CARDIO-COMPREHENSIVE

CARDIO-COMPREHENSIVEANATOMYSA and AV nodes are supplied by RCA..infarction of which will cause BRADYCARDIA or HEART BLOCKLAD is where the CORONARY ARTERY OCCLUSION TAKES PLACEPosterior part of heart is LA (enlargement causes dysphagia or hoarseness due to Recurrent Laryngeal Nerve compression)PHYSIOLOGYPHYSIOLOGY CO = SV * HRFICKS PRINICIPLECO = rate of oxygen consumption/(arterial oxygen content venous oxygen content)

PHYSIOLOGYMAP = 2/3 DIASTOLIC + 1/3 SYSTOLICPULSE PRESSURE = SYSTOLIC DIASTOLIC (INVERSLY PROPORTIONAL TO COMPLIANCE)Pathology: PP INCREASED in hyperthyroidism, aortic regurgitation, arteriosclerosis, sleep apnea, exercisePP DECREASED in aortic stenosis, cardiogenic shock, cardiac tamponade, advanced heart failureSV = EDV - ESV

PhysioSTROKE VOLUMESV-CAP SV is affected by Contractility, Afterload, and PreloadSV increases C increases, P increases, A decreasesContractility increased with Catecholamines (adrenaline), Digitalis (blocks Na/K pump)Physio ACE inhibitors and ARBs decrease both PRELOAD and AFTERLOAD PRELOADApproximated by EDVvEnodilators decrease prEload (NITROGLYCERIN)AFTERLOADApproximated by MAP (increase in MAP leads to LV hypertrophy)vAsodilators decreases Afterload (HYDRALAZINE)

RESISTANCEDepends on pressure, viscosity, and length of vesselsViscosity is increased in: Polycythemia, Hyperprotinemic states (Multiple Myeloma), SpherocytosisViscosity is decreased in: AnemiaHEART SOUNDSS1 mitral closure (QRS) and tricuspid closure S2 aortic and pulmonary valve closureS3 early diastole during rapid ventri phase (CHF, mitral regurg)S4 late diastole (LV Hypertrophy)A wave Atrial contractionC wave RV ContractionX descent Atrial relaXationV wave increased RA pressure going against tricuspid ValveY descent blood flow descending from RA to RV

ECG abnormalitiesAtrial fib X-descent is lost

Tricuspid regurg V-wave is very elevated (pressure of blood in veins is elevated)

Tricuspid stenosis X-descent will decrease (cant lose pressure in veins)

MURMURSMitral Regurg Holosystolic, high-pitched, blowing murmur. Loudest at apex. Enhanced by increased TPR (squatting, hand grip)Tricuspid Regurg Caused by RV dilation. Enhanced during inspiration.Aortic stenosis Crescendo-Decrescendo systolic ejection murmur. Loudest at base, radiates to carotids. Pulsus parvus et tardus (weak and delayed pulses). Due to age related calcific aortic stenosis.VSD Harsh, holosystolic murmur. Loudest at tricuspid area. Increased afterloadMitral valve Prolapse Crescendo late systolic murmur with midsystolic click. Enhanced by decreased venous return (standing, valsalva)Aortic Regurg High pitched blowing early diastolic decrescendo murmur. Wide pulse pressure, head bobbing. Due to aortic root dilation, bicuspid aortic valveMitral stenosis Follows Opening Snap (half leaflet in motion during diastole). Delayed rumbling late diastolic murmur. Enhanced during expiration.PDA Machine-like murmur. Loudest at S2. Due to Cogenital rubella or prematurity. Heard in infraclavicular area.ECGP-wave ATRIAL DEPOLARIZATIONPR-interval conduction delay through AVQRS-complex VENTRICULAR DEPOLARIZATIONQT-interval contraction of ventriclesT-wave VENTRICULAR REPOLARIZATIONU-wave caused by Hypokalemia, Bradycardia

