cardio Flashcards
s1
mitral and tricuspid closure, beginning of systole
s2
aortic and pulmonary closure, beginning of the diastole
s3
in the early diastole during rapid ventricular filling, mitral regurgitation or HF can be normal in children
s4
late diastole (arterial kick), beast heard at the apax associ. with noncompliance and hypertrophy
Turbulence caused by blood entering stiffened LV.
what is splitting?
it is a physiological splitting of the second heart tone in younger people during inspiration
Rheumatic fever is and common findings are?
group A beta-hemolytic streptococci, affects mitral> aortic>tricuspid valve
early leasion cause regurgitation and late mitral stenosis
anitschkow cells (enlarg. macroph. with ovoid, wavy, rod-like nuclei, increased anti atreplysin O (ASO) titers
type 2 hyper.
M-protein
Cardiac tamponade common finding?
pulsus paradoxus
Which is the most common tumor in heart diseases?
Myxomas, IL6 producing tumor
kawasaki disease is?
asian children < than 4 y
rash, adenopathy, strawbery toungue, fever, hand and food erythema
takayasu arthritis
asian fem. <40 y, pulseless disease, fever, arthritis, skin nodules
bac. endocarditis id usul. caused and symptoms?
S. aureus (large vegi.), Viridans (smaller vegi)
sympt: splinter hemorrhages, osler nodes, janeway leasons
most common the mitral valve,
less common tricuspid=iv use
What is dressler?
several weeks of autoimm. phenomenon resulting from periardits
adenosine does what?
iscreases k+ out of the cell leading to hyperpolerization the cell and decreasing Ica+, decrease in g AV node conduction used in SVT
Mg2+ is used?
effective torsades de pointes and digixin tox?
IVabradine is used for?
ist prolongs slow depolarization (phase IV) by selectiv. inhibit. funny channels (If)
calcium channel blockers mech. of action?
Class IV, Antiarrhythmics
Verapamil and diltiazem decrease conduction velocity, increases ERP, increases PR interval
potassium channel blockers mech. of action?
Antiarrhythmic, class3, amiodarone, ibutilide, dofetilide, sotalol
increase AP duration, increase ERP, increase QT interval
afib, aflut, VT
beta blockers mech. of action?
Antiarrhythmics, class3, metrolol -lol
drease SA and AV, decrease cAMP, decrease Ca2+, drease phase 4 slope
SVT, afib, aflut
flecainide and profenone mech and use?
class IC Strong Sodium blockade, prolong ERP AV
SVT, afib
Lidocaine mech. and use?
Class IB, weak sodium channel blockade, dcreases AP duration
Vent arrhytmia, best post MI
kussmaul sign
increase in JVP on inspiration instead of a decrease, increased in constrictive pericarditis, restrictive cardiomyopathy
hereditary hemorrhagic telangiectasia
Oler-Weber-Rendu sy. autosomal dominant dis. of the blood vessels, blanching, epitaxis, skin discolaration
Hypovolemic s.
PCWP (preload) decreased, CO decreased, SVR (afterload) increased
cadiogenic s.
preload increased or decreased, co decreased, SVR increased
obstructive s.
eg. Cardiac tamponade, pulmonary embolism
preload increased or decreased, co decreased, SVR increased
Distributive shock
preload decreased, co increased or decreased, SVR decreased
MI 0-24hrs
early coagularive necrosis, gross: none, reperfusion injury, ca+ influx increases, free radicals
complication VA, HF, cardi. shock
MI 1-3hrs
extensive coagulative necrosis acute, gross: hyperemia, acute inflammation with neutrophils.
complication: post mi fibri. pericarditis
MI 3-14hrs
hyperemic border with yellow-brown softening
Macrophages, then granulation tissue
Compli:Free wall rupture—>tamponade
MI 2 weeks
recanlization, grray white scar, contracted complete scare
Compli: Dressler syndrome, HF etc.
