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What are the "Big 6" in regards to risk factors for CAD?
FSH DAD
F - Family Hx of premature CAD/MI (M < 45; F < 55)
S - Smoking (Cigarettes)
H - HTN, Homocysteine levels elevated
D - DM/Metabolic syndrome
A - Age (M: > 45; F: > 55)
D - Dyslipidemia - Elevated LDL; Low HDL
What is the normal ejection fraction? What is the ejection fraction value that corresponds to increased mortality?
Normal = > 50%
<50% is associated w/ mortality
What vessel corresponds to a poor prognosis in regards to CAD?
LAD - b/c it covers 2/3 of the heart
What type of CAD is being described: CP that lasts < 10/15 min that is described as heaviness/pressure that is brought on by exertion, and relieved by rest or NTG?
A. Unstable Angina
B. Stable Angina
C. Prinzmetal's Angina
B. Stable Angina
What diagnostic procedures can be used as a screening tool for CAD?
Exercise stress ECHO/EKG
What is the GOLD STANDARD diagnostic procedure for CAD?
Coronary Angiography
The coronary cath looks at what? Coronary angiography looks at what?
Cath --> determining a cardiac diagnosis
Angiography --> presence and severity of CAD; looks at delineating coronary anatomy
What procedures can be used with "reversible" ischemia?
CABG and PTCA
If a patient is unable to exercise, what procedure can you use as a screening test for CAD?
Pharmacological Stress Test w/ IV adenosine, dipyramidole, dobutamine
What device can be used to detect silent ischemia and silent arrhythmias not assable by an in office EKG?
Holter Monitor
What are the components of metabolic syndrome?
hypercholesterolemia
hypertriglyceridemia
impaired glucose tolerance
diabetes
hyperuricemia
HTN
What is a nonpharmacological treatment that can be used for the tx of CAD?
TLC - EXERCISE is crucial and DIET modification (decrease fat, cholesterol)
What pharmacological therapies are first line for all CAD patients?
TLC, Aspirin, BB, Nitrates
(2nd line: add CCB)
What is the TOC is severe CAD?
CABG
The pathophysiology of stable vs unstable angina?
Stable: due to increased demand
Unstable: reduced resting coronary flow
What three patient profiles can be diagnosed with unstable angina (USA)?
1) Pts with chronic angina with increasing freq, duration, and intensity of CP
2) Pts with new-onset angina that is severe or worsening
3) Patients w/ ANGINA AT REST
What diagnostic procedures should be utilitzed for USA?
Higher risk for AE w/ Stress test sooo....
1) Stablize w/ medical management before stress test
or
2) undergo cardiac cath initially
What management should be taken with USA?
Admit w/ IV access and O2
Medical Management: "HANG"
Heparin (LMWH)
Aspirin
NTG - FIRST LINE THERAPY
Glycoprotein IIb/IIa
+
BB - FIRST LINE THERAPY
+
Cardiac Cath
After acute event, what tx are used for USA?
Aspirin, BB, nitrates
What form of angina is characterized by "transient coronary vasospasm", the episodes occur at rest, and ass w/ ventricular dysfunction?
A. Stable Angina
B. Unstable Angina
C. Prinzmetal's Angina
C. Prinzmetal's Angina
What is the HALLMARK of prinzmetal's angina?
transient S-T ELEVATION on ECG during chest pain, which respresents transmural ischemia
What is the DEFINITVE TEST for prinzmetal's angina?
CORONARY ANGIOGRAPHY - displays coronary vasopasm when the pt is given "IV ERGONOVINE"
What management can be used for prinzmetal's angina?
Nitrates, CCB
What is the MOST COMMON CAUSE of a MI?
Acute Coronary Thrombosis
Remember time is muscle w/ an MI
o 20-40 min: irreversible cell damage
o 3-6 hours: necrosis
MI is associated with 30% mortality, 1/2 of the deaths are (pre/post) hospital?
Pre
What are the clinical features of a MI?
