Cardiology Flashcards Preview

Boards 2 > Cardiology > Flashcards

Flashcards in Cardiology Deck (179):

Truncus Arteiosis

-Forms the outflow tracts of the LV
-Imigration of neural crest cells, endocardial cushion tissue and membranous ventricular septation allow for proper looping and function


Sinus Venosus

-Forms the smooth part of the RA (Right SV) and the coroncary sinus (Left SV)


Bulbus Cordis

-Smooth parts of ventricles


Primitive atria and ventricles

-Rotate during development
-Trabechulated muscle


Anterior and Common cardinal veins

-Make SVC


Posteior Cardinal Vein

-Makes IVC


Vitelline Veins

-Make Portal Circulation


Aortic Arches

-1,2 are relatively meaningless with portions of external carotid coming off of pharyngeal arches
3: Common Carotid
4: Aortic arch and proximal brachiocephalic
6: Pulmonary arteries


Interventricualar Septation

-Muscular portion forms from the bottom up and is rarely assicated with VSD
-Membranous poriton forms near the top with endochardial cushion (AV) and NC cells
-Membranous is most common site of defect
-Eisenmienger occurs when VSD leads to pHTN leading to RV hypertrophy which will flip the shunt to R to L


Atrial Septation

-Septum primum grows from top toward bottom and ednocardial cushin tissues. Is flexible and may not form right with EC in downs elading to primum type of defect
-Secundum forms from top down and bottom up and is rigid
-Together form a one way valve allowing to bypass pulmnary circulation
-Fuse at birht with LA greater than RA
-If don't fuse is PFO
-Secundum is also common defect with fixed splitting
-PFO can cause DVT to go to systemic circulation


Fetal Erythroposesis

-Begins in yolk sac from 3 weeks to 10 weeks
-Liver becomes dominant in early gestation (4-40 wks)
-Spleen provides minimal support
-Bone marrow begins to produce in week 20 and is the definitive site
-Fetal Hgb has decreased affinity for 2,3BPG leading to increased Oxygen binding capabilities


Fetal Circulation

-Oxygenated blood comes through umbilical vein and joins IVC dumpin into RA.
-In RA can tak 2 routes, through RV or to LA
-If goes through RV then out to lungs with majority divered via the DA to aorta
-If through PFO goes through LA to LV to aorta
-Systemic circulation becfore draiing into umbilical arteries for delivery back to placenta


Three Shunts

-Ductus Venosus allows blood to bypass the portal circuit in the liver
-Ductus Arteriosus allow blood from pulmonary artery to enter the aorta and bypass the lungs
-Foramen Ovale allows majority of oxygen rich blood to flow to LA to LV to aorta to systemic
-PReductal coarctation, majority flows through RV and out through DA to body, no development of collaterals leads to early cyanosis. Post ductal means that collaterals through the internal intercostals and internal throacic develop to allow for communication with superior and infereior epigastrics. These pateints will present later with differential BP


Fetal Derivatives in permanent tissue

-Umbilical Vein: Ligamentum tere hepatatis whihc is part of falciform ligament
-Umbilical arteries are medial umbilical ligaments
-Allantois/urachus is median umbilical ligament. Persistence can lead to urachal cyst or adenocarcinoma of the superioer pole of bladder
-Ligamentum Arteriosum: Is close DA (Decrease in PGE with elevated O2 leads to closure). Is a site of anchor of arta, so can be nidus for traumatic tear
-Ligamentum Venosum: Liver Shunt


Cardiac Projections

-RA is superior and medial
-RV forms majority of anterior projection
-LV forms majority of diaphragmatic porjection (Inferior border)
-LA in conctact with reccurent laryngeal (Hoarsness) and Esophagus (Dysphagia)


Cardiac Circulation

-RCA: Nodal, RV (Marginal), and majority (85%) posterior IV septum
-LCX: LV free wall, L dominant supplies posterior IV septum
-LAD: ANteiror LV and Anterior 2/3 IV septum



-HR * SV
-MAP = 1/3 systolic + 2/3 diastolic
-Exercise serves to increase CO by increasing HR and decreasing TPR. Eventually TPR maximized and only increase is with increased HR



-A function of the amount of Ca in cardiac cells
-Increased Contractilty: Caetacholamines (Increase Ca release from SR), Digoxin increases intracellular Na leading to impaired Ca exchange and increased Ca).
-Preload also increases CO by starling law of stretch of sarcomeres
-Decreasd extracellular Na can also increase intracellular Ca
-Contractility is decresed with decreased Ca: Beta blockers, Ca channel blockers (non DHP; verapamil and diltiazem), Acidosis, hypoxia (60 seconds stop contracting), Heart Failure



-EDV a function of volume and venoconstriction
-Decreased with nitrates (Venodilation)
-Increased with caetacholamines (Venoconstriction)
-Increase with exercise and volume overload



-MAP, function of arteriolar constricion
-Arteriolar constriction (Caetacholamines)
-Arteriolar dilation (Hydralzaine, minodoxil)


