CARDIOVASCULAR (13%) Flashcards

Question

GIANT CELL ARTERITIS (TEMPORAL ARTERITIS)

Answer 1

MEDIUM + LARGE VESSEL VASCULITIS PATHOPHSYIOLOGY - Vasculitis = typically an autoimmune disease - immune system recognizes own vasculature as foreign, and attacks (molecular mimicry) = associated with medium and large vessel vasculitis - Mostly affects cranial arteries (head + neck) Idiopathic +/- autoimmune viral infection causes monocyte activation and inflammatory cytokine production, inflammation and tissue destruction resulting in symptoms - Once vessels are damaged = exposed collagen + tissue factor ==> increases chances of blood coagulation - blood vessel walls get weaker as they are more damaged ==> higher risk for aneurysm - as vessel wall heals = gets harder / stiffer from fibrin deposition Vasculitis affects extracranial branches of the carotid artery: temporal artery, occipital artery, ophthalmic artery, posterior ciliary artery - MC location for vasculitis = *** TEMPORAL REGION *** supplied by carotid arteries ⦁ Patients > 50 (if < 50 in stem = not GCA) ⦁ Women > men ** ASSOCIATED WITH POLYMYALGIA RHEUMATICA ** = inflammatory condition that causes muscle pain + stiffness in proximal muscles - neck / shoulders / upper arms / proximal legs - stiffness in morning* - Many patients with GCA have polymyalgia rheumatica, but not necessarily the other way around SYMPTOMS ⦁ Throbbing unilateral Headache (temporal branch) ⦁ Severe tenderness over ipsilateral temple ⦁ Amaurosis Fugax*** / vision changes (ophthalmic artery) ⦁ Jaw claudication / pain with chewing (facial artery) ⦁ low grade fever / fatigue / weight loss / anorexia *** COMPLICATION = BLINDNESS *** *** COMPLICATION = AORTIC ANEURYSM *** PHYSICAL EXAM ⦁ thickened temporal artery - sticks out ⦁ tenderness of temporal region ⦁ pulseless temporal region DIAGNOSIS ⦁ *** ELEVATED ESR *** > 50, usually > 100 ⦁ elevated CRP ⦁ normochromic normocytic anemia ⦁ Will NOT have elevated CK (creatine kinase) - which occurs with muscle breakdown (MI / Rhabdo) (does not occur in polymyalgia rheumatica either) * ** GOLD STANDARD = TEMPORAL ARTERY BIOPSY ** - shows giant cells in elastic lamina (between tunica intima + tunica media) - not large single cells, but granulomas, or groups of monocytes packed tightly together to look like one giant cell Giant cell granulomas as immune system attempts to wall off "foreign" invaders * * Giant cell arteritis = SEGMENTAL or SKIP LESIONS ** - meaning that only sections of the artery are affected, so when performing temporal artery biopsy, need to take long sections in order to see affected segments - meaning if negative on biopsy, patient may still have GCA, and biopsy only showed unaffected area COMPLICATIONS ⦁ blindness!!!! - give steroids prior to biopsy, as results may take a while, and patient may be blind by then. DO NOT WAIT FOR BIOPSY RESULTS, GIVE STEROIDS FIRST IF GCA IS SUSPECTED ⦁ Aortic aneurysm - poor blood flow to ophthalmic artery --> ischemia --> irreversible blindness TREATMENT ⦁ high dose steroids = PREDNISONE - ESR used to monitor response to steroids RULE OF 50 WITH GCA 1) Age greater than 50 2) Sed rate greater than 50 3) Steroids greater than 50 (will start patient typically on 60 mg of prednisone) Patient will present as → a 67-year-old female with a severe throbbing headache and visual impairment in the left eye. The patient describes worsening of pain with chewing or combing her hair. Lately, she reports feeling very weak and tired especially in the mornings. At times she cannot even raise her arms to reach the cabinets in her kitchen. On physical exam, she has decreased visual acuity of the left eye, scalp tenderness on the left, and an absent pulse in the left temporal area. Laboratory testing is significant for an elevated erythrocyte sedimentation rate. She is admitted and immediately started on systemic glucocorticoids.

Answer 2

⦁ V1 - V4 = Anterior (V3-V4) / Septal Leads (V1-V2) ⦁ II / III / AVF = Inferior Leads ⦁ I / AVL / V5 / V6 = Lateral Leads ⦁ Anterior septal leads (V1 - V4) = LAD = SALAD (Septal Anterior LAD) ⦁ Inferior leads (II / III / AVF) = RCA*** (70%) + Left Circumflex ⦁ Lateral leads (I/AVL/V5/V6) = Left Circumflex + LAD ⦁ Anterior wall ST elevation in leads V1 through V4 ⦁ Inferior wall ST elevation in leads II, III, and AVF ⦁ Lateral wall ST elevation in leads I, AVL, V5, and V6 ⦁ Posterior wall ST depressions V1 through V3

Answer 3

MC CAUSES OF AV BLOCK = - Idiopathic fibrosis and sclerosis of conduction system (about 50% of patients) - Ischemic heart disease (40%) The remaining cases of AV block are caused by - Drugs (eg, beta-blockers, calcium channel blockers, digoxin, amiodarone) - Increased vagal tone - Valvulopathy - Congenital heart, genetic, or other disorders First-degree and second-degree blocks are partial Third-degree blocks are complete o FIRST DEGREE HEART BLOCK - PR interval > 0.20 - In a stable patient = most likely benign = needs no tx - Unstable patient with severe bradycardia = needs pacing o SECOND DEGREE HEART BLOCK ⦁ Mobitz I (Wenkebach) - longer, longer, longer, drop - PR interval gets longer, longer, longer, then QRS drops - Treatment = unnecessary unless the block causes symptomatic bradycardia and transient or reversible causes have been excluded In many cases, type 1 second-degree heart block is a normal variant. Other times, the etiology is likely related to increased vagal tone and in most cases requires no treatment. It can also occur in a myocardial infarction and usually resolves after the infarct period ⦁ Mobitz II - when some Ps don't get Qs - P wave not followed by QRS wave (dropped) - Almost always progresses to 3rd-degree heart block. - TX = Patients will need a pacemaker (even if asymptomatic!) o THIRD DEGREE HEART BLOCK (COMPLETE BLOCK) - Ps and Qs don't agree - P intervals are consistent - QRS intervals are consistent - Ps and QRSs don't line up ``` THIRD DEGREE HEART BLOCK TREATMENT ⦁ Asymptomatic - none ⦁ Symptomatic - atropine or isoproterenol ⦁ Permanent - pacemaker - TX = patients will need a pacer - need to rule out ischemic disease ```