ECG localization
Anteroseptal (LAD)
V1-V2
ECG localization
Anteroapical (distal LAD)
V3-V4
Anterolateral (LAD or LCX)
V5-V6
Lateral (LCX)
I, aVL
InFerior (RCA)
II III aVF
Posterior (PDA)
V7-V9, ST-depression V1-V3 with tall R waves
DCM
dilated cardiomyopathy
most common.
all 4 chambers are dilated, decreased EF, which is not related to CAD.
—–>eccentric hyperthrophy
ABCCCD
AD=Titin dis. Alcohlol Coxsachie Chagas Coccaine Doxorubicine=Dose dependent DCM Traztuzumab= Dose inde. DCM, reversable
Peripartum cardiomyopathy: TX like HF+ Transplant is currative
HOCM
accemetric septal hypertrophy leads to outflow obstruction, history: SUDDEN Death, young syncopy
AD. mutation on the sacomere gene
Pt: Varsity (young) athlete
syncopal vol decraese—–> give them Volume
sounds like aortic stenosis, S4, Mitral regurgitation because the valve does not close properly
Gross: Septal hypertophy
Histo: Myocyte (fibrilar), sarcomere disarray and fibrosis
restrictive/infil. cardiomyopathy
Speckled pattern, high pressure, icreased EF
Path: Infiltration, Stiff ventricle
Impaired filling in diastole
CAuse: Sarcoid, amyloid, hemomachromatosis, cancer and fibrosis (loefler)
PT: icreased EF=70, 80%
Gross: No hypertrophy, no dilation, infiltration,
histo:normal myocytes, extra stuff
Takotsuboś
ventricalar apical ballooning, old female,+STEMI, clean coronariers
Myocarditis
viral (coxackie)——>biosy of the lymphocytes
increase in troponin, noST, Young, decreased RF
Bacterial endocarditis
Acute—
S aureus (high virulence). Large vegetations on previously normal valves A. Rapid onset.
Bacterial endocarditis
Subacute
—viridans streptococci (low virulence).
Smaller vegetations on congenitally abnormal or diseased valves. Sequela of dental procedures. Gradual onset.
Bacterial endocarditis
FROMJANE with♥
Fever Roth spotsOsler nodes Murmur Janeway lesions Anemia Nail-bed hemorrhage Emboli Requires multiple blood cultures for diagnosis.
If culture ⊝, most likely Coxiella burnetii, Bartonella spp.
Bacterial endocarditis
involves which valve and is associ. with?
Mitral valve is most frequently involved.
Tricuspid valve endocarditis is associated with IV drug use (don’t “tri” drugs).
Associated with S aureus, Pseudomonas, and Candida.S bovis (gallolyticus) is present in colon cancer, S epidermidis on prosthetic valves.
Native valve endocarditis may be due to HACEK organisms (Haemophilus, Aggregatibacter [formerly Actinobacillus], Cardiobacterium, Eikenella, Kingella).
Syphilitic heart disease
3° syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of vessel wall and dilation of aorta and valve ring.
May see calcification of aortic root, ascending aortic arch, and thoracic aorta. Leads to “tree bark” appearance of aorta.Can result in aneurysm of ascending aorta or aortic arch, aortic insufficiency.
Acute pericarditis
Inflammation of the pericardium.
Commonly presents with sharp pain, aggravated by inspiration, and relieved by sitting up and leaning forward. Often complicated by pericardial effusion.
Presents with friction rub. ECG changes include widespread ST-segment elevation and/or PR depression.
Causes include idiopathic (most common; presumed viral), confirmed infection (eg, coxsackievirus B), neoplasia, autoimmune (eg, SLE, rheumatoid arthritis), uremia, cardiovascular (acute STEMI or Dressler syndrome), radiation therapy.Treatment: NSAIDs, colchicine, glucocorticoids, dialysis (uremia).
Myocarditis
Inflammation of myocardium —>global enlargement of heart and dilation of all chambers. Major cause of SCD in adults < 40 years old.
Presentation highly variable, can include dyspnea, chest pain, fever, arrhythmias (persistent tachycardia out of proportion to fever is characteristic).