Resistance and flow

-P=QR (PRessure = Flow*Resistance)
-Resistance = (viscosity * length)/Radius^4
-Dilation leads to massive loss of R
-Polycythemia, spherocytosis, increased protein (Multiple Myeloma) leads to increased viscosity
-Anemia leads to decreased viscosity


Resistance Circuits

Series: R = R1+R2 etc
-Parallel: which is sirculation 1/r=1/r1+1/r2 etc


Cardiac and vascular function curves

-Ascending line is contracility
-Descending line is volume status (Can be effected by venocosntriction)
-X intecept is means systemic filling pressure
-Blood volume is also a function of TPR, decreased TPR leads to effectively increased blood volume and vice versa
-Y axis is CO and venous return (Which are equal)
-X axis is Right Atrial Filling Pressure/EDV


Cardiac Cycle

-Contractility is a slope from the origin to S2
-Afterload is EDP/MAP
-EDV is preload


JVP Trace

-A wave is atrial contraction
-C wave is ventricular contraction that causes a bulge at the tricuspid valce
-X descent is from atrial relaxation
-V wave is atrial filling (gradual)
-Y descent is from rapid ventricular filling
-All curve is in pressure and so corresponds not to volume but to atrial contraction/relaxation


Kussmaul Sign

-Increase in JVP with inspiration
-Filling defect. Tamponade, CHF, etc


A wave changes

-A waves will be absent in A fib
-Cannon A waves will occur in heart blocks where there is contraction of the atria against a closed AV valve


Pulsus Paradoxus

-Inspiration leads to decrease in systolic BP of greater than 10 mmHg
-Inspiration decreases pressure in pulmonary veins and causes blood to pool which leads to a decrease in LV preload. This leads to a decrease in systolic BP which is sensed by baroreceptors leading to increased HR
-Seen in Cardiac Tamponade (Decreased filling leaves little reserve to pool)
-Also seen in obstructive lung diseases (Increased pooling exacebates the effect
-This effect occurs in the pulmonary venous system, the opposite occurs in the arterial system as pressures will rise beause of elevaed RV filling



Electrical signal always occur before contraction.
-QRS is at the very begining of atrial contraction and T wave, repolarization is in the middle
-This leads to discoordination between LV pressure/volume curve and EKG


Normal Splitting

-Inspiration leads to increased RV filling leading to a longer time to eject, causing a delay in emptying and heart sounds
-Pulmonic goes later


Widened splittin

-When there is exagerated closure of the pulmonic valve
-Pulmonic stenosis, RV dysfunction, RV failure, RBBB


Fixed splitting

-Splitting does not vary with inspiration
-Allows for pressures between RA and LA to equilibrate at all times, no change in splitting


Reversal (Paradoxical spltiting)

-There is a delay in closure of the aortic valve leading to the Aortic S2 to be delayed, during breathing when P2 gets longer they will come together
-Seen in aortic stenosis and LBBB


Right 2nd intercostal space

-Aortic listening area
-Systolic: AS


Left second intercostal space

-Pulmonic listening area
-Systolic is PS
-Diasolitc is PR
-Also can hear ASD and PDA


Left sternal border (not T)

Systolic: Hypertrophic Cardiomyoathy (worse with valsalva, decreased return)
-Diastolic: Aortic and Pulmonic Regurg


T Left sternal border (5th rib)

Systolic: Tricuspid regurg (endocarditis)
Diastolic: Tri Stenosis,
-Pansystolic: VSD
Diastolic: ASD


M Apex (Midclavicular line) 5th intercostal space

Systolic is mitral regurg
Diastolic is mitral stenosis



-Handgrip is going to increase vascular resistance and afterload leading to increse in regurg flow murmurs. Makes AS and Hypertrophic better
-Inspiration increases righ sided
-Valsalve decreases return to RV, increases hypertrophic cardiomyopathy and MVP


Mitral Regurg

-Systolic blowing murmur heard best at the apex. Midclavicular 5th intercostal
-MVP is common cause
-Endocarditis, RF
-Rupture of papillary muscle
-LV dilation (CHF)


Trcuspid Regurg

-Systolic, tricuspid
-RF, Endocarditis, RV dilation



-Systolic openins snap and crescendo decrescendo murmur
-Weak and delayed pulses
-May cause dyspnea, angina, and syncope
-Most comonly age related, increased with RF and bicupid valve



-Pansystolic murmur at Left strenal border
-Increased with handgrip exercise
-Membranous most common



-Systolic crescendo murmur loudes near S2
-Many causes and most commonl valvular lesion
-Can lead to MR
-Worse with valsalva (No opposing fluid in LA)



-Diastolic decrescendo murmur heard best at L sternal border. Immediate after S2
-Bounding pulses and headbobbing
-Worse with handgrip improved with vasodilators
-RF, Aortic Anyeruism and dilation, Syphilis



-Rumbling diastolic murmur at mtitral area following opening snap
-Complication of lonstanding RF
-Can cause LA dilation and A fib