(1) intense substernal CP - "crushing" or "elephant on chest"
(2) Radiation to neck, jaw, arms, or back - MOST COMMON on LEFT side
(3) Some experience epigastric discomfort (make sure to r/o w/ GERD sx)
(4) Dyspnea
(5)diaphoresis
(6)weakness, fatigue
(7) N/V, sense of impending doom
(8) syncope
What patient population can have an asx or atypical MIs?
(1) post-op
(2) DM
(3) Elderly
(4) Women
In the case of a MI w/ sudden cardiac death, what is the MOST COMMON CAUSE?
V. Fib
What are the characteristic EKG findings for a MI?
Peaked T waves - occur EARLY and may be missed
ST Elevation (STEMI) - TRANSMURAL MI - diagnostic of an acute infarct
Q Waves - evidence of NECROSIS (SPECIFIC) - usually seen LATE, not acutely
T wave inversion - sensitive NOT specific
ST Depression (NSTEMI) - SUBENDOCARDIAL injury
(NSTEMI/STEMI) is larger and more devestating to the patient's health?
STEMI
NSTEM tends to be smaller than a STEMI and presents similar to USA, how can you differentiate the two?
Cardiac Enzymes
What is the GOLD STANDARD for MI diagnosis?
CARDIAC ENZYMES (<-- Per Stepup to Medicine)
ANGIOGRAPHY (<-- Per Ovalle)
What cardiac enzyme increases w/in 4-8 hour - peaks at 24 hours - and returns to nl at 48-72 hours?
CK-MB (best when measured 24-36 hours)
Measure @ admission - every 8 hours for first 24 hours
What is the MOST IMPORTANT cardiac enzyme?
Troponin (I&T) <-- greater sensitivity and specificity than CK-MB
Increase w/in 3-5 hours - peak at 24-48 hours - return to nl at 5-14 days
Obtain levels on admission - every 8 hours for 24 hours
Troponin (I/T) is falsely elevated in patients w/ renal failure?
Troponin I
What is the initial treatment of an MI upon admission?
MONA - Morphine, Oxygen, Nitro, Aspirin
What is the acute management for a RCA infarction?
IV NL Saline + MOA (Morphine, O2, ASA)
NITRO IS C/I IN A RIGHT SIDED MI
What is the acute management for a NSTEMI/Non-Q wave MI?
MONA (THROMBOLYTICS ARE C/I)
BB/CCB/STENT
What are the indications for stents and thrombolytics?
CP 30-6 hours: ST elevation of 1mm or greater in 2 leads in STEMI --> use thrombolytics
o CP < 30 min → STENT in STEMI/NSTEMI
o CP > 6 hours - risk to benefit ratio in STEMI
NEVER USE USE THROMBOLYTICS IN NSTEMI***
TPA - most expensive and most effective
Streptokinase: least expensive an less effective
Explain the presentation for a cocaine induced MI? What is the MOST COMMON CAUSE of death?
o Tachycardia, HTN, vascular constriction
o Sudden death due to V.Fib
What is initiated in all patients with an MI to prevent the progreessio of thrombus, however has NOT been shown to decrease mortality?
LMWH (enoxaparin)
What drugs are used post-MI for maintance therapy?
ASA - decreases mortality - prevents platelet aggregation to prevent thrombosis formation
BB - decreases mortality - decreases HR/Contractility/afterload
ACEi - initiate w/in hours of hospitalization if no c/i - been shown to decrease mortality - esp important in DIABETICS
Statins - reduce risk of other coronary events
What is the MOST COMMON CAUSE of inpatient mortality post-MI?
Pump Failure (CHF)
Mild: tx w/ ACEi and Diuretic
Severe: can lead to cardiogenic shock - hemodynamic monitoring
If a pt is post MI w/ a second or third degree heart block, what is the appropriate treatment measures if it is an anterior MI? Inferior MI?
Anterior MI: pacemaker (temp then permanent) - worse prognosis
Inferior MI: atropine IV, if not controlled then temporary pacement (better prognosis)
How can a physician know if a patient is having a recurrent infaraction?
repeat ST-Elevation on EKG post 24 hours of the MI
In a papillary muscle infact, what is the common resulting murmur and what is the management
MR
ECHO - Emergeny MV replacement - afterload reduction w/ nitroprusside or intra-aortic balloon pump.
