Quick cards Flashcards
Any change in carotid upstroke/pulse has to do with?
Aortic valve
Similarly anything that radiates to carotids = AORTIC VALVE
“Fixed splitting of S2”
= ASD
bc blood going thru defect & coming bacd around & causing valve to close slightly slower
S3 = ?
Volume overload -
Occurs during increased passive filling (increase preload)
CHF
S4 = ?
Occurs in stiff, noncompliant ventricle during atrial kick
= (atrial squeeze right at end of diastole to get rest of blood from atria –> ventricles)
S1 = ?
AV valve closure
Mitral
Tricuspid
S2 = ?
Semilunar valves closing
Aortic
Pulmonic
Physiologic splitting of S2 = ?
Delay in aortic valve closure in YOUNG active healthy person w/ large inspiration
Paradoxical splitting
ABNORMAL
Delay in aortic valve closure w/ large exhalation in young active = HOCM!!!
Fixed splitting
Delayed consistently w/ every beat in a L-R shunt (ASD)
MR. ASTR - PS - mnemonic that’s helpful for what?
These are the murmurs that are all systolic - if they give you a systolic murmur and a location, then you know what it’s from immediately
If they give you a diastolic murmur and a location, switch it from REGURG –> STENOSIS or vice versa but with same valve!!!
MR-TR - should be closed during systole b/c so backflow = REGURG
AS-PS - open during systolic so systolic murmurs a/w these valves = STENOSIS
Any valve disorder that causes or results in enlargement of either atria will lead to?
Afib
Any valve disorder that causes increased fluid in either ventricle will lead to?
Dilated CMP and HFrEF
Any valve disorder which causes increased pressure in either ventricle (stenotic aortic or pulmonic valve) will cause?
LVH and lead to HFpEF at first and then HFrEF later if not treated
Calcified (stenotic) aortic valve by age 40…(so young?)..you’re thinking?
Bicuspid aortic valve - taking bigger pressure hit over longer period of time = AS at much younger age than normal
Systolic murmur
HARSH, loud
Radiates to neck
Slow, rising, prolonged carotid pulse
+syncopal episode walking up stairs
AORTIC STENOSIS
Anything radiating to carotids/neck = aortic
Anything that affects carotid upstroke = aortic issue
Systolic w/ aortic features (MR. ASTR-PS) = aortic stenosis
Aortic murmurs in general are?
Harsh, loud
High-pitched
Mitral murmurs in general are?
Low-pitched
Aortic stenosis = which structural cardiac issues over time?
LVH, LAE, LAD on EKG
AS = CP - ?
AS = SAD
Syncope (on exertion)
Angina
Dyspnea (on exertion)
Fatigue
Weakness
Loud harsh systolic murmur w/ exertional angina
Aortic stenosis
not an MI
Regurgitation = ? volume or pressure overload in general
Volume overload = S3
Stenosis = ? in general
Pressure overload = ventricular remodeling = stiffening of tissue = S4
Pressure overload = concentric LVH
Similar pathology as seen in LVH due to increase pressure 2/2 hypertension - so can think of that as an example
Signs of aortic regurg
AR = Al roker = WIDE pulse pressure signs
DIASTOLIC, HIGH-pitched, at BASE, wide pulse pressure, S3 common
Regurg = volume overload = ventricular remodeling = LVH (cardiomegaly) - tolerated well for many years
MR. ASTR-PS = systolic so if at base and diastolic = opposite = AR
Which maneuvers increase venous return (therefore increasing all murmurs except MVP, HOCM)
Squatting Laying down (legs up)
Which maneuvers decease venous return? (therefore decreasing all murmurs except HOCM, MVP)
Valsalva
Standing
Inspiration does what?
Increases preload = all right sided murmurs = louder, L-sided murmurs quieter
Exhalation does what?