-Continous machine like murmur
-Heard best at midclavicular line or near pulmonic listening area (2nd intercostal space)
-Congenital rubella, prematurity
-PGE keeps open and indomethacin closes


Ventricular AP

-Phase 0: Depolarization due to opening of V gated Na Channels. Connection through gap junctios allows for opening
-Phase 1: Na channels close and K channels open. QRS
-Phase 2: V gated (L type) Ca channels open and oppose K channels leading to plateau. Ca influx signals Ca release from SR to allow for contraction. QT interval and contraction
-Phase 3: L type Ca channels close and K channels cause repolarization. T wave
-Phase 4: K permiability maintains resting potential


Differences beteen Ventricular and Nodal

-Nodal there is no V gated Na channels. Leads to slowed conduction through AV node, leading to delay for vent filling
-T type and L type Ca channels both present. T type allow for intiail V opening
-HCN present which is permiable to Na and gated by hyperpolarization and cAMP ( B1 are Gs and M2 are Gi)
-Absence of phases 1 and 2


Nodal Action Potential

Phase 0: Opening of T-Type and L-type Ca channels allow for depolarization
-Phase 1,2 are gone
-Phase 3: K channels open and Ca close to allow for repolarization
-Phase 4: HCN allows for Na influx in response to depolarization and cAMP



-Is only electrical information from a gross perspective. Contractile and individual information is not presnt.
-P Wave: Atrial Depol
-PR: Nodal delay because of lack of Na channels in AV node
-QRS: Conduction through Venticles, perkinje and gap jcts
-T wave: Ventricular depolarization
-U Wave: hypokalemia and bradykardia
-QT interval is contraction period, when Ca is intracelular



Perkinje (only conduction) faster than atria (Conduction and contraction) faster than ventricle (Contraction and conduction) faster than AV (Delay)


Pacemaker rates

SA, AV, His, PErkinje/Vent



-Twisting rythm commonly caused by long QT, can devolve into V tach, must get out
-Precipitated by Long QT


Long QT Congenital

-Problems most commonly in K channel, can also be problem in Na channel
-Most common syndrome also presents with deafness


Drugs Causing Long QT

-Macrolides (Clarythromycin)
-Class IA: Quinidine, Procainamide, Disopyramide
-Class 3: Amiodarone, stalol, Ifebittide, Dofetilitide
-Antipsychotics (Haloperidol)
-TCA (most common cause of death in ovedose). Treat overdose with NaHCO3 to trap in urine


A fib

-Irregular atrial contractions with no observable P wave
-JvP will also show no A wave
-Irregularly irregular rythm as AV nodal repolarization sets ventricular rate
-Caused by dilation commonly: MR, MS, DCM/CHF, Alcohol, Sleep Apnea
-Major risk is thrombus formation because of turbulent and static flow, must be anticoagulate
-Rythm control can be accomplished with Beta blockers or Ca channel (Diltiezam and verapamil)
-Also can shock out of rythm
-Like many arrythmias, usually prsents with palpiations, syncopal episodes, light headedness



-Regular sawtooth pattern (Cannon A possible)
-Convert with class IA (Quinidine, procainamide, disopyrmaide) or III (Amiodarone, sotalol)
-Can control with beta and Ca blockers (Verapamil and diltiazam)


V Fib

Shock and CPR


First Degree AV nodal block

-PR lenghtened to greater than 0.2


Second Degree Type 1 (Wenckebach)

-Progressively lengthening PR with an eventual drop in beat.
-Usually assymptmatic


Second Degree type 2

-Somewhat random, but may be controlled loss of QRS after P waves. There is not lengthening. As if AV node forgot to contract
-AV nodal damage cause
-Can convert to thrid degree, often symptomatic with syncope, often need pacemaker


Third Degree

-No connection between atria and venticles (Cannon A)
-Often have synope, SOB, dyspnea, etc
-Treat with pacemaker


Wolf Parkinson White

Delta waves before QRS show there is an accessory pathway
-Can allow for SVT to be conducted and can cause retrograde (Through av node) re-entrant circuits. dangerous wth SVT



-Certain cells depolarize and repolarize while conduction is still occuring
-Commonly caused by fibrosis (MI, infection, etc) that leads to odd ciruits


Sick Sinus

-Irregular and impaired QRS and Ventricular rythm that originates in sinus node
-Many causes, but damage to sinus node (MI of RCA) common



-Carotid body is carried by CN9 and responds to HTN and hypotension
-Aortic Body is carried by CN 10 and responds only to hypertension
-End on nucleus solitarius and signal through Dorsal motor nucleus to vagus to decrease HR



-Central in CZT detect CO2 and pH of CSF, most important under normal conditions, stimulate breathing
-Peripheral can respond to CO2 and O2. Normally not used unless driven by O2 breathing.
-COPD, Sleep Apnea, Heroin OD are driven by O2