Answer 4

``` CAUSES OF SECONDARY HYPERTENSION ⦁ Chronic Kidney Disease ⦁ Cushing's Disease ⦁ Medications ⦁ Renal Artery Stenosis ⦁ Drugs (ETOH / Cocaine) ⦁ Hyperaldosteronism ⦁ Polycythemia Vera ⦁ Hyper / Hypothyroidism ⦁ Coarctation of the Aorta ⦁ Sleep Apnea ⦁ Pheochromocytoma ⦁ Hyperparathyroidism ```

Answer 5

Mitral Stenosis = narrowing of mitral valve MC cause = ** RHEUMATIC FEVER ** - in MS; rheumatic fever causes inflammation/fibrosis to fuse valve leaflets together = called commisural fusion - In MR; rheumatic fever causes inflammation/fibrosis to not properly close together MITRAL STENOSIS - usually normal valve area = 4-6 cm - in MS, commissural fusion narrows valve area to 2 cm The increased volume in the Left Atria pushing on the mitral valve --> increased pressure in LA. Higher pressures flowing through a fibrotic valve cause an OPENING SNAP after S2, followed by a diastolic rumble as blood is forced through smaller open Constant increased volume / pressure in the left atrium --> dilation of left atrium as well as back up of blood into the pulmonary system --> pulmonary congestion / edema --> symptoms such as Dyspnea (MC*) Extra blood in pulmonary system causes higher pulmonary pressures (pulmonary HTN), meaning the right ventricle has to pump harder to get blood through the pulmonic valve (SL valve) --> RVH --> can ultimately lead to right-sided heart failure With LAE, the pacemaker cells in the LA stretch and become irritable --> increased risk of A-fib (the right and left atrium don't contract properly anymore) --> stagnant blood --> increased risk of thromboembolism formation --> can dislodge to systemic circulation If atrium dilates and becomes really large = can compress the esophagus and lead to difficulty swallowing (dysphagia) - MC cause of mitral stenosis = RHEUMATIC FEVER - Rheumatic Fever can cause chronic rheumatic heart disease, leading to scarring + fusion of the valve leaflets - 40% of patients with rheumatic heart disease get pure or predominant Mitral valve stenosis - 2/3 of all patients with Mitral Stenosis = FEMALE - rheumatic fever - not commonly seen in the US - mostly foreign countries, but there have been some outbreaks. Rheumatic fever first affects mitral valve, then aortic, then tricuspid, then pulmonic. ETIOLOGIES of MITRAL STENOSIS ⦁ *** Rheumatic Heart Disease *** (mostly females) ⦁ Congenital ⦁ Left atrial myxoma ⦁ Valvulitis (rare) = Carcinoid, SLE, RA, Amyloid PATHOPHYSIOLOGY - narrowed mitral orifice --> obstruction of flow from LA to LV --> blood backs up into left atrium --> volume overload / increased left atrial pressure --> backs up into lungs --> pulmonary congestion --> pulmonary HTN --> CHF (heart has to work extra hard to pump blood to the lungs) - Normal Valve area = 4-5cm - Mild mitral stenosis = 1.5-2.5 cm with minimal symptoms - Moderate mitral stenosis = 1.0-1.5 cm - usually does not produce symptoms at rest - Severe mitral stenosis = < 1.0 cm - usually takes a long time for stenosis + symptoms to occur, but can occur rapidly (acute) - progressive lifelong disease that is usually slow/stable in early years, with progressive acceleration in later years* - 20-40 year latency from rheumatic fever to symptom onset with mitral valve stenosis. An additional 10 years before disabling symptoms occur ``` SYMPTOMS of MITRAL STENOSIS o Pulmonary Symptoms ⦁ ** Dyspnea (MC) - SOB, Orthopnea, PND ⦁ Pulmonary edema ⦁ Hemoptysis ⦁ Cough ⦁ Frequent bronchitis ⦁ Pulmonary HTN ``` o A-Fib (secondary to atrial enlargement --> thromboembolic events (CVA) o Right sided Heart failure = due to prolonged pulmonary HTN o Mitral Facies = ruddy, flushed cheeks with facial pallor (chronic hypoxia) o Signs of LAE (left atrial enlargement) = dysphagia (esophageal compression) + Ortner's Syndrome = recurrent laryngeal nerve palsy due to compression by the dilated left atrium --> hoarseness PHYSICAL EXAM 1) Prominent (Loud) S1 = due to delayed forceful closure of mitral valve - may have split S2 prior to OS (opening snap) 2) OPENING SNAP (OS)**** - high pitched sound of the opening of a stenotic valve (present in both aortic and mitral stenosis) - Valve area is proportional to S2-OS interval: the tighter the valve = will take longer to fill LV = therefore the shorter the interval - opening snap = diastolic for mitral stenosis, systolic for aortic stenosis (ejection click = think aortic stenosis only) 3) MID-LATE DIASTOLIC RUMBLE** @ APEX (low-pitched) - as blood is filling from LA to LV, and moving through stenosed valve - especially in LLD position (L lat decubitus) ⦁ decreased venous return -> decreased murmur intensity (ex: Valsalva, standing, inspiration) DIAGNOSIS 1) ECHO** = see narrowed mitral valve (increased LA pressure, may have pulmonary HTN) 2) EKG = Left Atrial Enlargement (P mitrale) = larger initial upward deflecting P wave in AVR + notched P wave in lead II 3) CXR = LAE + pulmonary congestion - Palpation = small volume pulse, palpable S1 - tapping apex, palpable pulmonic component of S2 Auscultation = loud S1, Early-mid diastolic RUMBLE @ apex, and opening snap. The length of the murmur is proportional to severity MITRAL STENOSIS COMPLICATIONS ⦁ atrial dysrhythmias from degree of atrial stretch causing pacemaker cells to become irritated ⦁ A-fib --> risk of embolization (related to age, presence of Afib, and previous embolic events) ⦁ CHF (right sided heart failure) - due to pulmonary HTN ⦁ Hemoptysis - from pulmonary HTN causing ruptured bronchial veins, or streaking/pink froth from pulmonary edema or infections ⦁ Endocarditis ⦁ Pulmonary Infections MITRAL STENOSIS PATHOPHYSIOLOGY 1) left atrium has to increase pressure to push blood through narrowed valve --> Left Atrial Hypertension --> LA stretch + A-fib --> limited LV filling / limited CO 2) A-fib can lead to thrombus formation 3) LA HTN --> pulmonary interstitial edema + pulmonary HTN ⦁ passive pulmonary HTN = obligatory to preserve forward flow ⦁ reactive pulmonary HTN = leads to vascular changes to protect interstitium from edema, which leads to right sided heart failure 4) LA stretch --> A-fib leads to increased HR, which decreases LV filling. Decreased atrial "kick" --> thrombus formation + embolus MITRAL STENOSIS EKG ⦁ LAE ⦁ RVH (due to pulmonary HTN) ⦁ PVCs - premature ventricular contractions ⦁ A-flutter and/or A-fib - A-flutter/A-fib = more frequent in patients with mod/severe MS for several years. A-fib develops in 30-40% of patients with symptoms Normal mitral valve = 4-5mm/4-6mm wide. Symptoms do not become apparent until valve stenosis is < 2.5 mm. Mild = 1.5-2.5, moderate = 1.0-1.5, severe = < 1.0 TREATMENT FOR MITRAL STENOSIS ⦁ surgery - mitral valve repair or replacement (if symptomatic) - balloon valvuloplasty / valvotomy = best in YOUNGER patients and in patients with noncalcified valves ⦁ Balloon valvuloplasty/valvotomy - effective long term improvement - the earlier it is done, the better = BEST TX IN YOUNGER PATIENTS and in patients with non-calcified valves o Medical Management = for symptoms, but still need surgery! ⦁ Diuretics / sodium restriction for LHF/RHF ⦁ Digitalis / Digoxin / BB / CCB - to control rate for A-fib ⦁ Anticoags for A-fib to prevent thrombus formation ⦁ Endocarditis prophylaxis Patient will present as → a 72-year-old female who presents to your office for a routine check-up. While she otherwise feels well, it has been a long time since she last received medical care. On exam her you note an apical, rumbling diastolic murmur with a split s1 that occurs following an opening snap. The rumbling is loudest at the start of diastole and is heard best at the left sternal border and apex MITRAL STENOSIS MURMUR Diastolic low pitched decrescendo rumbling murmur with opening snap heard best at the apex (mitral area) with a patient in a lateral decubitus position Mechanism: When the leaflets of the mitral valve thicken, stiffen, and become distorted from the effects of rheumatic fever, the valve fails to open sufficiently in diastole. Cause: Rheumatic heart disease May present with: Exertional dyspnea, orthopnea and paroxysmal nocturnal dyspnea secondary to pulmonary congestion, hoarse voice, atrial fibrillation Best heard at APEX in LEFT LATERAL DECUBITUS

Answer 6

Systolic regurgitation of blood back into the LA when LV is contracting; blood being sent both to aorta and back into left atrium CAUSES ⦁ ***MC = MVP *** ⦁ Rheumatic Fever ⦁ Damaged valve after heart attack or cardiomyopathy - if papillary muscles damaged, can't properly anchor chordae tendineae --> regurgitation ⦁ Left sided Heart Failure / Left Ventricular Dilation ⦁ collagen vascular disease: Marfan's, etc. PATHOPHYSIOLOGY 1) Retrograde blood flows from LV into LA, which then returns to LV during diastole 2) ==> LV volume overload ==> LA dilation 3) blood backs up into pulmonary circuit ==> increased pulmonary pressure 4) decreased cardiac output, due to diminished forward flow CLINICAL MANIFESTATIONS ⦁ Holosystolic Murmur (lasts for entirety of systole) ⦁ BLOWING HOLOCYSTOLIC (PANCYSTOLIC) MURMUR DURING SYSTOLE @ apex ⦁ Acute pulmonary edema ⦁ dyspnea ⦁ fatigue ``` CHRONIC SYMPTOMS ⦁ a-fib ⦁ progressive dyspnea on exertion ⦁ fatigue ⦁ CHF ⦁ pulmonary HTN ⦁ hemoptysis ``` ``` PHYSICAL EXAM ⦁ *** BLOWING, HOLOSYSTOLIC (PANSYSTOLIC) MURMUR @ APEX *** ⦁ ** radiates to the AXILLA ** ⦁ Widely Split S2 ⦁ MC cause of S3 sound ``` o Increased murmur = squatting, expiration, handgrip (like aortic regurgitation) (unlike aortic stenosis = decreased with handgrip) o Decreased murmur = Valsalva, standing, inspiration * Radiates to the axilla DIAGNOSIS ⦁ *** ECHO *** = shows hyperdynamic LV ⦁ EKG = LAE, LVH, may have a-fib ⦁ CXR = nonspecific, may have cardiomegaly and pulmonary congestion TREATMENT ⦁ *** REPAIR PREFERRED over replacement **** ⦁ Medications - decrease afterload (ACEI / ARB / Nifedipine / Hydralazine) - decrease preload (diuretics) - Afib = Digoxin

Answer 7