Multiple causes:Viral (eg, adenovirus, coxsackie B, Compression of the heart by fluid (eg, blood, effusions [arrows in A] in pericardial space) CO.Equilibration of diastolic pressures in all 4 chambers.Findings: Beck triad (hypotension, distended neck veins, distant heart sounds), HR, pulsus paradoxus. ECG shows low-voltage QRS and electrical alternans B (due to “swinging” movement of heart in large effusion).Treatment: pericardiocentesis or surgical drainage.Pulsus paradoxus— in amplitude of systolic BP by > 10 mm Hg during inspiration. Seen in constrictive pericarditis, obstructive pulmonary disease (eg, Croup, OSA, Asthma, COPD),
B19, HIV, HHV-6); lymphocytic infiltrate with focal necrosis highly indicative of viral myocarditisParasitic (eg , Trypanosoma cruzi, Toxoplasma gondii)Bacterial (eg , Borrelia burgdorferi, Mycoplasma pneumoniae, Corynebacterium diphtheriae)Tox i n s (eg, carbon monoxide, black widow venom)
Rheumatic fever
Drugs (eg, doxorubicin, cocaine)
Autoimmune (eg, Kawasaki disease, sarcoidosis, SLE, polymyositis/dermatomyositis)
Complications include sudden death, arrhythmias, heart block, dilated cardiomyopathy, HF, mural thrombus with systemic emboli.
Cardiac tamponade
Compression of the heart by fluid (eg, blood, effusions in pericardial space) decreases CO.
Equilibration of diastolic pressures in all 4 chambers.
Findings: Beck triad (hypotension, distended neck veins, distant heart sounds), HR, pulsus paradoxus.
ECG shows low-voltage QRS and electrical alternans B (due to “swinging” movement of heart in large effusion).
Treatment: pericardiocentesis or surgical drainage. Pulsus paradoxus— in amplitude of systolic BP by > 10 mm Hg during inspiration. Seen in constrictive pericarditis, obstructive pulmonary disease (eg, Croup, OSA, Asthma, COPD), cardiac Tamponade
Heart failure
Clinical syndrome of cardiac pump dysfunction —>congestion and low perfusion.
Symptoms include dyspnea, orthopnea, fatigue; signs include S3 heart sound, rales, jugular venous distention (JVD), pitting edema. Systolic dysfunction—reduced EF, EDV; contractility often 2° to ischemia/MI or dilated cardiomyopathy. Diastolic dysfunction—preserved EF, normal EDV; compliance ( EDP) often 2° to myocardial hypertrophy.
Right HF most often results from left HF. Cor pulmonale refers to isolated right HF due to pulmonary cause.
ACE inhibitors or angiotensin II receptor blockers, β-blockers (except in acute decompensated HF), and spironolactone mortality. Loop and thiazide diuretics are used mainly for symptomatic relief. Hydralazine with nitrate therapy improves both symptoms and mortality in select patiens
Congenital long QT syndrome
Most commonly due to loss of function mutation of
K+ channels (affects repolarization). Includes:
Romano-Ward syndrome—autosomal dominant, pure cardiac phenotype (no deafness).
Jervell and Lange-Nielsen syndrome—autosomal recessive, sensorineural deafness
Congenital heart diseases
RIGHT-TO-lEFT SHuNTS
Early cyanosis—“blue babies.”
is associ. with?
The 5 T’s:
- Truncus arteriosus (1 vessel)
- Transposition (2 sw itched ves sels)
- Tricuspid atresia (3=Tr i)
- Tetralogy of Fallot (4=Te t r a)
- TAPVR (5 letters in the name)
Persistent truncus arteriosus
Truncus arteriosus fails to divide into pulmonary trunk and aorta due to failure of aorticopulmonary septum formation; most patients have accompanying VSD
D-transposition of great vessel
Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior)—->separation of systemic and pulmonary circulations. Not compatible with life unless a shunt is present to allow mixing of blood (eg, VSD, PDA, or patent foramen ovale). Due to failure of the aorticopulmonary septum to spiral (“egg on a string” appearance on CXR) A.