Normal Pulmonary pressure




-Swanz-gantz catheter measures LA pressure
-Can determin MS as LA pressure will be greater than LV pressure during diastole


Cushing Reflex

-Increased ICP leads to vasoconstriciton of arterioles which leads to ischeima causing SANS activation. This increases systemic BP and causes baroreceptor firing leading to decrease in HR
-increased ICP leads to HTN and Bradychardia
-Also can cause ulcers because of vagal activation



-SANS is normal systemic control
-Local metabolites in systemic circulation and brain: lactate, K, CO2, NO, Adenosine
-In lungs the opposite happens, hypoxic vasoconsriction shunts blood to proper location. Causes pulmonary edema of altitude


Right to left shunts. Early Cyanosis

-TOF, Tricuspid Atresia, Transposition, TAPVR, Truncus



-Associated with Digeorges, results in anterosupero displacment of the infundibular septum
-Pulmonary Stenosis (Most important determining factor)
-Overriding Aorta
-RVH (Causes early R to L shunt)
-Patients get tet spells, mild cases may not be seen, patients will squat and increase systemic resistance to increase flow through stenosed pulmonary artery
-Tx: Surgical


Tricuspid Atresia

-Tricuspid valve never forms, results in hypoplastic RV
-Requres ASD and VSD to allow flow from RA to LA to LV to RV to lungs.



Truncus and septation (NC) failed to rotate, Seen commonly in mothers with DM
-Leads to two distinct circulations, requries a shunt for survival
-Maintain PDA with alpostadil (PGE) and surgical treatment



-Pulmonary veins attach to coronary sinus and drain into RA, requres ASD or VSD to allow oxygenated blood to enter systemic ciruclation


Patent Truncus

-Normally sepation with endochardial cushion tissue and NC. Fails to form
-OFten assoiated with membranous VSD


Ebsteins Anomaly

-Mothers taking lithium
-Tricuspid valve is placed lower on RV this leads to a massiv RA but shrunken RV


Blue Kids. L to R shunts

-Occurs because of Eisenmiengers syndrome
-Early R to L leads to pHTN and RVH leading to reversal of shunt
-Cyanosis, clubbing, polycythemia



Most common, commonly seen in FAS
-Pansystolic murmur at sternal border



-Highly asscoated with Downs and other trisomies or chromosomal anomalies. Ostium primim
-Downs also get other endocardial cushion (VSD, Truncus, AV)
-Fixed splitting
-PFO is a more mild form that is not clinically present but can cause paradoxical emboli to clot the systemic circulation



-Normally carries oxygen rich blood from RV to Aorta in fetal life
-RVH, pHTN, and machinlike murmur. If not corrected, differential cyanosis, with most in lower extremeties. Brachiocephalic comes off before PDA
-Maintained with rubella, prematurity, and low oxygen
-Closed with indomethacin
-Can over time cause eisenmingers


Preductal Coarctation

Coarctaion occurs before the DA. No collaterals develop in fetal life
-Early cyanosis
-Associatde with Turners syndrome


Postductal coarctation

Coarctation after DA, and after brachiocephalics
-Leads to collateral circulation development with internal thoracic (Rib notching of intercostals). Communicates with epigastrics
-Patients will not present with early cyanosis but can resent with late BP differences between upper and lower extremeties
-Associated with bicuspid aortic valve



-Digeorge - TOF
-Downs - ASD
-Rubell - PDA
-Turner - PReductal coarcataion
-Marfans - MVP and Regurg
-DM - Transposition



BP - greater than 140/90. Commonly there is isolated systolic in elderly because of reduced arterial compliance
-Primary is most common and multifactorial
-Secondary usually due to reduced renal flow or renal dysfunction.
-Women think fibromuscular dysplasia
-Men think renal artery atherosclerosis


Hyperlipidemia signs

-Atheromas are lipid laden plaques in intima of blood vessels
-Xanthomas are lipid laden histiocytes in skin. Eyelids, tendons, and arcus senilis (eye) seen in major hyperlipidema


Hyaline arteriosclerosis

- Transudate of proteins ad NEG in DM/HTN leads to fibrosis (SM) of vessel wall
-Leads to progressive narrowing of intima
-Causes beign nephrosclerosis in kideny leading to decreased renal blood flow and progresive loss of nephrons
-HTN only effects afferent arteriole while DM effects afferent and efferent
-Leads to increased renin release and propigation of HTN


Hyperplatic arteriolsclerosis

-Malignant HTN causes fibrinous necrosis of intima and media
-And causes onion skin proliferation of smooth muscle cells
-Leads to flea bitten kidney and acute renal fialure


Mockenbergs medial calfications

-Not clnically significant, but will show up on X ray as calcifications in media, not intima
-Radial and ulnar most common



-Endothelial injury (most common at bifurcations and turbulence) leads to platelet activation and leakage of LDL into intima. MAcrophages enter intima and oxidize LDL becoming foam cells (this is fatty streak stage). Inflammation and platelet activation etc (FGF and PDGF) lead to proliferation of smooth muscle cells from media and causes fibrosis and formation of cap (Complex atheroma)
-Intimal thickening and vascular luminal narrowing
-Abdominal > Coronary > Popliteal > Carotid


