Cholesterol / Dyslipidemia

Cholesterol / Dyslipidemia
Screening:
·       If ≥35 q5 years
·       If ≥20 w/ CAD RF q5 ys
Dx
·       Total > 200
·       LDL >130
·       TG >150
·       HDL <40
Tx
1˚: 12-week diet & exercise
2˚ Meds
When it is an option, the right answer is always:
1. Lifestyle = Diet / Exercise
2. Adherence = Medication and Lifestyle
·       So, you wanna 1) start those who need statin on HIGH-INTENSITY Statins –> if they are intolerant (hepatitis, renal, myositis) –> 2) reduce the intensity for them and be MODERATE-Intensity
Who Needs a Statin?
1. Vascular Disease = MI, CVA, PVD, CS
2. LDL > 190
3. LDL 70-189 + Age + Diabetes
4. LDL 70-189 + Age + Calculated Risk = “Risk Factors”
Risk Factors for Coronary Artery Disease
1. Diabetes
2. Smoking
3. Hypertension
4. Dyslipidemia
5. Age > 55 for women, > 45 for men
Drugs

Valvular disorders

Benign Vs Pathologic murmurs
Benign
Pathologic
Hx
      Normal appetite, energy, activities and growth
      No important Family Hx
      Diaphoresisi and fatigue with feeding or workout, poor weight gain, chest pain, dizziness, syncope, shortness of breath
      Family Hx of sudden cardiac death, heart defects, etc
Feature
      Early or mid-systolic
      Grade I or II intensity that decrease on standing and Valsalva maneuver 
      Low pitched, musical, pure, or squeeky tone at LLSB (still’s murmur) or high pitched at LUSB (Pulmonary flow murmur)
      Harsh, holosystolic, diastolic
      Grade III intensity or higher
      ️ with standing and Valsalva maneuver
Other findings
      None
      Loud, fixed split, or single S2
      ⤵️ or absent femoral pulses
 Workup
      None indicated
      ECG (to assess for hypertrophy)
      Echocardiogram (to assess for structural abnormalities)
      Cardiology Referral
Murmur
Location
Leg Raise
Valsalva
Tx
Path
Presentation
Def Tx
Mitral Stenosis
diastolic w/ openin snap
Apex
Get worse
Improves
Preload Reduction
Rheumatic Fever
Afib, CHF
SOB
Replace
Aortic Stenosis
Systolic / Crescendo-decrescendo
Aortic w/ radiation to Carotids
Get worse
Improves
Preload Reduction
Calcification Bicuspid
Angina, CHF
Syncope
Replace
Mitral Regurg
Systolic
Apex to Axilla
Get worse
Improves
Preload Reduction
Infxn Infarction
CHF
Replace
Aortic Regurg
Diastolic
Aortic
Get worse
Improves
Preload Reduction
Infxn Infarction
CHF
Replace
HCOM
Systolic
Apex
Improves
Get worse
Increase Preload
Congenital
SOB, Sudden Death
Replace
Mitral Valve Prolapse
Systolic
Apex
Improves
Get worse
Increase Preload
Congenital
CHF
Replace
Venous Return / Preload
Afterload
Drugs
Increase
(leg raise/ squat)
Decrease
(Valsalva/standing)
Increase
Decrease
Diuretics
ACEIs
(Handgrip)
(amyl Nitrate)
MS, AS
️(AS)
️(AS)
Yes, but better
Negligible Effect in (MS)
AS (Replace)
MR, AR
VSD
HOCM
MVP
Auscultation findings:
Innocent murmur
·       3-7 yo ped
·       systolic, grade 2, never diastolic
·       can happen when ⤴️ CO (fever)
·       best heard @ Left Lower sternal border
·       reassure
Pulmonary flow murmur
·       also innocent murmur
·       heart at 2nd left intercostal
·       while pt laying down
·       high-pitch, early systolic
Venous hum
·       why?
·       heard in neck / anterior chest
·       disappear w/ compression of jugular v
Machinary murmur
·       PDA
ASD
·       Ejection murmur
·       Wide fixed spilitting of P2
Prosthetic Valve Dysfunction
?
      Transvalvular regurgitation (cusp degeneration)
      Paravalvular leak (annular degeneration, IE)
      Obstruction/stenosis of the valve (valve thrombus)
Clx
      New murmur (regurgitant or stenotic)
      Macroangiopathic hemolytic anemia
      HF symptoms, thromboembolism
 Dx
      Echocardiography
Chronic AR
?
      Congenital bicuspid aortic valve
      Post inflammatory (rheumatic heart disease, endocarditis)
      Aortic root dilation (Marfan syndrome, syphilis)
 Path
      Backflow from aorta into LV à ⤴️ LV EDV
      LV compensates w/ eccentric hypertrophy à ⤴️ SV & CO
      Eventual LV dysfunction à ⤵️  SV & COà HF
 Clx
      Diastolic decrescendo murmur (best heard w/ pt sitting up, leaning forward, full expiration + at 3rd-4th left intercostal space)
      Widened pulse pressure (⤴️ SBP & ⤵️ DBP)
      Rapid rise-rapid fall (“water-hammer”) pulsation
      Abrupt carotid distension & collapse, “pistol-shot” femoral pulses
MS
🔉
·       Holosystolic murmur
·       Apex
·       S3
S/S
·       SOB
·       pHTN
·       Eccentric LV hypertrophy
·       ⤴️ LA pressure → HF
Dx
TTE