AbnormalitiesTorsades de pointes Ventricular tachycardia, shifting sinusoidal waveforms on ECG, can progress to Ventricular Fibrillation.Congenital long QT interval Inherited disorder of myocardial repolarization due to ion channel defects. Sudden cardiac death risk.Wolff-Parkinson-White Syndrome Abnormal fast accessory conduction pathway from atria to ventricle bypassing the rate slowing AV-node.PATHOLOGYCongenital Heart DiseasesRIGHT LEFT shuntsEarly cyanosis (Blue Babies)5 TsTruncus arteriosus (1 vessel)Transposition (2 switched vessels)Tricuspid atresia (3 sided valve closed)Tetralogy of Fallot (4= tetra)TAPVR (5 letters)Persistent Truncus arteriosusFailure of truncus arteriosus to divide into pulmonary trunk and aorta Patients can have accompanying VSDTransposition of Great VesselsAorta leaves RV, and Pulmonary trunk leaves LVSeparation of systemic and pulmonary circulationsNot compatible with life unless a shunt is placedFailure of Aorticopulmonary septum to spiralTricuspid atresiaAbsence of tricuspid valve and hypoplastic RV

Tetralogy of FallotCaused by anterosuperior displacement of the infundibular septumSquatting helps increasing SVR, decreasing R-L shunt, improving cyanosisPulmonary infundibular stenosisRVH Boot shaped heartOverriding aortaVSDCongenital Heart DiseasesLEFT RIGHT shuntsLate cyanosis (Blue kids)VSD > ASD > PDA

VSDMost common congenital heart defectAsymptomatic at birth, symptoms manifest weeks laterMost self resolveLarger lesions LV overload Heart failureASDDefect in the interatrial septumLoud S1, wide fixed split S2Occurs in septum secundumSymptoms range from none to heart failureSepta have missing tissue rather than unfused (like in patent foramen ovale)Patent ductus arteriosusIn fetal period, shunt is RL (normal)Neonatal period there is decreased lung resistance, making the shunt LR, leading to RVH, and LVH, leading to heart failureMachine like murmurPatency maintained by PGePatency ended by IndomethacinCoarctation of AortaPreductal (Infantile)Aorta narrowing proximal to the insertion of ductus arteriosusAssociated with Turner syndromePostductal (Adult)Aorta narrowing distal to the insertion of ductus arteriosusAssociated with Notching of ribs (collateral circulation), hypertension in upper extremities, and radiofemoral delayArteriosclerosisCommon sites: Abdominal Aorta > Coronary artery > popliteal artery > carotid arteryMonckebergCalcification of media of arteries especially radial and ulnarIntima not involved pipestem arteries on x-rayArteriosclerosisHyaline: thickening of small arteries in essential HTN or DMHyperplastic: onion skinning as seen in severe HTN AneurysmsAbdominal aneurysmAssociated with arteriosclerosis, most commonly in hypertensive male smokers > 50 y/o ageThoracic aneurysmCystic medial degeneration due to HTN (older patients) or Marfan syndrome.Associated with tertiary syphilis (obliterative endarteritis of the vasa vasorum)

Aortic dissectionLongitudinal intraluminal tear forming a false lumenAssociated with hypertension, bicuspid aortic valve, inherited connective tissue disorders (Marfans)Tearing chest pain radiating to the backMediastinal wideningCan result in pericardial tamponade, aortic rupture, and deathIschemic heart disease manifestationsAnginaStable Secondary to atherosclerosis. Pain on exertion. Relieved by rest. ST depression.Unstable Thrombosis with incomplete coronary artery occlusion. Pain at rest. ST depression.Prinzmetal Secondary to coronary artery spasm. Due to tobacco, cocaine, triptans. Relieved by CCBs, nitrates, smoking cessation. ST elevation.Coronary steel syndromeDistal to coronary stenosis, vessels are maximally dilated at baseline.Sudden Cardiac deathDeath from cardiac causes within 1 hour of onset of symptoms, most commonly due to a lethal arrhythmia (ventricular fibrillation). Associated with cardiomyopathy.