Atheroscleroic complications

-Rupture, generally at neck leads to activation of clotting cascade and thormbus formation leading to occlusion
-Imparied diffusion leads to medial weakness and anyeurism, most common in aorta abdominal (Also no vasa recta)
-Stenosis leads to decreased blood flow and claudication and angina


Thoracic Anyeursim

-Commonly occurs on the ascending aorta and requires large presures
-Risk with HTN, Connective tissue disease and cystic medial necrosis, syphilis (endartaritis), bicuspid aorta
-Can cause regurg, rupture leading to tamponade or fatal hemorrhage


Cystic Medial Necrosis

-Occurs in CT diseases, most notably marfans
-Mucinous material in the midst of medial CT leads to weakness of arteries
-Will stain with mucin stain
-Also why MVP occurs in Marfans


Aortic Dissection

-HTN leads to tear in intimal wall and blood flow into media
-Risk factors are syphilis, HTN, cystic medial necrosis, anyrurisms, bicuspid valve
-Tamponade and fatal hemorrhage are consequences
-Most commonly occurs at ascending aorta and will present with tearing back pain. CT will show false lumen and mediastinal widening.



-Stable is ST depression, occlusion greater than 75% with cap (ST depression)
-Unstable angina - occlusion 75% with rpture and thrombosis (ST depression)
-Prinzmetal's- vasospasm (ST Elevation, transmural), sumitriptan is contraindicated


Coronary Steal

-Vasodilators cause a shunting of blood from areas of stenosis to other areas. Override autoregulatory vasodilation
-Mechanism of drug induced cardiac stress tests



-Tissue death that will show changes in enzymes
-Transmural is elevation and subendocardial is depression


Sudden Death

Most commonly caused by arrythmia
-Cause in hypertrophic cardiomyopathy


Chronic Ischemic HEart Disease

-Chronic ischemia leads to death of cells and CHF



Areas of poor perfusion stop contracting but don't die, if reperfused, can begin functioning again


O-12 Hrs post MI

No Necrosis, can die from arrythmia or heart failure


12-24 hrs

Coagulative necrosis and contractin bands, no inflammation,
Markers elevated
-Risk of death is still arryhtmia


1-3 days

-Neutrophil infiltration
-Risk of fibrinous pericarditis with transmural infarct


3-7 days

-Macrophages infiltrate and granulation tissue begins to form
-Macrophages phagocytose and remodel tissues, predisposes to wall rupture (Tamponade, VSD, papillary rupture leading to regurg)


7-14 days

Scar is formed from type 1 collage, greatest risk for anyureisms.
-May cause arryhtmias or clots and decreased CO


6 weeks

-Scar formed, risk of dresslers syndrome



-EKG is best in first 6 hours
-Troponin I and CKMB begin to rise at 4hrs. Tropinin is specific and will stay elevated for 7-10 days. CK-MB is less specific, but will drop by 24-48 hrs and can show a reinfarct



-I-V4 are anterior wall and correspond to LAD, also II and AvF
-V5,6 are lateral wall and LCX
-II, III, AvF are inferior wall (RCA or LAD)


Dilated Cardiomyopathy

-Systolic Failure with eccentric hypertrophy, sarcomeres in parallel, large on CXR
-Decreased EF and increased EDV
-Wet Beri Beri
-Alcohol (isolated effect)
-Myocarditis (Coxsackie B)
-Cocaine use
-Idopathic (Majority)
-Tx: Digoxin, ACEI, Diuretics, Transplant
Dx: S3


Hypertrophic Cardiomyopathy

-Concentric hypertrophy of irregular myocytes, tangled appearance
-Dynamic outflow obstruction caused by Mitral leaflet hitting septum
-Systolic murmur hear at sternal border (Same spot as regurg), Worse with valsalva, and improves with handgrip
-Most common cause of death is arrythmia
-S4 will be heard and there may be a history of syncope, apical impulses
-Diastolic dysfunction
-Most commonly due to mutations in myosin B, also Freidrichs ataxia
-Tx: Beta blockers, Ca channel Blockers


Restrictive Cardiomyopathy

-Deposition of material in endocardium leads to diastolic failure with relatively maintained size and ejection fraction
-Loefflers (asthma, eosinphilia, MBP)
-Endocardial Fibroelastosis (Seen in young kids 2years less)


Arrythmogenic Right Ventricular Hypertrophy

-Genetic mutation in desmosomal or gap junction/intercalated disk proteins leads to apoptosis and fibrofatty replacement of RV
-Causes arrythmia and significant loss of mypcytes and replacement with fat



-Systolic function with decreased SV, EF, CO with increased SV
-CLinically will see DOE, Fatigue, Crackles (hemosiderin laden marophages), orthopnea, Nocturnal dyspnea
-Right heart most commonly caused by left heart, can also be cor pulmonale
-JVP, Edema, Cardiac Cirrhosis (Centrolobular necrosis from venous congestion)
-Tx: Beta blockers, ACE I , Spironolactone
-Diuretics and vasodilators for symptomatic relief