Mitral valve = 2 leaflets (anterior + posterior) During systole, the mitral valve closes to prevent backflow of blood into the LA as the LV contracts to send blood to the body MVP (mitral valve prolapse) = *** MC CAUSE OF MITRAL REGURGITATION *** MVP doesn't always cause mitral regurgitation, but it usually does! (can have mitral regurgitation without MVP) Mitral valve prolapse (MVP) affects 2-6% of the United States population. Most cases are benign, however, MVP can lead to acute mitral regurgitation (MR), sudden cardiac death, infectious endocarditis and stroke GENETICALLY INHERITED Normal Pathophysiology - normally, the papillary muscles and the connective tissue called chordae tendineae attached to the mitral valve keep it closed during systole, and keep it from PROLAPSING (moving backwards into the atrium) IN MVP, the connective tissue is WEAKENED, called MYXOMATOUS DEGENERATION - unknown why this weakening happens - but often related to CT disorders such as * ** MARFAN syndrome and EHLERS - DANLOS syndrome *** Myxomatous degeneration results in elongated larger leaflet area and lengthened chordae tendineae, which can sometimes rupture, therefore allowing prolapse of the mitral valve into the left atrium Mechanism: It is caused by an abnormal systolic ballooning of part of the mitral valve into the left atrium SYMPTOMS OF MVP ⦁ typically asymptomatic throughout their life! ⦁ *** mid-systolic click *** as valve prolapses and is then suddenly stopped by chordae tendineae (vs systolic ejection click with stenoses) ⦁ click may be followed by MID-LATE SYSTOLIC MURMUR ↑ Preload → ↓ murmur; ↓ preload → ↑ murmur Anything that causes LV to be smaller will result in valve leaflets being closer together, so during systole ==> an earlier and longer murmur (Valsalva, Standing) Squatting = increased preload (more blood volume in heart) so LV enlarges, which also relaxes the valve leaflets farther apart. During systole, it takes longer for valves to come together ==> later and shorter murmur symptoms of anxiety, panic attacks, palpitations, exercise intolerance, syncope and neuropsychiatric manifestations. Symptoms related to a progression into MR include dyspnea, fatigue, exercise intolerance, orthopnea and paroxysmal nocturnal dyspnea. MVP is classically described as an apical mid-systolic click which may or may not be followed by a late-systolic murmur. ``` o If Symptomatic ⦁ anxiety ⦁ panic attacks ⦁ palpitations ⦁ exercise intolerance ⦁ lightheadedness ⦁ syncope ⦁ chest pain worsened with exertion ⦁ orthopnea / PND ``` ``` o Symptoms associated with MR progression ⦁ fatigue ⦁ dyspnea ⦁ PND ⦁ CHF ``` Patients with mitral valve prolapse are typically asymptomatic throughout their lives, although a wide range of symptoms is possible. When symptoms do occur, palpitations from arrhythmias are most common along with lightheadedness. Syncope is not part of this disease process MIDSYSTOLIC EJECTION CLICK heard best at APEX (mitral area) ``` DIAGNOSIS ⦁ normal EKG ⦁ normal CXR ⦁ **** ECHO **** ⦁ mid-systolic click best heard at apex ``` ``` PHYSICAL EXAM ⦁ low body weight ⦁ pectus excavatum ⦁ hypotension ⦁ scoliosis ⦁ kyphosis ``` TREATMENT o If asymptomatic = reassurance + serial echo's o Patients with autonomic dysfunction = ⦁ *** trialed on beta-blockers *** ⦁ counseled on caffeine, alcohol and tobacco abstinence ⦁ given a 24-hour cardiac monitor Patient will present as → a 22-year-old female who complains of generalized, sub-sternal chest pain that is worsened with exertion. She appears anxious; she denies ETOH, tobacco and illicit drug use. You auscultate her heart and hear a mid-systolic click

Answer 8

⦁ Mitral Stenosis - opening snap - low-pitched diastolic decrescendo rumble - rheumatic fever ⦁ Mitral Regurgitation - blowing holosystolic (pansystolic) systolic murmur (holosystolic = lasts throughout systole) - radiates to AXILLA - *** S3 *** ⦁ Aortic Stenosis - Crescendo-decrescendo systolic murmur - opening snap + ejection click - narrow pulse pressure - radiates to CAROTIDS ⦁ Aortic Regurgitation - soft, blowing, high-pitched decrescendo diastolic murmur - widened pulse pressure ⦁ MVP - *mid-systolic click* ⦁ click may be followed by MID-LATE SYSTOLIC MURMUR expiration / squatting = increased murmur inspiration / standing / Valsalva = decreased murmur

Answer 9

Prinzmetal’s angina is a condition of cyclical chest pain secondary to coronary vasospasm. Any acute angina must be evaluated and empirically treated with an anti-ischemic regimen of antihypertensive, antiplatelet and antithrombotic medications. Once the diagnosis of coronary vasospasm is made, long term management of the anginal attacks include calcium channel blockers, namely nifedipine, and long-acting nitrates like isosorbide dinitrate. Statin medications (A) do play a role in the overall management of patients with Prinzmetal’s angina, as there is some correlation with atherosclerosis. However, statins do not work at decreasing vasospasm, and as such, they would not be a viable choice in decreasing the chest pain attacks. Nonselective beta-blockers like propranolol (C) are contraindicated in the treatment of Prinzmetal’s angina. Anticoagulants like warfarin (D) play no role in decreasing the vasospasm and subsequent angina associated with Prinzmetal’s. Prinzmetal Angina (Variant Angina) Patient with a history of HTN, smoking, DM, obesity, or cocaine use Complaining of squeezing, pressure-like chest discomfort at rest ECG will show transient ST-segment elevations and cardiac enzymes will be normal Diagnosis is made by cardiac stress test Most commonly caused by coronary artery spasm Treatment is calcium channel blockers and nitrates

Answer 10

Angina = chest pain Angina = caused by decreased blood flow, and therefore oxygen to the heart muscle STABLE ANGINA or chronic angina = MC type of angina MC underlying cause of stable angina = Atherosclerosis of 1 or more of coronary arteries Other causes = anything that may cause thickened heart muscle wall = requires more oxygen ⦁ hypertrophic cardiomyopathy (HOCM) ⦁ aortic stenosis ⦁ hypertension Usually occurs when patient has > 70% stenosis of coronary artery (70% of an artery is blocked by plaque buildup) The small remaining opening may be enough to supply the heart with oxygen/blood during rest, but during exercise or stressful situations, when the heart demands more blood flow / oxygen ==> symptoms! ⦁ ** Subendocardial Ischemia ** SYMPTOMS OF STABLE ANGINA ⦁ Chest pain with exertion or stress ⦁ chest pain resolves with rest ⦁ pain in left arm / jaw / shoulders / back ⦁ SOB / Diaphoresis when symptomatic ⦁ Pain / symptoms last < 20-30 min! - subside with rest, or when exertion / stress resolves Injury to cardiomyocytes = Reversible! not dead! (unlike myocardial infarction) o EKG ⦁ ST segment depression (limited to subendocardial ischemia) in PRECORDIAL leads o TREATMENT ⦁ Nitroglycerin (vasodilator) for acute symptoms - for management ⦁ Beta Blocker = 1st line! (CCB = 2nd line or if black) ⦁ Statin ⦁ Aspirin - Selective (B1) = Metoprolol, Atenolol, Bisoprolol, Esmolol - Nonselective (B1 + B2) = Propranolol, Carvedilol, Labetalol - Nondihydropyridines (CCB that works on heart) = Verapamil (long-acting) + Diltiazem Stable angina = relieved by rest + nitroglycerin! CHRONIC STABLE ANGINA that remains symptomatic after BB / CCB / Nitro ==> RANOLAZINE Ranolazine is approved for the treatment for chronic stable angina for those who have failed standard medical therapy. It has been shown to be effective in reducing anginal symptoms and improving exercise capacity when added to conventional medical therapy. Ranolazine can prolong the QT interval and it should be used with caution in patients with kidney or liver disease Patient will present as → a 50-year-old woman with a history of hyperlipidemia and diabetes type 2 complaining of "chest pain attacks." She says that these attacks tend to occur while walking up five flights of stairs to get to her apartment, they last for 15-20 minutes and are relieved by rest. She describes the pain as sharp and substernal. A baseline EKG is unremarkable. Suspecting the diagnosis, you perform an exercise stress EKG and observe transient ST depressions in the anterolateral leads after significant exertion

Answer 11

Angina = chest pain Angina = caused by decreased blood flow, and therefore oxygen to the heart muscle Unstable Angina = usually caused by rupture of an atherosclerotic plaque, followed by thrombosis, occluding even more of the vessel Clot forms on top of plaque; may not completely occlude vessel, but if it doesn't = still even further occlusion has occurred ==> even less blood flow / oxygen to the heart ⦁ ** Subendocardial Ischemia ** = should be treated as an emergency! due to HIGH RISK OF PROGRESSION TO MI - Unstable Angina = heart tissue is STILL ALIVE, but is starved for oxygen = Ischemic! (decreased blood flow / oxygen), not yet infarction (heart tissue has already begun to necrose / die) SYMPTOMS OF UNSTABLE ANGINA ⦁ Chest pain with exercise/stress, and DURING REST! ⦁ chest pain DOES NOT RESOLVE with rest ⦁ pain in left arm / jaw / shoulders / back ⦁ SOB ⦁ Diaphoresis ⦁ Pain / symptoms last Injury to cardiomyocytes = Reversible! not dead! (unlike myocardial infarction) ⦁ does NOT show elevated cardiac enzymes (unlike infarction) o EKG ⦁ ST segment depression (limited to subendocardial ischemia) in PRECORDIAL leads (similar to NSTEMI) o TREATMENT ⦁ **BETA BLOCKER** = 1st line or CCB for prevention All unstable angina = Antihypertensive (BB) + Statin + Aspirin ⦁ Nitroglycerin (vasodilator) = for acute if continued angina after BB or CCB therapy = for pain relief, but does not help with long-term treatment for further prevention Unstable angina may not always be completely relieved by rest or nitroglycerin, helping to differentiate it from stable angina Patient will present as → a 58-year-old man with a history of coronary artery disease, hypertension, and hyperlipidemia presents to an emergency department for evaluation of chest pain. He reports somewhat suddenly experiencing dull left-sided chest discomfort while at rest at home that was not relieved with taking nitroglycerin. His vital signs are T 37.1, HR 94 beats per minute, BP 133/87, and O2 saturation 97% on room air. His ECG shows no ST-segment changes; serum troponin is not elevated. His chest pain subsequently resolves and he is admitted to the cardiac service for further management.

