Cardiology Notes

Cardiology Basics: Baroreceptors: sense changes in arterial pressure. Vagal maneuvers (carotid massage) decreases HR Autoregulation: process by which blood flow remains constant in a organs despite changing arterial pressure to the organ. In  the heart, the local vasodilators are nitric oxide, oxygen, and adenosine. Cardiac output and respiration: ● CO = HR x SV, and is different on left and right side. Normal physiologic variation: during inspiration, LEFT sided stroke volume decreases because: ○ Negative intrathoracic pressure increases venous return, reducing blood flow to the left side of the heart ○ Dec in thoracic pressure increases compliance of the pulmonary vascular bed, reduces left sided return ○ Inc venous return on the right pushes the septum towards the left side ● Left sided CO is relatively unchanged despite dec SV during inspiration because CO is maintained by inc HR. THIS EXPLAINS: ○ Physiologic splitting of S2: inspiration separates S2 into A2 followed by P2. ○ Murmur Augmentation: L sided murmurs are bed heard @ end of inspiration ○ Sinus Arrhythmia: during inspiration, the compensatory inc in heart rate speeds up the rhythm and slows during expiration ○ Pulsus Paradoxus: > 10 mmHg decline in SBP with inspiration. Ex) cardiac tamponade, tension pneumothorax ○ Cautious use of IV nitroglycerin and morphine in R sided and inferior MI: bc right side is dependent on preload and stroke volume to maintain CO, nitrogen and morphine decreases preload. Renin-angiotensin-aldosterone system (RAAS) ● Regulates blood pressure and water (fluid) balance. Activated with dec in systolic blood pressure Diagnostic Test ● Electrocardiogram: rhythm disorder, INITIAL TEST IN EVALUATING CARDIAC DISEASE ● Angiography: gold standard, for CAD, PAD, renal artery stenosis and abdominal aortic aneurysm ● Echocardiogram: most useful for heart failure for echo ○ TTE: primary noninvasive test for assessing cardiac anatomy and function ○ TEE: more invasive but better image for structures, good for posterior structures ● Stress testing: most useful noninvasive test in evaluation pts with suspected CAD ● Exercise stress testing (ECG): treadmill and radionuclide myocardial perfusion imaging ● Pharmacologic stress testing: for people unable to exercise. Vasodilators (adenosine or dipyridamole) cause dilation but not in diseased arteries. ● Stress echocardiography: localizes the regions of ischemia (dobutamine) ● Chest Radiographs: aortic dissection, CHF, rule out other causes pulm, GI ● Ultrasound: used to assess arterial pulses or to evaluate AAA. Venous duplex for suspected DVTs Cardiovascular (13%) Cardiomyopathy Disease Information Pathophysiology S/Sx Dg Tx Dilated ● MOST COMMON: 95% ● MC in men ● Etiologies: idiopathic, enterovirus, alcohol, pregnancy, cocaine, anthracyclines (doxorubicin) ● Systolic dysfunction→ ventricular dilation ● Heart failure: systolic heart failure; + S3, fatigue, signs of left and right HF. Lateral displaced PMI ● Embolic events, arrhythmias, chest pain on exertion ● Echo: LV dilation, decreased EF, regional or global left ventricular hypokinesis ● CXR: cardiomegaly, pulmonary edema, pleural effusion ● ECG: sinus tachy or arrythmias ● Standard HF tx: ACEI, diuretics BB, digoxin, Na+ restriction, implantable defib if EF < 30-35% ● Differential: HF due to cardiac disease or Takotsubo  cardiomyopathy: apical left ventricular ballooning after catecholamine surge (broken heart syndrome) Hypertrophic ● 4% ● Inherited GENETIC disorder of inappropriate hypertrophy of ventricles ● Subaortic outflow obstruction → narrows the LV outflow tract ● Diastolic dysfunction: stiff ventricular chamber → impared relaxation ● ● ● ● ● ● Often as/x → cardiac death Dyspnea: MC initial complaint Angina pectoris Syncope Arrhythmias Sudden cardiac death due to ventricular fibrillation ● PE: HARSH systolic crescendo-decrescendo murmur ● Lowers intensity if you do hand grip, increase venous return, because inc LV volume preserves outflow ● Increases intensity if you decrease venous return (valsalva and standing) ● Echo: asymmetrical wall thickness, especially septum. Systolic anterior motion of mitral valve. ● ECG: LVH, atrial enlargement ● CXR: cardiomegaly ● Early detection ● Counseling to avoid dehydration and extreme exertion/exercise very important! ● Medial: BB is first line ● Caution with digoxin, nitrates and diuretics, you don’t want to decrease preload bc that will increase the blockage ● Surgical: myomectomy ● Alcohol septal ablation Restrictive ● 1% ● Etiology: amyloidosis is MC cause, sarcoidosis, idiopathic myocardial fibrosis, hemochromatosis, scleroderma, chemo ● Impared diastolic function with relatively preserved contractility ● The rigidity impedes ventricular filling (decreased compliance) ● Right-sided failure MC ● Kussmaul’s sign: JVP increases with inspiration: stiff, inelastic RV → impaired filling causes backflow of the blood. ● CXR: normal ventricular size, large atria, pulm congestion ● ECG: low voltage ● ECHO: ventricles nondilated with normal wall thickness, marked dilation of both atria, diastolic dysfunction ● No specific tx ● Tx underlying disorder ● Symptomatic: diuretics, vasodilators EKG Cheat Sheet: EKG Basics Standard Calibration Vertical: Amplitude/Voltage Horizontal: Time 1 Small Box H: 1 mm x 1mm 0.04 seconds V: .1 mV amplitude Speed 25 mm/s 1 Large Box H: 5 mm x 5 mm .20 seconds V: .5 mV Name of Lead RA LA RL LL V1 V2 V3 V4 V5 V6 Location Right arm Left arm RL, lateral calf muscle Left Leg 4th ICS RSB 4th ICS LSB Midway between V2 and V4 5th ICS LMCL Level with V4, left anterior axillary line Level with V3, left midaxillary line Leads Anatomical Representation of the heart V1, V2 (septal), V3, V4 (anterior) Anterior I, aVL, V5, V6 Left lateral II, III, aVF Inferior AVR, V1 Right Atrium PR Segment Represents AV node conduction delay, allows for atrial kick and ventricular filling PR interval P wave + PR segment, can help determine if they have an AV block Nl .12-.20 seconds QRS Complex Ventricular depolarization, Q wave is deflection and always negative. Good to look at for BBB or hyperkalemia. Nl: 0.6-12 seconds J point Start of ST segment ST Segment Early RV and LV replorization, normally isoelectric, depression of >1mm suggests myocardial ischemia, ELEVATION >1 mm in limb leads or 2 mm in precordial leads suggests infarction T wave Rapid ventricular repolarization, transition point between absolute and relative refractory periods. Negative T waves (flipped T’s) suggest ischemia, may be peaked in hyperkalemia. QT Interval Represents total ventricular activity, start of QRS to end ot T Order of Interpretation Rate Look @ lead I, rhythm strip. Beats 60-99 bpm. Use sequence or 6 second strip Rhythm Look at p wave and relationship to QRS. Measure