Without surgical intervention, most infants die within the first few months of life
Tricuspid atresia
Absence of tricuspid valve and hypoplastic RV; requires both ASD and VSD for viability
Tetralogy of Fallot
Caused by anterosuperior displacement of the infundibular septum.
Most common cause of early childhood cyanosis.
1) Pulmonary infundibular stenosis (most important determinant for prognosis)
2) Right ventricular hypertrophy (RVH)—boot-shaped heart on CXR
3) Overriding aorta
4) VSD
Pulmonary stenosis forces right-to-left flow across VSD—> RVH, “tet spells” (often caused by crying, fever, and exercise due to exacerbation of RV outflow obstruction)
Squatting: increases SVR, right-to-left shunt, improves cyanosis. Associated with 22q11 syndrome
LEFT-TO-RIGHT SHuNTS
Acyanotic at presentation; cyanosis may occur years later. Frequency: VSD > ASD > PDA.
Ventricular septal defect
Asymptomatic at birth, may manifest weeks later or remain asymptomatic throughout life. Most self resolve; larger lesions C may lead to LV overload and HF.
O2 saturation is increased in RV and pulmonary artery.
Atrial septal defect
Defect in interatrial septum D; wide, fixed split S2. Ostium secundum defects most common and usually an isolated finding; ostium primum defects rarer and usually occur with other cardiac anomalies.
Symptoms range from none to HF. Distinct from patent foramen ovale in that septa are missing tissue rather than unfused.
O2 saturation increased in RA, RV, and pulmonary artery. May lead to paradoxical emboli (systemic venous emboli use ASD to bypass lungs and become systemic arterial emboli). Associated with Down syndrome
Patent ductus arteriosus
In fetal period, shunt is right to left (normal). In neonatal period, pulmonary vascular resistance shunt becomes left to right progressive RVH and/or LVH and HF.
Associated with a continuous, “machine-like” murmur.
Patency is maintained by PGE synthesis and low O2 tension.
Uncorrected PDA E can eventually result in late cyanosis in the lower extremities (differential cyanosis).
PDA is normal in utero and normally closes only after birth.
Coarctation of the aorta
Aortic narrowing near insertion of ductus arteriosus (“juxtaductal”). Associated with bicuspid aortic valve, other heart defects, and Turner syndrome.
Hypertension in upper extremities and weak, delayed pulse in lower extremities (brachial-femoral delay). With age, intercostal arteries enlarge due to collateral circulation; arteries erode ribs ——>notched appearance on CXR. Complications include HF, risk of cerebral hemorrhage (berry aneurysms), aortic rupture, and possible endocarditis.
Turner syndrome
Bicuspid aortic valve, coarctation of aorta
22q11 syndromes
Truncus arteriosus, tetralogy of Fallot
Marfan syndrome
MVP, thoracic aortic aneurysm and dissection, aortic regurgitation
Aortic stenosis
Systolic murmer, LV concentrichypertrophy
Cause: RHD, Age
white, excertion
Crescendo-decrescendo systolic ejection murmur and soft S2
Aortic regurgitation
Dia murmer, LV dialation, head boding (increased sys and decrease dia). waterhammer pulses
decresdo murmer in the right sternal border
High-pitched “blowing” early diastolic decrescendo murmur.
Mitral stenosis
Follows opening snap (OS; due to abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips).
Delayed rumbling mid-to-late diastolic murmur ( interval between S2 and OS correlates with severity).
LA»_space; LV pressure during diastole. Often a late (and highly specific) sequela of rheumatic fever.
Chronic MS can result in pulmonary congestion/hypertension and LA dilation—->atrial fibrillation and Ortner syndrome
Mitral/tricuspid regurgitation
Holosystolic, high-pitched “blowing murmur.”
