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Cardiology

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What are the 6 steps to reading an ECG?
1. Rate
< 60 bradycardia
60-100 normal
> 100 tachycardia

2. Rhythm
sinus = P before every QRS; QRS after every P
irregular = regularly v irregularly
ectopic beats

3. Axis (leads I and aVF)
normal = +QRS in I and aVF
LAD = +QRS in I; -QRS in aVF
RAD = -QRS in I; +QRS in aVF

4. Intervals (PR, QRS, QT, I, V1, V5, V6)
normal: PR 120-200 msec; QRS <120 msec
AV block: PR > 200 or P w/o QRS
LBBB: QRS >120; no R wave in V1; tall R wave in I, V5,V6
RBBB: QRS > 120; RSR' "rabbit ears"; wide R wave in V1; wide S wave in I, V5, V6
Long QT syn: QTc > 440

5. Ischemia/Infarction
Ischemia: new inverted T waves; poor R wave progression in precordial leads; ST elevation/depression
Transmural Infarct: Q waves > 40 msec; ST elevation + T wave inversion

6. Chamber Enlargement
Right Atrial (p pulmonale): P wave > 2.5 mm amplitude in II
Left Atrial (m pulmonale): P wave > 120 msec in II; notched "m" P waves in II
LVH: amplitude of S in V1 + R in V5 or 6 > 35 mm
RVH: RAD (-QRS in I; +QRS in aVF) + R wave > 7 mm in V1
Explain finding JVD on physical exam
JVD > 7 cm above the sternal angle

Suggests R-sided HF, pulmonary HTN, volume overload, tricuspid regurg, pericardial dz
Explain finding a hepatojugular reflex on physical exam
Fluid overload, impaired right ventricular compliance
Explain finding a Kussmaul's sign on physical exam
Increase JVP on inspiration.

Suggests R-ventricular infarction, post-op tamponade, tricuspid regurg, constrictive pericarditis
Explain finding a systolic murmur on physical exam
Systolic Murmurs
1. Aortic Stenosis
2. Mitral Regurg
3. Mitral Valve Prolapse
4. Flow Murmur
Explain finding a diastolic murmur on physical exam
Diastolic Murmurs (always pathogenic)
1. Aortic Regurg
2. Mitral Stenosis
Explain finding gallops on physical exam
S3 Gallop (floppy ventricle)
- dilated cardiomyopathy, mitral valve dz
- nl in young/pregnant pts and in high output states

S4 Gallop (stiff ventricle)
- HTN, diastolic dysfunction, aortic stenosis
- nl in younger/athletes pts
Explain finding edema on physical exam
Pulmonary
- L-heart failure

Peripheral
- L/R heart failure, peripheral venous dz, constrictive pericarditis, tricuspid regurg, hepatic dz, lymphedema, nephrotic syndrome, hypoalbuminemia, drugs
Explain finding abnormal peripheral pulses on physical exam
Increase
- compensated aortic stenosis, coartaction (arms > legs), PDA

Decreased
- peripheral arterial dz (PAD), late-stage HF

Pulsus Paradoxus (dec sBP on inspiration)
- pericardial tamponade, asthma, COPD, tension PTX, foreign body in airway

Pulsus Alterans (alternating weak/strong)
- cardiac tamponade, impaired L-ventricular systolic function
- poor prognosis

Pulsus Parvus et Tardus (weak and delayed)
- aortic stenosis
What are the bradyarrhythmias and conduction abnormalities
Sinus bradycardia

First degree AV block

Second degree AV block (Mobitz I)

Second degree AV block (Mobitz II)

Third degree AV block

Sick sinus syndrome/tachycardia-bradycardia syndrome
What is sinus bradycardia?
Etiology
- normal response to conditioning
- sinus node dysfunction
- meds: beta-blocker; CCB

S/S
- asymptomatic; light-headed; syncope; chest pain; hypotension

ECG
- sinus rhythm; ventricular rate < 60 bpm

Tx
- asymptomatic = none
- atropine (inc HR); pacemaker (if severe)
What is first degree AV block?
Etiology
- can be normal; inc vagal tone
- meds: beta-blockers; CCB

S/S
- asymptomatic

ECG
- PR interval > 200 msec

Tx
- none necessary
What is second degree (Mobitz I/Wenckebach) AV block?
Etiology
- meds: digoxin; beta-blockers; CCB
- inc vagal tone
- right coronary ischemia/infarction

S/S
- asymptomatic

ECG
- progressive PR interval lengthening until a dropped beat occurs, then PR interval resets

Tx
- stop offending drug
- atropine as indicated
What is second degree (Mobitz II) AV block?
Etiology
- fibrotic dz of conduction system
- acute, subacute, prior MI

S/S
- occasional syncope
- frequent progression to 3rd degree AV block

ECG
- unexpected dropped beats w/o a change in PR interval

Tx
- pacemaker
What is third degree AV block?
Etiology
- no electrical communication bw atria and ventricles
- infection: lyme dz
- 2nd degree Mobitz II heart block

S/S
- syncope, dizziness, acute heart failure, hypotension, cannon A waves

ECG
- no relationship bw P waves and QRS complexes

Tx
- pacemaker
What is sick sinus syndrome/tachycardia-bradycardia?
Etiology
- heterogeneous d/o leading to intermittent supraventricular tachy- and bradyarrhythmias

S/S
- syncope, palpatations, dyspnea, chest pain, TIA, and stroke (2/2 tachy- or bradycardia)

ECG
- transient tachycardia/bradycardia

Tx
- pacemakers (most common indication)
How do you calculate CO (cardiac output)?
CO = SV x HR

CO = rate of O2 consumption/(arterial O2 - venous O2)
How do you calculate MAP (mean arterial pressure)?
MAP = CO x TPR (total peripheral resistance)

MAP = 2/3 diastolic pressure + 1/3 systolic pressure
- heart spends 2X longer in diastole than systole
- normal MAP = 70-100
How do you calculate SV (stroke volume) and what are factors affecting SV?
SV = CO/HR

SV = EDV - ESV

SV factors (CAP)
- Contractility
- Afterload: MAP
• dec by vasodilators (eg hydralazine)
- Preload: venticular EDV
• dec by venodilators (eg nitroglycerin)
Explain the Starling curve.
CO or SV is proportional to Preload or ventricular EDV
- CO is proportional to the initial length of the cardiac muscle (preload)