Answer 12

PRINZMETAL ANGINA = Chest pain due to CORONARY ARTERY VASOSPASMS that lead to ischemia (decreased blood flow / oxygen to the heart) Smooth muscle around coronary arteries constrict ==> reduce blood flow enough to cause ischemia Patients may or may not have atherosclerosis RISK FACTOR = SMOKING *** - Others = marijuana / meth / cocaine - tend to occur in younger patients (unlike unstable / stable angina) Vasospastic angina (Prinzmetal) = can happen at any time, not just with exertion. Can occur at rest - Prinzmetal Angina is associated with - * **** SMOKING ***** ***** REYNAUD'S PHENOMENON ***** ***** MIGRAINES ***** *** usually AWAKENS PATIENT AT NIGHT, or OCCURS IN THE MORNING - ** Magnesium deficiency ** = associated with Prinzmetal Angina CAUSE OF VASOSPASM ⦁ not well understood ⦁ likely involves vasoconstrictors (like platelet thromboxane A2) UNLIKE STABLE AND UNSTABLE ANGINA, PRINZMETA ANGINA OCCURS WHEN - the vasospasm constricts the coronary artery so severely that ALL LAYERS of the heart wall being supplied are affected (and not just subendocardial ischemia) = **TRANSMURAL ISCHEMIA** Injury to cardiomyocytes = Reversible! not dead! (unlike myocardial infarction) o GOLD STANDARD FOR DIAGNOSIS = ANGIOGRAPHY **** - will have no findings o EKG ⦁ ST segment elevation (transmural ischemia) in PRECORDIAL leads o TREATMENT ⦁ *** CCB = 1st line *** = Diltiazem* ⦁ Nitroglycerin (vasodilator) do NOT give beta blockers (Propranolol) = can exacerbate vasospasm in Prinzmetal's Angina PRINZMENTAL ANGINA = Intermittent chest pain, does not resolve with rest. EKG = ST Elevation, may or may not have elevation of cardiac enzymes Tx = CCB + nitro for acute pain relief vs STEMI = chest pain NOT cyclical, and would show troponin elevation

Answer 13

Congenital heart disease is classified as either cyanotic or acyanotic. Cyanotic congenital heart disease is secondary to a right to left shunt. Tetralogy of Fallot is a cyanotic congenital heart disease that is defined by four key findings: pulmonic stenosis with right ventricular outflow obstruction, right ventricular hypertrophy, a ventricular septal defect, and an overriding aorta. Tetralogy of Fallot is the most common cyanotic heart defect. It may present up to three to four months after birth. Signs and symptoms of tetralogy of Fallot include cyanosis, poor feeding, hemoptysis, squatting to relieve symptoms, a single S2 on cardiac auscultation, and scoliosis. Patients with unrepaired tetralogy of Fallot may experience “tet spells.” These episodes typically occur during periods of stress that result in crying and breath-holding. They are defined by acute respiratory distress because of an increase in right ventricular outflow tract obstruction. The pulmonic stenosis murmur becomes weaker at these times due to increased shunting through the ventricular septal defect. Diagnosis of tetralogy of Fallot is with echocardiogram. An ECG may reveal right ventricular hypertrophy or right axis deviation. A chest radiograph will often show a boot-shaped heart due to right ventricular hypertrophy. Management of a tet spell is to decrease pulmonary resistance and increase systemic resistance to blood flow. A crescendo-decrescendo murmur with a harsh systolic ejection quality is heard along the left upper sternal border First, you should place the child in the knees-to-chest position. Supplemental oxygen and morphine should be given. Phenylephrine may be used to increase systemic vascular resistance. Surgical therapy is the mainstay of long-term treatment for these patients. What is the key treatment for critical coarctation of the aorta? Answer: Prostaglandin E1 (keeps DA open) Tetralogy of Fallot Patient with a history of episodes of cyanosis (tet spells) and squatting for relief PE will show pulmonic stenosis, right ventricular hypertrophy, overriding aorta, and VSD CXR will show "boot-shaped" heart Comments: Most common cyanotic congenital heart disease Mnemonic: PROVe:: Pulmonic stenosis, Right ventricular hypertrophy, Overriding aorta, VSD

Answer 14

opening between right atrium and left atrium - how does this form? 1) Septum primum forms between atria, grows downward towards endocardial cushion 2) Ostium primum = gap between atria that closes as septum primum continues to grow downwards 3) Ostium secundum forms in septum primum higher up 4) Septum secundum forms closer to the RA next to the septum primum, covers the ostium secundum, but has its own gap further down called the Foramen Ovale 5) Makeshift valve present! - only allows blood to flow from RA to LA Oxygenated blood from placenta through umbilical vein can then go from right atrium through the foramen ovale in the septum secundum that is lower down, then travels up to go through the ostium secundum of septum primum to get to the left atrium at birth, the septum primum and septum secundum slap shut and close off the foramen ovale ASD = atrial septum doesn't close all the way; remains open even after birth 90% of ASD cases = due to ostium secundum septum secundum doesn't fuse properly with septum primum ===> foramen ovale doesn't close correctly The most common location for an ASD is a patent foramen ovale 10% of ASD cases = due to ostium secundum that doesn't grow all the way down to the endocardial cushion (more common in Down Syndrome - ostium primum issue) ASD = 10-15% of all congenital heart defects ASD = MC congenital heart defect IN ADULTS**** (MC congenital heart defect overall = VSD) ASD = 2nd MC congenital heart defect after VSD ⦁ **** 25% of all patients with DOWN SYNDROME have this type of heart defect (ASD) **** Down syndrome also associated with VSD and atrioventricular defect ***** ASD ASSOCIATED WITH DOWN SYNDROME ****** ***** ASD ASSOCIATED WITH FETAL ALCOHOL SYNDROME ****** **** TRICUSPID ATRESIA = ASSOCIATED WITH ASD **** Tricuspid atresia is the congenital cardiac disorder most commonly associated with an atrial septal defect. * *** CONGENITAL RUBELLA = ASSOCIATED WITH ASD ***** - Congenital rubella is a TORCH infection that can cause PDA and ASD ASD = LEFT - TO - RIGHT SHUNT (ACYANOTIC) - because Left sided pressure > Right sided pressure at birth, with ASD, oxygenated blood goes to the right side of the heart --> extra trip to the lungs to be oxygenated (left to right shunt = acyanotic!) CLINICAL MANIFESTATIONS ⦁ **** FIXED SPLIT S2 ***** at LEFT 3RD ICS ⦁ loud S1, widely split fixed S2 with no variance with respiration (widely split FIXED S2) - fixed = doesn't vary with respirations - fixed split S2 = ASD - paradoxically split S2 = Aortic Stenosis - widely split S2 = Mitral Regurgitation Fixed split S2 = - extra blood going to right side of the heart causes a delay in the blood getting through the pulmonic valve ===> delay in pulmonic valve closure compared to aortic valve closure ⦁ SYSTOLIC MURMUR (increased blood flow across pulmonic valve - at LEFT 3RD INTERCOSTAL SPACE - systolic ejection crescendo-decrescendo murmur at pulmonic area (left UPPER sternal border) Widely split and fixed S2 into A2, Ps (lub, dub-dub) Murmur: grade II-III/VI systolic ejection murmur at left 2nd or 3rd intercostal space ⦁ Increased oxygen saturation to right side of heart - Most patients are asymptomatic or symptoms are minimal in childhood until > 30 y/o Most patients with small ASDs are asymptomatic until the age of 30 ⦁ Over 30 y/o: present with dyspnea and chest pain ⦁ Over 50 y/o present with atrial arrhythmias - afib and RVF Infants / children - recurrent respiratory infections, failure to thrive, and exertional dyspnea Adolescents / adults = exertional dyspnea, easy fatigability, palpitations, atrial arrhythmias, syncope, heart failure COMPLICATIONS OF ASD ⦁ Paradoxical Embolism (Stroke) - in case of DVT - clot could break off, enter RA/RV, and would then be worried about PE - with ASD - clot could go from RA to LA, enter the systemic circuit, and potentially lodge in the brain - Paradoxical = clot starts off in right side, but ends up in left side ⦁ EISENMENGER'S SYNDROME - excess blood volume on right side causes pulmonary HTN / increased right sided pressure. if right sided pressure > left sided pressure ==> cyanotic! - dyspnea - deoxygenated blood enters systemic circuit (ASD / VSD / maybe PDA) Smaller ASDs may close on their own, so children are often monitored for some time before surgical intervention DIAGNOSIS ⦁ *** Echo *** = gold standard ⦁ CXR - may show cardiomegaly - dilated RA and RV, increased pulmonary markings, *** RBBB *** TREATMENT ⦁ Spontaneous closure - Smaller ASDs may close on their own in the 1st year, so children are often monitored for some time before surgical intervention - most close spontaneously (< 3 mm) ⦁ Surgery (for larger openings) if symptomatic - plugging or patching the opening - usually done at age 2-4 Most small centrally located ASDs (< 3mm) close spontaneously Asymptomatic children with a small shunt require only observation and periodic echocardiography. Although these children are theoretically at risk of paradoxical systemic embolization, this event is rare in childhood. Thus, it is not standard practice to close a small, hemodynamically insignificant defect. Moderate to large ASDs (evidence of right ventricular volume overload on echocardiography) should be closed, typically between ages 2 - 6 yr Patient will present as → a healthy 7-year-old girl who has reached all developmental milestones. On examination, the precordium is hyperdynamic with a prominent right ventricular heave. A grade III/VI systolic ejection murmur is present in the 2nd left intercostal space (pulmonic position) with an early to mid-systolic rumble and a fixed splitting of the second heard sound (s2) during inspiration and expiration