Mitral—loudest at apex and radiates toward axilla. MR is often due to ischemic heart disease (post-MI), MVP, LV dilatation.
Tricuspid—loudest at tricuspid area. TR commonly caused by RV dilatation. Rheumatic fever and infective endocarditis can cause either MR or TR
Non–ST-segment elevation MI (NSTEMI)
Non–ST-segment elevation MI (NSTEMI) Subendocardial infarctsSubendocardium (inner 1/3) especially vulnerable to ischemiaST depression on ECG
ST-segment elevation MI (STEMI)
ST-segment elevation MI
(STEMI)
Transmural infarcts
Full thickness of myocardial wall involved
ST elevation, pathologic Q waves on ECG
Class IA
Quinidine, procainamide, disopyramide. “The queen proclaims Diso’s pyramid.
Moderate Na+ channel blockade. increase AP duration, increase effective refractory period (ERP) in ventricular action potential, increase QT interval, some potassium channel blocking effects.
ClINICAl uSE
Both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.
Class IB
Lidocaine, phenytoin, mexiletine. “I’d Buy Liddy’s phine Mexican tacos.”
Weak Na+ channel blockade. decrease AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue.
ClINICAl uSE
Acute ventricular arrhythmias (especially post-MI), digitalis-induced arrhythmias.
IB is Best post-MI.
Class IC
Flecainide, propafenone.
“Can I have fries, please?”
Strong Na+ channel blockade. Significantly prolongs ERP in AV node and accessory bypass tracts. No effect on ERP in Purkinje and ventricular tissue. Minimal effect on AP duration.
ClINICAluSESVTs, including atrial fibrillation. Only as a last resort in refractory VT.
AdvERSE EFFECTS
Proarrhythmic, especially post-MI (contraindicated). IC is Contraindicated in structural and ischemic heart disease
Antiarrhythmics—β-blockers (class III)
Metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol.
MECHANISM
Decrease SA and AV nodal activity by cAMP, Ca2+ currents. Suppress abnormal pacemakers by slope of phase 4. AV node particularly sensitive— PR interval.
Esmolol very short acting.
ClINICAluSESVT, ventricular rate control for atrial fibrillation and atrial flutter.
Antiarrhythmics— potassium channel blockers (class III)
Amiodarone, Ibutilide, Dofetilide, Sotalol.
AIDS.
MECHANISM
increases AP duration, increases E R P, increases QT interval.
ClINICAl uSE
Atrial fibrillation, atrial flutter; ventricular tachycardia (amiodarone, sotalol).
AdvERSE EFFECTS
Sotalol—torsades de pointes, excessive βblockade.
Ibutilide—torsades de pointes.
Amiodarone—pulmonary fibrosis, hepatotoxicity, hypothyroidism or hyperthyroidism (amIODarone is 40% IODine by weight), acts as hapten (cor neal deposits, blue/gray skin deposits resulting in photodermatitis), neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, HF).
Remember to check PFTs, LFTs, and TFTs when using amiodarone.
Amiodarone is lipophilic and has class I, II, III, and IV effects.
Antiarrhythmics—calcium channel blockers (class IV)
Diltiazem, verapamil.
MECHANISMDecrease conduction velocit y, increses ERP, increases PR interval.
ClINICAluSE
Prevention of nodal arrhythmias (eg, SVT), rate control in atrial fibrillation.
AdvERSE EFFECTS
Constipation, flushing, edema, cardiovascular effects (HF, AV block, sinus node depression
Adenosine
increases K+ out of cells—–> hyperpolarizing the cell and ICa, decreasing AV node conduction. Drug of choice in diagnosing/terminating certain forms of SVT. Very short acting (~ 15 sec).
Effects blunted by theophylline and caffeine (both are adenosine receptor antagonists). Adverse effects include flushing, hypotension, chest pain, sense of impending doom, bronchospasm.
Cardiac glycosides
Digoxin.
MECHANISM
Direct inhibition of Na+/K+ ATPase—->indirect inhibition of Na+/Ca2+ exchanger. [Ca2+]i—>positive inotropy.