Exercise/sympathetic stimulation increase preload -> increased SV and increased CO
How do you calculate EF (ejection fraction)?
EF = SV/EDV = (EDV - ESV)/EDV

EF is an index of ventricular contractility

normal EF > 55%
What are the 2 main categories of tachyarrhythmias and examples of each?
Supraventricular ("Atrial") Tachyarrhythmias
[Atrial]
- Sinus tachycardia
- A-fib (atrial fibrillation)
- Atrial flutter
- Multifocal atrial tachycardia
[AV Junction]
- AVNRT (atrioventricular nodal reentry tachycardia)
- AVRT (atrioventricular reciprocating tachycardia)
- Paroxysmal atrial tachycardia
- WPW (Wolf-Parkison-White) syndrome

Ventricular Tachyarrhythmias
- PVC (premature ventricular contractions)
- VT (ventricular tachycardia)
- V-fib (ventricular fibrillation)
- Torsades de pointes
What is sinus tachycardia?
Etiology (atrial)
- normal response to fear, pain, exercise
- 2/2 hyperthyroidism, hypovolemia, infection, PE

S/S
- palpitations; SOB

ECG
- sinus rhythm
- ventricular rate > 100 bpm

Tx
- underlying cause
What is a-fib?
Etiology (atrial)
- Acute AF: PIRATES (Pulmonary dz, Ischemia, Rheumatic heart dz, Anemia/Atrial myxoma, Thyrotoxicosis, Ethanol, Sepsis
- Chronic AF: HTN, CHF

S/S
- asymptomatic
- SOB, chest pain, palpatations
- CVA
- irregularly irregular pulse

ECG
- no p waves
- variable and irregular QRS

Tx (ABCD = anticoagulate, beta-block, cardioconvert/CCB, digoxin)
- Anticoagulate if
• CHADS2 score > 2 (CHF, HTN, Age > 75, DM, Stroke/TIA)
• persists > 48 hrs to prevent CVA
- Rate control (beta-block, CCB, digoxin)
- Cardiovert if
• new onset < 48 hrs
• TEE r/o left atrial clot
• after 3-6 weeks of warfarin w INR 2-3
What is atrial flutter?
Etiology (atrial)
- circular movement of electrical activity around the atrium at a rate of approx 300X/min

S/S
- asymptomatic
- palpitations, syncope, lightheadedness

ECG
- regular rhythm
- "saw tooth" appearance of P waves
- atrial rate 240-320 bpm
- ventricular rate approx 150 bpm

Tx
- ABCD as in A-fib
- Anticoagulate if
• CHADS2 score > 2 (CHF, HTN, Age > 75, DM, Stroke/TIA)
• persists > 48 hrs to prevent CVA
- Rate control (beta-block, CCB, digoxin)
- Cardiovert if
• new onset < 48 hrs
• TEE r/o left atrial clot
• after 3-6 weeks of warfarin w INR 2-3
What is multifocal atrial tachycardia?
Etiology (atrial)
- multiple atrial pacemakers or reentrant pathways
- COPD; hypoxemia

S/S
- asymptomatic

ECG
- 3 or more unique P wave morphologies
- rate > 100 bpm

Tx
- underlying do
- rate control: beta-blocker; verapamil (CCB)
What is AVNRT (atrioventricular nodal reentry tachycardia)?
Etiology (AV junction)
- reentry circuit in the AV node depolarizes the atrium and ventricle nearly simultaneously

S/S
- palpitations, SOB, angina, syncope, lightheadedness

ECG
- rate 150-250 bpm
- P waves buried in QRS or right after QRS

Tx (same as AVRT)
- attempt to stop arrhythmia: carotid massage; Valsalva; adenosine
- cardiovert if hemodynamically unstable
What is AVRT (atrioventricular reciprocating tachycardia)?
Etiology (AV junction)
- ectopic connection between atrium and ventricle causing a reentry circuit
- WPW

S/S
- palpitations, SOB, angina, syncope, lightheadedness

ECG
- retrograde P wave after a normal QRS
- WPW: preexcitation delta wave

Tx (same as AVNRT)
- attempt to stop arrhythmia: carotid massage; Valsalva; adenosine
- cardiovert if hemodynamically unstable
What is paroxysmal atrial tachycardia?
Etiology (AV junction)
- rapid ectopic pacemaker in atrium (not the sinus node)

S/S
- palpitations, SOB, angina, syncope, lightheadedness

ECG
- rate > 100 bpm
- P wave w unusual axis before each normal QRS

Tx
- adenosine to unmask underlying atrial activity
What is WPW (Wolf-Parkison-White) syndrome?
Etiology (AV junction)
- similar to AVRT
- Bundle of Kent = ectopic connection between atrium and ventricle causing a reentry circuit -> ventricles depolarize earlier -> characteristic delta wave on ECG

S/S
- palpitations, SOB, angina, syncope, lightheadedness
- syncope w prodromal symptoms or signs of sz but unremarkable PE and abnormal ECG

ECG
- preexcitation delta wave

Tx
- advise against vigorous physical activity
- beta-block
- refer for electrophysiological study
What is PVC (premature ventricular contractions)?
Etiology (ventricular)
- ectopic beats arise from ventricular foci
- assoc w hypoxia, electrolyte abnormalities, hyperthyroidism

S/S
- asymptomatic; palpatations

ECG
- early wide QRS not preceded by P wave
- PVC followed by compensatory pause

Tx
- underlying cause
- symptomatic: beta-blockers; other antiarrhythmics
What is V-fib (ventricular fibrillation)?
Etiology (ventricular)
- assoc w CAD, structural heart dz, cardiac arrest/asystole

S/S
- syncope, absence of BP, pulselessness

ECG
- totally erratic wide complex tracing

Tx
- immediate electrical cardioversion and ALCS protocol
What is VT (ventricular tachycardia)?
Etiology (ventricular)
- assoc w CAD, MI, structural heart dz

S/S
- non-sustained VT: often asymptomatic
- sustained VT: palpitations, hypotension, angina, syncope; can progress to VFib and death

