All cardiac terms:

Know the following definitions

• Preload: the filling V of the ventricle at the end of diastole

  • Determinants: Total BV returning, distribution of BV, atrial compliance, compliance

• Afterload: the amount of resistance against which the ventricle pumps (against the aorta > pulm artery)

  • Dependent on: aortic P & V of ventricle cavity/thickness of ventricular wall

• SV: amount of blood pumped per minute

• EDV-ESV

• CO: average 5 L/min, amount of blood pumped per min

  • CO=SV x HR

  • Affected by preload, afterload, HR, contractility

    • Contractility = force generated by the ventricular performance

      • Frank-starling mech can inc, VH inc

• EF: a %, not CO

  • EF = SV/EDV x 100

  • Normal: 55-70%

  • Measure via: MUGA, Echo, Cath

• MAP: mean arterial pressure

  • MAP = DBP + 1/3PP

  • Generally 60-100 mmHg in healthy pts

• PP: pulse pressure

  • PP = SBP -DBP

  • Usually around 40 in healthy pts

• Sterling’s law: “the greater the stretch the greater the force of the next contraction”

  • Ie: greater the EDV (pre) the great the V of blood ejected (SV)

  • Inc this = inc contractility -> inc SV -> inc CO

• Renin-Angiotensin Aldosterone System-RAAS

  • Renin released from JG apparatus in low V states -> tell liver to switch angio to angio 1 -> ACE cleave 2 peptides = angio 2 (vasoconstrictor) -> aldosterone inc -> Na and water retention

Cardiac signs & symptoms

forms of dyspnea (dyspnea = abnormally uncomfortable awareness of breathing; may cause pt to tripod)

• Orthopnea: dyspnea upon assuming the supine posture

• Trepopnea: dyspnea occurs only in lateral decubitus position

  • Most often in pts w/ heart disease

• Platypnea: dyspnea that occurs only in the upright position

• Bendopnea: dyspnea caused by bending over as in tying one’s shoe

Other cardiac sx

• Palpitations: characterized by an awareness of the heartbeat

  • Can be due to rate or rhythm changes, inc contraction force, other cardiac

  • Can be due to Psychiatric conditions: anxiety, depression, panic disorder

  • NEED to describe onset, duration, associated sx w/ circumstances in which they occur

    • Intermittent/sustained, reg or irreg, abrupt onset/term vs gradual

• Syncope: sudden loss of consciousness

  • Usually cardiac -> vasovagal due to hypoperfusion

• Schamroth’s sign: indicates clubbing is present!!

  • Touch finger tips together (nail side) -> do not form Schamroth’s window = clubbing

• Clubbing: enlargement of distal phalanges w/ flattening of nail at the cuticle

  • Late finding

  • Associated w/ cyanotic heart dz, advanced chronic pulm dz, biliary cirrhosis, colitis, sickle cell, thyrotoxicosis

• Cardiovascular causes of chest pain

  • Angina, MI, Pericarditis (knifelike, friction rub), Aortic dissection (knifelike)

Signs of HF

• right vs left heart failure signs

  • usually a mix of the 2

    • only just right when due to lung problem (Cor pulmonale)

  • Right

    • JVP, hepatojugular reflux, liver congestion, ascites, leg edema

  • Left

    • PND, orthopnea, bibasilar rales

Risk factor stratification: ASCVD

• Big 6

  • modifiable

    • smoking/tobacco use, HTN, DM, HLD

  • NON modifiable

    • Age, FMHx

• ASCVD > 10 = high risk for CVD events, prevent score: >20% = high risk for CVD events

  • 10 yr risk: > 7.5% intermediate; >20 % high

JVP waveforms and significance of each

• Large “a” wave

  • Tricuspid stenosis, pulm HTN, pulm stenosis

• Cannon wave

  • A fib, complete heart block, VVI pacing, vent tachy

  • Occurs when the RA contracts against closed tricuspid valve

• Steep “x”, “y” descent

  • Constrictive pericarditis, cardiac tamponade

• Large “v” wave, “cv” wave

  • Tricuspid regurgitation

• Kussmaul’s sign!!!