Acute Bacterial Endocarditis

-Presents on non damaged valves and is associated with highly virulen strains like staph aureua
-Commonly presents in IV drug users on tricuspid valve
-Candida, S Aureus, and Pseudomonas are common offenders
-Vegetations are a comination of fibrin, platelts and trapped bacteria
-Can cause abrupt new strong murmur associated with cardiac failure and cardiogenic shock
-Fever and systemic Signs will be present
-Emboli can be infective
-Emboli: Oslers, janway, splinter hemorrhages, retinal hemorrhages


Subacute Bacterial Endocarditis

-More insidious onset with low virulence strains, usually only damages damaged valves (RF, etc)
-PResents with low grade systemic signs including fever, and classic signs of endocarditis, also may have anemia of chronic disease
-Also presents with a new murmur, most commonly of the mitral valve
-Strep Viridans: Post dental damaged valves
-Staph Epi: Prosthetic heart valves
-Strep bovis: Colon Cancer
-HACEK are culture negative


Murantic or noninfectous, thromotic endocarditis

-Small verucous vegetations that may effect both sides of heart
-Involve arota then mitral valve
-Can throw small clots and will be culture negative
-Liebman Sacs: Lupus and immune complexes
-Hypercoagulable state (pregnancy)
-Mucinous adenocarcinoma: Pancreatic is classic


Rheumatic Fever

-Type 2 hypersenstivity due to molecular mimicry of GAS M protein
-M protein antibodies cross reac with cardiac muscle, glycogen etc
-Neutrophil and macrophage infiltration
-Jones Diagnostic criteria must be seen in the context of previous GAS infection or positive ASO titers
-Joints (polyarthritis migrating upwards)
-Heart (pancarditis)
-Nodes (subcutaenous painless nodes)
-Erythema Marginatum (macular rash, may form rings, etc)
-Syndehams Chorea
-Predisposes to early mitral regurgitation (Blowing systolic murmur) or Mitral Stenosis (Rumbling diastolic murmur with opening snap)
-Pandcarditis: Endocarditis, and pericarditis
-Most common cause of death is myocaridits. Characterized by granulomatous aschoff bodies with large asnitschkow cells (Histiocytes with catepillar nucleus)



-Inflammation of the pericardial Sac
-Presents with sharp chest pain that is worse with lying down and breathing. Improves with moving forward (Carried by phrenic nerve)
-Serous: Most commonly after viral infection, lupus. If serous is chronic then there can be fibrosis that causes contrictive periarditis with a preicardial knock
-Fibrinous: exudative fibrin deposition: Uremia, Radiation, MI
-Purulent: Can be from staph or strep, rare now
-ECG will show diffuse ST changes


Cardiac Tamponade

-Accumulation of fluid in the pericardial sac leads to reduced ability to fill
-Causes equalization of pressures in all four chambers during diastole
-Hypotension and tachychardia with cardiogenic shock
-Causes: Free wall rupture post MI, DIssection or anyurism, Tumor, infection
-Positive kussmals sign: Increased in JVP with inspiration
-Positive Pulsus paradoxus, drop in systolic BP greater than 10 mmHg with inspiration
-PP: Seen in tamponade and restrictive lung disease


Syphilitic Heart Disease

-Treponema pallidum, tertiery syphilis
-Causes an endarteritis in vaso vasorum leading to ischemia and necrosis of media leading to anyurism
-May be calcified, "tree bark" appearance
-May cause rupture or tamponade into pericardial sac
-Aortic Regurg with head bobbing



-Most common is a myxoid tumor seen most commonly in the left atrium. Myocytes are permanent cells, so tumor is in stromal cells
-May cause a ball valve mechanism murmur and obstruction. Commonly present with complaints of frequent syncopal episodes
-Cardiac Rhabdomyoma: seen mroe commonly in kids, associated with tuberous sclerosis, AD mutation in TSG
-Mets are possible, but more commonly involve the peicardium
-Can be lymphoma or melanoma
-If occlusion of RV/RA can present with kussmauls sign
-May be syndromic and associated with endocrinopathies (Carries syndrome)



-Increase in JVP with inspiration, paradoxical
-Tamponade, Tumors, Resrictive cardiomyopathy
-Constrictive pericarditis



-Vasospasm of peripheral arterioles leding to transient sicheima with pain, white, then blue fingers
-If disease is isolated and idiopathic
-If syndeom, is associated with systemic CT disase (Lupus, Scleroderma, CREST)


Temporal Arteritis

Necrotizing Vasculitis of large vessels, branches of carotid, granulomas
-Jaw claudication, unilateral headache, blindness
-Tx steroids
-Assiciated with polymyalgia Rheumatica
-Massively elevated ESR in elderly