ECG
- 3 or more consecutive PVCs
- wider QRS complexes in regular but rapid rhythm
- AV dissociation possible

Tx
- antiarrhythmics: amiodarone, lidocaine, procainamide
- cardioversion
What is torsades de pointes?
Etiology (ventricular)
- assoc w long QT syndrome
- proarrhythmic response to meds, hypokalemia, congenital deafness, alcoholism

S/S
- palpatations, dizziness, syncope
- sudden cardiac death

ECG
- polymorphous QRS "twisting"
- VT w rates 150-250 bpm

Tx
- magnesium initially
- correct hypokalemia
- withdraw offending med
- cardioversion is unstable
What is CHF?
clinical syndrome caused by inability of the heart to pump enough blood to maintain fluid and metabolic homeostasis

risk factors: CAD, HTN, DM, cadiomyopathy, valvular dz

many classifications:
AHA/ACC; NYHA; systolic v non-systolic dysfunction; left v right failure; functional severity
What is the definition CHF?
A clinical syndrome due to inherited or acquired abnormality of cardiac structure or function causing an inability of the heart to pump enough blood to maintain fluid and metabolic homeostasis.

Systolic dysfunction:
- EF < 50%
- Inc LVEDV

Non-systolic dysfunction:
- Dec ventricular compliance
- NL systolic function
What is CHF due to systolic dysfunction?

Cause
S/S
PE
Dx
Tx
Low EF < 50% and Inc LVEDV (preload)

Caused by inadequate contractility and Inc afterload -> heart compensates dec EF and inc preload by hypertrophy and ventricular dilation -> compensation ultimately fails -> Inc myocardial work/worsening systolic function and eventual failure

S/S
- exertional dyspnea (earliest and most common)
- orthopnea, paroxysmal nocturnal dyspnea (PND), rest dyspnea
- chronic cough, fatigue, peripheral edema, nocturia, abdominal fullness

PE
- parasternal lift, elevated/sustained LV impulse, S3/S4 gallop, JVD, peripheral edema

Dx
- clinical
- CXR: cardiomegaly, pulmonary vessel cephalization, pulmonary effusions, vascular congestion, interstitial edema, prominent hila
- Echocardiogram: dec EF and ventricle dilation
- Labs: BNP > 500 pg/mL; inc creatinine; dec Na
- ECG: nondiagnostic but helps w etiology

Tx (acute):
- aggressive diuresis (loop and thiazides)
- ACEI (ARBs if cannot tolerate ACEI)
- beta-blockers contraindicated if DEcompensated CHF but indicated once pt is euvolemic
- LMNOP for pulmonary congestion (P = position upright)

Tx (chronic):
- control comorbidities
- beta-blockers and ACEI/ARBs (prevent remodeling and dec mortality)
- daily ASA
- statin
- diuretic (loop +/- thiazide)
- spironolactone (dec mortality in NYHA III-IV)
- anticoagulate if previous embolic event
- consider ICD if EF < 35%
- consider mechanical ventricular assist device/transplantation if unresponsive to max tx
What are the risk factors for CHF?

What are the S/S of CHF?
Risk factors: CAD, HTN, DM, cardiomyopathy, valvular heart dz

S/S
- exertional dyspnea (earliest and most common)
- orthopnea, PND, dyspnea at rest
- chronic cough
- fatigue
- peripheral edema
- nocturia
- abdominal fullness
What is CHF due to non-systolic dysfunction?

Cause
S/S
Tx
Dec ventricular compliance w normal systolic function due to impaired ventricular relaxation (ischemia, aging, hypertrophy) or impaired passive filling (scarring from MI, restrictive cardiomyopathy) -> Inc LVEDP but nl CO, and nl/inc EF

S/S
- stable/unstable angina, SOB, DOE, arrhythmias, MI, HF, sudden death

Tx
- first line = diuretics
- maintain HR and BP w beta-blockers, ACEI, ARBs, CCBs
- Digoxin usually ineffective
What are the classifications of CHF?
AHH/ACC classify according to clinical syndrome

Left- vs Right-sided

Systolic v Non-systolic

NYHA
I
- no limitation of normal activity
- no symptoms w normal activity
II
- slight limitation of activity
- comfortable at rest or mild exertion but normal activity may cause symptoms
III
- marked limitation of activity
- comfortable only at rest and even mild activity may cause symptoms
IV
- severe limitation of activity; discomfort w any activity
- symptoms at rest
What is the NYHA Functional Classification of CHF?
Class I
- no limitation of activity
- no symptoms w normal activity

Class II
- slight limitation of activity
- comfortable at rest or mild exertion

Class III
- marked limitation of acitivity
- comfortable only at rest

Class IV
- severe limitation/discomfort w any activity
- symptoms present at rest
Compare CHF due to systolic dysfunction v non-systolic dysfunction in regards to:

Age
Comorbidities
PE
CXR
ECG/Echo
Age
- systolic < 65
- non-systolic > 65

Comorbidities
- systolic: dilated cardiomyopathy, valvular dz
- non-systolic: restrictive or hypertrophic cardiomyopathy, renal dz, HTN

PE
- systolic: displaced PMI, S3 gallop
- non-systolic: sustained PMI, S4 gallop

CXR
- systolic: pulmonary congestion, cardiomegaly
- non-systolic: pulmonary congestion, nl heart size

ECG/Echo
- systolic: Q waves, dec EF < 40%
- non-systolic: LVH, nl EF > 55%
How can S/S distinguish left- from right-sided heart failure
Left-sided HF (dyspnea predominates)
- left-sided S3/S4 gallop
- bilat basilar rales
- pleural effusions
- pulmonary edema
- orthopnea
- PND

Right-sided HF (fluid retention predominates)
- right-sided S3/S4 gallop
- JVD
- hepatojugular reflex
- peripheral edema
- hepatomegaly (inc CVP -> inc resistance to portal flow -> "nutmeg" liver)
- ascites
How can you differentiate left- vs right-sided CHF from symptoms?
Left-sided CHF (dyspnea predominates)
- left-sided S3/S4 gallop
- bilateral basilar rales
- pleural effusions
- pulmonary edema
- orthopnea
- PND