What is the name of the "postmyocardial infarction syndrome" that is immunologically based and consists of fever, malaise, pericarditis, leukocytosis, and pleuritis occuring weeks to months post-MI?
Dresslers Syndrome
TOC = ASA
Name the leads and corresponding artery for which ST-Elevation/Depression can be seen for the following infarctions:
Anterior MI?
Lateral MI?
Inferior MI?
Posterior MI?
Anterior: V1-V4 - LAD
Lateral: I, avL, V5, V6 - Circumflex
Inferior: II, III, avF - RCA
Posterior Large R wave in V1/V2 - RCA
What MI location is the MOST COMMON?
Anterior - LAD
In CHF there is systolic and diastolic dysfunction...what are they defined by and what is the MOST COMMON CAUSE of each?
Defined by Ejection fraction
Systolic: <50% or decreased EF
MCC - post MI
Other: DCM/Myocarditis
Diastolic: Nl/increased EF
MCC = HTN leading to myocardial hypertrophy
Other: AS, MS, AR, RCM/HCM
What are the sx of left-sided heart failure?
What is the MCC of left-sided HF?
Left sided heart failure - dyspnea, orthopnea, paraxoysmal noctural dyspnea, nocturnal cought (nonproductive)
Adv CHF - confusion and memory impairment
NYHA Class IV - diaphoresis and cool extremeities at rest
MCC = CAD/HTN
What are the signs of left sided heart failure?
Dislaced PMI to the left
Pathologic S3 (ventricular gallop) - S4 can be present
Crackles/rales at lung bases (pulmonary edema, moderate severity of left ventricular HF)
Dullness to percusssion and decreased tactile fremitus of lower lung feilds
increased pulmonic component of heart sounds indicates pulmonary HTN
What are the S&S of right sided heart failure?
What is the MCC?
Peripheral Pitting Edema (secondary to venous insuff)
Nocturia (due to increased venous return from leg elevation)
MCC = Left sided HF or Cor pulmonale (pure)
JVD
Hepatomegaly/Hepatojugular reflex
Ascites
Right ventricular heave
Name the NYHA described..."symptoms occur w/ vigorous activities, such as playing a sport, pts are nearly asymptomatic?
A. I
B. II
C. III
D. IV
A. I
Name the NYHA described..."symptoms occur w/ prolonged or moderate exertion, such as climbing a flight of stairs or carrying heavy packages. Slight limitation in activity"?
A. I
B. II
C. III
D. IV
B. II
Name the NYHA described...."symptoms occurs w/ usual activities of daily living, such as walking across the room or getting dressed. Marketedly Limited"?
A. I
B. II
C. III
D. IV
C. III
Name the NYHA described...."symptoms occur at rest. Incapacitating.?
A. I
B. II
C. III
D. IV
D. IV
What are the CXR findings for CHF?
Cardiomegaly
KERLY B LINES
Prominent interstitial markings
Pleural Effusion
What is the INITIAL TEST OF CHOICE/GOLD STD for CHF?
Echo
What is very important about the ECHO and CHF?
It measures EJECTION FRACTION
<40% = systolic dysfunction (MOST COMMON)
>40% = diastolic dysfunction
What can be used to precisely measure the EF and left ventricular function?
Radionucleotide ventriculography using technetium-99m
What lab is pathognomic for CHF?
Elevated BNP
What is the acute tx for CHF?
LMNOP
L - Lasics
M - Morphine
N - Nitro
O - O2
P - Position
What is the initial LT treatment for mild CHF (I/II)?
Mild restriction of sodium intake (<4 g Na+)
Physical activity
Loop Diuretic
ACEi
Loop and ACEi are the FIRST LINE TREATMENTS
What is the initial LT treatment for mild-mod CHF (II/III)?
Start w/ a loop diuretic and ACEi
Add a Beta Blocker if moderate disease is present.
What is the initial LT treatment for moderate-severe CHF (III/IV)
Add Dig to loop and ACEi
Can add Dig at anytime for systolic dysfunction
In patient with Class IV sx who are still symptomatic despite the previously mentioned treatment, what can you add?
spironolactone
What are the S&S of Dig toxicity?