  • Rise of JVP on inspiration, constrictive pericarditis, cardiac tamponade

Pulses and their disorders

Pulses

• Reg irreg: barely palpable

  • 2^nd degree AV block, vent bigeminy, A flutter

• Irreg irreg: barely palpable

  • A fib, frequent vent ecotopic beats

• Slow rising: low gradient upstroke

  • AS

• Pulsus paradoxus: exaggerated fall in pulse V on inspiration (>10)

  • Cardiac tamponade, acute asthma

• Corrigan’s pulse: unusually large carotid pulsation

• water-hammer pulses (collapsing): wide pulse pressure

  • steep up and down stroke

  • lift arm so the wrist is above heart

  • AR, patent ductus arteriosus

• bounding: large volume

  • anemia, hepatic failure, type 2 resp failure

• Pulsus alternans: alt large and small V pulses

  • Bigeminy

• pulsus bisferiens: double peaked pulse -2^nd peak can be smaller, larger, or same

  • AR, hypertrophic cardiomyopathy

Signs secondary to pulses

• Traube’s sign: pistol-shot burit over femoral pulse

• Quincke’s sign: pulsatile blanching and reddening of fingernails upon light pressure

• De musset’s sign: head bobbing caused by carotid pulsations

• Muller’s sign: pulsatile bobing of the uvula

• Duroziez’s sign: to & fro murmur over femoral artery, heard best w/ mild pressure applied to the artery

NYHA Classifications I through IV

**based on how limited they are during physical activity (SOB/angina), determines prognosis

• Class I: pts w/ NO limitation of activities; they suffer no sx from ordinary activities

• Class 2: pt w/ slight, mild limitation of activity; they are comfortable w/ rest or w/ mild exertion

• Class 3: pt w/ marked limitation of activity; comfortable on at rest

• Class 4: pts/ who should be at complete rest, confined to a bed or chair; any physical activity brings on discomfort and sx occur at rest

All heart sounds

normal & abnormal (valvular murmurs and effects with maneuvers, gallops, bruits, venous hum), grading of murmurs

Normal vs Abnormal

Normal: S1 & S2

• S1: mitral – tricuspid

• S2: aortic – pulm (in split A heard first)

Abn: S3 & 4

• Gallops

  • S3: ventricular gallop sys-to-lEE

    • CHF, V overload, sloshing dilated wall

  • S4: atrial gallop di-as-sto-lEE

    • LVH, stiff rigid noncompliant wall

• Bruits

  • waterfall like sound over arteries

• Venous hum

  • Mostly in kids, after 2 y/o

  • Infraclavicular, louder on right

  • Continuous, musical hum of grade 1-2

  • Turning neck, supine, and compressing jugular resolves the murmur

Others

• Fixed splitting = ASD

• Opening snap = MS

• Ejection clicks= AS

• Mid-systolic clicks=MVP

• Friction rubs = pericarditis

Valvular murmurs + maneuver effects

• Best dx test for valvular dz? -> ECHO tte or tee

• Nearly all diastolic murmurs are pathologic, many systolic are benign

  • Pathologic: all pan or holosystolic, late systolic

• RILE: right on inspiration, left on expiration (when louder)

• Inc murmur: inspiration, squatting & lying w/ legs elevated (inc preload)

  • Handgrip ->inc afterload: stenotic (-MS) dec, regurg inc

• Dec murmur: standing, Valsalva (dec pre)

  • Amyl nitrate (dec after)

    • Stenotic (-MS) inc, regurg dec

  • HOCOM & MVP do opposite

    • Inc w/ Valsalva and standing, amyl nitrates

    • Dec w/ squatting, passive leg raising, handgrip

    • Respirations have no effect

Systolic

• AS (MC): ejection clicks, paradoxical splitting, inc on expiration

  • Triad: exertional dypsnea, syncope, angina

  • Crescendo-decrescendo, systolic

  • Heard at: RUSB radiating to neck, paradoxical split S2

  • Pulsus parvus et tardus

  • Dx: tee tx: valve replacement

• MR (MC) MVP is most common cause

  • Holosystolic murmur, loud high pitched

  • Heard at: Apex, radiates to left axilla

  • Dx: Tee & color doppler echo

  • LVH, LAE, cardiomegaly

  • Tx = surgical repair >>> replacement

• Tri regurg

  • High pitch, blowing holosystolic or pansystolic murmur

  • heard at: LLSB

  • Louder w/ inspiration

  • Endocarditis

    • Osler, janeyway, roth

• VSD

• Pulmonic stenosis

  • Crescendo decrescendo ejection murmur

  • Heard at: Left upper sternal border

  • Inc with inspiration and radiates diffusely

  • tx: Valvuloplasty or replacement

Diastolic

• AR:

  • widened splitting

  • High pitched decrescendo diastolic

    • Apical low pitched diastolic rumble

  • Accentuated by sitting up/leaning forward

  • Austin flint murmur

  • Pulsus alternans & bisferens pulses

• MS:

  • Open snap; loud crisp S1, inc S2

  • Low pitched diastolic rumble

  • Heard best at the apex in the left lateral decumitus position

  • Accentuated w/ squatting and decreased w/ Valsalva or expiration

  • Bisferens pulsus or irregulary, irregular pulses if afib

  •  Occasional Ortner syndrome

  • Palpitations, HF, dyspnea on exertion

• Pulmonic regurg

  • Crescendo decrescendo early diastolic murmur

  • Heard at LUSD

  • Inspiration louder, Valsalva softer

  • Graham steell murmur of pulm HTN

    • More high pitched

• Tri stenosis

Other:

• PDA = continuous

• HOCOM = midsystolic, crescendo-decrescendo

• MVP

  • Click murmur or “Barlow’s syndrome”

  • MC valve abnormality

  • Mid systolic click & late systolic mumur at apex

  • Valsalva -> click heard earlier and more holosytolic and louder

Grading of murmurs (Levine scale)

• 1 = very soft only detected after very careful auscultation

• 2 = soft murmur that is readily evident

• 3= moderately intense murmur not associated w/ palpable thrill

• 4= loud murmur; palpable precordial thrill is present

• 5= loud cardiac murmur, palpable thrill; audible when rim of stethoscope lightly touches chest

• 6= loud murmur, palpable thrill, audible w/o stethoscope

HOCOM & MVP

·       HOCOM

·       MVP

All cardiac labs and tests

(cardiac enzymes, BNP, CXR, CIMT, CAC, MUGA, Holter monitors, Continuous Ambulatory BP (CABP) monitoring, LVEF, 2D echo & TEE.

·       Lecture 3: just make a knowt over the whole damn thing basically

IE prophylaxis and types (acute, subacute endocarditis)

Prophylaxis

• Prophylactic abx given to:

  • Pts w/ predisposing congenital or significant valvular abnormalities who undergo invasive procedures

  • New guidelines: routine prophylaxis is no longer recommended during a procedure

    • ONLY high risk groups get IE prophylaxis

    • All dental procedures involving manipulation of gingival tissue or periapical regionl of teeth or perforation of oral mucosa only

    • Procedures involving the respiratory tract or infected skin, skin structures, or MSK tissue. NOT for GI procedures or GU

    • Both only for pts w/ underling cardiac conditions associated w/ the highest risk of adverse outcome from IE

      • Not valvular disease

      • CHD: unrepaired, prosthetic material first 6 months post, repaired w/ residual defects at the site of patch /device

      • Cardiac transplant

      • Hx of IE or prosthetic valves

  • Take 1 hr prior to procedure: amoxicillin; PCN allergy: Clinda

Dx

• S/sx: fever, petechiae, Osler’s, Janeway, Roth spot’s lesions of retina

• Dx: TEE and Duke criteria

Duke criteria

• Major: 2 + blood cultures, echo show vegetation, abscess or dehiscence of a prosthetic valve

• Minor: predisposing condition, fever, 1 + blood culture, + echo no meeting major criteria, immunologic signs (rheumatoid factor, roth spots, osler’s nodes, glomerulonephritis)

• Dx: 2 major, 1 major 3 minor, 5 minor

Tx

• Tx: no IVDA – native valve empiric, culture pending

  • 1^st line: Beta lactam: Pen G or another cillin + Aminoglycoside (Gentamicin)

  • Alt: if PCN allergy: Vanc + aminoglycoside (Genta)

• Tx: IVDA – native valve empiric tx w/ culture pending

  • Vanc + Genta

    • Monitor Vanc trough levels

• Tx: prosthetic valve: trible abs empiric tx, culture pending

  • Vanc + Gentamicin + Rifampin

• TX overall

  • give empirical regimen until blood culture results are final

  • Nonemergent: 4-6 weeks Abx IV

  • Emergent: if unresponsive to IV after 7-10 days are more likely to need surgical valve replacement for eradication of vegetations