Right-sided CHF (fluid retention predominates)
- right-sided S3/S4 gallop
- JVD
- hepatojugular reflex
- peripheral edema
- hepatomegaly
- ascites
Compare CHF due to systolic dysfunction vs non-systolic dysfunction based on:

Age
Comorbidities
PE
CXR
ECG/Echo
Age:
- systolic < 65
- non-systolic > 65

Comorbidities
- systolic: dilated cardiomyopathy, valvular dz
- non-systolic: restrictive or hypertrophic cardiomyopathy, renal dz, HTN

PE
- systolic: displaced PMI, S3 gallop
- non-systolic: sustained PMI, S4 gallop

CXR
- systolic: pulmonary congestion, cardiomegaly
- non-systolic: pulmonary congestion, nl heart

ECG/Echo
- systolic: Q waves, dec EF (< 40%)
- non-systolic: LVH, nl EF (> 55%)
How do you Dx CHF?
Clinical syndrome

CXR: cardiomegaly, cephalization of pulmonary vessels, pleural effusions, vascular congestion, interstitial edema, prominent hila

Echo: reduced EF, ventricular dilation

Labs: BNP > 500 pg/mL; inc creatinine; red Na

ECG: non-diagnostic but helps w etiology
How do you Tx Acute CHF?

How do you Tx Chronic CHF?
Acute CHF
- tx underlying cause
- aggressive diuresis (loops and thiazides)
- ACEIs or ARBs
- beta-blockers if pt euvolemic (contraindicated in decompensated CHF)
- LMNOP

Chronic CHF
- limit dietary Na and fluid intake
- beta-blockers
- ACEIs/ARBs (help prevent remodeling; dec mortality)
- daily ASA
- statin
- spironolactone (dec mortality)
- anticoagulate if prior embolic event
- ICD if EF < 35%
- mechanical ventricular assist device/cardiac transplantation if unresponsive to max tx
How do the different cardiomyopathies differ based on:

Major abnormality
LVED size
LVES size
EF
Wall thickness
Major abnormality
- dilated: impaired contractility
- restrictive: impaired elasticity
- hypertrophic: impaired relaxation

LVED size
- dilated: inc
- restrictive: inc
- hypertrophic: dec

LVES size
- dilated: inc
- restrictive: inc
- hypertrophic: dec

EF
- dilated: dec
- restrictive: dec or nl
- hypertrophic: inc or nl

Wall thickness
- dilated: dec/variable
- restrictive: inc/variable
- hypertrophic: inc
What is dilated cardiomyopathy?

Causes
S/S
PE
Dx
Tx
Most common cardiomyopathy

Causes: most idiopathic
- secondary (ABCD): Alcohol abuse, wet Beriberi, Coxsackie B viral myocarditis, Chronic Cocaine use, Chagas' dz, Doxorubicin
- hemochromatosis, peripartum cardiomyopathy, HIV, parasites
- most common secondary = ischemia and HTN

S/S
- gradual development of CHF symptoms

PE
- displaced LV impulse, JVD, S3 > S4 gallop, mitral/tricuspid regurgitation

Dx
- LV dilation and reduced EF required for Dx
- Echo diagnostic
- ECG: non-specific ST-T changes, low-voltage QRS, sinus tachycardia, ectopy, LBBB
- CXR: enlarged, "balloon-like" heart and pulmonary congestion

Tx
- CHF symptoms (diuretics, ACEIs/ARBs, beta-block; digoxin; avoid CCB in HF)
- anticoagulation if AF or thrombus present
- ICD if EF < 35%
What is restrictive cardiomyopathy?

Causes
S/S
PE
Dx
Tx
Reduced elasticity of myocardium -> diastolic/impaired diastolic filling w/o systolic dysfunction (nl EF)

Causes: infiltrative dz (amyloidosis, sarcoidosis, hemochromatosis); or scarring/fibrosis (radiation); or Loffler's syndrome (endomyocardial fibrosis w prominent eosinophilic infiltrate)

S/S and PE: right > left-sided HF (JVD, peripheral edema)

Dx
- Echo is diagnostic: rapid early filling and near-normal EF
- CXR/MRI/cardiac cath: etiology (sarcoid etc)
- Cardiac bx
- ECG: LBBB; low voltages in amyloidosis

Tx
- tx limited, mostly palliative
- diuretics for fluid overload
- vasodilators to dec filling pressures
What is hypertrophic cardiomyopathy?

Causes
S/S
PE
Dx
Tx
Thickened ventricular walls -> Impaired LV relaxation and filling = Non-systolic dysfunction

Commonly thickened IV septum -> LV outflow obstruction -> impaired ejection of blood

Congenital = 50% HOCM is autosomal dominant
- most common cause of sudden death in young, healthy athletes
- assoc w Friedreich's ataxia
Other causes = HTN, aortic stenosis

S/S
- asymptomatic
- syncope, dyspnea, palpitations, angina, sudden cardiac death

PE
- sustained apical impulse
- S4 gallop
- systolic crescendo-decrescendo murmur (inc: dec preload eg standing/Valsalva or dec: inc preload eg passive leg raise)

Dx
- Echo is diagnostic: asymmetrically thickened septum and dynamic obstruction of blood flow
- ECG: LVH
- CXR: left atrial enlargement (2/2 mitral regurg)

Tx
- beta-blockers for initial symptomatic relief
- CCBs second line
- surgery: dual-chamber pacing, partial excision, EtOH ablation of myocardial septum, ICD placement, mitral valve replacement
- avoid intense athletics/exertion
What are 4 signs of hyperlipidemia?
Atheromas: plaques in blood vessel wall

Xanthomas: plaques or nodules composed of lipid-laden histiocytes in the skin
- especially the eyelids = xanthelasma

Tendinous xanthoma: lipid deposits in tendon
- especially Achilles

Corneal arcus: lipid deposits in cornea, nonspecific (arcus senilis)
What are the 3 types of atherosclerosis?
Arteriolosclerosis:
- essential HTN or DM = hyaline thickening of small arteries
- malignant HTN = hyperplastic "onion skinning"

Artherosclerosis:
- fibrous plaques and atheroma in the intima of medium and large muscular arteries (abd aorta > coronary > popliteal > carotid)
- risk factors: smoking, HTN, DM, HL, FHx
- complications: aneurysms, ischemia, infarction, PVD, thrombus, emboli
- S/S: angina, claudication, or asymptomatic

Monckeberg:
- calcification in the media of the arteries (esp radial/ulnar)
- "pipestem" arteries
- usually benign; doesnt obstruct blood flow or involve intima
What is CAD?