N/V Anorexia
Cardiac: ectopic ventricular beats, AV block, Afib
CNS: green/yellow vision, disorientation
What are the characteristic findings for PACs? What management would you recommend?
EKG: early p-waves that differ in morphology from the normal sinus P-wave - QRS is normal
Management: can occur in healthy individuals and some patients can be asx so they do not require treatement
If palpatations - prescribe BB
What are the EKG findings for PVCs? Tx?
Wide, Bizzare QRS complexes followed by compensatory pause are seen; a P-wave is not usually seen because it is buried within the wide QRS complex.
Increased Incidence w/ Age
>10 PVC/hour --> Pathologic
Exercise should improve PVCs, if not then pathologic
Tx: Symptomatic - BB
Pts w/ repetitive PVCs are at increased risk for what?
Sudden Death by V. Fib (Esp when >10/hour)
Define the following terms in regards to PVCs:
Couplet?
Bigeminy?
Trigeminy?
Couplet: two successive PVCs
Bigeminy: Sinus beat followed by a PVC
Trigeminy: sinus beat followed by two PVCs
What EKG finding is defined as "irregularly irregular"?
A. Fib (Atrial rate is > 400 and vent rate is 75-175)
MOST COMMON ARRYTHMIA
Pts with A. Fib are at increased risk for what?
thromboembolism and hemodynamic compromise
What is "holiday heart syndrome"?
A. Fib caused by excessive alcohol intake
What are the clinical features of A. Fib?
Fatigue and Exertional Dyspnea
Palpitations, dizziness, angina, or syncope
Irregular, irregular pulse
Blood stasis leads to formation of intramural thrombi, which can embolize to the brain
Absense of an "A Wave" in JVP measurement.
In a hemodynamically unstable patient in A. Fib what manaement would you take?
Immediate electrical cardioversion to sinus rhythm
In regards to A. Fib and rate control, what is the target rate? Perferred Tx?
60-100 bpm
CCB - Perferred Tx (Alt: BB)
In a hemodynamically stable patient, what management steps should you take?
Rate Control w/ CCB
Duration of A.Fib <48 hours --> Cardioversion
Duration of A.Fib > 48 hours --> Anticoagulate x 3 weeks w/ Warfarin (INR 2-3) then cardiovert
or
Duration of A.Fib > 48 hours --> get a TEE --> If thrombosis in left atrium then anticoagulate x 3 weeks and then cardiovert; If no thrombis in left atrium then cardiovert immediatly.
Explain the CHADS score for A. Fib?
Used to assess patients risk and when to anticoagulate w/ "Warfarin" verus "electric shock"
DO NOT ANTIVERT PATIENTS WITH HIGH RISK! (CHAD SCORE >/= 2+
ALWAYS ANTICOAGULATE CHADS 2+ PATIENT
Criteria for CHADS Score - BQ
Congestive Heart Failure (1 point)
Hypertension (1 point)
Age over 75 years (1 point)
Diabetes Mellitus (1 point)
Stroke or TIA history (2 points)
Mitral Stenosis or prosthetic heart valve carry similar risk and also indicate Warfarin
Interpretation
CHADS Score >2 (CVA risk >5% per year): Warfarin with goal INR 2.0 to 3.0
CHADS Score 1 (CVA risk >4% per year): Warfarin or Aspirin
CHADS Score 0: Aspirin 81 to 325 mg daily
*NEW ONSET A.FIB W/ NO PRIOR DOCUMENTATION - CARDIOVERT**
What is the MOST COMMON CAUSE of A. Flutter?
COPD = MCC
Other: rheumatic heart disease, CAD, CHF, ASD
What is the EKG findings for A. Flutter?
Pathogneumonic - "saw-tooth" flutter waves best seen in II/III/avF
Rate will be 250-350
What is the MCC of multifocal atrial tachycardia?
COPD
How can you diagnose multifocal atrial tachycardia?
three different P-wave morphologies are required to make an accurate diagnosis
Rate is 100-200
Can also be diagnosed w/ vagal maneuvars or adenosine to slow AV block
*Note that a wandering pacemaker is similiar but the rate is <100*
Explain orthodromic and antidromic AVRT.