Aortic Diseases / Injuries

Aortic dissection
Approach
·       1st: look at the vitals
·       if hypertensive –> Labetalol (keep systolic 120-100)
·       if BP is not controlled w/ labetalol –> Add nitroprosside
o   never give it w/o BB → since it induces reflexive tachycardia → causing more damage
Dx Work-up
Spiral CT w/ contrast
·       Pt is Clx stable
·       Often 1˚ & done in ER
TEE
·       Clx unstable (VS UNSTABLE)
·       Allergic to contrast
·       has kidney failure
·       Must intubuate
MRI
·       Chronic
·       Clx stable
Acute Aortic Dissection
Clx
·       PMHx: Hypertension, genetic do (Marfan)
·       intense, sharp, tearing chest or back pain
·      >20 difference in Systolic BP bw arms
 Dx
·       ECG:
·       CXR: mediastinal widening
·      CT angiography or TEE for final diagnosis
 Tx
·       Pain control (morphine)
·       IV BB (Esmolol)
·       ± Sodium nitroprusside (if SBP >120 mm Hg)
·       Emergent surgical repair for ascending dissection
AAA
RF
·       Advanced age (eg, >60)
·       Smoking, male 🤵🏻, HTN
·       Hx of atherosclerosis or Autoimmune
S/S
Mostly Asx
Rapid expansion
·       Dull abdominal/back pain (can be referred)
·       Distal embolization
Rupture
·       Sudden, severe abdominal/back pain ± shock
·       Umbilical/flank hematoma
·       Syncope
Tx
·       Smoking cessation
·       Elective repair for size >5.5 cm (Asx)
·       Urgent repair for sx & HD stable
·       EMERGENT repair for sx & HD unstable
AAA
Aortic Dissection
S/S
·       Pulstile abdomenal mask,
·       Can present as back pain,
·       Incidentally found on CT.
·       >65 male
·       Atherosclerotic
·       RF: SMOKING
·       HTN
·       TEARING Chest pn radiating to back
·       Asymmetric BP in arms
·       Widened mediastinum
Dx
·       US
·       X-ray: prevertebral aortic calcification
·       NOT CT
·       NOT ARTERIOGRAM
BEST? CT ARTERIOGRAM
NOT ARTERIOGRAM
Tx
Strategy:
If VS stable: CT
If VS unstable → SURGERY + US
If small AAA –> wait & screen.
If big AAA or growing fast, I shall operate.
>3.5 cm –> screen q1 year
>4.5 cm –> screen q6 months
>5.5 / growin fast (0.5 per 6 m) –> SURGERY
Type A (Ascending): OR –> offer aortic valve replacement
Type B (Descending): IV BB
Traumatic carotid injuries
Mechanism
·       Penetrating trauma
·       Fall with object in mouth (eg, toothbrush, pencil)
·       Neck manipulation (eg, yoga, sports)
Clx
·       Gradual-onset hemiplegia
·       Aphasia
·       Neck pain
·       “Thunderclap” headache
Dx
·       CT or MR angiography

Arrhythmias (To be updated)