Increases venous return to left side = all L-sided murmurs louder& right sided murmurs quieter
**Why L-sided murmurs are best heard after maximal expiration
MS ==>
MS = diastolic opening snap / diastolic rumble - heard best at APEX, radiates to axilla - low-pitched = use bell
MS. DOSSA - laying on left side - slut - got strep - rheumatic fever
Rheumatic fever = MCC
Pulm edema, hoarseness, cough, LAE, afib:
So much pressure backed up into LA b/c can’t get thru stenotic valve - so it backs up into pulm - so get pulmonary symptoms & get hoarseness b/c l recurrent pharyngeal nerve gets stretched out
MR etiologies - acute vs chronic
Acute:
Infective endocarditis
Chordae tendinae rupture
Papillary mu ischemia/infarction
Chronic:
MC form - can be asx for years or forever
Marfan’s syndrome
Rheumatic, congenital, MVP
Acute MR
NO LA enlargement - blood just backs up due to huge sudden volume overload
Remember blood coming from lungs into LA -> LV
So if Mitral valve not working, blood backs up into..? LUNGS = ACUTE PULMONARY EDEMA
Chronic MR
Blood flows back from LV to LA during systole = volume overload = prominent S3
LA will become enlarged
LV will dilate to accomodate
Results in dilated heart failure (EF < 40%) =
Afib
DOE
Fatigue
Chronic MR management
Yearly Echo
Cards referral if > mild
MVP = ? murmur? CP?
MVP = MSC (mid-systolic click)
Up to 10% of females 2/2 floppy valve
ASX in most - found incidentally
CP = palpitations, CP, dyspnea, fatigue
MVP management
If murmur, send to cards
Bb for palps
SSRI’s for anxiety
MV repair
Tricuspid stenosis = ?
RAE, RVH –> right HF = dependent edema, hepatometaly, ascites (fluid backs up to body if RHF)
Holosystolic murmur along LLSB, increases w/ inspiration
(inspiration = increased preload = all R-sided murmurs get louder)
Valve replacement
Left heart failure, fluid backs up to?
BODY - systemic
LIVER -portosystemic
LEFT side = blood coming from LUNGS
RIGHT side = blood coming from BODY
Stenotic mitral valve, fluid backs up to?
Left atria
Then lungs
LEFT side = blood coming from LUNGS
RIGHT side = blood coming from BODY
Who gets abx ppx with dental procedures?
Prosthetic cardiac valves
Previous infective endocarditis
Congenital anomalies - shunts, unrepaired cyanotic heart disease
Controlling sx in HFrEF
Reduce cardiac workload:
Dec afterload! (control HTN)
Reduce preload: (control excessive fluid!!)
- Diet, diuretics, vasodilators
Increase contractility (+inotropes)
Which med is given to improve QOL in the later stages of CHF?
Digoxin = positive cardiac inotrope
Does NOT PROLONG life, makes QOL better - makes heart pump harder so decreases sx but heart might poop out sooner
Also + inotrope = milrinone
In cardiogenic shock - can use pressors = IV + inotropes = Epi, NE, dobutamine, and dopamine
Vasodilator drugs
CCB
Alpha-1 blockers
Hydralazine
Minoxodil
Nitropress
What is BiDil? Who should get it?
BiDil = medication for AA w/ HF
BiDil = isosorbid dinitrate + hydralazine = dec BP & dec vascular resistance
Nitrates are used for?
They are anti-anginal agents- for PPX and treatemnt
NTG - SL tab, patch, ointment - used to treat acute CHF/angina, MI –> paste you can rub off! - Caution can cause hypotension
Isosorbid dinitrate - for AA w/ CHF or PO tab for angina
Nitrates MOA - get converted to nitrous oxide = smooth muscle relaxation & vasodilation =
Dec preload
Dec afterload
Nitrates C/I in inferior MI (preload dependent) and hypotension
Note: PDE-5 inhibitors (sildenafil, tadalafil) work on same pathway to cause vasodilation! Used in P. aa. HTN. Not used w/ nitrates = severe hypotension
Initial management stable afib
RATE CONTROL
BB (metoprolol)
CCB (Diltiazem)
Dig in CHF/Hypotension
Preferred agent for rate control in Afib if elderly with significant comorbid conditions of CHF or severe hypotension?