ClINICAl uSE HF ( increases contractility); atrial fibrillation ( decreases conduction at AV node and depression of SA node).
AdvERSE EFFECTSCholinergic effects (nausea, vomiting, diarrhea), blurry yellow vision (think van Glow), arrhythmias, AV block.
Can lead to hyperkalemia, which indicates poor prognosis. Factors predisposing to toxicity: renal failure ( excretion), hypokalemia (permissive for digoxin binding at K+-binding site on Na+/K+ ATPase), drugs that displace digoxin from tissue-binding sites, and clearance (eg, verapamil, amiodarone, quinidine).
ANTIdOTE Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+.
Bile acid resins Cholestyramine, colestipol, colesevelam
Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more
decreases LDL, slightly increses HDL andTG.
Ezetimibe
Prevents cholesterol absorption at small intestine brush border
decreases LDL
Fibrates Gemfibrozil, bezafibrate, fenofibrate
Activate PPAR-α—->upregulate LPL —->TG clearanceActivate PPAR—->induce HDL synthesis
decreases immensely TG, decreases LDL and increases HDL
PCSK9 inhibitorsAlirocumab, evolocumab
Inactivation of LDL-receptor degradation—->removal of LDL from bloodstream
Fish oil and marine omega-3 fatty acids
Believed to decrease FFA delivery to liver and decrease activity of TG-synthesizing enzymes
slightly increases LDL and HDL
Calcium channel blockers
Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine
(dihydropyridines, act on vascular smooth muscle);
diltiazem, verapamil (nondihydropyridines, act on heart).
MECHANISM
Block voltage-dependent L-type calcium channels of cardiac and smooth muscle—->muscle contractility.
Vascular smooth muscle—amlodipine = nifedipine > diltiazem > verapamil.Heart—verapamil > diltiazem > amlodipine = nifedipine.
ClINICAluSE
Dihydropyridines (except nimodipine): hypertension, angina (including vasospastic type), Raynaud phenomenon. Nimodipine: subarachnoid hemorrhage (prevents cerebral vasospasm). Nicardipine, clevidipine: hypertensive urgency or emergency.
Nondihydropyridines: hypertension, angina, atrial fibrillation/flutter.
AdvERSE EFFECTS
Gingival hyperplasia. Dihydropyridine: peripheral edema, flushing, dizziness. Nondihydropyridine: cardiac depression, AV block, hyperprolactinemia (verapamil), constipation
Hydralazine
MECHANISM
increases cGMP—->smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction.
ClINICAluSE Severe hypertension (particularly acute), HF (with organic nitrate). Safe to use during pregnancy. Frequently coadministered with a β-blocker to prevent reflex tachycardia.
AdvERSE EFFECTS Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, headache, angina, drug-induced lupus
Hypertensive emergency
Treat with labetalol, clevidipine, fenoldopam, nicardipine, nitroprusside.
Nitroprusside
Short acting vasodilator (arteries = veins); increases cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide)
Fenoldopam
Dopamine D1 receptor agonist—coronary, peripheral, renal, and splanchnic vasodilation. decreases BP, increases natriuresis. Also used postoperatively as an antihypertensive. Can cause hypotension, tachycardia, flushing, headache, nausea.
Nitrates
Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate.
MECHANISM
Vasodilate by increases NO in vascular smooth muscle increases cGMP and smooth muscle relaxation. Dilate veins»_space; arteries. preload.
ClINICAluSE
Angina, acute coronary syndrome, pulmonary edema.
AdvERSE EFFECTS
Reflex tachycardia (treat with β-blockers), hypotension, flushing, headache, “Monday disease” in industrial nitrate exposure: development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend—->tachycardia, dizziness, headache upon reexposure.
Contraindicated in right ventricular infarction, hypertrophic cardiomyopathy, and with concurrent PDE-5 inhibitor use.