R-R interval and P-P interval Cardiac Axis Refers to the general direction of the heart depolarization wavefront. It is where the majority of the muscle bulk of the heart lies P Wave Normal is 3 small boxes and 2.5 high. Positive in I and II. Negative in aVR PR Interval Normal .12-.2 seconds (3-5 boxes). LONG = heart block, SHORT= Wolff-parkinson-white QRS Complex Normal: QRS is less than ⅓ QRS amplitude or <1 small square. WRS is 3 small boxes wide and S amplitude in V1 + amplitude in V5 < 3.5 Narrow < 3 boxes, wide > 3 boxes Small complex < 5 mm or <0.5 mV in limb leads or < 10 mm or <.1mV in chest leads Can have morphologies such as: ● Delta waves ● Q waves: old MI’ ● R waves ● S waves ● J point: point between QRS and ST segment NARROW QRS: (<120): BBB, ventricular origin of rhythm, LVH, pacemaker WIDE QRS: (>120): drugs, WPW, profound hyperkalemia ST segment Normally < 2-3 small boxes. This is isoelectric and this is where you look to distinguish NSTEMI or STEMI QT interval Normal is <2 large squares, 9-11 small boxes. QT interval decreases when heart rate increases ECG signs U wave: isn’t always seen, symmetrical and positive in lead II and follows t waves. It is thought to represent repolarization of the papillary muscles or purkinje fibers. Prominent U waves: hypokalemia, hypercalcemia, thyrotoxicosis, digitalis, epinephrine Inverted U: may represent myocardial ischemia or left ventricular volume overload. Calcium and potassium can also cause this Axis Lead I Lead II Lead III Normal + + +/- R axis deviation: normal in children and tall thin adults - + + L axis deviation: normal variation in pregnancy, obesity, ascites, abd distention, + - - P Wave Pulmonale Tall peaked P waves due to enlarged atrium Mitrale Wide p wave often bifid due to mitral stenosis or left atrial enlargement PR Interval: Longer First Degree P wave precedes QRS but P-R interval is prolonged and remains CONSTANT from beat to beat. Therefore, arterial pulse is delayed Second Degree Mobitz Type I (Wenchenbach): runs in cycle, first P-R is normal, and then it lengthens so long there is a dropped QRS. Going, going, going, gone Second Degree Mobitz Type II: P-R interval is constant, duration is normal/prolonged and periodically there is no conduction between the atria and ventricles, resulting in a p wave with no associated QRS. BB are contraindicated. Third Degree NO association between p and QRS complexes: complete heart block. PR Interval: Shorter Wolff-Parkinson-White Syndrome Delta waves, short PR of 0.08 seconds, and long QRS complex at 0.12 seconds. Accessory pathway (BUNDLE OF KENT) allows early activation of the ventricle. Look for DELTA WAVE.bTx: procainamide and avoid AV nodal blockers ABCD (adenosine, BB, CCB, Digoxin) Lown-Ganong- Levine Syndrome Characterized by short PR interval with normal QRS complex. Like WPW, LGL is an AVRT (leading to a short PR interval) but the accessory pathway (undles of james0 connects to the bundles of HIS, so the QRS is narrow in LGL (unlike wise in WPW) QRS complex: BBB LBBB: WilLiaM (WLM) Indirect activation of the left ventricle to contract later than the right. If new, rule out MI Qs or rS complex in V1: W shaped RSR wave in V6: M shaped If QRS >.0.12 seconds, check V5,6 for R’R and predominantly negative QRS in V1-V3 RBBB: MarRoW (MRW) Indirect activation causes right ventricle to contract later than left Terminal R wave in V1: M shaped Slurred S wave in V6: W shaped If QRS >.0.12 seconds, check V1,2 for R’R and V5-V6 slurred S waves ST segment STEMI ST elevation in > or = 2 chest leads greater than or equal to 2 mm elevation. ST elevation in > or = 2 limb leads greater than or equal to 1 mm elevation. Pathological Q waves = previous MI NSTEMI Suspected: ST depression, T wave inversion without ST depression MI 1 mm ST segment depression, symmetrical, tall T wave and long QT interval. A ST depression is more suggestive of myocardial ischemia than infarction Pericarditis ST elevation with concave shape, seen in all leads, sitting up makes people feel better Digoxin Downsloping ST segment depression, also known as reverse tick or reverse check Ions Hyperkalemia Narrow and tall peaked T waves Hypokalemia Narrow T waves flattened together with appearance of a prominent U wave Hypercalcemia Not obvious, associated with shorter QT intervals Hypokalemia Not obvious, associated with longer QT intervals Conductive Disorders/ Arrhythmias Disease Information Pathophysiology Tx Afib ● Irregularly irregular rhythm ● NO p waves ● MOST COMMON CHRONIC ARRHYTHMIA ● Ashman’s phenomenon: occasional aberrantly conducted beats (wide QRS) after short R-R cycles ● Ineffective quivering can cause thrombi to form, causing ischemic strokes ● Etiologies: cardiac disease, pulmonary disease, cardiomyopathies, electrolyte imbalances, thyroid disorders ● Types: ● Paroxysmal: self terminating within 7 days +/- recurrent ● Persistent: fails to self-terminate ● Permanet: persistent > 1 year ● Lone: paroxysmal, persistent or permanent without evidence of heart disease ● STABLE ● Rate control is the initial management over rhythm control ○ BB: metoprolol (caution if they have reactive airway disease) ○ CCB: diltiazem ○ Digoxin: prefered for pts with hypotension or congestive heart failure ● Rhythm control, younger patients with lone afib ○ Direct current cardioversion (DCC) ○ Medicine: ibutilide, flecainide, sotalol, amiodarone ○ Radiofreq ablation → perm pacemaker ● UNSTABLE: DCC ● ANTICOAG: CHA2DS2-VASc or CHADS2 to determine risks for embolization Aflutter ● Flutter (saw tooth) waves ● Rate is regular ● Stable: vagal, BB, CCB ● Unstable: direct current (synchronized) cardioversion ● Definitive management: radiofrequency ablation Paroxysmal supraventricular tachycardia ● Heart rate > 100 bpm ● Rhythm usually regular with narrow QRS complexes ● P wave is hard to see ● Paroxysmal: sudden onset and termination (preceded by PAC) ● Supraventricular: rhythm originates above the ventricles ● 2 types: ○ AV nodal reentry tachycardia (AVNRT): 2 pathways both within the AV node. MC type ○ AV Reciprocating Tachycardia (AVRT): 1 pathway within the AV node and second outside the AV node ● Conduction patterns: orthodromic → impulses go down normal AV node and returns leading to NARROW complex tachycardia. While antidromic → impulses go down accessory pathway first and return to the atria via nl pathway → WIDE complex tachycardia ● Stable (narrow complex): vagal maneuvers (stimulate acetylcholine → dec heart rate). Adenosine is first line tx for SVT. ● Stable (wide complex): antiarrhythmics (amiodarone) Procainamide in WPW ● Unstable: direct current (synchronized) cardioversion ● Definitive management: radiofrequency ablation Wandering Atrial Pacemaker (WAP) ● Multiple ectopic atrial foci generate impulses that