Digoxin
= + cardiac inotrope
Improves LVEF, reduces hospitalizations for CHF but NO IMPROVEMENT IN MORTALITY
For standard CHF tx - still use ACEI + BB + DIURETIC
Which drug reduces # hospitalizations in CHF?
Digoxin
Standard maintenance management of CHF
ACEI
BB
Diuretic
Stable afib: After rate control what are other considerations?
Rhythm control - use direct synchronized cardioversion most commonly - can do if:
Afib < 48 hrs, anticoagulated 3-4 weeks & TEE shows no clots in LA
IF UNSTABLE CARDIOVERT RIGHT AWAY
Or can use anti-arrhythmic agent (amiodarone, ibutilide, flecainide etc)
CHA2DS2-VASc components?
CHF HTN Age > or equal to 75 - 2pt DM Stroke, TIA, thrombus - 2pt
Vascular dz (MI, PAD)
Age > or equal to 65-74
Sex (female 1 pt)
Total of 9 points max
> or equal to 2 = moderate to high risk of clot - chronic oral anti-coag recommended
1 = low risk = based on clinical judgement - benefit vs risk
0 = low risk - no anticoagulation
Drugs that prolong QT…why prolonged QT is dangerous? How prolonged QT can present clinically?
Drugs: Macrolides Fluoroquinolones TCAs First gen antipsychotics Anti-arrhythmics (amio) --> GET EKG BEFORE STARTING
ELECTROLYTE ABNL can also prolong QT!!! AKA Hypocalcemia, hypo-Mg2+, hypo-K+
Presents clinically as recurrent syncope - get electrolytes & EKG…or can present as SCD in otherwise young healthy b/c can be congenital
Can lead to torsades - polymorphic ventricular tachycardia that leads to vfib –> death
Two types of SVT
AV nodal reentry tachycardia (AVNRT) –> two pathways WITHIN node = MC type
Extra pathways = extra impulses sent to ventricles
AV reciprocating tachycardia (AVRT) = less common, MORE dangerous - accessory pathway OUTSIDE AV node = WPW
**Often preceded by a PAC that kicks it on –> SVT is frequently fast on, fast off
Orthodromic AVNRT, AVRT = ? wide or narrow? Stable or unstable? Tx?
Can to orthodromic (normal direction thru AV Node) ==> leads to STABLE, NARROW complex SVT
Tx: Vagal maneuvers, Adenosine
Antidromic AVNRT, AVRT = wide or narrow QRS? Stable or unstable?
WIDE QRS (going wrong direction thru AV node)
Usually less stable but if pt is doing okay (HD stable), can try meds first –> NO ADENOSINE, need an anti-arrhythmic (Look at ALCS algorithm)
Tx: Amiodarone
**If suspect WPW, then PROCAINAMIDE = tx
WPW = what on EKG?
Delta wave = wide QRS
Upward slope of QRS
Short PR interval
MAT a/w what dz? definitoin = what?
Multifocal atrial tachycardia = rate > 100, > 3 p wave morphologies
A/w SEVERE COPD
Unstable SVT or unstable WPW
Direct synchronized cardioversion
If stable and WPW - use procainamide
Which drugs must you avoid in WPW?
AV nodal blockers - ABCD
Adenosine
Beta blockers
CCB
Digoxin
These are avoided b/c they can cause preferential conduction through the fast (pre-excitation) pathway = worsening of the tachy-arrhythmia
Causes of increased JVP
JVP & crackles = CHF
JVP & normal pulm exam = tamponade or constrictive pericarditis
JVP & decrease breath sounds = tension PTX
Young asian male w/ sudden cardiac syncope = ?
