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S1 First aid > cardio > Flashcards

cardio Flashcards

1
Q

s1

A

mitral and tricuspid closure, beginning of systole

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2
Q

s2

A

aortic and pulmonary closure, beginning of the diastole

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3
Q

s3

A

in the early diastole during rapid ventricular filling, mitral regurgitation or HF can be normal in children

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4
Q

s4

A 
late diastole (arterial kick), beast heard at the apax associ.
with noncompliance and hypertrophy

Turbulence caused by blood entering stiffened LV.

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5
Q

what is splitting?

A

it is a physiological splitting of the second heart tone in younger people during inspiration

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6
Q

Rheumatic fever is and common findings are?

A

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

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7
Q

Cardiac tamponade common finding?

A

pulsus paradoxus

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8
Q

Which is the most common tumor in heart diseases?

A

Myxomas, IL6 producing tumor

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9
Q

kawasaki disease is?

A

asian children < than 4 y

rash, adenopathy, strawbery toungue, fever, hand and food erythema

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10
Q

takayasu arthritis

A

asian fem. <40 y, pulseless disease, fever, arthritis, skin nodules

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11
Q

bac. endocarditis id usul. caused and symptoms?

A

S. aureus (large vegi.), Viridans (smaller vegi)
sympt: splinter hemorrhages, osler nodes, janeway leasons

most common the mitral valve,

less common tricuspid=iv use

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12
Q

What is dressler?

A

several weeks of autoimm. phenomenon resulting from periardits

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13
Q

adenosine does what?

A

iscreases k+ out of the cell leading to hyperpolerization the cell and decreasing Ica+, decrease in g AV node conduction used in SVT

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14
Q

Mg2+ is used?

A

effective torsades de pointes and digixin tox?

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15
Q

IVabradine is used for?

A

ist prolongs slow depolarization (phase IV) by selectiv. inhibit. funny channels (If)

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16
Q

calcium channel blockers mech. of action?

A

Class IV, Antiarrhythmics

Verapamil and diltiazem decrease conduction velocity, increases ERP, increases PR interval

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17
Q

potassium channel blockers mech. of action?

A

Antiarrhythmic, class3, amiodarone, ibutilide, dofetilide, sotalol

increase AP duration, increase ERP, increase QT interval

afib, aflut, VT

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18
Q

beta blockers mech. of action?

A

Antiarrhythmics, class3, metrolol -lol

drease SA and AV, decrease cAMP, decrease Ca2+, drease phase 4 slope

SVT, afib, aflut

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19
Q

flecainide and profenone mech and use?

A 
class IC
Strong Sodium blockade, prolong ERP AV

SVT, afib

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20
Q

Lidocaine mech. and use?

A

Class IB, weak sodium channel blockade, dcreases AP duration

Vent arrhytmia, best post MI

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21
Q

kussmaul sign

A

increase in JVP on inspiration instead of a decrease, increased in constrictive pericarditis, restrictive cardiomyopathy

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22
Q

hereditary hemorrhagic telangiectasia

A

Oler-Weber-Rendu sy. autosomal dominant dis. of the blood vessels, blanching, epitaxis, skin discolaration

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23
Q

Hypovolemic s.

A

PCWP (preload) decreased, CO decreased, SVR (afterload) increased

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24
Q

cadiogenic s.

A

preload increased or decreased, co decreased, SVR increased

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25
Q

obstructive s.

A

eg. Cardiac tamponade, pulmonary embolism

preload increased or decreased, co decreased, SVR increased

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26
Q

Distributive shock

A

preload decreased, co increased or decreased, SVR decreased

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27
Q

MI 0-24hrs

A

early coagularive necrosis, gross: none, reperfusion injury, ca+ influx increases, free radicals

complication VA, HF, cardi. shock

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28
Q

MI 1-3hrs

A

extensive coagulative necrosis acute, gross: hyperemia, acute inflammation with neutrophils.

complication: post mi fibri. pericarditis

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29
Q

MI 3-14hrs

A

hyperemic border with yellow-brown softening
Macrophages, then granulation tissue

Compli:Free wall rupture—>tamponade

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30
Q

MI 2 weeks

A

recanlization, grray white scar, contracted complete scare

Compli: Dressler syndrome, HF etc.