Answer 15

VSD = gap in ventricular septum that forms when septum doesn't properly close during development, creating a tunnel between the LV and RV Membranous portion grows downward from endocardial cushion, and muscular ridge grows upward from the apex Majority of VSD = caused by a defect in the membranous portion of the septum = ** PERIMEMBRANOUS ******* ``` VSD = MC CONGENITAL DEFECT OVERALL AMONG BABIES (adults = ASD) ``` 30-50% of VSDs can spontaneously close during childhood, which makes VSDs less common in adults VSDs = Also associated with FETAL ALCOHOL SYNDROME and DOWN SYNDROME (just like ASD) PATHOPHYSIOLOGY ⦁ deoxygenated blood from body --> RA --> RV --> Lungs --> LA --> LV --> Either back to LA or to body VSD = Left to Right shunt = Acyanotic! - Leads to higher oxygenation in right ventricle / pulmonary artery - oxygenated blood takes an extra trip to the lungs CLINICAL MANIFESTATIONS ⦁ ** LOUD HIGH-PITCHED HARSH HOLOSYSTOLIC MURMUR at LEFT LOWER STERNAL BORDER *** (blowing holosystolic = mitral regurgitation) ⦁ small VSD may be asymptomatic ⦁ larger VSD = more severe symptoms that present earlier on in life = CHF (tachycardia / tachypnea / rales / cardiomegaly) ⦁ worsening fatigue ⦁ displaced point of maximal impulse (PMI) ⦁ may develop Pulmonary HTN ⦁ EISEMENGER'S SYNDROME (if pulmonary HTN develops, volume/pressure on right side eventually overcomes pressure on left side, and switch from left-right to right-left shunt, and become acyanotic!) In the absence of pulmonary hypertension, a ventricular septal defect leads to a left to right shunt. DIAGNOSIS ⦁ Echo ⦁ EKG = LVH (in attempt to pump more blood to body). May also have RV dilation ⦁ CXR = may show Cardiomegaly TREATMENT = Surgery ⦁ 30-40% close spontaneously, especially if small VSD present = no treatment!! wait for closure ⦁ Pediatric cardiology referral is appropriate for serial examinations and echocardiograms q6-12m ⦁ Infants with a large VSD who develop CHF and growth retardation should be treated first with DIGOXIN + DIURETICS - If this fails, surgical intervention is necessary within the first 6 months of life Risk for bacterial endocarditis = give antibiotics if having any dental work done Patient will present as → a 4-year-old boy who is brought to your office by his parents because he gets tired very easily and cannot keep up with the other children. On exam, you hear a loud, harsh, holosystolic murmur at the left lower sternal border without radiation to the axillae

Answer 16

Atrial flutter is a dysrhythmia characterized by an atrial rate of 250-300 bpm The MC site of pathology = a reentrant circuit in the right atrium about the tricuspid valve annulus. ``` CAUSES ⦁ hypertensive heart disease ⦁ ischemic heart disease ⦁ rheumatic heart disease ⦁ cardiomyopathy ``` The resulting tachycardia typically causes decreased cardiac output with ``` SYMPTOMS ⦁ tachycardia ==> decreased cardiac output ⦁ palpitations ⦁ dyspnea ⦁ presyncope ⦁ fatigue ``` DIAGNOSIS = EKG ⦁ regularly shaped and spaced P waves which have the appearance of a sawtooth pattern ⦁ regular QRS waves (unlike a-fib = unregular) - These P waves will intermittently be followed by narrow QRS complexes - ventricular rate = classically 150 ``` A-fib = irregularly irregular A-flutter = regularly irregular ``` TREATMENT ⦁ CARDIOVERSION - electrical (synchronized) - chemical (amiodarone or procainamide) ⦁ BB or CCB for rate control

Answer 17

Brugada syndrome is a hereditary condition that leads to abnormal myocardial depolarization and predisposes otherwise young healthy individuals to VENTRICULAR FIBRILLIONAT + sudden cardiac death The incidence of Brugada syndrome is highest in ASIAN POPULATIONS Most patients with Brugada syndrome are ASYMPTOMATIC, and the disorder is identified incidentally via an abnormal ECG There may also be a family history of sudden cardiac death DIAGNOSIS = EKG ⦁ coved ST segment elevation followed by an inverted T wave in leads V1 to V3 TREATMENT ⦁ **** refer to cardiology! *** - for further testing to rule out structural heart problems and confirm the diagnosis of Brugada syndrome. ⦁ avoid sodium channel blockers (procainamide / flecainide) ⦁ *** definitive = ICD *** - implantable cardioverter defibrillator device

Answer 18

Premature ventricular contractions (PVCs) appear as abnormal QRS complexes and T waves that occur in another underlying rhythm PVCs have 6 characteristics: (1) Occur earlier than the next expected normal QRS (2) Wider than a normal QRS (3) QRS morphology is generally bizarre (4) Preceding P wave is absent (5) Deflection of the ST segment and T wave is opposite that of the QRS (6) Followed by a compensatory pause In general, PVCs are benign. However, *** when more than 3 occur simultaneously at a rate greater than 100, it is considered ventricular tachycardia *** MVPs (mitral valve prolapse) = commonly associated with PVCs

Answer 19

an acute onset tachydysrhythmia that can affect any age group. The dysrhythmia is caused by a REENTRANT CONDUCTION PATHWAY, most commonly in the atrium or atrioventricular node. COMMON TRIGGERS - atrial or atrioventricular premature beats - hyperthyroidism - caffeine - drugs COMMON SYMPTOMS - palpitations - dizziness - dyspnea - syncope - angina - fatigue - nausea - sweating - chest pain ``` MC symptoms = palpitations and dizziness - The chest pain which accompanies this class of dysrhythmias is usually due to the tachycardia itself. ``` TREATMENT o if Hemodynamically stable ⦁ Hemodynamically stable patients should first attempt VAGAL MANEUVERS**** (Valsalva) ⦁ If unsuccessful, AV-nodal blocking agents can be administered such as ADENOSINE or BB/CCBs ⦁ Radiofrequency catheter ablation o If Hemodynamically unstable ⦁ CARDIOVERSION (immediate) = synchronized

Answer 20

Ventricular tachycardia (VT) is usually initiated by irritable ventricular automaticity foci VT is a frequent complication of acute MI and dilated cardiomyopathy These foci may become irritable by several factors, three of which are hypokalemia, hypoxia and ischemia. Hypoxia may result from airway obstruction, lack of air (as in suffocation or drowning) and pulmonary compromise (as in pulmonary embolus or pneumothorax). Myocardial ischemia or infarction occurs in disease states such as chronic ischemic heart and coronary disease, or in emergent states, as in hypovolemic shock or cardiogenic shock. The more common causes of irritation are coronary insufficiency (vasospasm as with cocaine, atherosclerosis or thrombosis and embolus) and myocardial infarction. Once a ventricular foci is irritated enough, it will take over as the dominant pacemaker, suppressing the sinoatrial node, and resulting in a tachycardia usually between 150-250 bpm. DIAGNOSIS = EKG ⦁ QRS > 120 ⦁ Rate > 100 (usually 150-200) TREATMENT ⦁ hemodynamically stable = Amiodarone -> Lidocaine -> Procainamide (ALP) ⦁ hemodynamically unstable or if refractory to medical = synchronized cardioversion (starting = 100J) ⦁ pulseless = defibrillation (= unsynchronized cardioversion)

Answer 21

⦁ CLASS I = Na+ channel blocker ⦁ CLASS II = Beta adrenoreceptor blocker ⦁ CLASS III = K+ channel blocker ⦁ CLASS IV = Ca++ channel blocker EXAMPLES OF CLASS I (Na+ channel blocker) - Procainamide - Lidocaine - Phenytoin - Flecainide - don't give in CAD / heart disease! - due to increased risk of Vtach Ia = Quinidine / Procainamide Ib = Lidocaine / Phenytoin Ic = Flecainide / Propafenone (Can I have Fries Please) EXAMPLES OF CLASS II = beta blockers EXAMPLES OF CLASS III (K+ channel blocker) - Amiodarone - Dronedarone - Dofetilide

Answer 22

Ventricular tachycardia can be diagnosed when capture beats or fusion beats are seen in the setting of a wide complex tachycardia. This is especially helpful when trying to distinguish between ventricular tachycardia and supraventricular tachycardia with aberrant conduction. Supraventricular tachycardia with aberrancy can produce a wide complex tachycardia that mimics ventricular tachycardia. It is important to distinguish between the two because ventricular tachycardia is a more serious condition and treatment is different. During ventricular tachycardia, there is AV dissociation in which independent pacing of the atria and ventricles occurs. The SA node still paces the atria, but the larger ventricular complexes often hide the P waves. However, P waves can be seen occasionally. When a sinus paced depolarization is able to conduct to the ventricles, it can produce a normal-appearing QRS; this is called a CAPTURE BEAT. More commonly, an atrial depolarization is able to conduct only partially before it encounters depolarization coming from the ventricles; this produces a FUSION BEAT, which is a blending of a normal QRS with a PVC like complex. Capture beats + fusion beats do not occur during SVT, making their presence useful in differentiating them

Answer 23

normal potassium levels = 3.5 - 5 SYMPTOMS = lethargy, weakness, paralysis ``` EKG FOR HYPERKALEMIA ⦁ peaked T waves ⦁ wide QRS complex ⦁ prolonged PR interval ⦁ dropped p wave ``` TREATMENT ⦁ immediate = ** Calcium gluconate ** or chloride - helps to prevent fatal cardiac conduction abnormalities in response to the hyperkalemia, UNTIL excess K can be driven into cells or out of body ``` o for redistribution ⦁ Insulin ⦁ Albuterol ⦁ Sodium bicarbonate - drives excess K+ into the cells ``` o for elimination ⦁ Loop or thiazide diuretics (Lasix / HCTZ) ⦁ kayexalate (sodium polystyrene) ⦁ dialysis - removes excess K+ from the body (total body K+)

Answer 24

normal potassium levels = 3.5 - 5 EKG FOR HYPERKALEMIA ⦁ ** QT PROLONGATION ** ⦁ U waves QT prolongation = at risk for Torsades de pointes**

Answer 25