Tachyarrhythmias
Bradyarrhythmias
Heart Block:
Mobitz type I
Mobitz type II
Level of block
Usually AV node
Below the level of AV node (Bundle
of His)
ECG
Progressive prolonged PR interval leads to a nonconducted P wave
(“group beating”)
PR interval remains constant with intermittent nonconducted P waves
QRS complex
Narrow
Narrow
Exercise or atropine
Improves type I AV block
Worsens type II AV block
Vagal maneuvers 
Worsens
Paradoxically improves
Risk of complete heart block
Low risk
Higher risk, indication for pacemaker

Cardiomyopathy

 Dilated
Features
Etiologies of Dilated (Congestive) Cardiomyopathy
• Idiopathic: most common
• Alcoholic (dx of exclusion / complete abstinence from alcohol leads to NORMALIZATION)
• Peripartum
• Postmyocarditis due to infectious agents
• Doxorubicin
• Metabolic: chronic hypophosphatemia, hypokalemia, hypocalcemia, uremia
S/S
HF
Dx
·       Clx
·       X-ray: cardiomegaly / pulmonary congestion
·       Echo
Tx
Tx just like HF
 HOCM
Features
·       Chromosome 14
·       Sarcomere gene mutation
·       AD (variable penetration)
S/S
·       Can be Asx
·       Systolic Ejection murmur that ⤴️ by ⤵️ preload / afterload
·       Fatigue, chest pain, SOB, Syncope
·       Sudden death.
Dx
·       ECG: LV hypertrophy
·       Echo: ⤴️ LV outflow tract gradient, Systolic anterior motion of Mitral valve
·       Family screening
Tx
·       BB
·       CCB
·       Surgery
Avoid:
Digitalis
• Diuretics (do not ⤵️ PRELOAD)
• Vasodilators
• Exercise
 Restrictive
Features
• Infiltrative:
·       sarcoidosis/amyloidosis;
·       Hemochromatosis;
·       Neoplasia
• Scleroderma
• Radiation
S/S
HF
Dx
Echo
Tx
There is no good therapy; ultimately results in death from CHF or arrhythmias; consider heart transplantation.
Viral Myocarditis
Clx
      Relatively young adults (age <60)
      Viral prodrome (Fever, malaise, myalgias)
      CHF → can lead to dilated heart
      Chest pain
      Sudden cardiac death
 Dx
      ECG: Nonspecific
      Echo: 4-chamber dilation
      Cardiac MRI: Late improvement of the epicardium
      Biopsy: Lymphocytic infiltration, viral DNA or RNA
 Tx
      CHF 💊 (Diuretics, ACEI, 8B)
      Temporary ventricular assist device, if needed
      If no recovery → Heart transplant

Pericardial Disorders

Etiology for Pericarditis
Infections
Viral (coxsackie)
Bacterial (Strep/Staph)
Tuberculosis
Fungus
Autoimmune
 Lupus, Rheumatoid, Scleroderma
Procainamide, Hydralazine Uremia
 Trauma
Blunt, Penetrating
Cancers
Lung, Breast, Esophagus Lymphoma
Others
Many
Pericardial Disease Treatment
Pericarditis
NSAIDs + Colchicine
Pericardial effusion
Pericarditis
Recurrent Effusion
Pericardial Window
Tamponade
Pericardiocentesis
Constrictive Pericarditis
Pericardiectomy
Acute Pericarditis
Features
many causes (check table)
S/S
Pleuritic chest pain
Dx
ECG
Tx
NSAID + Colchicine
Constrictive pericarditis Features
Etiology
      Idiopathic or viral pericarditis
      Cardiac surgery or RTx
      Tuberculosis (in endemic areas)
Pathogenesis
      Thickened, rigid pericardium forms a noncompliant casing surrounding the heart, limiting ventricular expansion during diastolic filling
Hemodynamic signs
      ⤴️ Jugular venous pressure
      Kussmaul sign
      Pulsus paradoxus
      Pericardial knock
Pericardial Effusion
Features
·       Fluid may accumulate in the pericardial cavity in virtually all forms of pericardial disease.
S/S
JVP / SOB / Pulsus Paradoxus (exagerated BP fall during inspiration by >10)
Dx
ECHO
Tx
·       Fluid aspiration
·       Management of acute pericarditis etiology
·       If recurrent: pericardial window
 Post-pericardiotomy syndrome
?
Inflammation → reactive pericarditis
S/S
·       Infants: abdominal pain / vomiting
·       Older children: pericarditis
·       Can progress to temponade (beck’s triad)
CXR
Cardiomegaly
Tx
Pericardiocentesis