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31
Q

ECG localization

Anteroseptal (LAD)

A

V1-V2

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32
Q

ECG localization

Anteroapical (distal LAD)

A

V3-V4

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33
Q

Anterolateral (LAD or LCX)

A

V5-V6

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34
Q

Lateral (LCX)

A

I, aVL

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35
Q

InFerior (RCA)

A

II III aVF

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36
Q

Posterior (PDA)

A

V7-V9, ST-depression V1-V3 with tall R waves

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37
Q

DCM

dilated cardiomyopathy

A

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

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38
Q

HOCM

A

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

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39
Q

restrictive/infil. cardiomyopathy

A

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

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40
Q

Takotsuboś

A

ventricalar apical ballooning, old female,+STEMI, clean coronariers

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41
Q

Myocarditis

A

viral (coxackie)——>biosy of the lymphocytes

increase in troponin, noST, Young, decreased RF

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42
Q

Bacterial endocarditis

Acute—

A

S aureus (high virulence). Large vegetations on previously normal valves A. Rapid onset.

43
Q

Bacterial endocarditis

Subacute

A

—viridans streptococci (low virulence).

Smaller vegetations on congenitally abnormal or diseased valves. Sequela of dental procedures. Gradual onset.

44
Q

Bacterial endocarditis

FROMJANE with♥

A 
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.

45
Q

Bacterial endocarditis

involves which valve and is associ. with?

A

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).

46
Q

Syphilitic heart disease

A

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.

47
Q

Acute pericarditis

A

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).

48
Q

Myocarditis

A

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:ƒViral (eg, adenovirus, coxsackie B, Compression of the heart by fluid (eg, blood, effusions [arrows in A] in pericardial space) Ž 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 myocarditisƒParasitic (eg , Trypanosoma cruzi, Toxoplasma gondii)ƒBacterial (eg , Borrelia burgdorferi, Mycoplasma pneumoniae, Corynebacterium diphtheriae)ƒTox i n s (eg, carbon monoxide, black widow venom)ƒ
Rheumatic feverƒ
Drugs (eg, doxorubicin, cocaine)ƒ
Autoimmune (eg, Kawasaki disease, sarcoidosis, SLE, polymyositis/dermatomyositis)

Complications include sudden death, arrhythmias, heart block, dilated cardiomyopathy, HF, mural thrombus with systemic emboli.

49
Q

Cardiac tamponade

A

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

50
Q

Heart failure

A

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

51
Q

Congenital long QT syndrome

A

Most commonly due to loss of function mutation of

K+ channels (affects repolarization). Includes:

ƒRomano-Ward syndrome—autosomal dominant, pure cardiac phenotype (no deafness).ƒ

Jervell and Lange-Nielsen syndrome—autosomal recessive, sensorineural deafness

52
Q

Congenital heart diseases

RIGHT-TO-lEFT SHuNTS

Early cyanosis—“blue babies.”

is associ. with?

A

The 5 T’s:

  1. Truncus arteriosus (1 vessel)
  2. Transposition (2 sw itched ves sels)
  3. Tricuspid atresia (3=Tr i)
  4. Tetralogy of Fallot (4=Te t r a)
  5. TAPVR (5 letters in the name)
53
Q

Persistent truncus arteriosus

A

Truncus arteriosus fails to divide into pulmonary trunk and aorta due to failure of aorticopulmonary septum formation; most patients have accompanying VSD

54
Q

D-transposition of great vessel

A

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

55
Q

Tricuspid atresia

A

Absence of tricuspid valve and hypoplastic RV; requires both ASD and VSD for viability

56
Q

Tetralogy of Fallot

A

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

57
Q

LEFT-TO-RIGHT SHuNTS

A

Acyanotic at presentation; cyanosis may occur years later. Frequency: VSD > ASD > PDA.

58
Q

Ventricular septal defect

A

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.

59
Q

Atrial septal defect

A

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

60
Q

Patent ductus arteriosus

A

In fetal period, shunt is right to left (normal). In neonatal period,  pulmonary vascular resistance Ž shunt becomes left to right Ž 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.

61
Q

Coarctation of the aorta

A

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.

62
Q

Turner syndrome

A

Bicuspid aortic valve, coarctation of aorta

63
Q

22q11 syndromes

A

Truncus arteriosus, tetralogy of Fallot

64
Q

Marfan syndrome

A

MVP, thoracic aortic aneurysm and dissection, aortic regurgitation

65
Q

Aortic stenosis

A

Systolic murmer, LV concentrichypertrophy

Cause: RHD, Age

white, excertion

Crescendo-decrescendo systolic ejection murmur and soft S2

66
Q

Aortic regurgitation

A

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.