Sacubitril
A neprilysin inhibitor; prevents degradation of bradykinin, natriuretic peptides, angiotensin II, and substance P —->vasodilation, ECF volume
Used in combination with valsartan (an ARB) to treat HFrEF
Standing Valsalva (strain phase)
decreases preload ( decreases LV volume)
MuRMuRS THAT INCREASE WITH MANEuvER:
MVP ( decreases LV volume) with earlier midsystolic clickHCM ( LV volume)
MuRMuRS THAT dECREASE WITH MANEuvER:
Most murmurs ( flow through stenotic or regurgitant valve)
Passive leg raise
increases preload ( LV volume)
incresease Most murmurs ( increases flow through stenotic or regurgitant valve)
dcreases:
MVP ( LV volume) with later midsystolic clickHCM ( LV volume)
Squatting
increases preload, afterload ( LV volume)
increases Most murmurs ( increases flow through stenotic or regurgitant valve)
Hand grip
increases afterload reverse flow across aortic valve ( LV volume)
increases Most other left-sided murmurs (AR, MR, VSD)
AS ( decreases transaortic valve pressure gradient) HCM (increases LV volume)
Inspiration
increases venous return to right heart, decreases venous return to left heart
increases Most right-sided murmurs
decreases Most left-sided murmurs
Wide splitting
pulmonic stenosis
Seen in conditions that delay RV emptying (eg, pulmonic stenosis, right bundle branch block).
Causes delayed pulmonic sound (especially on inspiration). An exaggeration of normal splitting
Fixed splitting
ASD
Heard in ASD. ASD—–> left-to-right shunt—–>RA and RV volumes——> flow through pulmonic valve—–>delayed pulmonic valve closure (independent of respiration)
Paradoxical splitting
aortic stenosis
Heard in conditions that delay aortic valve closure (eg, aortic stenosis, left bundle branch block). Normal order of semilunar valve closure is reversed:
in Paradoxical splitting P2 occurs before A2. On inspiration, P2 closes later and moves closer to A2, “paradoxically” eliminating the split. On expiration, the split can be heard (opposite to physiologic splitting).
Subclavian steal syndrome
subclavian artery
Stenosis of subclavian artery proximal to origin of vertebral artery—> hypoperfusion distal to stenosis—> reversed blood flow in ipsilateral vertebral artery—->reduced cerebral perfusion on exertion of affected arm.
Causes arm ischemia, pain, paresthesia, vertebrobasilar insufficiency (dizziness, vertigo). >15 mm Hg difference in systolic BP between arms.
Associated with arteriosclerosis, Takayasu arteritis, heart surgery
Coronary steal syndrome
Distal to coronary stenosis, vessels are maximally dilated at baseline.
Administration of vasodilators (eg, dipyridamole, regadenoson) dilates normal vessels—->blood is shunted toward well-perfused areas —>ischemia in myocardium perfused by stenosed vessels.
Principle behind pharmacologic stress tests with coronary vasodilators.
Sudden cardiac death
VT
Death occurs within 1 hour of symptoms, most commonly due to lethal arrhythmia (eg, ventricular fibrillation). Associated with CAD (up to 70% of cases), cardiomyopathy (hypertrophic, dilated), and hereditary ion channelopathies (eg, long QT syndrome, Brugada syndrome). Prevent with ICD
Chronic ischemic heart disease
Progressive onset of HF over many years due to chronic ischemic myocardial damage.
Myocardial hibernation—potentially reversible LV systolic dysfunction in the setting of chronic ischemia. Contrast with myocardial stunning, a transient LV systolic dysfunction after a brief episode of acute ischemia.
Congenital long QT syndrome
Most commonly due to loss of function mutation of K+ channels (affects repolarization). Includes:
Romano-Ward syndrome—autosomal dominant, pure cardiac phenotype (no deafness).
Jervell and Lange-Nielsen syndrome—autosomal recessive, sensorineural deafness.
Rhabdomyomas
Most frequent 1° cardiac tumor in children (associated with tuberous sclerosis).
Histology: hamartomatous growths. More common in the ventricles.