are conducted to the ventricles ● ECG: heart rate < 100 bpm and >3 P wave morphologies ● Multifocal Arterial Tachycardia (MAT) ● Same as wandering atrial pacemaker except HR is > 100 bpm. ● ECG: HR > 100 bpm and > 3 P wave morphologies ● MAT is associated with severe COPD ● Difficult to tx, calcium channel blocker (verapamil) or BB usd if LV function is preserved Junctional Dysrhythmias ● AV node/junction becomes the dominant pacemaker of the heart in AV junctional rhythms ● Etiologies: sinus disease, coronary artery disease, MC rhythm seen with digitalis toxicity, myocarditis ● ECG: regular rhythm. P  waves inverted if present or are not seen ● Associated with narrow QRS ● Nl is 40-60 bpm (reflecting the intrinsic rate of the AV junction). Accelerated is 60-100 and tachy is > 100 ● Premature beats: PVC ● Premature beat originating from the ventricle: wide bizarre QRS occurring earlier than expected. With a PVC, T wave is in the opposite direction of the QRS ● Associated with a compensatory pause: overall rhythm is unchanged ● Potentially lethal because stroke volume and coronary flow are compromised ● No tx needed, most ventricular arrhythmias occur after a PVC Sinus arrhythmia ● Same as normal sinus rhythm except the rhythm is irregular ● HR increases during inspiration ● HR decreases during expiration ● Normal variant, can be seen with bradycardia. ● If bradycardia and symptomatic → atropine Torsades de pointes ● V tach that “twists” around baseline ● MC due to hypomagnesemia, hypokalemia. ● IV magnesium Ventricular Fibrillation ● Can be coarse or fine ● Heart looks like it is quivering ● ● Unsynchronized cardioversion (defib) + CPR Ventricular tachycardia ● > 3 consecutive PVCs at a rate of > 100 bpm. Must evaluate the pt if hemodynamically stable vs unstable and if it is sustained v non sustained. ● Ventricular tachycardia: prolonged QT interval is a common predisposing condition ● Stable sustained VT: antiarrhythmics (amiodarone, lidocaine, procainamide) ● Unstable VT with a pulse: synchronized cardioversion ● VT (no pulse): defibrillation (unsynchronized cardioversion) CPR tx as vent fibrillation Disease Information Pathophysiology S/Sx Dg Tx ASD ● Hole in the atrial septum ● Etiology: ostium secundum MC (80%) ● Ostium primum: associated with mitral regurgitation ● 2nd MC cause of CHD ● Shunt: Left to Right (NONCYANOTIC) ● Most pts asymptomatic or minimal in childhood until > 30 y ● Infants/young children will have failure to thrive, resp infections, exertional dyspnea ● Adults: exertional dyspnea, easy fatigability, palpation, syncope ● PE: systolic ejection crescendo-decrescendo flor murmur @ pulmonic area. Widely split fixed S2 does not vary with respiration ● CXR: cardiomegaly ● ECG: incomplete RBB ● Crochetage sign: notching of the peach of the R wave in inferior lead ● ECHO is the gold standard ● Spontaneous closure likely in the 1st year so may observe if small ● Surgical correction if symptomatic (usually between 2-4 y) Coarctation of aorta ● Congenital narrowing of the descending thoracic aorta. ● M:F 2:1 ● 70% also have a bicuspid aortic valve ● NONCYANOTIC ● Inc LV afterload with SNS activity and RAAS activation → HTN, LVH, CHF ● Secondary HTN ● Bilateral claudication, dyspnea on exertion, syncope ● Infats: failure to thrive ● Infants: PREductal ● Adults: POSTductal ● PE: systtolic murmur that radiates to the back/scapula/chest. BP higher in upper >> lower extremities ● Delayed/weak femoral pulses, decrease flow distal to obstruction in the lower extremities ● CXR: rib notching (increased collateral circulation via intercostal arteries) “3 sign’ narrowed aorta looks like the notch of the number 3 ● ECG: LvH ● ANGIO: GOLD STANDARD ● Surgical correction ● Balloon angioplasty ● Prostaglandin E1: preoperatively Congenital heart disease PDA ● Communication between descending thoracic aorta and pulmonary artery ● Left to Right (NONCYANOTIC) ● Prematurity, perinatal distress, hypoxia delays closure, Rubella infection in the 1st trimester ● Continued prostaglandin E2 production promotes patency Tetralogy of Fallot ● MOST COMMON CYANOTIC CONGENITAL HEART DISEASE ● ● ● ● ● VSD ● Hole in the ventricular septum ● MC cause of congenital heart disease ● Types: ○ Perimembranous: MC hole near tricuspid valve ○ Muscular: multiple holes swiss cheese ○ Inlet (posterior) ○ Supracristal (outlet) Congenital Cyanotic Heart Disease (All the T’s) 1. Truncus Arteriosus: 1 vessel instead of 2 normal vessels (aorta and pulmonary artery) ● Mostly asymptomatic ● Poor feeding, weight loss, frequent lower respiratory tract infections, pulmonary congestion ● Eisenmeger’s syndrome: pulmonary HTN → left to right shunt switches and become right to left shunt (cyanotic) ● Continuous machinery murmur loudest and pulmonic area ● Wide pulse pressure: BOUNDING Peripheral pulses ● CXR: normal or cardiomegaly ● ECG: LVH, LAE ● ECHO: GOLD STANDARD ● Indomethacin is 1st line to close the PDA ● Surgical correction if it fails, best before 1-3 y.o. ● Blue baby syndrome (cyanosis) ● TET SPELLS: paroxysms of cyanosis: older children relieve spells by squatting ● Eisenmenger syndrome: seend with PDA, VSD, TOF ● HARSH holosystolic murmur @ left upper sternal border ● RV heave, digital clubbing ● CXR: BOOT SHAPED HEART ● ECG: RVH ● Echo: GOLD STANDARD ● Surgical repair performed in the first 4-12 months of life ● PGE infusion to prevent ductal closure if pts in cyanotic prior to surgery ● Left to right shunt (NONCYANOTIC) ● Small (restrictive): asymptomatic or mild, found incidentally due to murmur. 80% will spontaneously close. Called Restrictive because normal pressure is maintained bc defect is small ● Moderate: excessive sweating or fatigue especially during feeds ● Large: nonrestrictive → CHF ● PE: loud high-pitched harsh, holosystolic murmur @ lower left sternal border. ● CXR: may be normal, may show LAE, RVH ● Echo: determines size and location. PREFERRED OVER CAT ● ECG: LVH with mild to moderate VSD +/RVH/LVH ● MRI: only used of echo nondiagnostic. Same diagnostic info as cat ● Cardiac Catheterization: only done if other tests are nondiagnostic ● Restrictive VSD (Left > Right sided pressure) = good prognosis ● 1. Most small VSDs close by themself within 10 years ● 2. Surgery 2. Transposition of the Great Arteries: 2 vessels switched (aorta and pulmonary artery) 3. Tricuspid Atresia: absence of the TRIcuspid valve leading to hypoplastic right ventricle 4. Tetralogy of Fallot: 4 issues highlighted above 5. Total anomalous pulmonary venous return: 5 vessels involved, ALL 4 pulmonary veins connect to 1 vessel (SVC) instead of left atrium Right to left (CYANOTIC) 1. RV outflow obstruction 2. RV hypertrophy VSD Overriding aorta Coronary Artery Disease Disease Information Pathophysiology S/Sx Dg Tx Coronary Artery