67
Q

Mitral stenosis

A

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&raquo_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

68
Q

Mitral/tricuspid regurgitation

A

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

69
Q

Non–ST-segment elevation MI (NSTEMI)

A

Non–ST-segment elevation MI (NSTEMI) Subendocardial infarctsSubendocardium (inner 1/3) especially vulnerable to ischemiaST depression on ECG

70
Q

ST-segment elevation MI (STEMI)

A

ST-segment elevation MI
(STEMI)
Transmural infarcts
Full thickness of myocardial wall involved

ST elevation, pathologic Q waves on ECG

71
Q

Class IA

A

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.

72
Q

Class IB

A

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.

73
Q

Class IC

A

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

74
Q

Antiarrhythmics—β-blockers (class III)

A

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.

75
Q

Antiarrhythmics— potassium channel blockers (class III)

A

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.

76
Q

Antiarrhythmics—calcium channel blockers (class IV)

A

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

77
Q

Adenosine

A

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.

78
Q

Cardiac glycosides

A

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+.

79
Q

Bile acid resins Cholestyramine, colestipol, colesevelam

A

Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more

decreases LDL, slightly increses HDL andTG.

80
Q

Ezetimibe

A

Prevents cholesterol absorption at small intestine brush border

decreases LDL

81
Q

Fibrates Gemfibrozil, bezafibrate, fenofibrate

A

Activate PPAR-α—->upregulate LPL —->TG clearanceActivate PPAR—->induce HDL synthesis

decreases immensely TG, decreases LDL and increases HDL

82
Q

PCSK9 inhibitorsAlirocumab, evolocumab

A

Inactivation of LDL-receptor degradation—->removal of LDL from bloodstream

83
Q

Fish oil and marine omega-3 fatty acids

A

Believed to decrease FFA delivery to liver and decrease activity of TG-synthesizing enzymes

slightly increases LDL and HDL

84
Q

Calcium channel blockers

A

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

85
Q

Hydralazine

A

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
86
Q

Hypertensive emergency

A

Treat with labetalol, clevidipine, fenoldopam, nicardipine, nitroprusside.

87
Q

Nitroprusside

A

Short acting vasodilator (arteries = veins); increases cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide)

88
Q

Fenoldopam

A

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.

89
Q

Nitrates

A

Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate.

MECHANISM

Vasodilate by increases NO in vascular smooth muscle Ž increases cGMP and smooth muscle relaxation. Dilate veins&raquo_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.

90
Q

Sacubitril

A

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

91
Q

Standing Valsalva (strain phase)

A

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)

92
Q

Passive leg raise

A

increases preload ( LV volume)

incresease Most murmurs ( increases flow through stenotic or regurgitant valve)

dcreases:
MVP ( LV volume) with later midsystolic clickHCM ( LV volume)

93
Q

Squatting

A

increases preload, afterload ( LV volume)

increases Most murmurs ( increases flow through stenotic or regurgitant valve)

94
Q

Hand grip

A

increases afterload Ž 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)

95
Q

Inspiration

A

increases venous return to right heart, decreases venous return to left heart

increases Most right-sided murmurs

decreases Most left-sided murmurs

96
Q

Wide splitting

A

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

97
Q

Fixed splitting

A

ASD

Heard in ASD. ASD—–> left-to-right shunt—–>RA and RV volumes——> flow through pulmonic valve—–>delayed pulmonic valve closure (independent of respiration)

98
Q

Paradoxical splitting

A

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).

99
Q

Subclavian steal syndrome

A

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

100
Q

Coronary steal syndrome

A

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.

101
Q

Sudden cardiac death

A

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

102
Q

Chronic ischemic heart disease

A

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.

103
Q

Congenital long QT syndrome

A

Most commonly due to loss of function mutation of K+ channels (affects repolarization). Includes:ƒ

Romano-Ward syndrome—autosomal dominant, pure cardiac phenotype (no deafness).ƒ

Jervell and Lange-Nielsen syndrome—autosomal recessive, sensorineural deafness.

104
Q

Rhabdomyomas

A

Most frequent 1° cardiac tumor in children (associated with tuberous sclerosis).

Histology: hamartomatous growths. More common in the ventricles.

S1 First aid (20 decks)

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