, L2R VSD shunting of blood Right Ventricle = Tricuspid or PV regurg

Increased afterload - increased resistance the ventricle contracts against to eject blood in systole -Essential HTN -Aortic Stenosis -HOCM

leads to concentric thickening of ventricular wall -sarcomere duplicate in parallel to long axis of cells causing individual muscle cells to be thicker

Systolic heart failure (SHF)

low ejection fraction (EF <40%; some use <50%). The EF equals the stroke volume (SV) divided by the left ventricular end-diastolic volume (LVEDV). The normal value ranges from 55% to 80%.

Heart Tumors

metastasis most common - especially to pericardium --> pericarditis *cardiac myxoma is most common primary* - mesychymal origin : tumor is sessile or pedunculated. "Ball-valve" effect blocks the MV orifice in LA (most posterior chamber so use transesophageal ultrasound) • Blocks diastolic filling of the LV, simulating MV stenosis *Rhabdomyoma* 1. Most common primary tumor of the heart in infants and children - associate with Tuberous Sclerosis -

Diastolic heart failure (DHF)

normal EF (>60%) at rest. In addition, there is usually an S4 atrial gallop, due to increased resistance to filling in late diastole. There is an increase in left atrial and left ventricular end-diastolic pressure. Pulmonary congestion commonly occurs when the heart cannot meet the metabolic demands of peripheral tissue (e.g., when the patient exercises) at which point the EF is decreased.

Transposition of the great vessels

presents with extreme cyanosis and "egg-on-a-string" appearance on CXR. -leads to pulmonary and systemic circulation existing in parallel Infant must have arteriovenous communication to be compatable with life including patent ductus arteriosus (PDA) or persistent foramen ovale (PFO) Risk factors are -Down's Syndrome -Alpert's Syndrome - cri-du-chat, -trisomy 13/18

The severity mitral stensosis is based on....

pressure in LA aka the length of time between A2 and opening snap (more pressure = less time)

Nonpharmacologic therapy in CHF

restricting sodium (<2 g/day) and water (<2 L/day) -decreased CO leads to renal retention of H20 and water to increase CO via preload

B-blockers in HF -Carvedilol (a1, B12 antagonist) -Metoprolol (B1 antagonist)

use if HF is symptomatic or if LVEF is decreased, or if history MI AE) fluid retention Studies demonstrate reverse cardiac remodeling & reduction in mortality & hospitalization (30-40% in patients with NYHA II-IV HF) decrease HR (negative inotropic effect) & inhibit renin release (block B1 receptors) • Prevent deleterious effects of norepinephrine on cardiac muscle fibers .. decreases remodeling, hypertrophy -start at low dose and increase over weeks beware initial exacerbation of symptoms (do not suddenly remove) -Bblockers inhibit Gs, decreasing cAMP/PKA decrease Na/Ca current in AV node decreasing slope of phase 4 and 0

How does digoxin slow the heart rate?

via vagal stimulation of AV node (increase in parasympathetic activity M2 receptors)

Dobutamine

• (-) isomer is an B1-receptor agonist and a weak B1 agonist • (+) isomer is an B1-antagonist and a potent B1 agonist At therapeutic levels the stimulation of β1-receptors predominate, leading to a potent inotropic effect (with little change in heart rate). Net vascular effect is vasodilation (β2-receptors) • Used in short-term management of patients withcardiac decompensation

Diastolic HF -look for normal EjF does not usually respond to positive inotropic drugs

• Diuretics • β-adrenoceptor antagonists (β-blockers) • Calcium-channel antagonists