-Necrotizing granulmoaous inflammation of large vessel branches of aorta
-Most commonly presents in young asian females,
-Associaed with loss of pulses
-Many signs, fatigue, Night sweats, arthritis, skin nodes


Polyarteritis Nodosa

-Younger paients
-Involve muscular arteries
-GI, Renal, and visceral involvment, spares pulmonary
-Hepatitis B associated
-Skin also possible
-Immune complex mediated
-Transmural inflammation with fibrinous necrosis. Lesions of different ages (beads on string)


Kawasaki Disease

-Conjunctivitis and cervical lymphadenopathy, desquamating rash on palms and soles. Lips and strawberry tongue
-Treat with aspirin and IVIG to prevent clots
-Coronary Anyeurism



-Thrmobosing vasculitis of distal arterioles
-Autoinfarction of digits with gangrene
-Raynauds with intermeiten colaudication
-Tx: Smoking cessation


Microscopic Polyangitis

-Cutanous nodules and no granulomas but still necrotizing
-Pauci immune proliferative glomerulonephritis



-Granulomatous necrotizing vasculitis
-Lung, Nasal, Glomerulopehritis
-CXR: Large nodular Densities


Churgg Strauss

-P-ANCA, Eosinophilia
-Granuloma necrotizing vasulitis
-Pauci immune glomerulonephritis, palpable purpura
-GI, Kidney's and heart



-IgA immune complexes deposit in blood vessels
-Palpable purpura on extensor surfaces and GI pain with melena
-IgA mediated glomerulonephrits
-Post viral is often onset


Strawberry Angioma

-Kids, VEGF, capillary proliferation, regresses by 6-8 years


Cherry Angioma

-Adults, Doesn;t Regress


Pyogenic Hemangima

-Associatd with pregnancy
-Often occur in mouth and GI, often ulcerate and bleed


Cystic Hygroma

-Lymphangioma in neck, associated with turners
-Can occur anywhere in Turnere


Glomus Tumor

-Tumor of smooth muscle in finger nails
-Painful small, blue/red tumor


Bacillary Angiomatosis

-Bartonella Hensalae in AIDS pts



-Malignan dangerous blood vessel tumor
-Seen in liver post PVC exposure and seen in rest of body post radiatoin



-Lymph malignant tumor, associated with longstandin lymphedema


Kaposi Sarcoma

HHV-8, gamma herpes, intercalates in genome
-AIDS patietns and middle eastern men
-Mouth, Skin, and GI are common locations


Stuge Webber

-Post zygotic mutation leading to capillary proliferatino along V1
-Angiomas in eye predispose to early glacoma
-Angiomas in leptomeninges predispose to siezures
-Also a cause of AVM leading to stroke or high output cardiac failure



-AD changes in grwoth factor signallig
-GI and mouth bleeds often first signs
-AVM leading to cerebral hemorrhage major risk


Polyarteritis nodosa

-Fibrinous necrotizing vasculitis of medium sized muscular arteries
-Caused by immune complex deposition
-Normally asscoiaed with Hep B infecction
-Involves visceral circulation mostly with skin involvment
-Spares pulmonary
-GI, Renal, Skin complaints are classic, there can also be neurologic complaints and systemic inflammation


Essential HTN treatment

-Ca channel blockers



-K Sparing Diuretics
-B Blockers



-B Blockers
-alpha blockers


DHP Ca CHannel Blockers Nifedipine

-Block V gated Ca channel and prevent Ca realease into smooth muscle cells of vasculature, mainly lead to a decrease in afterload
-Can be used for HTN especially malignant HTN where vasodilation is required
-Used for prinzmetal angina and raynauds diseasae


Non DHP. Diltiazam and verapamil

-Block V gated channels in the heart
-Reduce myocardial contractility and decrease conduction through AV node
-Can treat A fib for rate control



-Causes in crease in arteriolar cGMP leading to a drop in afterload
-Drug of choice for HTN in pregnancy along with methyldopa
-Can cause lupus like syndrome with Ab to histones
-Can also cause compensatory tachycardia leading to increased work of heart



-D1 agonist. Gs
-Causes dilation of smooth muscle and increased naturesis
-Used in malignant HTN



-Release NO leading to increased cGMP and vasodilation
-used in malignant HTN and angina
-May cause cyanide poisoning if overdose, treat with thiosulfate to generate a more metabolizable product in the liver
-Also treat with nitrates to bind to RBC



-No release, paticularly in Veins leading to decreased preload
-Used to treat angina
-May cause increaed HR and contractility
-Give with beta blockers to effect both



-Cholesterol absorbed from gut and packaged into chylomicrons with B-48, C (LPL coeznyem), E (Uptake by liver. Deliver lipid to tissues and becoming remnant, then taken up by liver (E)



VLDL made in liver to deliver fat and cholestrol to tissue.
-C to mediate LPL
-E to mediate reuptake
-B - 100 to mediate deliver to tissues (Required for secetion)
-Once delivered tri and chol to tissues becomes IDL then LDL if lose E and C