Disease: Leads to Angina pectoris (chest pain) Can be STABLE OR UNSTABLE ● Inadequate tissue perfusion (ischemia) due to an imbalance between blood supply and demand. ● Etiologies: atherosclerosis MC cause, cigarette smoking, hyperlipidemia, hypertension, males, age, fm hx ● Classes: ○ I: VERY strenuous activity, no limitations of activity ○ II: prolonged activity, slight limitation of physical activity ○ III: daily activity, marked limitation ○ IV: at rest, can’t carry out activity ● Formation of atherosclerotic plaque: ○ Fatty streak formation: lipid  deposition in WBC. Asx ○ Formation of an early plaque: LDL enters the endothelium in the fatty streak → oxidizes and attracts shit to create foam cells, attracting more inflammation ○ Formation of fibrous (Mature) Plaque: proliferating smooth muscle cells and CT proliferation. Fibrous cap narrows luman +calcification for stabilization ● Myocardial ischemia: narrowing of the lumen dec flow typically >70% when symptomatic ● Substernal chest pain, pressure, burning, tightness that is POORLY localized, nonpleuritic, and exertional. ● Radiates to the arm (forearm and hand), teeth, lower jaw, back. ● Typically short in duration ● Levine’s sign: clenched first over chest. ● Pain is relieved with rest or nitroglycerin ● Can have associated symptoms: dyspnea, nausea, diaphoresis, numbness, fatigue ● PE: often normal ● ECG is initial test, then stress test ● Angiography is the gold standard ● ECG: ST depressions, resting is normal in 50% with stable ● Stress test: most useful noninvasive screening tool. Positive if it induces ST depression, hypotension/hypertension, arrhythmias, or symptoms ● Myocardial perfusion imaging stress: pts with baseline ECG abnl to localize region of ischemia. CI IN ASTHMATICS ● Stress echocardiogram: assesses LV function, valve dz ● PCTA (percutaneous transluminal coronary angioplasty): for pts with 1 or 2 vessel disease NOT involving the left main coronary artery in whom ventricular function in normal/near nl ● CABG: left main coronary artery disease, symptomatic or critical stenotic (>70%) 3-vessel disease or dec left ventricular EF <40% ● Pharm management of stable chronic angina ○ Nitroglycerin (nitrates):. SUBLINGUAL most effective. No relief after 3rd dose → ACS. CI: SBP < 90, RV infarction, use of sildenafil, and other PDE-r inhibitors ○ BB: FIRST LINE FOR CHRONIC MANAGEMENT ■ Cardioselective: M/A ■ NONselective: P/N ○ CCB: Nondihydropyridines (Diltiazem, Verapamil) ○ Aspirin: prevents platelet activation/ aggregation ○ Acute Coronary Syndrome (ACS): includes UNSTABLE angina, NSTEMI, and STEMI ● Symptoms of acute myocardial ischemia 2nd to acute plaque rupture and varying degrees of coronary artery thrombosis (occlusion) ● MIs can lead to Dressier syndrome: POST MI pericarditis + fever + pulmonary infiltrates ● Etiologies is either atherosclerosis (caused by plaque rupture) or coronary artery vasospasm (cocaine-induced or prinzmetal) ● Anginal pain: NOT RELIEVED WITH REST/NITROGLYCERI N ● Freq is highest in AM and pain @ rest = > 90% occlusion ● Silent MIs = women, elderly, diabetics, obese (abd pain, jaw pain, dyspnea WITHOUT CHEST PAIN) ● PE: Normal ● ECG: NSTEMI or unstable angina: ST depression or T wave inversion ● ECG: STEMI: ST elevation > 1mm in > 2 anatomically contiguous leads, new LBBB is STEMI equivalent!! ● On ECG STEMI will show the progression: t wave will be peaked, → ST elevation → Q waves → T wave inversions ● Cardiac markers: standard is 3 sets every 8 hours. Troponins are most sensitive and specific ● TIMI is used for risk stratification for pts with UA or NSTEMI to determine if they need invasive angiography ● Tx UA or NSTEMI: antithrombotic therapy and adjunctive therapy ● Antiplatelet aspirin, ADP inhibitors (clopidogrel, prasugrel, ticlopidine), GP IIB/IIIa inhibitors (eptifibatide, tirofiban, abciximab) ● Anticoag: unfrac heparin, LMW heparin (enoxaparin, dalteparin), fondaparinux (direct Xa inhibitor) ● Adjunctive therapy: BB, Nitrates, Morphine, CCB (can’t take BB, has prinzmetal angina) ● Tx of STEMI: Reperfusion, antithrombotics, and adjunctive ● Reperfusion: mainstay done within 12 hours, either PCI or thrombolytics. PCR within 3 hrs, best is 90 min. Get thrombolytics only if PCI is not an option (alteplase, reteplase, streptokinase). ● Antithrombotic tx: aspirin, heparin, glycoprotein IIB, IIIa inhibitors ● Adjunctive: BB, ACEI to slow progression of CHF after STEMI by decreasing remodeling. DEC MORTALITY. Angina pectoris: Prinzmetal variant ● Coronary artery spasm → transient ST elevation without MI (but can occur) ● Females ● > 50 y.o., smokers ● Vasospastic associated with migraines and raynaud’s) ● Cocaine induced MI has the same patho → vasospasm due to cocaine activation of the sympathetic nervous system and alpha 1 receptors. ● Chest pain that is nonexertional often occuring @ rest. Occurs in MORNING or WAKES THEM UP AT NIGHT ● ECG: transient ST elevation ● Angio: vasospasm with IV Ergonovine admin ● Symptoms and ST elevations resolve with CCB or nitro ● CCB is the drug of choice!!! ● Avoid BB in Cocaine induced MI bc there is an inc risk of vasospasm (UNOPPOSED A1 CONSTRICTION) Heart Failure Disease Information Pathophysiology S/Sx Dg Tx LEFT Sided H Failure ● HF is inability of heart to pump to meet metabolic demands. ● MC cause is coronary artery disease and hypertension (others is valvular disease) ● Increase pulmonary venous pressure from fluid backup into lungs ● Dyspnea is MC s/sx ● Pulm congestion → rales, rhonchi, pink frothy sputum (surfactant), wheezing. ● CHF is the most common cause of transudative pleural effusions ● PE: hypertension, cheyne-stokes breathing, S3/S4, lateral displaced PMI ● Increased adrenergic activation: dusky, pale skin, diaphoresis, tachycardia, cool extremities ● Echo: MOST USEFUL TEST. Measures EF ● Systolic: decrease EF, thin walls, dilated ● Diastolic: normal/ inc EF, thick walls, small LC ● CXR: good for congestive HF, shows kerley B lines, butterfly pattern, cardiomegaly, pleural effusion, pulm edema ● BNP: identify CHF as cause for dyspnea RIGHT Sided H Failure ● HF is inability of heart to pump to meet metabolic demands. ● MC cause of R sided heart failure is L sided heart failure ● Systolic: decrease EF + S3 gallop, Systolic is MC form of HF. CAUSE: MI, dilated cardiomyopathy, myocarditis ● Diastolic: normal or increase EF + S4 = forced atrial contraction into a stiff ventricle. Cause: hypertension, elderly, heart disease ● High output: the metabolic demands exceed function (thyrotoxicosis, wet beriberi, severe anemia, paget’s disease) ● Low output: inherent problem of myocardial contraction, ischemia, chronic hypertension ● Acute: often systolic ● Chronic: typically seen with dilated cardiomyopathy or valvular disease ● NYHA