Long QT syndrome is a disorder of myocardial repolarization characterized by a prolonged QT interval on ECG and an increased risk of sudden cardiac death QTc is usually > 460 ms This syndrome is associated with an increased risk of a characteristic life threatening polymorphic ventricular tachycardia known as torsades de pointes or "twisting of the points.” ``` The primary symptoms in patients with long QT syndrome include ⦁ palpitations ⦁ syncope ⦁ seizures ⦁ cardiac arrest ``` Factors conferring the highest risk for sudden cardiac death include a history of sudden cardiac arrest, recent syncope, and QTc interval greater than 500ms. Beta blockers, such as propranolol, have shown to reduce both syncope and sudden cardiac death. The goal of beta blocker therapy is to blunt the maximal heart rate achieved during exertion and are thought to interrupt the "trigger" for torsades de pointes and shorten the QT interval Prolong QT interval is associated with polymorphic ventricular tachycardia, including torsades de pointes, and sudden cardiac death ``` CAUSES OF LONG QT INTERVAL ⦁ many medications (class 1a + 1c antiarrhythmics) ⦁ antidepressants ⦁ antipsychotics ⦁ hypokalemia ⦁ erythromycin etc ``` TREATMENT ⦁ *** PROPRANOLOL *** or beta blocker*** ⦁ implanted cardioverter defibrillators QT prolongation = at risk for Torsades de pointes** (treatment for torsades = magnesium sulfate)

Answer 26

Multifocal atrial tachycardia (MAT) is a subset of atrial tachycardia, with more than 2 foci of impulse formation. EKG ⦁ at least 3 distinctively different P waves with varying P’-R, R-R, and P’-P’ intervals ⦁ rate = 100-180 MAT is often associated with pulmonary disease: *** COPD *** and hypoxemia, either directly from these conditions or as a result of beta-adrenergic agonist or chronic methylxanthine treatment MAT often resolves when the underlying condition is treated. MAT is easily confused for atrial fibrillation because both rhythms may be irregular and tachycardic, but P waves exist in MAT, not atrial fibrillation. MULTIFOCIAL ATRIAL TACHYCARDIA = has P waves (vs Afib = no p waves) TREATMENT ⦁ Oxygen ⦁ treat underlying condition (COPD) ⦁ rate control (BB / CCB) WANDERING PACEMAKER is similar to MAT in that there are 3 different P wave morphologies However, the rate in wandering pacemaker is 60–100 beats per minute, slower than MAT.

Answer 27

Atrial fibrillation is associated with arterial thromboembolism and ischemic stroke; therefore, anticoagulation is recommended in most cases. ``` CHA2-DS2-VAS = MC used ⦁ CHF = 1 point ⦁ HTN = 1 point ⦁ Age ≥ 75 = 2 points ⦁ DM = 1 point ⦁ S2 = Stroke / TIA / Thrombus = 2 points ⦁ Vascular dz (prior MI / PAD) = 1 point ⦁ Age 65-74 = 1 point ⦁ Sex (Female) = 1 point Max = 9 ``` ≥ 2 = moderate to high risk => chronic oral anticoagulation recommended 1 = low risk => discuss with patient 0 = low risk => none needed, but ask patient *** If mitral stenosis = Warfarin, regardless of CHA2DS2VAS score The HAS-BLED risk score is based upon seven risk factors for bleeding, including age > 65 years, and has been recommended for assessing the risk of bleeding in atrial fibrillation management. ``` HAS-BLED ⦁ HTN = 1 ⦁ Abnormal kidney or liver function = 1 or 2 (for each) ⦁ Stroke = 1 ⦁ Bleeding = 1 ⦁ Labile INRs = 1 ⦁ Elderly (> 65) = 1 ⦁ Drugs or alcohol = 1 or 2 (for each) ``` Score of 0 or 1 = Low = consider anticoags Score of 2 = Moderate = consider anticoags Score of 3+ = High = ANTICOAGS!

Answer 28

Sick sinus syndrome occurs as a result of disease of the sinoatrial (SA) node It is associated with TACHYCARDIA - BRADYCARDIA SYNDROME - a form of sick sinus syndrome in which the sinus rate varies from fast to slow and back again often associated with ischemic heart disease and heart valve disease Scarring, degeneration, or damage to the sinoatrial node from sarcoidosis, amyloidosis, and cardiomyopathies can cause sick sinus syndrome. The most common atrial arrhythmia seen in sick sinus syndrome patients is *** ATRIAL FIBRILLATION *** EKG ⦁ irregular rhythm with pauses in sinus activity ⦁ alternate between tachy and brady (and not just looks like going into SVT) May manifest as Palpitations and SYNCOPE TREATMENT o Asymptomatic = observation o Symptomatic = *** PACEMAKER *** = mainstay of tx Asymptomatic patients suspected to have sick sinus syndrome should be monitored using a Holter monitor. ⦁ too slow = pacemaker**** = mainstay ⦁ too fast = BB or CCB

Answer 29

ECG will show rhythm > 100 beats per minute and frequent variation in the QRS axis and morphology Most commonly caused by acquired or congenital long QT interval syndrome Treatment is ⦁ Unstable: defibrillation ⦁ Stable: intravenous MAGNESIUM SULFATE and stopping the offending drug

Answer 30

Wolff-Parkinson-White (WPW) syndrome is a ventricular preexcitation syndrome that involves an anatomic accessory pathway that bypasses the AV node and forms a direct electrical connection between the atria and ventricles Patients with this accessory pathway are at high risk of supraventricular tachydysrhythmias, the most common of which is atrioventricular reentrant (or reciprocating) tachycardia (AVRT). Atrial fibrillation is also common and is seen in approximately 25% of symptomatic WPW tachydysrhythmias. Atrial fibrillation in WPW has a very rapid ventricular rate due to the ability of the accessory pathway to conduct the impulse faster than the AV node. It is usually a wide-complex tachycardia due to impulses conducted through both pathways fusing to form a depolarization. QRS morphology in atrial fibrillation with underlying WPW typically varies from beat to beat due to variable conduction through the accessory tract versus the AV node. Orthodromic WPW is clinically indistinguishable from AVNRT and can be treated in a similar fashion. - looks like SVT (narrow QRS complex tachycardia) - Orthodromic WPW = MC WPW tachydysrhythmia - TX ⦁ 1st = vagal maneuvers ⦁ 2nd = Adenosine followed by BB / CCB ⦁ 3rd = Cardioversion if unstable ⦁ DEFINITIVE = RADIOFREQUENCY ABLATION Antidromic WPW is more dangerous as it can lead to tachyarrhythmias and death as above. Therefore, any medication that slows AV nodal conduction is contraindicated in antidromic WPW - looks like V-tach (wide QRS complex tachycardia) = do NOT give “ABCD”-- adenosine, beta-blockers, calcium channel blockers, and digoxin EKG ⦁ *** Delta Wave *** = slurred upstroke of QRS (check) ⦁ short PR interval ⦁ wide QRS BYPASS TRACT= *BUNDLE OF KENT* TREATMENT ⦁ *** Radiofrequency Ablation *** Wolff-Parkinson-White (WPW) Syndrome ECG will show short PR interval, delta wave, wide QRS Most commonly caused by an accessory pathway (bundle of Kent) connects atria to ventricles, bypassing AV node Definitive treatment is radiofrequency ablation

Answer 31

Afib / Aflutter / atrial tachycardia after excessive alcohol use TREATMENT = OBSERVATION!

Answer 32

Digoxin is a cardiac glycoside derived from the foxglove plant. It is used to increase the force of myocardial contraction in systolic heart failure and to decrease AV nodal conduction in atrial fibrillation. used in treating atrial fibrillation and congestive heart failure. It works by inactivating the Na+ K+ ATPase pump on the cardiac cell membrane which leads to increased intracellular calcium and extracellular potassium. In individuals taking digoxin, there is a characteristic ECG pattern commonly referred to as the “digoxin effect.” The presence of the “digoxin effect” on the ECG is not a marker of toxicity, rather it indicates that the patient is taking digoxin. The “digoxin effect” is characterized by ⦁ (1) downsloping ST depression with a characteristic “slurred” appearance ⦁ (2) flattened, inverted, or biphasic T waves ⦁ (3) shortened QT interval The overall morphology is commonly compared to the shape of a mustache.

Answer 33

Patients with coarctation of the aorta may present with circulatory failure and shock upon closure of a patent ductus arteriosus (PDA). In many cases, the coarctation of the aorta occurs juxtaductal (adjacent to the PDA). The PDA may serve to widen the juxtaductal area of the aorta so that blood may flow forward from the left ventricle. However, in other cases, the PDA serves as a conduit for right-to-left shunted blood from the right ventricle. In the latter case, infants classically present with differential cyanosis due to well-oxygenated blood reaching the upper body (pink) from the ascending aorta, and deoxygenated blood reaching the lower body (blue) via the PDA and descending aorta. This is because the PDA often inserts distal to the origin of the left subclavian artery from the aorta. When the ductus arteriosus closes, this can lead to circulatory failure and shock. *** TURNER'S SYNDROME *** *** INTRACRANIAL ANEURYSMS *** *** RELIES ON PDA *** If COA present = give prostaglandin E1 to keep DA patent (don't give indomethacin = will close PDA) Ductal Dependent Lesions (cyanotic) Transposition of the great vessels (most common cause in newborns) Tetralogy of Fallot (most common in children >1 year old) Tricuspid atresia Interrupted aortic arch Coarctation of the aorta Hypoplastic left heart syndrome Shock, “gray baby” within hours to days after birth PGE1 The classic exam finding is blood pressure higher in the arms than legs, and pulses bounding in the arms and decreased in the legs. Rib notching (inferior aspect of the rib) is the classic radiographic finding in patients with coarctation of the aorta classic xray findings: The “figure-3” sign, characterized by prestenotic aortic dilation, coarctation indentation and poststenotic aortic dilation. PE will show higher blood pressure in the arms than in the legs EKG will show LVH CXR will show notching of ribs Diagnosis is made by echo Treatment is balloon angioplasty with stent placement,or surgical correction Comments:Associated with Turner's syndrome

Answer 34