Acute vs Subacute

Acute

• MCC in IVDA: Staph Auerus

  • Tricuspid 80-90% valve affected in IVDA

• Develops very rapidly

• Causes valve damage

• Occurs in pts w/ normal hearts and already damaged hearts

  • IV drug abusers, prosthetic valves, septic conditions

Subacute

• MCC: Streptococcus viridans

• Develops gradually

• Heart usually already damaged

  • Congenital conditions, prosthetic valves, rheumatic heart disease

ARF and Jones criteria

Disease and Dx

• Dz: sequela of Group A beta-hemolytic strep (GAS) infection that causes chronic post-infectious inflammatory disease

  • No single sx make the dx, but evidence of strep is required

  • Most commonly affects the mitral valve

  • Typically 2-3 weeks post infection

• Dx: 2 major or 1 major and 2 minor + positive blood culture for GAS using Jones Criteria

  • can also use Labs:

    • NAAT vs RADT: isolation of GAS

    • Antibody titers: ASO, Anti-DNase B, AH, ASTZ

    • Acute phase reactants: high CRP & ESR    

Jones Criteria

• Major

  • Mneumonic: CCEPS plus strept

    • Carditis: Carey-combs murmur: short mid-diastolic mitral murmur

    • Chorea: involuntary movements, sudden, aimless, irregular

      • Rare but most diagnostic manifestation

    • Erythema marginatum: vary in size, clear centers

      • Trunk/proximal extremities, never on face, blanch

    • Polyarthritis: migratory, large joints >, can be a single joint

      • Lasts 1-5 weeks, 1^st line: prompt response to tx doses of NSAIDS

    • Subcutaneous nodules: pea-sized, painless, non-tender

      • Prominent over bony prominences

• Minor

  • Arthralgias, fever, elevated ESR or CRP, prolonged PR interval, hx of ARF

Treatment

Tx: 75% subside w/in 6 weeks, 90% 12 weeks, chronic usually affects mitral valve -> MS

• 1^st line: acute therapy and primary prevention

  • Abx: Penicillin

    • Allergy -> Cephalosporin or Macrolide (azith, erythro)

  • Anti-inflammatory

    • ASA or corticosteroids (Prednisone) short course for arthritis

• Secondary prevention of recurrences

  • MC -monthly PCN shots

  • Duration uncertain up to 10yrs to life

  • Tx strep early!!

• Recurrent prevention of episodes that had Carditis:

  • Benzathine Pen G x 4 weeks

    • PCN allergy: Ceph or Macrolide

  • Durations:

    • Carditis and persistent heart disease: 10 yrs from last episode of ARF or until 40 y/o; whichever is longer

    • Carditis w/o persistent heart disease: 10 yrs from last episode of ARF or until age 21; whichever is longer

    • No Carditis: 5 years from the last episode of ARF or until 21, whichever longer

All congenital heart diseases including Coarctation of Aorta & Patent Foramen Ovale

Acyanotic

Acyanotic: congenital heart disease with a L to R shunt

AS:

• most develop sx during 5^th or 6^th decade

• Dx: TTE

• Sx: chest pain, syncope, CHF

• Tx: mild- none; severe- valve replacement

PS:

• usually isolated congenital lesion

• Sx: mild/mod -Asx; severe- progressive dyspnea & fatigue, -> RVH & dysfunction

• PE: RV lift, norm S1, soft P2 & delayed as severity increases; opening click, mid systolic high pitched crescendo-decrescendo @LUSB

• Dx: 2D TTE

• Tx: symptomatic w/ severe obstruction (>50mmHg) -> surg repair or percutaneous balloon valvuloplasty

ASD:

• F:M = 3:1

• Types:

  • Ostium secundum -involve fossa ovalis (PFO)

    • Known to cause thromboembolic events

    • Idiopathic strokes in YA and children

  • Ostium primum -involve AV junction

  • Sinus venosus -involve superior septum

• Sx: Asx until adulthood, sx usually secondary to RV dysfunction -fatigue, dyspnea

  • Afib common, irreversible pulm vascular obstruction w/ R to L shunting and cyanosis (Eisenmenger’s complex)