functional class: ○ I: no symptoms, no limitations ○ II: mild symptoms, slight limitations ○ III: cause marked limitation of activity with minimal exertion, only comfy @ rest ○ IV: symptoms @ rest ● Initial insult leads to inc afterload, inc preload &/or dec contractility. To compensate, the heart 1) ACTIVATES sympathetic NS, 2) HYPERTROPHY and REMODELING, and 3) RAAS activates → fluid overload, ventricular remodeling/hypertrophy ● Dec Afterload ○ ACE & diuretics >> BB ○ ACE: “pril” ○ ARB: “sartan” ○ BB: “lol”, add after ACE ● Dec Preload ○ Loop diuretics: furosemid,  bumetanide, torsemide ○ Potassium sparing: spironolactone, eplerenone ○ Hydrochlorothiazide ● Positive Inotropes ○ Digoxin: no mortality benefit. Watch 4 toxicity, hypokalemia worsens toxicity. ○ Dobutamine ○ Dopamine ● Increase systemic venous pressure → signs of systemic fluid retention ● Peripheral edema ● Jugular Venous Distention ● GI/Hepatic congestion → anorexia, N/V, RUQ tenderness, hepatojugular reflux CCB are not generally used unless angina with HF or nl EF Implantable cardioverter Defibrillator in pts with EF < 35% Systolic HF can use ivabradine which is a selective sinus nose inhibitor Hypertension Disease Information Hypertension ● Primary (essential): hypertension due to idiopathic etiology (95%) ● Secondary (5%): Htn due to an underlying, identifiable cause. Suspect this if refractory to meds. Renal is MC cause. ○ Renal artery stenosis: ■ Fibromuscular dysplasia MC in young ■ Atherosclerosis in elderly ● Patho: inc sympathetic, inc angiotensin II, inc mineralocorticoid activity S/Sx Dg Tx ● Typically silent ● Complications: ○ Cardiovascular: CAD, HF, MI, LVH, PVD ○ Neuro: TIA, stroke, ruptured aneurysm ○ Nephro: Htn 2nd Mc cause of end stage renal disease in the US ○ Optic: retinal hemorrhage, blindness, retinopathy ● Elevated BP >2 readings on > 2 different visits. ● Normal 120 / 80 ● Pre-HTN 120-139 / 80-89 ● Stage 1 140-159 / 90-99 ● Stage 2>160 / >100 ● Goal < 140/90 in general population, diabetics, or chronic renal disease ● Goal <150/90 if > 60 years old ● *Lifestyle modification: weight loss, DASH diet, exercise, limit alcohol consumption ● Meds: ○ Diuretics: tx of choice - hydrochlorothiazide ○ ACEI ○ ARB ○ CCB: dihydropyridines (vasodilator, doesn’t affect heart, “PINE”) and non-dihydropyridines (affects the heart, verapamil and diltiazem) ○ BB: cardioselective = ■ A, M, E ○ A1 blockers: “sin” On PE: ● Funduscopic exam shows papilledema (advanced stage of malignant hypertension) ○ I: arterial narrowing ○ II: A-V nicking ○ III hemorrhages and soft exudates ○ IV: papilledema (malignant) ● Skin: uremic appearance, stiae, carotid bruits ● Cardiopulmonary: loud S2 ● Abdomen: pheochromocytoma, PKD, bruits in renal artery ● Arterial pulses: dec or absent femoral pulses, BP upper ? lower → coarctation, edema Deciding what to give ● Initial UNCOMP non-AA: (1 of 4) thiazide, ACE, ARB, CCB Comorbidities: ● A fib: BB or CCB ● Angina: BB, CCB ● Post MII: BB, ACE ● Systolic HF: ACE, ARB, BB ● DM: ACE, ARB ● Isolated htn in elderly: diuretics ● Osteoporosis: thiazide ● BPH: a1 blockers ● AA: THIAZIDES, CCB ● Young, caucasian males: thiazide → ACE, ARB → BB ● Gout: CCB, losartan is the only ARB doesn't cause hyperuricemia Hypertensive Urgency ● High blood pressure with NO APPARENT ACUTE END ORGAN DAMAGE ● No end organ damage ● > 180 / 120 with NO end organ damage ● Dec BP by 25% over 24-48 hours using ORAL agents ● Goal of management is BP reduction to <160/<100 ● Drugs: Clonidine (REBOUND HTN IS STOPPED ABRUPTLY), captopril, furosemide, labetalol, nicardipine Hypertensive Emergency ● Usually > 180/120 (no specific #) BUT THERE IS END ORGAN DAMAGE ● Neurological: encephalopathy, hemorrhagic or ischemic stroke ● Cardiac: acute coronary syndrome, aortic dissection, heart failure ● Renal: acute kidney injury, proteinuria, hematuria ● Retinal: malignant HTN/ Grade IV retinopathy (papilledema) ● END ORGAN DAMAGE ● Dec BP by no more than 25% within the first hour, and additional 5-15% over the next 23 hours using IV agents. UNLESS they have an ischemic stroke. Only lowered if they are a candidate for thrombolytics. Acute aortic dissection you want to reduce rapidly in 20 min. ● Drugs: sodium nitroprusside is tx of choice, labetalol for prego ○ Nicardipine or clevidipine for neuro ○ BB, nitro, furosemide for cardio ○ Fenoldopam for renal Hypotension Circulatory shock is inadequate tissue perfusion to meet oxygen demand. Often associated with hypotension, and determined by low CO or low SVR. 4 Main types are hypovolemic (hemorrhage), cardiogenic (MI), Obstructive (pericardial tamponade), or distributive (septic, anaphylactic, or neurogenic shock) Disease Information Pathophysiology S/Sx Cardiogenic Shock ● Primary cardiac/myocardial dysfunction → inadequate tissue perfusion → dec cardiac output with increased systemic vascular resistance ● Etiologies: cardiac disease like: MI, myocarditis, valvedysfunctino, congenital heart disease, cardiomyopathy, arrhythmias ● ● ● ● ● ● ● ● Orthostatic hypotension ● Marked reduction of blood pressure from supine to upright position ● Impaired autonomic reflexes or reduced intravascular volume ● Causes from meds: antihypertensives, vasodilators, diuretics, ETOH consumption ● Neuro causes: diabetic autonomic neuropathy, parkinson, guillain-barre syndrome ● Dizziness, weakness, lightheadedness ● Syncope, change in mental status ● Weak pulses, cool extremities Vasovagal hypotension ● Faint because body overreacts to certain triggers (sight of blood or extreme emotional distress) ● Causes your heart rate and blood pressure to drop suddenly. Reduces blood flow to your brain causing you to briefly lose consciousness ● Vagus nerve (parasympathetic) ● ● ● ● ● Rapid breathing SOB Tachycardia LOC Weak pulse Low BP Sweating Pale skin Pal skin Lightheadedness Tunnel vision Nausea Blurred vision Dg Tx ● Clinical, may perform EKG, blood pressure and other tests ● Oxygen, isotonic fluids (ONLY SHOCK THAT ISN’T GIVEN LARGE AMOUNTS OF FLUID) ● Inotropic support: inc myocardial contractility and CO ○ Dobutamine, epinephrine Tx underlying cause ● Within 2-5 min of quiet standing there is EITHER ● Drop in SYSTOLIC > 20 ● Drop in DIASTOLIC > 10 ● Pulse rate should typically rise when stand, if it doesn't there is autonomic dysfunction ● If caused by volume, HR will increase ● Get a VMP, CBC, ECG ● Tx underlying disease, remove offending med, support BP ● Check for other causes but clinical dg ● Harmless and requires no tx Lipid Disorders: Hyperlipidemia can be hypercholesterolemia or hypertriglyceridemia Disease Information Pathophysiology S/Sx Dg Tx Hypercholesterolemia ● High cholesterol ● Hypothyroidism, pregnancy, kidney failure Hypertriglyceridemia ● High triglycerides ● 3DM, ETOH, obesity, steroids, estrogen ● Most are asymptomatic. Hypertriglyceride mia may cause pancreatitis. May develop xanthomas (achilles) or xanthelasma (eyelid) ● Screening based on RF and 10 YEAR CVD RISK ● Recommended ○ DM get at 40-75 ○ Without cardiovascular disease at 40-75 with > 7.5% risk ○ Older 21 with LFL > 190 ○ Any pt with any form of clinical atherosclerotic CVD ● Lifestyle modifications ● Lower LDL → Statins (HMGcoA reductase inhibitors, watch for rhabdo) ● Lower triglycerides → fibrates (Gemfibrozil,fenofibrate, watch for gallstones) ● Increase HDL → Niacin (causes hyperglycemia) ● Bile acid sequestrants (cholestyramine, colestipol, colesevelam, may inc triglycerides so use with pts w high LDL and nl triglycerides) ● Ezetimibe: inhibits intestinal cholesterol abs Traumatic, infectious, and inflammatory heart conditions Disease Information Pathophysiology S/Sx Dg Tx Acute and subacute bacterial endocarditis ● Infection of the endothelium/valve 2nd to colonization of bacterial ● MITRAL VALVE MC ● Types: ○ Acute: infection of nl valves with virulent organism (s. Aureus) ○ Subacute: indolent  infection of Abnl valve w less virulent organism (s. viridans) ○ Endocarditis in IV drug users: MRSA, pseudomonas, candida ○ Prosthetic valve endocarditis: early within 60 days, steph epidermis MC ● Micro ● Strep viridans: MC in subacute: oral flora ● Staph aureus: MC in Acute and IVDU ● Enterococci: MC in men with hx Gi/GU procedures ● HACEK organisms: Haemophilus, Actinobacillus, Cardiobacterium, Elkenella, Klingella. HACEK = gram organisms that are LARGE vegetations and are often hard to culture ● FEVER (FUO), anorexia weight loss, ECG abnl ● Peripheral manifestations: ○ Janewy lesions: painless red macules on the palms and soles ○ Roth spots: retinal hemorrhages ○ Osler nodes: tender nodules on pads of the digits ○ Splinter hemorrhage: hemorrhages of nail bed, clubbing ● Blood cultures before antibiotics ● 3 sets of at least 1 hour apart if the pt is stable ● ECg: look for conduction abnl ● Echo: TTE first, consider TEE ● Labs: CBCm leukocytosis, anemia, high ES/RF ● DUKE CRITERIA ● Major: sustained bacteremia, endocardial involvement (+ echo or new valve regurg) ● Minor: predisposing condition, fever, vasc and embolic phenomena, immunologic phenomena, positive blood culture not meeting major criteria, echo not meeting major criteria ● 2 major or 1 major + 3 minor or 5 minor! (80% accuracy) ● Empiric therapy: ○ Acute: nafcillin + gentamicin or vanco if you think MRSA ○ Subacute: penicillin or amp + gentamicin ○ Prosthetic: vanco + gentamicin + rifampin ○ Fungal: amphotericin B Acute pericarditis ● Acute fibrinous inflammation of the pericardium. May cause an effusion. Serious: noninfectious ● Etiologies: MC causes are idiopathic and virus, dressler syndrome (post MI), autoimmune, drugs ● Chest pain that is pleuritic, persistent and postural ● Pain radiates to trapezius, back, neck, shoulder ● Fever present ● Pericardial friction rub: heard best at end expiration while upright and leaning forward ● ECG: diffuse ST elevation in precordial leads (v1-v6) ● Echo: used to assess for complications of acute pericarditis (effusion or tamponade) ● Antiinflammatory drugs: aspirin or NSAIDS ● Colchicine is 2nd line ● Corticosteroid if symptomatic > 48 hours ● Dressler: Aspirin or colchicine Pericardial effusion ● Increased fluid in the pericardial space ● Etiologies: ○ Pericarditis, malignancy, infection, radiation therapy, dialysis/uremia, collagen vascular disease ● PE: Distant (muffled) heart sounds ● Electrocardiogram: Low voltage QRS complex, Electrical alternans ● Echo: inc pericardial fluid ● CXR: cardiomegaly ● Observe if small and no evidence of tamponade ● Pericardiocentesis if tamponade or large effusion Nonbacterial verrucous endocarditis (libman-sacks endocarditis) seen with SLE Penicillin and Vanco has gram + and gentamicin has gram -. Tx is typically 4-6 weeks Prophylaxis indications: ● Prosthetic heart valve ● Heart repairs using prosthetic material ● Prior hx of endocarditis ● Cong heart disease Procedures: ● Dental procedures ● Respiratory surgery Use amoxicillin 2g 30-60 min before procedure. NOT needed for GI/GU procedures Cardiac tamponade ● Pericardial effusion causing significant pressure on the heart -> restriction of cardiac ventricular filling → dec cardiac output ● Small rapidly developing effusion can cause tamponade ● Chronic (malignancy), the pericardium can stretch to accommodate up to 1 L without causing hemodynamic compromise ● Beck’s Triad: distant heart sounds, high JVP, systemic HYPOtension ● Pulsus paradoxus, > 100 mm decrease in systolic blood pressure with inspiration ● Dyspnea, fatigue, peripheral edema, reflex tachycardia ● Echo: presence of effusion + diastolic collapse of cardiac chambers ● Pericardiocentesis Constrictive pericarditis ● thickened , fibrotic, calcified pericardium that restricts ventricular diastolic filling ● ● Dyspnea MC symptoms ● Right sided heart failure signs ● Kussmaul’s sign: inc JVD during inspiration ● Pericardial knock: high pitch 3rd heart sound due to sudden cessation of ventricular filling in early diastole from thickened inelastic pericardium ● Echo: pericardial thickening ● CXR: pericardial calcification ● “Square root sign” on cardiac catheterization ● Pericardiectomy: definitive tx ● Diuretics 4 symptoms Rheumatic Fever ● Acute autoimmune inflammatory multi-systemic illness mainly affecting children 5-15 y.o. ● Starts with GABHS (aka strep pyogenes) stimulates antibodies that damage organs directly. ● Clinical manifestations are in the diagnosis criteria of JONES ○ Joints(Arthritis) ○ Oh my heart ○ Nodules ○ Erythema marginatum ○ Sydenham’s chorea Minor criteria: fever, arthralgia, high ESR, ECG show prolonged PR interval ● JONES Criteria: ● 2 Major or 1 major + 2minor ● PLUS evidence of recent GABHS infection ● Anti-inflammatory: aspirin ● Penicillin G antibiotic of choice!! Murmur Cheat Sheet: S1: Start of Systole Normal S 1 << S 2 @ base S 1 >> S 2 @ apex Loud Tachycardia, exercise, anemia , hyperthyroid Soft 1st degree heart block, CHF, CAD Varying CHB, irregular rhythms → afib Split Delay of tricuspid, sometimes normal, RBBB, PVCs S2: End of Systole Physiological splitting Accentuated on inspiration and usually disappears on expiration Wide Splitting Increase with inspiration and is persists through respiration. Delay of pulmonic valve closing → PS or RBBB. Early closure of AV → MR Fixed Splitting Respiration does not affect. ASD and RVF Paradoxical Splitting Splitting on expiration and disappears on inspiration. Closure of AV is delayed → LBBB S3 Normal in young. Old = LV overload. “Kentucky” sound. Very compliant LV = Dilated. Systolic CHF fluid overload S4 Vigorous atrial contraction onto stiff LV. “Tennessee” sound. Not heard in