Syncope

Generalized SZ
Trigger:
• Fever
• Hypoglycemia
• Sleep deprivation
Clx:
• +/- Aura
• Loss of consciousness & tone, tonic-clonic convulsions
• Postictal state
Vasovagal Syncope
Trigger:
standing
Physical/emotional
Clx:
-Presyncope (lightheadedness, pallor, diaphoresis)
-Immediate retum to baseline
Cardiogenic Syncope
Trigger:
• Exertion
• Dehydration
Clx:
-Sudden loss of
consciousness
without prodrome
– Immediate retum to
baseline after event
Syncope
Path
Hx
Physical
Dx
VV (Vaso Vagal)
– Visceral Organs (micturition, defecation, cough)
– Carotid Stimulus (turning head, shaving)
– Psychogenic (see blood)
– Situation- related
– Prodrome (eg, pallor, nausea, diaphoresis)
Vagal stimulation
produces asystole
or a ⤵️SYS BP of
50 mmHg
Tilt table
Orthostatics
⤵️ Volume
– Autonomic Nervous Dysfunction
Orthostatic
hypotension
Defined as
⤵️SYSBP by 20
⤵️DIA BP by 10
⤴️HR by 20
Sxs of orthostasis
Volume and Reassess, chase causes of hypotension if
refractory to fluid
Mechanical Cardiac
Exertional syncope
Murmur
Echo
Arrhythmia
Onset is sudden,
unprovoked,
None
24-hour Holter
Neuro (vertebrobasilar insufficiency
Onset is sudden,
unprovoked, very rare
Focal Neurologic Deficit
CTA
Pulmonary Embolism
Electrolytes (bG, TSH)
PE
None
PE
None
Wells criteria, CT scan
BMO
Vasovagal syncope
Clx
      Inciting event (stress, prolonged standing)
      Prodrome (pallor, nausea, diaphoresis)
      Rapid regain of consciousness (<1 minute)
Dx
      Primarily clinical diagnosis
      Upright tilt table testing in uncertain cases
Tx
      Reassurance
      Triggers avoiding
      Counterpressure techniques for recurring episodes
Types of syncope
Types
Causes
Characteristic
Cardiogenic
Mechanical (AS. PS, HOCM…)
Arrhythmias
No prodome
Vasomotor (the most common)
• Excessive vagal tone
• Impaired reflex control of the peripheral circulation
Has prodome: Lightheadness. nausea, sweating, ringing ears. Trigger: stressful situation
Orthostatic Hypotension
• Hypovolemia
• Decrease BP > 20/10 mmHg
Think in elderly. blood loss. use of diuretics, vasodilators
Neurogenic
 • Loss of sympathetic nervous system tone
Decrease BP due to vasodilation

Hypertension

Start w/
Thiazide
African-American
Thiazide
Essential Tremor
BB
Perioperative HTN
BB
Hyperthyroidism
BB
Migraine
BB/CCB
Raynaud’s
CCB
DM
ACEI
Osteoporosis
Thiazide
BPH
alpha 1 blocker


Malignant HTN
Hypertensive Encephalopathy
·       PMHx: Long standing uncontrolled HTN
·       End-organ damage (but no CNS Sx)
·       PMHx: Long standing uncontrolled HTN
·       Cerebral edema d/t breakthrough vasodilation from failure of autoregulation
·       Eye: retinal FLAME hemorrhage, Papilledema, exudates
·       AKI: nephrosclerosis (∆ AKF, Hematuria, Proteinuria)
·       NO CNS Sx
·       Headache
·       N/V
·       Non-localizing neurologic Sx (restlessness, confusion, SZ, coma)
·       can develop ICH/SAH

Antihypertensive that can cause hyperprolactinemia?
·       Methyldopa
·       Reserpine
·       Verapamil
 Secondary HTN DDx
Renal Disease
 ⤴️ Cr
Renal a. Stenosis
 SEVERE HTN + Abdominal bruit
Hyperaldosteronism
HTN + ⤴️ Na + ⤵️ k+
Pheochromocytoma
Episodic SEVERE HTN + HEADACHEs
Cushing
Typical Sx
Hypothyroidism
Fatigue, dry skin, cold intolerance
HyperPTH
Sx of hypercalcemia (kidney stones)
CoA
difference in BP b/w arms & legs