• PE: fixed split S2, mid systolic murmur @LUSB

• Dx: 2D TTE and color doppler echo

• Tx: surgical closure for pts w/ large defects

  • Ostium secundum, PFO, ASDs may be closed percutaneously

VSD:

• oxygenated blood from LV is shunted through VSD into RV

• rarely encountered in adults, 50% close spontaneously during childhood

• Most large defects are surgically corrected at an early age

  • If large: RV dilates and pulm BF inc; uncorrected: pulm vaso-occlusive obstruction -> Eisenmenger’s complex (don’t live long)

• Classified by location w/in IVS

  • Membranous or muscular IVS VSDs

  • AV canal VSDs

    • Common in Down syndrome

    • Associated w/ ostium primum ASDs

• PE: hyperdynamic precordium, holosystolic left parasternal murmur w/ thrill @LLSB

• Dx: 2DTTE and Doppler echo, cath necessary prior to surgical repair

• Tx: surgical closure, percutaneous transcatheter closure when pts are non-surgical candidates or if conduction abnormalities are a concern

PDA:

• more common in premature infants, maternal rubella is also a risk

• May be associated w/ coarctation of aorta and VSD

• Physio: failure to close results in persistent communication between aorta & pulm artery, hemodynamic consequences depend on size of ductus; large -> LV V overload and pulm vascular congestion

  • Persistent obstruction w/ Eisenmenger’s complex develops

  • LE cyanosis and clubbing, UE fine

• PE: loud continuous machinery-like murmur in left infraclavicular region

• Dx: 2D TTE and doppler echo; cath to confirm and exclude irreversible obstruction

• Tx: Tiny: IV Indocin (NSAIDS); Large: surgical closure unless irreversible pulm HTN; IE prophylaxis

Coarctation of aorta w/wo AS:

• fibrotic narrowing of the aortic lumen usually distal to the left subclavian artery

• 25% have bicuspid AV

• MC extracardiac abnormality is aneurysm of the circle of Willis

  • Screen pts for Berry aneurysms!!!

• Sx: produces obstruction to LV outflow ->

  • Rise in BP in proximal aorta and great vessels

    • Most cases are undx until workup for HTN

  • LVH develops; Untx: 2/3 pts w/ develop HF by 4^th decade

  • Complication: aortic dissection or rupture, CVA, IE

• PE: forceful carotid and UE pulses w/ weak and delayed LE pulses

  • Ejection murmur if bicuspid AoV

  • Systolic murmur @ LU back

• Dx: infants/kids: 2D echo and doppler; adults: MRI and cardiac cath

  • CXR: rib-notching or figure 3 sign

• Tx: surgical repair -adults; IE prophylaxis

Cyanotic

Cyanotic: reduced or diversion of oxygenated blood to the rest of the body

Eisenmenger’s syndrome:

• Initial: L -> R shunt, inc pulm blood flow

• Later (before puberty): pulm HTN -> reverse, so now R -> L flow w/ variable degrees of cyanosis (especially in LE) due to deoxy blood flowing to the body

• Due to ASD or VSD

• Sx: consequences of chronic cyanosis, thrombosis, pulm HTN, vaso-occlusive dz

• Tx: limited, meds for pulm HTN and vaso-occlusive dz, limit activity, phlebotomy, IE prophylaxis, surgery

  • Prognosis poor; high mortality

Ebstein’s anomaly

• Atrialized RV

• Associated w/ ASD, PFO, WPW

• Pathophysio: related to degree of tricuspid valve displacement

• Dx: CXR, ECG & TTE

  • CXR- giant RA & RV

• Tx: IE prophylaxis, possible surgical repair

Tetralogy of Fallot:

• 4 components PROV mnemonic (4 defects in 1)

  • Pulmonic valve or infundibular stenosis -> RV outflow obstruction

  • RVH

  • Overriding aorta across the VSD

  • VSD membranous

• Sx: cyanosis (worsens w/ exercise), clubbing, failure to gain wt, feeding difficulty

• Tx: surgery to repair RV outflow and VSD (infancy/childhood), IE prophylaxis

Transposition of the Great vessels (TGA)

• Aorta & pulm artery are switched

• Often coexists w/ other CHD’s (ASD, VSDA, PDA) to be able to deliver some oxy blood to body