What are the risk factors for CAD?

What are CAD risk equivalents?
CAD: narrowing of coronary arteries
- manifests as stable or unstable angina, SOB, DOE, arrhythmias, MI, HF, sudden death

Risk factors: age (M>45; F>55), male, inc LDL, HDL < 40, DM, HTN, FHx, smoking, PAD
- HDL > 60 is a negative risk factor (-1)

Risk equivalents: DM, PAD, AAA, symptomatic carotid artery dz
What are the different types of angina?
Angina occurs > 75% stenosis

Prinzmetal's variant
- occurs at rest 2/2 coronary artery spasm
- ST elevation on ECG during attack
- negative cardiac enzymes

Stable
- 2/2 atherosclerosis
- ST depression on ECG
- retrosternal chest pain w exertion

Unstable
- new onset chest pain or changing of prior stable angina
- thrombosis but no necrosis
- ST depression on ECG
- worsening chest pain at rest/minimal exertion
What are the S/S of angina pectoris (stable angina)?

What are the PE findings?

How do you Dx?

How do you Tx?
S/S
- classic triad: substernal chest pain, precipitated by exertion/stress, relieved by rest/nitrates
- radiating pain (jaw, shoulder), SOB, nausea/vomiting, diaphoresis, lightheadedness

PE
- carotid/peripheral bruits
- HTN

Dx
- exercise/drug stress test w ECG: ST changes is diagnostic
- serial cardiac enzymes to r/o acute MI
- atypical/silent MIs: women, DM, elderly, post-heart transplant pts

Tx
- admit until acute MI is r/o by serial cardiac enzymes
- acute: ASA, O2, IV nitroglycerin, IV morphine, consider IV beta-blockers
- chronic: ASA, nitrates, beta-blockers (CCBs are second line)
- risk factor reduction
* only ASA and beta-blockers have mortality benefit in tx of angina
What is ACS?
A spectrum of clinical syndromes caused by plaque disruption or vasospasm leading to acute myocardial ischemia:

- Unstable angina
- Non-STEMI
- STEMI
What is the difference between unstable angina and NSTEMI?

How do you Dx?

How do you Tx?
Unstable angina: new onset chest pain or changing of prior stable angina (pain w less exertion, longer lasting, less responsive to tx, occurs at rest)
- sign of impending infarction from plaque instability
- no elevation of cardiac enzymes (TnI or CK-MB)

NSTEMI: myocardial necrosis w elevation of TnI and CK-MB w/o ST elevations on ECG

Dx
- risk stratify by TIMI (thrombolysis in MI)
- cardiac enzymes (not elevated in UA/elevated in NSTEMI)
- ECG: ST changes

Tx
- acute (same as stable angina): admit, ASA, O2, IV NG, IV morphine, IV beta-blocker, as well as, clopidogrel, UFH, or enoxaparin based on TIMI
- IV heparin and angiography w possible revascularization (PCI or CABG)
What is STEMI?

What are the S/S and PE findings?

How do you Dx?

How do you Tx?

What are the possible complications?
ST elevations w cardiac enzyme elevation 2/2 prolonged myocardial ischemia and necrosis

S/S
- acute, substernal chest pain/tightness/pressure radiating to neck, jaw, arm, shoulder
- diaphoresis, N/V, SOB, DOE, lightheadedness, anxiety, syncope

PE
- arrhythmias, hypotension (cardiogenic shock), new CHF findings
* best predictor of survival = LV EF

Dx
- ECG: ST elevation or new LBBB; ST depression can indicate posterior wall infarct
- sequence of ECG changes: peaked T-waves -> ST-elevation -> Q-waves -> T-wave inversion -> ST-normalization -> T-wave normalization
- cardiac enzymes: TnI, CK-MB, CK index (CK-MB/total-CK)

Tx
- C'MON ABS: clopidogrel, morphine, O2, nitrates, ASA, beta-blockers, statins (chronic tx)
- beta-blocker contraindicated if pt in HF or cardiogenic shock -> ACEI/ARBs if not hypotensive
- emergent angiography and PCI w/in 90 min
- if PCI cant be done and thrombolytics arent CI'd and w/in 3 hrs from onset, then thrombolysis w tPA, streptokinase

Complications
- arrhythmias (most common)
- reinfarction, LV wall rupture, VSD, pericarditis, papillary rupture, LV aneurysm, mural thrombi
- Dressler's syndrome
What are the 7 components of the TIMI score?
History
- Age at least 65
- >3 CAD risk factors
- CAD
- ASA used in past 7 days

Presentation
- severe angina (at least 2 episodes w/in 24 hrs)
- ST deviation at least 0.5 mm
- elevated cardiac markers
What is the timeline of post-MI complications?
First day: HF
2-4 days: arrhythmias, pericarditis
5-10 days: LV wall rupture (-> acute pericardial tamponade causing electrical alternates, PEA); papillary muscle rupture (-> severe mitral regurg)
Weeks-Months: ventricular aneurysm; Dressler's syndrome (auto-immune fever, pericarditis, pleural effusion, leukocytosis, inc ESR)
What is dyslipidemia?

What are some causes?

What are the S/S and PE?

How do you Dx?