Brugada syndrome
EKG: RBBB & ST elevations (downsloping) in V1-V2
Why is digoxin good for rate control in people with hypotension or CHF?
Because it is a positive inotrope (inc contractility) but a negative chronotrope (dec rate)
First line chronic management angina
Beta blocker
Reduces mortality
Decreases sx
Prevents ischemic occurrences
Tx Prinzmental angina
CCB
Prevents/terminates ischemia induced by coronary vasospasm
Why do we use nitoglycerin in angina?
Nitro - SL
Reduces coronary vasospasm
Decreases demand/cardiac workload by dec preload
Increases myocardial blood supply - increased collateral blood flow to iischemic myocardium, coronary artery vasodilation
Both DHPs and Non-DHPs cause peripheral dilation - which group have direct effects on the heart as well?
Non-DHPs - Diltiazem, verapamil
Think Non-DHPs = Non-selective - affect heart (negative chorno/dromo/inotrope) and peripheral blood vessels
Therefore caution in CHF, in combination w/ BB (do same thing, different mech), pre-existing AV block= WORSE
Medication regimen chronic stable angina
Nitro SL PRN
Beta-blocker (FIRST LINE)
ASA
Tx NTEMI/STEMI caused by cocaine (coronary artery vasospasm)
BETA BLOCKERS CONTRAINDICATED (usually part of first line management in acute and
When are BB contraindicated in acute management of NSTEMI/STEMI?
Severe bradycardia (<50) - inferior / RV might present w/ this
Hypotension (SBP <90) Decompensated CHF Heart block (2nd-3rd deg) Cardiogenic shock Cocain-induced MI Severe asthma/COPD
Medications unstable angina/ NSTEMI
MONA +
Clopidogrel
(caution if CABG planned)
UFH
(dec mortality - add in pt w/ EKG change or + cardiac biomarkers)
Beta-blocker
(CCB in pt who cannot have Bb)
Nitrate (no dec in mortality, dec anginal sx)
R ventricular (inferior wall) MI - DO NOT give??
Nitrates
Caution w/ morphine too
Causes unsafe drop in preload
Give IV fluids to keep preload up
Management STEMI
MONA + EKG (w/in 10 imn) + troponin
Heparin
Consider clopidogrel
Beta blocker
ACEI
PCI = most important (w/in 90 min)
Complications of MI
Arrhythmias (Vfib) Ventricular aneurysm/rupture Cardiogenic shock Papillary muscle dysfunction Heart failure LV wall rupture
Post-MI pericarditis (dressler syndrome)
Signs left-sided HF
Pulmonary edema = chronic nonproductive cough (or pink frothy), dyspnea (MC symptom)
PE: S3, rales, rhonchi
Signs right-sided HF
Fluid backs up into systemic sx = JVD, LE pitting edema, hepatic congestion (hepatomegaly) + hepatogugular reflex
Management acute decompenstated HF
LMNOP
Lasix Morphine +/- Nitrates Oxygen Position
+ Inotropic support if severe!