• Dx: TTE

• Tx: surgery to correct the position of the vessels

HTN (essential, secondary, urgent, emergent, malignant) & all anti-HTN meds in algorithmic treatment

Essential vs Secondary

• SBP: first Korotkoff sound

• DBP: fifth Kortkoff soud

• PP: SBP-DBP

• MAP=DBP+1/3PP MidBP=avg BP

• BP readings

  • Normal BP: <120/<80; Elevated: 120-129/<80

  • HTN S1: 130-139/80-89; S2 >140/>90

  • Goals: <120/80; over 80 yo <140/90

• Dx hypertension: 2 or more high BP readings on 2 or more office visits about 2 weeks apart

  • Unless BP is severely high w/ unequivocal evidence of life-threatening end organ damage

  • Best way to dx: Home or continuous ambulatory BP monitoring

• Pathogenesis:

  • Arterial vasoconstriction/loss of elasticity -> Inc resistance (SVR) -> Dec flow to vital organs -> signal for more pressure -> neurohormonal responses

Essential: HTN w/ no identifiable or reversible cause

• Idiopathic or genetic, 95% of cases, FMHx

• Usually discovered in the 5^th decade, unremarkable PE

• Theorized cause: SNS hyperactivity, RAAS, defect in naturesis, intracellular Na/Ca, exacerbating factors: obesity, ETOH, inc Na intake, smoking, inactivity, NSAIDS, low K+

• Basic optional tests: fasting glucose, CBC, lipids, SCr w/ eGFr, serum Na K Ca, TSH, urinalysis

• Advanced tests: CXR, ECG

• Labs: uric acid, urinary albumin:Cr, ambulatory BP, home BP

Secondary: HTN w/ a known identifiable or reversible cause

• HTN is secondary to the problem or disorders

• Demands an aggressive workup, <20 or >50 must be considered

  • Also consider pts who are refractory to tx or need multiple meds

• Dx: CXR, EKG, Echo, Catecholamine levels, aldosterone levels urine electrolytes

• Consider: RA stenosis, fibromuscular dysplasia, renal insufficiency, renal parenchymal dz, endocrinopathies, coarctation of aorta

  • Adrenal: primary hyperalosteronism, cushings, pheochromocytoma

    • Primary hyperaldosteronism:

      • MCC -> Merkel Cell CA -unilateral adenoma (conn’s)

      • Excessive unregulated secretion of aldosteronone by adrenal cortex

      • Sx: muscle weakness and fatigue, polyuria, polydipsia

      • Dx: serum electrolytes, (maybe hypo K), adrenal CT/MRI,

        • Best: Ratio- Plasma aldosterone inc/renin dec

    • Cushings:

      • long term steroid tx or adrenal tumor

      • Sx: central obesity/moon face/buffalo hump, fatigue and proximal muscle weakness, hirsutism, purple skin striae, ecchymosis

      • Dx: inc serum/urine cortisol, dexa suppression test, hyperglyc, hypokalemia, adrenal CT/MRI, ACTH sampling

    • Pheochrom: adrenal tumor

      • Sx: sustained or paroxysmal HTN, sudden onset HA HTN sweating palpitations, anxiety, tremor, wt loss, ht intolerance, N, abd pain, CP, orthostatic hypotension w/ severe supine HTN

      • Dx: normal thyroid, urinary VMA, serum chromogranin A, CT MRI Nuc imaging, Urinary catecholamines & metanephrines and Cr during/after attack

      • Tx: removal

  • Renal: CKD, Renal AS, FMHx of PKD, analgesic use

    • RVD: HTN from excess renin due to low renal BF from stenosis

    • Suspect if: Sx LE atherosclerosis, renal bruit, severe/accel/malig HTN

    • ACE-I induced worsens renal function, reversible Cr elevation

    • Dx: elevated BUN/Cr, kid ultrasound, renal arteriogram (definitive), duplex RA sonogram

  • Other: OC, ETOH, NSAIDS, preggo, hyper Ca or TSH, OSA, obesity, coarctation of aorta, inc intracranial pressure

    • Coarc: localized narrowing of aortic arch

      • Young, HA, epistaxis, cold extremities, claudication

      • Diminished, delayed femoral pulse w/ differential BP between UE and LE, ejection murmur LSB and back