afib. Stiff ventricle = diastolic CHF pressure overload Diastole Grading of Murmurs 1 Very faint, “tuned in” 2 Quiet, but heard immediately 3 Moderately loud 4 Loud, THRILLS 5 Very loud: stethoscope partly off chest 6 May be heard with stethoscope FULLY off chest Harsh/Rumble Blowing Think stenosis Think regurgitation Murmur Accentuation Maneuvers Position Aortic: sitting up and leaning forward Mitral: lying on left side Increase Venous Return Increase venous return increases ALL murmurs (squatting, leg raise, laying down) EXCEPT HOCM Decrease Venous Return Decrease venous return decrease ALL murmurs (valsalva/standing) EXCEPT HOCM Inspiration Inspiration increase venous return on right therefore increases murmurs on RIGHT side Inspiration decrease venous return on left side therefore dec murmurs on LEFT side Expiration Expiration increases venous return on left side Expiration decreases venous return on right side Handgrip Increases afterload leading to decrease LB emptying and increase backward flow ● AS, MVP, HOCM decrease with handgrip. Because hand grip increases afterload, the increased afterload prevents blood flow from being ejected from the ventricles, lessening the blood flowing through the stenotic aortic valve and less blood ejected in hypertrophic cardiomyopathy, thus lessening both murmurs ● AR, MR inc with handgrip due to increase backflow. MS increases due to inc afterload Amyl, Nitrate Decreases afterload leading to increase LV emptying ● AS, MVP, hypertrophic cardiomyopathy murmur will inc with amyl nitrate ● AR, MR decrease with amyl nitrate Valvular Disorders Disease Pathophysiology S/Sx Dg Tx Aortic Regurg ● Etiologies: ○ Valve disease: rheumatic heart disease, endocarditis ○ Aortic root disease/dilation: hypertension, marfan syndrome, syphilis, sLE, aortic dissection, ankylosing spondylitis ● Regurg → fluid overload → dilation ● ● ● ● ● ● ● ● Acute → pulmonary edema and hypotension Chronic: clinically silent then turns to CHF PE: diastolic, decrescendo, blowing murmur @ LUSB Inc intensity: inc venous return (squatting) sitting forward, handgrip, expiration Dec intensity: dec venous return (valsalva, standing), inspiration, amyl nitrate BOUNDING PULSE: 2NDARY TO INC STROKE VOLUME WIDE PULSE PRESSURE +/- austin flint murmurs: mid-late diastolic rumble at the apex 2ry to retrograde regurgitant jet competing with antegrade flow from left atrium into the ventricle ● Signs: ○ Water hammer pulse: swift upstroke and rapid fall of radial pulse accentuated with wrist elevation ○ Corrigan’s pulse: similar to water hammer but carotid ○ Hill’s sign: popliteal artery systolic pressure > brachial by 60 mmHg most sensitive ○ Durozier’s sign: Gradual pressure over femoral artery→ systolic and diastolic bruit ○ Traube’s sound (pistol shot): double down heard @ femoral artery w partial compression ○ De Musset’s sign: head bobbing with heart beating ○ Muller sign: visible systolic pulsations of the uvula ○ Quincke’s pulse: visible fingernail bed pulsation with light compression ● Pulsus Bisferiens: double pulse carotid upstroke. Seen with AR + AS or severe AR ● Echo: regurg ● ECG: nonspecific ● CXR: nonspecific + cardiomegaly ● Medial therapy: afterload reduction with vasodilators ● Surgical therapy: definitive management if EF <55% Aortic Stenosis ● Etiologies: ○ Degenerative heart disease: calcification ○ Congenital: bicuspid valve ○ Rheumatic ● Stenosis → hypertrophy ● Dyspnea is MC symptom ● Aortic Stenosis Complications: Angina, Syncope, CHF ● PE: systolic “ejection” crescendo-decrescendo murmur @ RUSB that radiates to carotid ● Dec intensity: dec venous return, inspiration, handgrip ● Inc intensity: inc venous return, squatting, leg rise, expiration ● Sign of severity: late peaking murmur, pulsus parvus et tardus, paradoxically split S2 ● Pulsus parvus Et tardus: small, delayed, carotid pulses, narrow pulse pressure ● Echo: small aortic orifice, LVH, thickened Aov ● ECG: LVH ● Surgical therapy: aortic valve replacement only effective tx ● Mechanical is prolonged durability but thrombogenic ● Bioprosthetic less durable but minimally thrombogenic ● Percutaneous aortic valvuloplasty: 50% restenos Mitral Stenosis ● Etiologies: ○ Rheumatic heart Disease: MC by far ● Back up to the left atrium, increase pulmonary pressure ● ● ● ● ● ● ● Echo: narrowed mitral valve ● ECG: left atrial enlargement ● Surgical management: percutaneous balloon valvuloplasty/valvotomy: best tx in younger pts and in pts with noncalcified valves ● Open mitral valvotomy ● Mitral valve repair or replacement Meds DON’T help ● ● ● Slow progression → rapid Pulmonary symptoms dyspnea MC, hemoptysis, cough, frequent bronchitis, pulm htn A fib Right sided heart failure Mitral facies = ruddy (flushed) cheeks with facial pallor Left atrial enlargement: dysphagia,, ortner’s syndrome: recurrent laryngeal nerve palsy due to compression by the dilated left atrium → hoarseness PE: prominent LOUD S1 OPENING SNAP: HIGH PITCHED EARLY DIAGNOSTIC SOUND OF THE OPENING OF STENOTIC VALVE Early-mid diastolic rumble @ apex esp in LLD position Decrease murmur intensity: dec venous return Increase murmur intensity: inc venous return Acute:Pulmonary edema, Dyspnea, fatigue Chroni: A fib, progressive DOE, fatigue PE: BLOWING HOLOSYSTOLIC @ apex with regurg to the axilla Decrease murmur: dec venous return (valsalva, standing) Increase murmur: increase venous return (squatting, supine) Widely split S2 ● Echo: regurg jet, hyperdynamic LV ● Repair >> Replacement ● Medial: vasodilators to decrease afterload ● ● Mitral Regurg ● Etiologies ○ Leaflet abnl: prolapse is MC cause, rheumatic heart disease, marfan syndrome ○ Papillary muscle dysfunction: ischemia/infarction ○ Ruptured chordae tendineae ● ● ● ● ● ● Mitral Valve Prolapse ● Etiologies: ○ Myxomatous degeneration of the mitral valve apparatus with CT disease (marfan, ehlers-danlos, osteogenesis imperfecta) ○ MC young women ● Most a/sx ● Autonomic dysfunction: anxiety, atypical chest pain, panic attacks, palpitations, dizziness, fatigue ● PE: MID-LATE SYSTOLIC EJECTION CLICK best heard @ the apex ● Any maneuver, which makes LV smaller (valsalva,standing) results in earlier click ● Echo ● Reassurance only ● BB ONLY if autonomic dysfunction Pulmonary Regurgitation ● Etiologies: ○ Pulm htn, tetralogy of fallot, endocarditis ● GRAHAM STEELL MURMUR: brief decrescendo early diastolic murmur @ LUSB with full inspiration ● Inc murmur: inc venous return (squatting, supine, inspiration) ● Dec murmur: dec venous return (valsalva, standing, expiration) ● Echo ● No tx ● ALMOST ALWAYS CONGENITAL Pulmonic Stenosis ● Almost always congenital and a disease of the young (congenital rubella syndrome) ● PE: HARSH MIDSYSTOLIC EJECTION CRESC-DECRESCENDO MURMUR (@LUSB) RADIATES TO NECK ● Inc with inspiration ● Signs of R sided HG ● Systolic ejection click buried in S1 ● Echo ● Balloon valvuloplasty Tricuspid Regurgitation ● Right sided heart failure ● HOLOSYSTOLIC BLOWING HIGH-PITCHED MURMUR @ SUBXHYPOID (L MID STERNAL BORDER) ● NO RADIATION ● Inc intensity by inc venous return (squatting, inspiration) ● Carvallo’s sign: inc murmur intensity with inspiration. Helps distinguish TR from MR ● Echo ● Med: diuretics ● Surgical: repair > replacement Tricuspid Stenosis ● Right sided heart failure ● Echo ● MID DIASTOLIC MURMUR @ LLS (XIPHOID BORDER) 4TH ICS ● Inc intensity by increasing venous return (squatting, laying down, leg raising, inspiration) ● Med management: dec right atrial volume overload with diuretics and sodium restriction ● Surgical management Vascular Disease Disease Information Pathophysiology S/Sx Dg Tx Abdominal Aortic Aneurysm (AAA) ● Focal dilation of the aortic diameter @ least 1- 1.5 x diameter measured @ level of the renal arteries ● >3.0 cm generally considered aneurysmal. MC infrarenal ● RF: atherosclerosis is MC, Age > 60 y.o., smoking, males, hyperlipidemia, CT disorders ● Proteolytic degeneration of aortic wall, connective tissue, inflammation and an immune response ● a/sx until it ruptures ● Acute leakage/rupture: classic presentation is syncope or hypotension and tender/pulsatile abd mass ● Flank ecchymosis ● Often incidental finding on US, CT, or MRI ● Dg with US ● Angio is gold standard ● 5.5 = IMMEDIATE surgical repair ● 4.5 → Surgery referral ● 4-4.5 monitor by US every 6 months ● 3-4 monitor every year ● Give BB Aortic Dissection ● Tear in the innermost layer of aorta (intima) ● *65% is ascending ● 20% descending ● 10% aortic arch ● RF: hypertension, age 50-60 y.o., vasculitis (rare), collagen disorder ● Sudden onset of severe tearing (ripping, knife life) chest/upper back pain ● N/V, diaphoresis ● Variation in pulses ( > 20 mmHg difference between the right and left arm) ● CT scan with contrast ● MRI angio = GS ● CXR: widening of the mediastinum ● Surgery → acute proximal or distal with complication ● Medial → descending if no complications:esmol ol, labetalol 1st line Giant cell arteritis ● Same clinical spectrum as polymyalgia rheumatica (which is present in 50% of cases) ● MC seen in women > 50y.o. ● Etiologies: idiopathic, autoimmune, vasculitis of the extracranial branches of the carotid artery ● Granulomatous (cell-mediated), chronic vasculitis, mostly affecting cranial arteries ● Headache MC symptoms: new onset, localized ● Jaw claudication with mastication ● Acute vision disturbances: amaurosis fugax (temporary monocular blindness) ● Thickened temporal artery ● Labs and biopsy are supportive but this is a CLINICAL DIAGNOSIS bc BLINDNESS IS THE MC COMPLICATION ● High ESR > 100, High CRP ● Biopsy may have skip lesion, therefore if negative doesn’t exclude dg. Shows mononuclear lymphocyte infiltration, multinucleated giant cells, lamina cell degradation ● High dose corticosteroids start tx right away!!! Hallmark: headache, scalp tenderness, jaw claudication, fever, visual changes Peripheral artery disease ● Atherosclerotic disease of the lower extremities ● Atherosclerosis pathophysiology ● Intermittent claudication: MC presentation. Reproducible pain/discomfort in the lower extremity brought on the exercise/walking and relieved with rest ● Leriche’s syndrome: claudication (buttock, thigh pain), impotence, and decreased femoral pulses ● Acute arterial embolism: sudden occlusion is the 6 P’s (paresthesias, pain, pallor, pulselessness, paralysis, poikilothermia) ● Gangrene can occur when arterial perfusion is so poor spontanous necrosis can occur. ● PE: decrease pulses, + bruits, dec capillary refill ● Skin: atrophic skin changes, dry, shiny ● Color: pale on elevation ● LATERAL malleolar ulcers ● ABI: simple quick and noninvasive +PAD if ABI <0.90 ● Normal is 1-1.2 ● Gold standard = arteriography ● Platelet Inhibitors: cilostazol is mainstay of tx ● Aspirin ● Clopidogrel ● Also can do revascularization ● Supportive Peripheral Venous Disease ● Multiple types: ○ Superficial venous system: greater/lesser saphenous veins ○ Deep venous system: major arteries like femoral, iliac, popliteal, posterior tibial and superficial femoral ○ Perforating veins: communicate between deep and superficial sys ● Virchow’s triad 1. Intimal damage (trauma, infection, inflammation) 2. Stasis (immobilization) 3. Hypercoagulability: factor V leiden mutation, protein C or S deficiency, oral contraception use ● WORSE with standing/sitting, IMPROVES with walking (opposite of arterial disease) ● Cyanotic leg with dependency (dependent rubor is arterial) ● Ulcer is medial (arterial is lateral) ● Pominant edema (arterial has no edema) ● ● Phlebitis/Thrombophlebitis ● inflammation/swelling of vein caused by a blood clot. 2 main types: superficial thrombophlebitis and deep vein thrombosis (deep, larger veins) ● Superficial → IV catheterization, trauma ● Deep → most important thing it can cause is pulmonary embolism ● Superficial: Local phlebitis: tenderness, pain, induration, edema, and erythema ● Trousseau's sign: migratory thrombophlebitis associated with malignancy ● Deep:unilateral swelling/edema of lower extremities, calf tenderness, homan’s sign ● Superficial → Most don’t need workup ● Deep → venous duplex US: first imaging test showing noncompressible echo ● D-dimer: low sensitivity ● Venography is GS ● Superficial Supportive management is mainstay ● Deep Prevent PE with anticoagulation therapy WELLS criteria for DVT Varicose Veins ● Dilated tortuous superficial veins 2ndary to valve structure and function of the superficial veins ● Seen with high estrogen OCPs, pregnancy, high stress on legs, prolonged standing obesity ● Muscle contractions compress the deep veins and this pressure gets transferred to the superficial venous system → causing dilation ● Often a/sx but may be cosmetic issue for some patients. Dilated, tortuous veins ● Dull ache or pressure sensation worsened with prolonged standing and relieved with elevation ● Venous stasis ulcers ● Clinical ● Conservative or sclerotherapy Venous Insufficiency ● Vascular incompetence of either the deep or superficial veins. ● Etiologies: ○ MC occurs after superficial thrombophlebitis, after DVT or trauma to the affected leg ● Leg pain: burning, aching, throbbing, cramping, “heavy leg” ● Pain is worse with prolonged standing ● Pain improves with leg elevation ● Leg edema ● Stasis dermatitis ● Brownish hyperpigmentation ● Venous stasis ulcers @ MEDIAL MALLEOLUS ● Trendelenburg test: test perforator function and saphenofemoral vein competency. Elevate one leg @ 90 degree → occlude great saphenous vein at the upper thigh. After pt stands for 20 seconds, slow filling at the ankle suggests perforator competency ● Compression mainstay of tx