Digoxin - (HF + AFIB, dec hospitalizations but NO MORTALITY BENEFIT), dobutamine, dopamine etc
Long term management of CHF
- ACEI
(FIRST LINE TX OF CHF) - dec mortality , prevents rehospitalization, reverses pathology by decreasing renin/SNS activation = dec ventricular remodeling
PLUS
- Diuretic
(Most effective tx for SYMPTOMS caused by CHF - spironolactone also a/w dec mortality
Then add if needed:
+/- 3. Beta blocker
(dec mortality, added AFTER ACEI)
+ 4. Implantable cardioverter defibrillator in pt w/ EF < 35% (b/c they tolerate arrhythmias poorly)
Meds that decrease mortality in CHF
ACEI
Beta-blockers
Nitrates + Hydralazine (BIDIL)
Spironolactone
EKG changes pericarditis
MCC pericarditis
MCC - idiopathic, after viral infection (ENTEROVIRUSES - coxackie, echo)
CP: PPPP - pleuritic, persistent, postural (worse supine, relieved leaning forward), Pericardial friction rub
EKG: DIFFUSE ST elevations in PRECORDIAL (V1-V6) leads & assocated PR DEPRESSIONS
EKG findings pericardial effusion
Low voltage QRS
Electrical alternans
PE findings pericardial tamponade
Pulsus paradoxus
(exaggerated > 10mmHg dec in systolic blood pressure w/ inspiration - increased filling of R side of heart during inspiraiton dec left sided ventricular filling, leading to pulsus paradoxus)
+ Beck’s triad
Beck’s triad
Hypotension
JVD
Muffled heart sounds
Triad of pericardial tamponade!!!
Kussmaul’s sign
Increased JVD during inspiration
Inspiration = increased filling of the R heart --> r-I-ght = INc during INspiration
Rn disease where R heart cannot fill (constrictive pericarditis, restrictive CMP, R heart failure) = fluid backs up into jugulars b/c R heart cannot keep up
CP/PE constrictive pericarditis
Right sided heart failure signs: Dyspnea Kussmaul's sign Inc JVD Peripheral edema Hepatojugular reflux
PERICARDIAL KNOCK
High-pitched 3rd heart sound due to sudden cessation of ventricular filling in early diastole from thickened inelastic pericardium - sounds like an S3
Myocarditis - MCC, CP/PE, Tx
MCC Infections - enteroviruses - COXSACKIE- Also Lyme, SLE, rheumatic fever - similar to pericarditis
Myocarditis = muscle is inflamed = HEART failure!!!! –> impaired systolic function (heart muscle is sick) =…..
CP/PE: DOE, S3, tachycardia, hepatomegaly
Dx:
CXR = CARDIOMEGALY 2/2 dilated CMP
+ TROPONIN - helps distinguish myocarditis from chronic dilated CMP
Echo - ventricular dysfunction
Endomyocardial bx = GOLD standard
Tx: supportive + standard HF tx (diuretic, ACEI, inotrope if severe)
Someone w/ viral prodrome (fever, myalgias, malaise) for several days who now comes in hypotensive, SOB, tachycardic, found to have hepatomegaly on exam
MYOCARDITIS - had coxackie B –> which infiltrated heart muscle & now has HEART FAILURE
May also have si/sx pericarditis concurrently
HOCM Murmur
Harsh systolic crescendo-decrescendo murmur best heard at LLSB (sounds similar to AS but in different location & patient population)
Tx: Beta blockers = first line medical therapy, surgical = definitive (reserved for severe)
Dx criteria rheumatic fever
Two Major OR one major + two minor
JONES = MAJOR
Joint (migratory arthralgias (LE-UE, LG)
Oh my heart! Active carditis - myo, valves (mit)
Nodules (subcutaneous) - over joints
Erythema marginatum - annular rash on trunk
Sydenham’s chorea - jerky nonrhythmic mvmt
MINOR: Fever Arthralgia Inc ESR/CRP EKG prolonged PR interval
PLUS evidence of strep infection - rapid, cultures, ASO titer
Tx: Aspirin 2-6 weeks w/ taper + PCN G
HTN urgency
Lower BP by ~25% max over 24-48 hours using ORAL agents
Clonidine Catopril Furosemide Labetalol Nicardipine
Goal is to get < 160/100
HTN + OP
Thiazide diruetic
AA first line HTN
Thiazide
not 2/2 RAAS, ACEI less effective
Aortic stenosis complications
= ASC
Angina
Syncope
CHF
HTN + Systolic HF
ACEI !!!