How do you Tx?
Dyslipidemia = total cholesterol > 200 mg/dL; LDL > 130 mg/dL; TG > 150 mg/dL; HDL < 40 mg/dL

Causes: obesity, DM, alcoholism, hypothyroidism, nephrotic syndrome, hepatic dz, Cushing's syndrome, OCPs, diuretics, familial hypercholesterolemia

S/S
- no specific s/s
- xanthomas, xanthelasmas, lipemia retinalis

Dx
- fasting lipid profile if at least 35 yo
- fasting lipid profile if at least 20 yo w known risk factors (eg CAD) -> repeat every 5 years

Tx
- based on risk stratification
- first line = 3 month trial of diet and exercise in pts w no known atherosclerotic vascular dz
- lipid-lowering agents: statins, fibrates, ezetimibe, niacin, colesevelam/cholestyramine
Statins
Atorvastatin (Lipitor), Simvistatin (Zocor), Lovastatin, Pravastatin, Rosuvastatin (Crestor)

MOA: HMG-CoA reductase inhibitor (inhibits rate limiting step of cholesterol synthesis)
- dec LDL and TGs

S/E
- inc LFTs
- myositis; rhabdomyolysis
- warfarin potentiation
Fibrates
Gemfibrozil

MOA: lipoprotein lipase stimulator -> inc VLDL and TG catabolism
- dec TG
- inc HDL

S/E
- GI upset
- cholelithiasis
- myositis
- inc LFTs
Cholesterol absorption inhibitors
Ezetimibe (Zetia)

MOA: inhibits cholesterol absorption at small intestine brush boarder
- dec LDL

S/E
- diarrhea
- abdominal pain
- angioedema
Niacin
Niacin (Niaspan; vitamin B3)

MOA: dec FA release from adipose tissue / dec hepatic synthesis of LDL
- dec LDL
- inc HDL
Bile acid resins
Cholestyramine; Colesevelam; Colestipol

MOA: binds intestinal bile acids -> dec bile acid stores and inc catabolism of LDL from plasma
- dec LDL

S/E
- constipation
- GI upset
- LFT abnormalities
- myalgias
- dec absorption of other drugs from small intestines
How do you risk stratify dyslipidemia to determine LDL goal and treatment initiation?
0-1 risk factors
- LDL goal: < 160
- start lifestyle mod w LDL > 160
- start drug tx w LDL > 190

2+ risk factors
- LDL goal: < 130
- start lifestyle mod w LDL > 130
- start drug tx w LDL > 130

CAD or CAD equivalents
- LDL goal: < 100
- start lifestyle mod w LDL > 100
- start drug tx w LDL > 100
What is the JNC-7 classification of HTN?
Normal
< 120/<80
- encourage lifestyle modification
- no meds

PreHTN
120-139/80-89
- lifestyle modification
- no meds

Stage 1 HTN
140-159/90-99
- lifestyle modification
- thiazide diuretics for most
- ACEIs/ARBs, beta-blockers, CCBs, or combo may be considered

Stage 2 HTN
> 160/>100
- lifestyle modification
- 2 drug combo (thiazide diuretic + ACEI/ARB, beta-blocker, or CCB)
What is essential HTN?

Risk factors?

Dx?

Tx?
Primary or Essential HTN - no identifiable cause
- 95% of cases

Risk Factors
- FHx, high-Na diet, smoking, obesity, ethnicity (black > white), advanced age

S/S
- asymptomatic until complications
- end-organ damage (stroke, dementia, vision changes, proteinuria, CKD, renal bruits

Dx
- U/A, BUN/Cr, CBC, Chem panel

Tx
- r/o secondary causes
- lifestyle modifications (wt loss most effective)
- BP goal < 140/<90 for most
- BP goal < 130/<80 for DM or renal dz w proteinuria
- first line meds: diuretics, ACEIs, beta-blockers dec mortality
- periodically test for end-organ damage
What is Secondary HTN?
Secondary HTN = HTN due to identifiable cause
- only 5% of cases

CHAPOS:
Cushing's syndrome
- ACTH-producing pituitary tumor/ectopic ACTH-secreting tumor/cortisol-secreting adrenal tumor/exogenous steroids
- tx: surgical resection/dc exogenous steroids

Hyperaldosteronism (Conn's syndrome)
- aldosterone-producing adrenal adenoma
- classic triad: HTN, hypokalemia, metabolic alkalosis
- dx: inc aldosterone and dec renin levels
- tx: surgical resection

Aortic coarctation
- unequal arm BPs
- tx: surgical correction

Pheochromocytoma
- epi/norepi-secreting adrenal tumor
- headache, sweating, tachycardia
- dx: urinary metanephrines and catecholamines; plasma metanephrines
- tx: pretx w both alpha- and beta-blockers before surgical resection

OCP use
- women: > 35, obese, long-standing use
- d/c use

Stenosis of renal artery
- new onset of HTN < 25 yo or > 50 yo
- etiologies: fibromuscular dysplasia (younger) or atherosclerosis (older)
- dx: renal artery U/S or MRA
- tx: angioplasty or stenting; ACEI if unilateral; surgery possible
What are the hypertensive crises?
Hypertensive crises = spectrum of d/o in which elevated BP causes end organ damage (Dx'd based on end organ damage, not BP)

Hypertensive Urgency
- elevated BP w mild-moderate symptoms (headache, chest pain) w/o end-organ damage
- Tx: oral anti-hypertensives to gradually lower BP over 24-48 hrs

Hypertensive Emergency
- elevated BP w s/s of end-organ damage (AKI, ICH, papilledema, ECG changes)
- Tx: IV anti-hypertensives to lower MAP < 25% in first 2 hrs to prevent cerebral hypo perfusion or coronary insufficiency

Malignant Hypetension
- Dx: progressive renal failure and/or encephalopathy w papilledema
Loop Diuretics
Furosemide, Ethacrynic acid, Bumetanide, Torsemide

Site of Action: Loop of Henle

MOA:
- dec Na/K/2Cl cotransporter
- inc Ca excretion
- dec urine concentration

S/E
- ototoxicity
- hypokalemia
- hypocalcemia
- dehydration
- gout
Thiazide Diuretics
HCTZ, Cholorthiazide, Chlorthalidone

Site of Action: Early distal tubule

MOA:
- dec NaCl resorption -> dec diluting capacity of nephron
- dec Ca excretion

S/E
- hypokalemic metabolic alkalosis
- hyponatremia
- hyperGLUC (-glycemia, -lipidemia, -uricemia, -calcemia)
K-sparing Diuretics
Spironolactone, Amiloride, Triamterene (SAT)

Site of Action: Cortical collecting tubule

MOA:
- spironolactone: aldosterone receptor antagonist
- amiloride/triamterene: block Na channels

S/E
- hyperkalemia
- gynecomastia
- sexual dysfunction
Carbonic Anhydrase Inhibitors
Acetazolamide