Congestive Heart Failure

Clx Features of Acute decompensated heart failure
S/S
      Acute SOB, orthopnea, paroxysmal noctumal dyspnea
      HTN is common; hypotension suggests severe disease
      Accessory muscle use, tachycardia, tachypnea
      Diffuse crackles with possible wheezes (cardiac asthma)
      Possible S3, JVP distention, peripheral edema
 Tx
or ⤴️ BP:
      O2
      IV loop diuretic (Furosemide)
      Consider IV vasodilator (Nitroglycerin)
Hypotension/Shock
·       O2
      IV loop diuretic (Furosemide)
      IV vasopressor (Norepinephrine)
 HF w/ preserved EF
?
·       LV diastolic dysfunction: HTN / Restrictive / Hypertrophic cardiomyopathy
·       Valvular heart disease: Aortic / Mitral valves
·       Pericardium: Constrictive pericarditis
·       Systemic disorders (high-CO): Thyrotoxicosis, severe anemia, large AV fistula
Tx
·       Control BP & HR
·       Address concurrent conditions: AF & Ml
·       Tx hypervolemia w/ diuretics
·       Exercise / cardiac rehabilitation

Pt
Tx
Everybody
Salt <2g per day
H2O < 2L, per day
ACEI or ARB (best mortality benefit)
Beta -Blocker
Preload Reduction
Diuretics such as Furosemide
Nitrates such as Isosorbide Dinitrate
Dietary Modifications (NaC1, H20)
Afterload Reduction
ACEI or ARB
Hydralazine
Spironolactone
Special Considerations
EF < 35%
AICD (must be Class I-III)
Ischemic
ASA and Statin
Class IV
Inotropes like Dobutamine (ICU)
VAD bridge to transplant
Transplant
💊 that improve mortality in LV systolic failure/CHD
BB
ACEI
Minalocorticoid receptor blocker (eplerenone, spironolactone)
Statin
Dual Antiplatelets (Aspirin + Clopidogril)
In African-american pt 👨🏾‍⚖️: Hy nigga (Hydralazine +  Nitrate)
EXACERBATION
When a CHF pt comes w/ acute pulmonary edema?
Everyone
·      Lasix (Furosemide)
·      Morphine
·      Nitrates
·      O2
·      Position
If it fails →
·       Dobutamine
o   If fails + no hypotension → Hydralazine
o   If fails + hypotension → Dopamine

Poor prognostic factors in systolic heart failure
Clx
• Higher NYHA functional class
• Resting tachycardia
• Presence of S3
• JVP Elevation
• Low BP (<100/60)
• MR
Lab
• Hyponatremia
• Elevated BNP levels
• Renal insufficiency
ECG
• QRS duration >120 msec
Echo
• Severe LV dysfunction
• Concomitant diastolic dysfunction
• Reduced right ventricular function
• Pulmonary hypertension
Association
• Anemia
• Atrial fibrillation
• DM

Cor Pulmonale
?
·       PULMONARY-RELATED
·       COPD
·       Interstitial Lung dz
·       PE
·       OSA
Sx
·       SOB
·       Syncope on exertion (d/t ⤵️ CO)
·       Angina on exertion (d/t ⤴️ heart demand)
PEx
·       Peripheral edema (LL, Ascites)
·       ⤴️ JVP
·       Loud S2
·       Right-sided Heave
·       Hepatomegaly
·       TR Murmur
Dx
·       ECG: RBBB / RV hypertrophy / Right axis deviation
·       Echo: pHTN, dilated RV, TR
·       heart catherization: gold standard: RV failure.