Orthodromic AVRT (MORE COMMON):
Narrow Complex tachycardia in which the wave of depol travels down the aVnode and retrograde up the accessory pathway (narrow QRS - bypass going down normal conduction pathways) - Retrograde
Antidromic AVRT (LESS COMMON):
Wide Complex tachycardia in which wave of depol travels down the accessory pathway and retrograde up the AV node (The wider the QRS the farther the conduction is from the std conduction pathways and it is slower) - Anterograde
What is the treatment for AVRT?
Vagal Maneuvars
IV Adenosine = TOC
Prevention: DIG = TOC
Recurrent/Symptomatic = radiofreqencu catheter abalation of either the AV node or accessory tract
Explain WPW and the Tx?
Accessory pathways between the atrium and ventricle may occasionally be seen
MOST COMMON is 'bundle of Kent' seen in Wolff-Parkinson-White syndrome
SHORTENED PR INTERVAL AND A "DELTA WAVE" caused by early excitation of the ventricle via the accessory pathway.
TX: Radiofreqency catheter abalation
What is the arrhythmia that is defined as *"rapid and repetitive firing of 3+ PVCs in a row, at a rate of 150 - 250 bpm?
A. A. Fib
B. V. Fib
C. Trigeminy
D. V. Tach
D. V. Tach
What is the MOST COMMON CAUSE of V. Tach?
CAD w/ Prior MI = MCC
OTher: active ichemia, hypotsn, CM, CHD, prolonged QT syndrome, drug toxicity
Define sustained V.Tach. What are the associated risks?
Sustained VT lasts longer than 30 secondas and is almost always symptomatic!
Ass w/ MI/Hypotsn
Can be a life-treatening arrhythmia and can lead to V. Fib :0
Define non-sustained VT.
VT that lasts less than 30 seconds - brief, asx
Worse prognosis when CAD/LV dysfunction are present.
What are the clinical features of VT?
l. Palpitations, dyspnea, lightheadedness, angina, impaired consciousness (syncope or near-syncope)
2. May present with sudden cardiac death
3. Signs of cardiogenic shock may be present.
4. May be asymptomatic if rate is slow
5. Physical findings include cannon a waves in the neck (secondary to AV dissociation,
which results in atrial contraction during ventricular contraction) and an Sl that varies in intensity.
Name the EKG findings that are characteristic of VT.
Pathogneuomic = WIDE AND BIZARRE QRS COMPLEXES
QRS can be monomorphic or polymorphic
MONOMORPHIC - all QRS complexes are identical
POLYMORPHIC - the QRS complexes are different - beat to beat variation
How can you differentiate VT from PVST?
Unlike PVST, VT DOES NOT respond to vagal maneuvars or adenosine
What phenomenon is described as follows... ABERRANT VENTRICULAR CONDUCTION DUE TO A CHANGE IN QRS CYCLE LENGTH. Describes a particular type of wide complex tachycardia that is often seen in atrial fibrillation. It is more often misinterpreted as a premature ventricular complex.
ASHMAN'S PHENOMENON
What is the management option for hemodynamically stable sustained VT pts w/ SBP of > 90?
New ACLS says IV Amiodarone, IV procaimamide, or IV sotaolol
What is the management option for a non-hemodynamically stable sustained VT pt?
BOX TRUMPS PILL
IMMEDIATE synchronous DC cardioversion
Follow w/ Amiodarone to maintain sinus rhythm
As a general rule, what form of management should be given to all patient who are dx w/ sustained VT?
ICD
Exception - EF is normal, then you can consider amiodarone
In regards to VT as a whole what is the FIRST LINE THERAPY?
ICD
Amiodarone is considered the BEST 2ND LINE TX
Describe the patho behind V. Fib?
Multiple foci in the ventricles fire rapidly, leading to chaotic quivering of the ventricles and NO CO.
Reoccurance is high if unrelate to an MI and has a worse prognosis --> Pt will need a ICD/Amiodarone
Fatal if untreated can result in "SUDDEN CARDIAC DEATH"