Site of Action: Proximal convoluted tubule

MOA: NaHCO3 diuresis -> dec total NaHCO3

S/E
- hyperchloremic metabolic acidosis
- neuropathy
- NH3 toxicity
- sulfa allergy
Osmotic Diuretics
Mannitol

Site of Action: Proximal tubule

MOA: inc tubular fluid osmolarity -> inc urine flow

S/E
- pulmonary edema
- dehydration

Contraindicated in anuria and CHF
Beta-Blockers
Propranolol, Metoprolol, Nadolol, Atenolol, Timolol, Carvedilol, Labetalol

MOA: dec cardiac contractility and renin release

S/E
- bronchospasm
- bradycardia
- CHF exacerbation
- impotence
- fatigue
- depression
ACEIs
Captopril, Enalapril, Benazepril, Lisinopril, Fosinopril

MOA: blocks aldosterone formation -> dec peripheral vascular resistance and dec salt/water retention

S/E
- cough (vs ARBs)
- angioedema
- rashes
- leukopenia
- hyperkalemia
ARBs
Losartan, Valsartan, Irbesartan

MOA: blocks aldosterone formation -> dec peripheral vascular resistance and dec salt/water retention

S/E
- no cough (vs ACEI)
- rashes
- leukopenia
- hyperkalemia
CCBs
Dihydropyridine: Nifedipine, Felodipine, Amlodipine

Non-dihydropyridine: Diltiazem, Verapamil

MOA: dec smooth muscle tone -> vasodilation; dec cardiac output

S/E
Dihydropyridine: headache, flushing, peripheral edema
Non-dihydropyridine: dec contractility
Vasodilators
Hydralazine, Minoxidil

MOA: dilation of arteries/arterioles -> dec peripheral resistance

S/E
Hydralazine: headache, lupus-like syndrome
Minoxidil: orthostasis, hirsutism
alpha1-Adrenergic Blockers
Prazosin, Terazosin, Phenoxybenzamine

MOA: blocks NE on vascular smooth muscle -> vasodilation

S/E
- orthostatic hypotension
Centrally-Acting Adrenergic Agonist
Methyldopa, Clonidine

MOA: central alpha2-adrenergic receptors -> inhibits sympathetic nervous system

S/E
- somnolence
- orthostatic hypotension
- impotence
- rebound hypertension
What is pericarditis?

What are causes of pericarditis?

S/S?

PE?

Dx?

Tx?
Inflammation of pericardial sac

Causes: CARDIAC RIND
- Collagen vascular dz
- Aortic dissection
- Radiation
- Drugs
- Idiopathic (most common)/Infections (viral/TB)
- Acute renal failure
- Cardiac (MI)
- Rheumatic fever
- Injury
- Neoplasm
- Dressler's syndrome

S/S
- pleuritic chest pain, worsens while supine; dyspnea, cough, fever

PE
- pericardial friction rub, elevated JVP, pulsus paradoxus (dec SBP > 10 on inspiration)

Dx
- CXR, ECG, Echo r/o MI, PNA
- ECG: diffuse ST-elevation; PR-depression; T-wave inversion
- Echo: pericardial thickening or effusion

Tx:
- underlying causes and symptoms
- avoid corticosteroids w/in few days post MI (can cause wall rupture)
- pericardial effusion: monitor w/o symptoms, pericardiocentesis if e/o tamponade
What is cardiac tamponade?

What are risk factors?

S/S?

PE?

Dx?

Tx?
Excess fluid in pericardial sac -> compromised ventricular filling and dec CO
- rate of effusion is more important than size

Risk Factors:
- pericarditis
- malignancy
- SLE
- TB
- trauma (stab wound medial to left nipple)

S/S:
- fatigue, dyspnea, anxiety, tachycardia, tachypnea -> rapid progression to shock and death

PE:
- acute: Beck' triad (JVD, hypotension, distant heart sounds), narrow pulse pressure, pulsus paradoxes, Kussmaul's sign (JVD on inspiration)

Dx:
- Echo: right atrial/right ventricular diastolic collapse
- CXR: enlarged, globular, "water-bottle" shaped heart w large effusion
- ECG: electrical alternans is diagnostic for large effusion

Tx:
- Aggressive volume expansion w IV fluids
- Urgent pericardiocentesis (aspirate will be non-clotting blood)
- Decompensation may warrant pericardial window
What is the most common cause of valvular heart dz in US adults?
Mechanical degeneration

Previously rheumatic fever (affecting the mitral valve > aortic valve) but now mechanical degeneration
Aortic Stenosis

Etiology

Hx

PE

Dx

Tx
Etiology
- most often in the elderly; unicuspid/bicuspid valves can cause symptoms in childhood/adolescence

Hx
- asymptomatic despite significant stenosis
- once symptomatic, -> angina -> syncope -> CHF -> death w/in 5 yrs
- ACS (indication for valve replacement): angina, CHF, syncope

PE
- pulsus parvus et tardus (weak and delayed carotid pulse)
- single or paradoxically split S2
- systolic murmur radiating to carotids

Dx
- echocardiography

Tx
- aortic valve replacement
Aortic Regurgitation

Etiology

Hx

PE

Dx

Tx
Etiology
- acute: infective endocarditis, aortic dissection, chest trauma
- chronic: valve malformations, rheumatic fever, connective tissue d/o

Hx
- acute: rapid onset of pulmonary congestion, cardiogenic shock, severe dyspnea
- chronic: slowly progressive DOE, orthopnea, PND

PE
- blowing diastolic murmur at left sternal boarder
- Austin Flint murmur (mid-diastolic murmur)
- midsystolic apical murmur

Dx
- echocardiography

Tx
- vasodilators (dihydropyridines or ACEIs) for isolated AR until severe enough for valve replacement
Mitral Valve Stenosis

Etiology

Hx

PE

Dx

Tx
Etiology
- most commonly due to rheumatic fever

Hx
- dyspnea, orthopnea, PND
- infective endocarditis, arrhythmias

PE
- opening snap
- mid-diastolic murmur at apex
- pulmonary edema

Dx
- echocardiography

Tx
- anti-arrhythmias (beta-blockers, digoxin) for symptomatic relief
- mitral valve valvotomy and valve replacement if severe
Mitral Valve Regurgitation