Patent ductus arteriosus (PDA) is an acyanotic congenital cardiac condition. In this condition, the fetal connection between the pulmonary artery and aorta remains open, causing a continuous, “machine-like” murmur that is heard in both systole and diastole. Diagnosis is confirmed by appreciating pulmonary artery high-velocity jetting during Doppler echocardiography. Significant cases commonly result in labored breathing, symptoms of congestive heart failure and failure to thrive. Symptomatic PDA is treated surgically, with ligation being the most preferred method of closure. A continuous systolic-diastolic murmur is auscultated in a 3-week-old dyspneic infant. She is tachypneic and diaphoretic. Her mother reports weight loss and poor feeding. Doppler color-flow imaging reveals high velocity jets in the pulmonary artery. *** HIGH VELOCITY JETS IN PULMONARY ARTERY *** Patent Ductus Arteriosus Patient will be complaining of failure to thrive, poor feeding, tachycardia, and tachypnea PE will show continuous, rough, "machinery-like" murmur, heard best in the first interspaces of the LSB Diagnosis is made by echo Treatment is indomethacin

Answer 35

Physical activity limitations may be recommended for children with a past history of congenital heart disease. **** There are no restrictions on any sport activity, including competition and contact sports, in patients who have had surgical correction of tetralogy of Fallot and whose right ventricular pressure is < 50 mm Hg ****

Answer 36

BILIARY DISEASE

Answer 37

EBSTEIN'S ANOMALY During fetal development, there is a failure of the tricuspid valve to form properly, resulting in downward displacement of the leaflets and incompetency of the valve. This leads to a relatively small functional right ventricle, tricuspid regurgitation, and eventually symptoms of heart failure Ebstein's anomaly = cyanotic!

Answer 38

> 150 Fibrates = specifically for high triglycerides Statins = for LDL + Triglycerides Statins < Fish oil < Niacin < Fibrates Statins have the lowest effect on reducing triglyceride levels

Answer 39

FLUSHING PRURITUS

Answer 40

APNEA therefore, it is important to secure the airway with endotracheal intubation prior to its infusion

Answer 41

In this situation, the patient becomes preload dependent (essentially the right ventricle is impaired so there is “passive” flow into the left ventricle) Right ventricular infarction is represented on an ECG by noting ST elevation in right-sided leads (V3R and V4R). Because the right coronary artery often supplies the right side of the heart and the inferior wall of the heart, any ECG with ST elevations in leads II, III, and aVF (inferior leads) should have another ECG performed with right-sided lead placement. When these patients become hypotensive, the immediate treatment is intravenous hydration to increase preload Aggressive volume loading with normal saline boluses is used to restore blood flow to the right ventricle and inotropic support is indicated if hypotension persists. Early percutaneous coronary intervention or thrombolytic therapy should be initiated as soon as possible . In general, patients’ with right ventricular myocardial infarction are treated in a manner similar to those with acute ST-elevation myocardial infarction. This includes the early use of dual antiplatelet therapy, statin therapy, and an anticoagulant. A right ventricular infarct can be discovered by performing a right-sided ECG and looking for ST elevation in lead “RV4.” In these patients, a preload reducing medication like nitroglycerin can lead to a precipitous drop in blood pressure NITRATES ARE CONTRAINDICATED IN RIGHT VENTRICULAR INFARCT - avoid nitro / morphine = lower preload - avoid beta blockers = slow heart rate RIGHT VENTRICULAR INFARCT = PRELOAD DEPENDENT ==> TREAT WITH IV FLUIDS**** ``` Right Ventricular Infarction ⦁ Hypotension, JVD ⦁ Clear lungs ⦁ ST elevation in V4 - V6 ⦁ Preload dependent ⦁ Impaired filling of left ventricle ⦁ Reperfusion, dopamine/dobutamine ```

Answer 42

used to detect mortality rate after cardiac arrest (1) Systolic blood pressure in the emergency department ⦁ SBP > 90 mm Hg = 1 point ⦁ SBP < 90 mm Hg = 0 points (2) time from loss of consciousness to return of spontaneous circulation ⦁ < 25 minutes = 1 point ⦁ > 25 minutes = 0 points (3) neurologic responsiveness ⦁ positive neurologic responsiveness = 1 point ⦁ unresponsiveness = 0 points A score of 0 equates to 90% in-hospital mortality and 3% chance of neurologic recovery A score of 3 equates to 18% in-hospital mortality and an 89% chance of neurologic recovery

Answer 43

⦁ aspirin ⦁ beta blockers ⦁ statin ⦁ ACEI ST-Segment Elevation Myocardial Infarction (STEMI) - Patient will be complaining of substernal chest pain radiating to the neck and arm - Labs will show elevated troponin I or troponin T and CK, ST segment elevations > 1 mm in > 2 contiguous leads Treatment is: - PCI (Percutaneous Coronary Intervention) GOLD STANDARD - best if within 3 hours - Thrombolytic therapy - Aspirin

Answer 44

⦁ ST elevation in II, III, AVF (inferior leads) ⦁ ST depression in V4, V5 DO NOT GIVE NITRO*** because... may have right ventricular infarct! In a patient with an inferior STEMI, right ventricular infarct is suggested by the presence of ST elevation in lead III larger than that in lead II.

Answer 45

⦁ MYOGLOBIN - takes 1-2 hours after onset of ischemia to rise - peaks in 8-10 hours - returns to baseline after 1-2 days ⦁ CK-MB - most sensitive marker - takes 3-12 hours after onset of ischemia to rise - peaks in 1-2 days - returns to baseline after 5-14 days ⦁ TROPONIN - most sensitive marker - takes 3-12 hours after onset of ischemia to rise - peaks in 1 day (24 hrs) - returns to baseline after 2-3 days

Answer 46

PDE5 INHIBITORS ⦁ Sildenafil (Viagra) ⦁ Tadalafil (Cialis) PDE5 inhibitor = inhibits cyclic guanosine monophosphate (cGMP) specific phosphodiesterase type 5 It leads to an increased release of nitric oxide resulting in smooth muscle relaxation and therefore vasodilation The combination of sildenafil and nitroglycerin can result in profound hypotension Normally PDE5 breaks down cGMP => erectile dysfunction PDE5 inhibitors will prevent PDE5 from breaking down cGMP => increased cGMP => smooth muscle relaxation => increased blood flow to penis

Answer 47

⦁ Age 65+ ⦁ 3+ coronary artery disease risk factors ⦁ coronary artery disease (> 50% stenosis) ⦁ *** Aspirin usage in last 7 days *** ⦁ severe angina: 2+ episodes in 24 hrs ⦁ EKG ST segment changes > 0.5mm ⦁ troponin marker each = 1 point each additional point increases risk of new or recurrent MI in the next 14 days A higher score places the patient into a more invasive paradigm that usually includes cardiac catheterization, whereas a lower score favors a more conservative approach with medication options.

Answer 48

Aspirin: mortality, infarct size, reinfarction rate Clopridogrel if patient allergic to aspirin Heparin: DVT, reinfarction, stroke, LV thrombus, reocclusion Nitroglycerin: Coronary artery dilation/vascular smooth muscle relaxation preload/afterload myocardial O2 demand Contraindications: sildenafil use within 24 hrs, RV infarction Beta-blockers: Myocardial O2 demand, ventricular fibrillation IV indications: tachydysrhythmias, intractable HTN Morphine: Preload/afterload, sympathetic activity No mortality benefit Glycoprotein IIb/IIIa inhibitors: benefit in patients undergoing PCI PCI: Preferred over thrombolytics in all STEMI patients PCI center: <90 minutes contact to device time Non-PCI center: transfer to PCI center if contact to device time can be <120 minutes Non-PCI center: thrombolytics if contact to device time to be >120 minutes Thrombolytics: begin within 30 minutes of ED arrival if selected

Answer 49

1) Normal 2) Hyperacute T waves 3) J point elevation 4) ST elevation 5) Q wave formation 6) T wave inversion

Answer 50

⦁ *** PROSTHETIC VALVES *** ⦁ Previous infective endocarditis ⦁ congenital heart disease ⦁ unrepaired cyanotic congenital heart defects ⦁ first 6 months after congenital heart defect repair ⦁ cardiac transplantation patients TX = 2g of Amoxicillin 1 hour prior to procedure IVDA: S. aureus, tricuspid Native valve: Streptococci, mitral GI malignancy: S. bovis

Answer 51

Patient will be complaining of fatigue, fever, chest discomfort, dyspnea, and palpitations *** HEPATOMEGALY *** often occurs after an infection (usually viral, but can also occur from more serious infections) PE will show tachycardia that is disproportionate to fever or discomfort *** LEADS TO DILATED CARDIOMYOPATHY *** Echocardiogram will show decreased ventricular ejection fraction with hypokinesis and wall motion abnormalities Gold standard for diagnosis is an endomyocardial biopsy

Answer 52

PERICARDIAL KNOCK*** Idiopathic Infectious (viral / TB / fungal/ parasitic / etc) Constrictive pericarditis is pathologically distinct from acute pericarditis. Constrictive pericarditis is caused by the resultant inflammatory and reparative process from a pericardial injury. This leads to a fibrous thickening of the pericardium. Clinical presentation mimics heart failure and restrictive cardiomyopathy. Physical exam is associated with Kussmaul's sign (inspiratory neck vein distention) and pulsus paradoxus. Severe cases require surgical treatment with a pericardiectomy. CONSTRICTIVE PERICARDITIS RESULTS FROM SCARRING / LOSS OF ELASTICITY OF PERICARDIUM KUSSMAUL SIGN = increase in JVP during inspiration DIAGNOSIS = Echo*** - shows thickened pericardium

Answer 53

**** ASSOCIATED WITH SARCOIDOSIS / AMYLOIDOSIS **** hemochromatosis, scleroderma, chemo, radiation, etc. MC cause = Amyloidosis Ventricular rigidity: Stiff ventricle impedes diastolic ventricular filling; decreased compliance Disease of the myocardium that results in RESTRICTED ventricular filling Impaired filling ==> increased blood flow backs up into venous system ==> KUSSMAUL SIGN (jvp increases with inspiration) KUSSMAUL SIGN = also occurs with constrictive pericarditis + cardiac tamponade

Answer 54