      • Associated w/ Bicuspid AV and Berry aneurysms

      • Dx: EKG -LVH, CXR -figure 3, ECHO, Ct, MRI, aortic angio

Urgent vs Emergent vs Malignant

• Both elevated BP >180-220 or diastolic >120

• Urgency: marked HTN w/o end-organ damage, usually Asx

  • Tx: bring BP down slow w/in several hours, rarely requires emergency therapy

    • PO: clonidine, Captopril (avoid in RAS suspected), Metoprolol (avoid if cocaine use), hydralazine

    • Avoid SA DHP CCB b/c BP reduction is often abrupt

• Emergent: marked HTN w/ end-organ damage

  • Damage seen in heart, brain, kidneys, retina

    • HTN encephalopathy (HA, AMS, confusion), HTN nephropathy, HTN retinopathy

  • Tx: dec in MAP by no more than 25% in 1-2 hrs, then reduce BP to 160/100 over next 6-12 hrs

    • Avoid excessive reduction -> coronary, cerebral, renal hypoperfusion

    • Key use meds w/ predictable, dose-dependent transient effects (IV)

      • Nicardipine, Labetalol, Nitroglycerin -pts w/ ACS

• Malignant = same as HTN emergency

  • Elevated BP w/ encephalopathy, nephropathy or HTN retinopathy

  • Systolic w/ wide PP: arteriosclerosis, AR, thyrotoxicosis, hyperkinetic heart syndrome, fever, arteriovenous fistula, patent ductus arteriosus

Tx

• Tx to avoid complications

  • CVA, dementia, MI, CHF, retinal vasculopathy, aortic dissection, nephrosclerosis, ESRD, malignant HTN, HTN urgency/emergency

  • Associated w/ preeclampsia, metabolic syndrome

• Lifestyle changes

  • Optimize wt, DASH diet, Adequate K/Ca/Mg intake, low Na intake, start exercise program, quit smoking, limit ETOH, optimize lipids, manage stress

• Race and Ethnicity

  • AA: initial tx include a thiazie diuretic or CCB

  • 2+ antiHTN meds are recommened to achieve BP of 130/80 in most adults, especially AA

• Preggo:

  • give: methyldopa, nifedipine, or labetalol

  • NO: ACEI, ARBs, or direct renin inhibitors

• Diuretics: good for fluid reduction

  • Thiazide: (-thiazide)

    • lower BP by dec plasma V, long term reduce PVR

      • Preferred over LOOP in HTN *unless renal dysfxn

    • Most effective in: blacks, elderly, obese, smokers

    • AE: inc lipids, rash, ED, hypoK

    • Chlorthalidone is now preferred of HCTZ

• BB: reserved for CAD (-olol)

  • Dec HR and CO and renin release

  • More effective in: young, white, post MI, stable HF, migraines, anxiety

  • SE: brady, bronchospasm, heart blocks, nasal congestion, Raynaud’s, CNS sx, nightmares, fatigue, ED, adverse lipid level effects

• ACE I: HF and DM (-pril)

  • gaining favor as first line

  • Primary mechanism of action inhibit RAAS, stimulate synthesis of vasodilating prostaglandins

  • Most effective in: young, white, DM, HF

  • Reduced mortality, MI, CVA in pts w/ CAD, stroke or PVD w/ DM and one other risk factor; risk of renal failure in bilateral RAS

  • SE: hyperK, chronic dry cough, dizziness, skin rash, angioedema, taste alt

• Angio 2 Receptor blockers: if ACEI isn’t tolerated (-artan)

  • Lower BP by blocking effects of Angio 2 at the receptor site

  • Can improve CV outcomes in pts w/ HTN, DM

  • Have not been compared to ACEI in RCT in HTN

  • Does not cause cough, minimal rash and angioedema (no kinin effect), still risk of renal failure in bilat RAS

• CCB: (-dipine)

  • Act on peripheral vasodilation negative inotrope effects (can worsen/cause CHF)

  • Protective against stroke

  • Most effective in: AA, elderly isolated systolic HTN

  • Usually in combo w/ diuretic/ACEI

  • SE: HA, periph edema, brady, Constipation,

    • DHP agents -> HA, flushing, palpitations, periph edema

• Alpha adrenoceptor antagonists: (-zosin)

  • Relax smooth muscle, lower PVR, tx BPH, + HDL effect

  • SE: tachyphylaxis, marked orthostatic hypotension, syncope, HA, palpitaitons, nervousness, inc in HF and CVA, avoid in cataract surgery as can cause floppy iris syndrome