Digoxin toxicity
Cardiac
·       severe arrhythmias
 GI
·       Anorexia
·       Nausea & vomiting
·       Abdominal pain
 Neuro
·       Confusion
·       Faintness
·       Color vision changes

Coronary Artery Disease

Notes from OME (Provided for free)

Treatment of chronic stable angina
Beta blockers
      1st -line therapy
      ⤵️ Myocardial contractility & HR
Nondihydropyridine CCBs
      Alternative to beta blocker
      ⤵️ Myocardial contractility & HR
Dihydropyridine CCBs
      Added to beta blocker when needed
      Coronary artery vasodilation
      ⤵️ Afterload by systemic vasodilation
Nitrates
      Long-acting added for persistent angina
      ⤵️Preload by dilation of capacitance veins
Ranolazine
      Alternative therapy for refractory angina
      ⤵️Myocardial calcium influx

Stable angina
Unstable Angina/NSETMI
STEMI
·       Most patients with angina will have ECG changes during an attack? ST depression
·       Dx: Stress test:
o   Target: 85%*(220-age)
o   Contraindication: MI, dissection, AS, HOCM, uncontrolled HTN
o   Stop BB 24 h prior to procedure
o   Digoxin causes ST depression –> make it hard to interpret the results
o   Stress test in young females? False positive
·       Tx:
o   OP: BASA – BB / Aspirin / Statin / ACEI (everybody gets statin) –> if there’s pain (NGT) / If there’s stent (clopidogril)
o   For episodes: NTG
o   Long-term: NGT + BB –(no contraindications)–> Aspirin + Statins
o   Modify RFs
o   Cath –> to see if they need bypass
o   When to give antihyperlipidemia?
·       Bottom line: almost all patients with chronic stable coronary artery disease will likely need to be on statin therapy, unless contraindicated.
·       Target: LDL <100 / <70 if IHD + DM / ACS
·       If there are no detectable serum markers of myocardial injury 12–18 hours after symptom onset, the patient should be diagnosed with UA.
·       At the time of presentation, UA and NSTEMI may be indistinguishable and can be identically managed.
·       Thrombolytic therapy is beneficial in patients with STEMI, but is not effective in UA or NSTEMI and may be harmful.
·       In fact, untreated UA progresses to MI in 50% of cases –> Tx is IP
·       In NSTEMI –> ECG can be normal
·       Tx: BANC Cath
o   NGT
o   Aspirin for all pts + another antiplatelets: Clopidogrel + Heparin
o   BB
o   Take them to cath lab (ASAP)
·       Cardiac exam will usually be normal.
·       Tx:
1.     MONA BASH C
·       M: Morphine
·       O: O2
·       N: NGT
·       A: ASA
·       B: BB
·       A: ACEI
·       S: Statins
·       H: Heparin
·       C: Clopidogrel (or other antiplatelets)
2.     REPERFUSION:
·       EMERGENT CATH –> PCI
·       Fibrinolytics (within 60 min + no near facility to transfer)
o   Late presentation (>12 hours after symptom onset): Reperfusion therapy with either PCI or fibrinolysis is not recommended in patients who are asymptomatic and hemodynamically stable, and who present >12 hours after symptom onset.
o   Drugs to use w/ reperfusin:
·       Clopidogrel or prasugrel should be prescribed in addition to aspirin for patients undergoing PCI with a stent / Fibrinolytics. Ticagrelor is an alternative to clopidogrel or prasugrel.
·       If CABG –> NO Clopidogrel ❌❌❌❌
·       if Stent: keep clopidogrel for 12 m / if fibrinolytics: keep for 1 m
·       Give unfractionated heparin to all
·       GP IIb/IIIa inhibitors should be avoided with fibrinolytic therapy as there is evidence of excessive bleeding
o   If Left main coronary (or equivelant: 70% proximal LAD + LCX) –> CABG
o   If DM –> CABG
Absolute Contraindications to tPA
Relative
ICH
Poorly controlled HTN
Structural vascular lesion
Ischemic stroke > 3 months
Intracranial mass
Dementia
Ischemic stroke w/i 3 months
Major surgery w/i 3 weeks
Hemorrhagic stroke anytime
Internal bleeding w/i 3 weeks
Aortic dissection
Active bleeding
Hx of diabetic retinopathy

Notes from UW:

Complications of Femoral a. Cath
Cholesterol embolism
·       Pain + skin changes
·       livedo reticularis
·       Ischemic ulcers
·       Cyanosis
·       Gangrene
·      
Femoral pseudoaneurysm
·       loss of distal pulses
·       pulsitile mass post-cath
·       Systolic bruit
Retroperitoneal bleeding
·       back pain
·       sudden drop in Hct
·       purpura in lower back