Diuretic
DM + HTN
ACEI
Aortic dissection - medical management
For DESCENDING
Esmolol
Best drug to increase HDL
Niacin
Best drug to decrease LDL
HmgCOa reductase inhibitors
Statins
Best drug to decrease triglycerides
Fibrates
Duke criteria endocarditis
MAJOR:
Sustained bacteremia (2+ Bl Cx w/ organism known to cause endocarditis)
AND
Endocardial involvement (Echo = vegetations, NEW valvular regurgitation)
MINOR:
Predisposing condition (IVDA, abnl valve, indwelling catheter)
Fever (100.4)
Vascular & embolic phenomena
+ Bl cx not meeting major criteria
+ echo findings not meeting major (worsening of existing murmur)
TWO MAJOR or ONE major & THREE minor
Odd but can have + ESR/RF too…?
MCC subacute endocarditis
Indolent infection of ABnormal valve w/ less virulent organism
S. viridans
MC organism endocarditis prosthetic valve (PVE)
Staph epidermis if w/in 60 d of implant
If late, same as acute endo (staph aureus)
Mainstay of PAD treatment
Cilostazol
Control other RF (DM, HTN, HLD)
When to repair AAA (prerupture)
> 5.5 cm - immediate repair even if asx
Unique PE finding Aortic dissection
> 20 mmHg between left and right arm
Decreased peripheral pulses
Dx: CT scan w/ contrast = initial test of choice - MRI angiogram = gold standard
Tx: Esmolol if descending (type III/B) w/ target SBP 100-120 & pulse < 60 +/- sodium nitroprusside
If Type A, Type I/II - aka acute proximal = SURGERY
Signs coarctation of aorta
High UE BP
Low LE BP
A/w Bicuspid aortic valve
A/w TURNER syndrome - bicuspid valve looks like a T
Superficial thrombophlebitis
Thrombophlebitis = swelling/inflammation of a vein caused by a blood clot - superficial = superficial thrombophlebitis - deep = DVT
RF: Virchow’s triad, IV cath, trauma, pregnancy, varicose veins
Tx: supportive management = MAINSTAY - extremity elevation, warm compresses, NSAIDs, elastic compression stockings
Etiologies cardiogenic shock
Massive PE
Pericardial tamponade
Tension PTX
Aortic dissection
Tx underlying cause!!!
SIRS criteria
HR > 90
RR > 20
Temp > 100.4
WBC > 12,000
Sepsis = SIRS + focus of infection (a/w inc lactate)))
Septic shock = Sepsis + refractory hypotension despite resuscitation
Neurogenic shock
Form of distributive shock (along w/ septic, anaphylactic, endocrine)
Hypotension WITHOUT reflex tachycardia –> AKA HYPOTENSION w/ BRADYCARDIA = weird!!!
4 findings TOF
1 of 5 cyanotic heart diseases
Pulmonary aa. stenosis =RVOF obs
Overriding aorta
RVH
VSD
= DOE, cyanosis worsens w/ age
“Tet-spells”= cyanotic spells relieved by inc venous return
Murmur of VSD
Non-cyanotic - L–>R shunt
= HHHH
Harsh, High-pitched, Holosystolic best heard at LLSB (think of where ventricles are & which way it’s blowing L–>R)
PE of ASD
Left to right = NON-cyanotic (Lefties = good)
Systolic ejection crescendo-decrescendo murmur
ASD, AS, HOCM are all described as crescendo decrescendo - but all in DIFFERENT areas - ASD = pulmonic area, AS = aortic area (RUSB), HOCM = LLSB/Erb’s point
PDA murmur/ CP
Loud harsh continuous machinery murmur heard at pulmonic area
Bounding pulses - like a hammer - everything aggressive in PDA
IV indomethacin = tx, surgical correction if fails before 1-3 years of age
Cyanotic congenital heart lesions
The 5 T’s
Pulmonary atresia
Tricuspid atresia
KEEP PFO/PDA OPEN w/ prostaglandin until surgical correction