• Central sympatholytic: least favored!! (clonidine, methyldopa)

  • Alpha adrenergic agonist, reduces efferent peripheral sympathetic outflow

  • preferred use: clon- HTN urgencies *watch for rebound; methyl -preggo

  • SE: sedation, fatigue, dry mouth, postural hypotension, ED, rebound HTN, withdrawal, Methy -hepatitis, and hemolytic anemia

• Arteriolar dilators

  • Reduce vascular smooth muscle, peripheral vasodilation

  • Reflex tachy, + inotropic

  • SE: HA, palpitations fluid retention; Hydralazine: GI, Lupus-like; Minoxidil: hirsutism, fluid retention

  • Given in combo w/ diuretics/BBs

Lipid disorders and all anti-hyperlipidemic meds

Assessing LDL, HDL, TGs

• LDL we are most concerned w/; independent risk factor for CAD; greatest risk

• Bad: high LDL, low HDL, high TGs

  • Mixed HLD = 2 or all 3 not at goal

• Dyslipidemia = high levels of lipids including cholesterol and TG

• Values

  • TC<200 is normal, TC = 200-239 is borderline, TC >240 is high

  • LDL: best <70; <100 optimal, 160-189 high, >190 very high

    • <70 is goal

  • HDL: M <40 W <50 is low; >60 is high = good, cardioprotective

  • TG: <150 Norm; >150 high

    • In cases of high TG LDL may not be able to be calculated by lab

• Peds screening: 1 x 9-11; 1 x 17-21; FMH or DM screen earlier

• Total lipid profile: must fast for 9-12 hrs; most accurate

Metabolic syndrome

• Cluster of conditions: inc BP, high blood sugar, excess fat around waist, abn cholesterol

  • Ab or central obesity, atherogenic dyslipidemia (inc TG, small LDL particles, low HDL), inc BP, insulin resistance, prothrombotic state, proinflammatory state

    • FBS >110; M ab >40in; W ab >35 in

• Tx:

  • Statin – 1^st line!!!

    • HMG CoA reductase inhibitors (HMG CoA is a precursor to lipid formation)

    • Major effects: reduce LDL 18-55% & TG 7-30%

    • Use high intensity!!

      • High intensity: atorvastatin (40-80) and rosuvastatin (20-40)

    • SE: major-myopathy, rahbdo, inc LFTs

    • Contraindications: absolute -liver disease; relative -certain drugs

      • NOT FOR PREGGOS

    • GOAL: high ASCVD score, lower LDL (70)

    • Avoid grapefruit and its juice; take at night to max effects

• Fibric Acids (fibrates) – 2^nd line if statin fails (fib)

  • Major effect: lowers TG 20-505, raise HDL 10-20%

    • Risk of raising LDL

  • SE: dyspepsia, gallstones, myopathy

  • Contraindications severe renal or hepatic dz

  • Gemfibrozil 600 BID

• Gut brush border blocks (Ezetimibe)

  • Block cholesterol absorption; dec TG, dec LDL

  • SE: angioedema, pancreatitis, hepatitis

  • Contraindications: hepatic impairment

  • Monitor: LFTs every 3 mo for first year then every 6

• Bile Acid Sequestrants (chol)

  • Major action: reduce LDL, raise HDL, may inc TG

  • SE: GI, constipation, dec absorption of other drugs

  • Contraindications: dysbetalipoproteinemia, raise TG (>400)

  • Cholestyramine 4-16mg

• Nicotinic Acid (Niacin)

  • Major actions: lowers TG 20-50%, inc HDL, low LDL barely

  • SE: flushing, hyperglycemia, hyperuricemia, upper GI distress, hepatotoxicity

  • Contraindications: liver disease, severe gout, peptic ulcer

  • Take ASA prior to taking Niacin to reduce flushing, drink w/ plenty of water

• PCSK9 inihibitors -biologics

  • Praluent, Repatha

  • Adjunct to statin or other agents, no muscle problems

• ACL inhibitors

  • 20-25% reduction in LDL

  • SE: hyperuricemia, arthralgias

• Omega 3 & fish oils (DHA) and (EPA)

  • Lower TG and raise HDL, no effect on lowering LDL