-Loss of E and C leads to only B100 on surface
-Only function is to deliver chol to tissues



-Donate C, E to LDL to allow for reuptake by liver and reverse cholesterol delivery
-C is LPL co enzyme
-E allows for receptor mediated uptake in liver
-A allows for cholesterl ester formation (only HDL has this)



-Defect in MTP (Beta lipoprotine transfer molecule), prevens B-48 and B-100 from being loaded onto lipoproteins
-No chylomicrons secreted from GI and no VLDL secreted from liver
-Enterocytes and liver will be lipid laden and fatty. Fat soluble vitamin deficency and steaorrhea with failure to thrive
-Ataxia, acanthosis, night blindness



-Lack of apo C leads to inablilty for LPL to function and chylomicrons can't deliver TG to tissues
-Risk of pancreatitis, xanthomas, HSM
-No increased risk of atheoscleoris


Familial Hypercholiesterolemi

-AD with increasing severity if heterozygote
-Absesnce of LDL receptor prevents endoytosis of LDL leads to accumulation
-Fatty streaks and atheroslcerosis
-Xanthomas and corneal arcus



-Liver makes too much triglyceride (VLDL)
-Causes pancreatitiss



-COmpetitive inhibitor of HMG coA reductase which converts HMG CoA to Melevlonate
-Used to reduce LDL and stabalize plaques, given to pts with MI
-S/E: Rhabdomyolysis and Hepatotoxicity



-Interacts with GPCR and decreases metabolism of fats in lipids, prevents need and reduces requriement
-Decrease Lipolysis in peripheral tissues
-Increase HDL, also decreases TG and decreases LDL
-S/E: FLushing (COXI), Hyperglycemia and hyertriglyceridemia due to increased reliance on sugars for energy


Bile Acid Binders (Chol) Cholesteramie, colesipol

-Bind bile and prevent resorbtion
-Decrease LDL
-Bad taste, GI upset, Reduced fat soluble absorption
-Increase Risk of Cholesterol gallstones



-Activate PPARa leading to increased TG breakdown and increased LPL activity
-Greatly reduce triglycerides, also increase HDL and decrease LDL
-Gemfibrozil is a CYP inhbitor
-Cholesterol Gallstones, myositis, hepatotoxicity



-Block Chol absorption from gut
-Diahhrea and hepatotoxicity



-Binds to K site on Na/K ATPase and shuts off function. Leads to increased intracellular Na and decresed Na/Ca driving force, results in increased Ca and increased cardiac function
-CHF, A fib to decreae conduction through nodes
-Cholinergic (GI, etc) also yellow halos around eyes
-Hyperkalemia (poor sign)
-Decreased QT and elongated PR (Hyperkalemia), arrythmia
-Worse with hypokalemia, poor renal function, quinidine
-Overdose Tx: FAb, Mg, K, Lidocaine


Class I

-Bind to Na channel and effect phase 0
-Preferentially bind to depolarized chanels
-Inhibit firing in ectopic sites
-Hyperkalemia will increase toxicity for all drugs


A-Quinidine, procainamide, disopyramide

-enlongate refractroy perior and elongate QT interval
-Used to treat SVT and ventricular Arrythmias
-S/E for all are risk of Torsades due to long QT
-Quinidne: Tinnitus
-Procainamide: Lupus
-Disopyramide: Heart Failure


B; Lidocaine, Tocainide, mexiletine

-Block Na channels in damaged tissue and decrease AP
-Used to decrease arrythmias from damaged tissue post MI
-Slow conduction in perkinje etc
-Acute and digitalis induced arrythmias
-S/E: CNS depression, CV depression


C: Flecainainde, propafone

-Rarely used
-Arrythmogenic and contraindicated in MI


Class 2 Beta Blockers

-Esmolol shorter action
-Decreased cAMP leads to decrease phase 4 in pacemakers
-Slow cocnduction through AV node and slow sinus rate
-Increase PR interval
-Can cause heart block
-Exacerbate Asthma
-Mask Hypoglycemic signs in diabetics
-Treat overdose with glucagon
-Propranalol can exacerbate prinzmetals


Class III Amiodarone, Ifelitibitide, Dofelibitide, Soltalol

K Channel Blockers
-Block K channels and increase AP duration
-Long QT, all have Torsades as S/E



-alters lipid membrane and has functions of all classes
-S/E: Pulmonary fibrosis. High iodine weight leads to thyroid issues (Hyper/hypo), Deposits in eyes and skin leading to photosensitivity


Class 4 Ca Channel Blockers

-Non DHP (diltiazem and verapamil)
-Cause a decrease in conduction through the heart and block at AV node



-Binds PGY channel and increases K influx
-Leads to major depression of phase 4 and slowed heart rate in nodes
-Used to abolish SVT
-Short half life (15 sec)
-Can cause hypotension, flushing, and chest pain
-Caffeine and theophline will block effects, antagonize receptor



-Used in Torsades, Eclamptic siezures, Digoxin Tox