DiagnosisCardiac troponin 1 Rises after 4 hours and is increasing for 7-10 daysCK-MB Found in myocardium. Useful for diagnosing reinfarction following acute MI because levels return to normal after 48 hoursECG changes Include ST elevation (STEMI, acute transmural infarct). ST depression (subendocardial infarct). Pathologic Q waves (evolving or old transmural infarct).LEADS

CardiomyopathiesDilatedIdiopathic or congenitalAlcohol, Beriberi, Coxsackie B virus, Cocaine, Chagas, Doxorubicin (ABCCCD)Heart failure, S3, dilated heart on ECG, balloon appearance on CXRTx: Na restriction, ACE inhibitors, Beta-blockers, Diuretics, digoxinHypertrophicFamilial, autosomal dominantCan be associated with Friedreich ataxiaCause of sudden death in young athletesS4, systolic murmurRestrictiveCauses include: sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis, Loffler syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate), and hemochromatosis

CHFClinical syndrome of cardiac pump dysfunctionSymptoms include: dyspnea, orthopnea, and fatigueRales, JVD, and pitting edemaSystolic dysfunction low EF, poor contractility, often secondary to ischemic heart diseaseDiastolic dysfunction normal EF and contractility, impaired relaxation, decreased compliance.Right sided heart failure is due to cor pulmonaleBacterial endocarditisFever, Roth spots (retina), Osler nodes, Murmur, Janeway lesions, Anemia, Nail Splinter hemorrhages, Emboli. (FROM JANE)Acute S. aureus (high virulence), large vegetations on previously normal valves, rapid onset.Subacute Strep. Viridans (low virulence), smaller vegetations, sequela of dental procedures.Rheumatic feverA consequence of pharyngeal infection with Group A Beta Hemolytic StreptococciEarly death due to myocarditisAffects heart valves mitral > aortic >>>tricuspidEarly lesion is mitral valve regurgitation, late lesion is mitral stenosisAschoff bodies (granuloma with giant cells), ASO titer increase, M proteinChorea, Arthritis, Nodules, Carditis, Erythema, Rheumatic anemia (CANCER)

Acute pericarditisSharp pain, aggravated by inspirationRelieved by sitting up and leaning forwardPresents with friction rubWidespread ST-segment elevation and/or PR dpressionFibrinous caused by Dressler syndrome, uremia, radiation. Presents with friction rub.Serous viral pericarditis (resolves spontaneously)Suppurative/purulent usually cased by bacterial infections (Pneumococcus, Strepto)VasculitisLarge-vesselTemporal (giant cell) arteritis Elderly femalesUnilateral headache (temporal artery), jaw claudicationCould lead to irreversible blindness due to opthalmic artery occlusionFocal granulomatous inflammationTakayasu arteritisAsian females diltiazem > verapamilHeart: veramapil (veramapil = ventricle) > diltiazem > amoldipine = nifedipine Dihydropyridines (except nimodipine): HTN, angina, RaynaudsNondihydropyridines: HTN, angina, atrial fibrillation/flutterNimodipine: Subarachnoid hemorrhage (prevents cerebral vasospasm)HydralazineIncrease cGMP smooth muscle relaxationVasodilation of arterioles > veins, afterload reductionSevere HTN, CHF. First line therapy for HTN in pregnancy, with methyldopaGiven with Beta-Blockers to prevent reflex tachycardiaContraindicated in angina/CAD (reflex tachycardia)Can cause Lupus-like SyndromeHypertensive EmergencyNitroprusside: Short actingIncrease cGMP (direct release of NO)Can cause cyanide toxicity (releases cyanide)Fenoldopam:Dopamine D1 receptor agonistCoronary, peripheralm renal, and splanchnic vasodilationDecreases BP and increases natriuresisAntianginal therapyGoal is to reduce myocardial Oxygen consumptionDecrease end-diastolic volume, BP, HR, contractility

Lipid lowering agents

Cardiac glycosidesDigoxinDirect inhibition of Na/K ATPase indirect inhibition of Na/Ca exhanger/antiportIncreases Ca positive inotropyStimulates vagal nerve decreasing HR (initiating parasympathetic response)Cholinergic toxicity is a side effect