``` MAJOR ⦁ Carditis ⦁ Polyarthritis ⦁ Sydenham's chorea ⦁ Subcutaneous nodules ⦁ Erythema Nodosum ``` ``` MINOR ⦁ Fever ⦁ Arthralgia ⦁ Elevated ESR or CRP ⦁ Prolonged PR interval in ekg ``` Rheumatic Fever Patient with a history of GAS infection Complaining of fever, red skin lesions on the trunk and proximal extremities, and small, non-tender lumps located over the joints PE will show JONES criteria: Joints, Oh, no carditis!, Nodules, Erythema marginatum, Sydenham’s chorea Labs will show anti-streptolysin O, anti-DNase B, positive throat culture, or positive rapid antigen test Treatment is antibiotics, NSAIDs Comments: Modified Jones Criteria for a first episode of acute rheumatic fever: need 2 major or 1 major and 2 minor

Answer 55

non-shockable rhythm!!!! EKG looks normal, but pt is pulseless 1) CPR 2) epinephrine ``` Adult PEA Rhythm on monitor, no palpable pulse High quality CPR Minimize interruptions Epinephrine 1 mg every 3-5 minutes Not shockable rhythm ```

Answer 56

Innocent murmurs are typically systolic ejection murmurs located at the base of the heart, short and soft, grade 1/6 to 2/6, without radiation, with a normal S1 and S2, normal cardiac impulse, and no evidence of any hemodynamic abnormality. TX = NONE The benign characteristics of the murmur in this patient include a grade < 3/6, mid-systolic timing, lack of radiation, and the absence of additional abnormal heart sounds

Answer 57

a short, vibrating, physiologic murmur which can be heard over the mid precordium in children in the absence of any other abnormality. This is a common and benign condition.

Answer 58

used in the treatment of both ventricular and supraventricular dysrhythmias. It is classified as a class III antiarrhythmic drug due to is inhibition of outward potassium channels which prolongs the duration of the action potential. It also has properties of class I antiarrhythmics (sodium channel blockage), class II antiarrhythmics (beta adrenergic receptor blockage) and class IV antiarrhythmics (calcium channel blockage). It has superior efficacy compared to many other antiarrhythmic drugs and a low rate of ventricular proarrhythmia. It is not, however, without side effects. The MC side effect of intravenous administration = ***HYPOTENSION***, which can occur in up to a quarter of patients and may be attributed to the solvents used in the preparation.

Answer 59

SITTING --> STANDING Decrease in systolic blood pressure 20 Decrease in diastolic blood pressure 10 Inadequate physiologic response to postural changes Head-up tilt-table testing (B) can help confirm a diagnosis of suspected orthostatic hypotension when orthostatic vital signs are nondiagnostic. It should be done after orthostatic vital signs are checked

Answer 60

Adolescent athlete + syncope: HOCM (hypertrophic cardiomyopathy) Young woman + abdominal pain + syncope: ectopic pregnancy Older male + abdominal/flank pain + syncope: AAA Sudden onset severe HA + syncope: SAH Woman + prodrome of nausea, sweating, warmth + syncope: vasovagal Malignancy + sudden onset SOB + syncope: PE

Answer 61

AV MALFORMATION PREGNANCY THYROTOXICOSIS BERIBERI

Answer 62

DILATED CARDIOMYOPATHY

Answer 63

Left ventricular free wall rupture usually leads to hemopericardium with cardiac tamponade, characterized by the classic triad of jugular venous distention, hypotension and muffled heart sounds. The presence of rupture is first suggested by the development of sudden profound right heart failure and shock, often progressing rapidly to pulseless electrical activity and death. Treatment is emergent pericardiocentesis and hemodynamic support. Risk factors include first myocardial infarction, anterior location of the infarction, elderly age and female sex.

Answer 64

ELEVATED RIGHT HEART PRESSURE | not IV drug use

Answer 65

RHEUMATIC HEART DISEASE (just like with mitral stenosis)

Answer 66

RHEUMATIC HEART DISEASE

Answer 67

CALCIFIED VALVES (old age)

Answer 68

AORTIC ROOT DILATION

Answer 69

``` ANAPHYLAXIS = Epi 1:1000 1000 mcg per mL IM 0.3-0.5 mL 300-500 mcg = actual dose q 15 min - children = 0.01 mL/kg 1:1000 solution IM q15 minutes - adults = 0.3 to 0.5 mL 1:1000 solution IM q15 minutes ``` CARDIAC ARREST = Epi 1: 10,000 100 mcg per mL 10mL 1000 mcg (1mg) = actual dose

Answer 70

MECHANICAL HEART VALVES - constructed of entirely synthetic material - more likely to have paravalvular leaks - last longer (> 20 years) - lifelong anticoagulation!!! - click A paravalvular leak occurs when a portion of the prosthetic valve becomes unseated from the valve annulus BIOLOGIC / BIOPROSTHETIC VALVES - made up of human, porcine, bovine material - last 8-10 years - no anticoagulation - no click All prosthetic valves are associated with complications ranging from structural failure and thrombosis to systemic embolization, hemolysis, and endocarditis

Answer 71

o Aortic valve = RIGHT 2nd ICS o Pulmonic valve = LEFT 2nd ICS o Tricuspid valve = LEFT 4-5th ICS o Mitral Valve = LEFT 5th ICS - APEX

CARDIOVASCULAR (13%) Flashcards

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