Etiology

Hx

PE

Dx

Tx
Etiology
- most commonly due to rheumatic fever or chord tendinae rupture after MI
- infective endocarditis

Hx
- dyspnea, orthopnea, fatigue

PE
- holosystolic murmur radiating to the axilla

Dx
- echocardiography: regurgitant flow
- angiography: assess the severity

Tx
- anti-arrhythmics
- valve repair/replacement if severe
What are the 4 major vascular dz disorders?
Aortic Aneurysm

Aortic Dissection

DVT (deep vein thrombosis)

PAD (peripheral arterial dz)
Aortic Aneurysm
> 50% dilation of all 3 layers of the aortic wall
- most commonly assoc w atherosclerosis
- most are abdominal and >90% are below renal arteries

S/S
- asymptomatic, usually found incidentally on PE or radiology

Risk Factors
- HTN, HL, other vascular dz, FHx, smoking, males, age

PE
- pulsatile abdominal mass
- abdominal bruit
- ruptured aneurysm -> hypotension, severe, tearing abdominal pain radiating to the back

Dx
- all men 65-75 w h/o smoking screen for AAA w U/S
- abdominal U/S for dx or follow aneurysm
- CT w contrast: precise anatomy

Tx
- asymptomatic and < 5 cm, monitor
- if > 5.5 cm (abd), > 6 cm (thoracic), or smaller but rapidly enlarging, surgical repair
- symptomatic or ruptured aneurysms, emergent surgery
Aortic Dissection
Transverse tear in intima of a vessel -> blood entering media -> false lumen -> hematoma that propagates longitudinally
- most commonly due to HTN
- most common site of origin: above aortic valve; distal to left subclavian artery
- 40-60 yo males

Classification (Stanford) - A or B
- A (proximal): involves ascending aorta or arch, proximal to left subclavian
- B (distal): involves descending aorta only, distal to left subclavian

S/S
- sudden, tearing/ripping pain in anterior chest (ascending) or back (descending)
- HTN; if pt hypotensive, consider pericardial tamponade, hypovolemia from blood loss, or other cardiopulmonary d/o
- asymmetric pulses and BP
- if aortic valve is involved, AR murmur
- if aortic arch or spinal arteries involved, neurological deficits

Dx
- CTA is gold standard
- MRA if CTA is contraindicated
- TEE for anatomy

Tx
- manage HR and BP
- avoid thrombolytics
- beta-blockage before vasodilators to prevent reflex tachycardia
- Standford A (ascending, proximal to left subclavian): surgical emergency
- Stanford B (descending, distal to left subclavian): HR and BP control
DVT
Clot formation in large veins of extremities or pelvis

Virchow's triad:
- endothelial damage (surgery, trauma)
- veno/hemostasis (plane flights, bed rest, incompetent venous valves)
- hypercoagulability (malignancy, pregnancy, OCPs)

S/S
- unilateral lower extremity pain and swelling
- Homan's sign: calf tenderness w passive foot dorsiflexion (poor sensitivity/specificity)

Dx
- Doppler U/S
- Spiral CT or V/Q scan for PE
- d-dimer to r/o PE in low risk pts

Tx
- anticoagulate: IV UFH or SQ LMWH followed by PO warfarin for 3-5 mo
- IVC filters if contraindications to anticoagulation or recurrent DVTs while on anticoagulation
- DVT ppx for hospitalized pts: SQ UFH or LMWH, compression stockings, exercise as tolerated/early ambulation
PAD
Restriction of blood supply to extremities by atherosclerotic plaques
- lower extremities most commonly affected

S/S
- intermittent claudication (reproducible, relieved by rest)
- with progressive dz, pain at rest and more distal extremities
- dorsal ulceration due to hypoperfusion
- 6 Ps of acute ischemia: Pain, Pallor, Paralysis, Pulse deficit, Paresthesia, Poikilothermia
- "blue toe syndrome" = acute ischemia 2/2 cholesterol emboli
- chronic ischemia: muscle atrophy, pallor, cyanosis, hair loss, gangrene/necrosis
- aortoiliac: buttock claudication, dec femoral pulses, male impotence (Leriche's synd)
- Femoropopliteal: calf claudication, dec pulses below femoral)

Dx
- ABI = P(leg)/P(arm) < 0.4 -> rest pain
- ABI can be falsely nl or high if arteries are calcified
- Doppler U/S: stenosis/occlusion
- Surgical evaluation: arteriography and digital subtraction

Tx
- exercise helps develop collateral circulation
- ASA, cilostazol, thromboxane inhibitors for symptoms
- angioplasty and stenting
- surgery (arterial bypass) or amputation
Lymphedema
Disruption of lymphatic circulation -> peripheral edema and chronic infection of the extremities
- often a complication of lymph node dissection
- underdeveloped countries: parasitic infection -> lymphatic obstruction
- congenital malformation: Milroy's dz -> lymphedema in childhood

S/S
- unexplained swelling of upper extremities in post-mastectomy pts
- immigrants w progressive swelling of lower extremities w no cardiac abnormalities (filariasis)
- children w swelling (Milroy's dz)

Dx
- clinical
- r/o other edema causes (cardiac, metabolic d/o)

Tx
- symptom management (exercise, massage, pressure garments)
- diurectics are ineffective and relatively contraindicated
- monitor for cellulitis w prompt gram(+) Ab coverage
Syncope
A sudden, temporary loss of consciousness and postural tone 2/2 cerebral hypoperfusion

- Cardiac: valvular, arrhythmias, PE, cardiac tamponade, aortic dissection
- Non-cardiac: orthostatic/hypovolemic hypotension, neurologic (TIA/stroke), metabolic abnormalities, neurocardiogenic syndrome (vasovagal/micturition syncope), psychiatric

S/S
- triggers, prodrome, assoc symptoms
- cardiac: brief/absent prodrome, exertion, lack of assoc w changes in position, h/o cardiac dz

Dx
- Holter monitor or event recorder
- echocardiogram
- stress test (ischemia)
- tilt-table testing (neurally mediated syncope)

Tx
- underlying cause, most commonly beta-blockers for rate control
- cardiac syncope is assoc w 1-yr sudden cardiac death rates up to 40%