Cardio - Blueprint

gACC/AHA 2017 Hypertension categories

• Normal: < 120/80 mm Hg

• Elevated BP: systolic 120–129 mm Hg, diastolic < 80 mm Hg

• Stage 1 HTN: systolic 130–139 mm Hg, diastolic 80–89 mm Hg

• Stage 2 HTN: systolic ≥ 140 mm Hg OR diastolic ≥ 90 mm Hg

first-line tx for high BP (general)

ALWAYS lifestyle modifications

meds start at >130/80 AND clinical CVD or 10 year CVD risk >10%

thiazides, CCB, ACEI, ARB

first line BP tx black pt

CCB or thiazide

(d/t efficacy in lowering BP in this pop)

first line BP for CKD/albuminuria

ACEI/ARB

first-line BP tx for pts with MI

BB

ACEI

ACEI MOA

Renoprotective effect although can see a slight decrease in kidney function before becomes protective

used in HTN, kidney dz, HF

blocks conversion of angiotensin I → II

“pril”

ACEI adverse effects

cough

angioedema

hyperkalemia

adverse effects if with ARB

orthostatic (postural hypotension) etiology

nadequate autonomic reflexes,

volume depletion (dehydration, hemorrhage, vomiting),

certain medications (antihypertensives, CCBs,

antidepressants, opiates)

orthostatic hypotension

• Decrease in systolic blood pressure ≥ 20 mm Hg OR

• Decrease in diastolic blood pressure ≥ 10 mm Hg

orthostatic hypotension tx

• 1st: stop causative meds → INC salt, stockings, exercise

• #2: low dose fludricortisone or micodrine

hypertensive urgency def + sx

>180/110-120 and NO signs of acute organ damage

sx: HA, atypical CP, epistaxis, dizziness

hypertensive urgency tx

PO meds (captopril, labetalol, clonidine [relaxes BP], prazosin)

• Follow up → 1-7 days

clonidine = centrally acting alpha-2 adrenergic agonist

hypertensive emergency acute organ damage

hemorrhagic or ischemic stroke, acute coronary syndrome, aortic dissection, diffuse microvascular injury (anemia, thrombocytopenia, acute kidney injury, new onset retinopathy), hypertensive encephalopathy

hypertensive emergency tx

• Admit to ICU → BP stabilization with IV antihypertensives

  • Lower BP (reduce MAP) by no more that 20-25% over 1 hour, then 160-100 within 6 hours, then to target BP in 48 hours

• Nicardipine and labetalol → shown to be most effective at lowering BP

• Once stable → start a chronic PO med

renal artery stenosis (RAS)

• MC cx of secondary HTN (along with 1º aldosteronism) in adults

  • Pursue screening in patients with: drug resistant HTN, unusual presentation (YA), abdominal bruit, low serum potassium (indicating 1º aldosterone)

RAS causes

• atherosclerosis, fibromuscular dysplasia (FMD), kidney trasplant

• if FMD = young, F <60

• atherosclerosis = old, CV RF

• kidney transplant: surgical, native dz, immune

• neonates = congenital 

possible drug resistant hypertension

RAS PE

abdominal bruit

RAS dx - “next appropriate”, highest sensitivity, gold standard

Doppler U/S,

MRA (highest sensitivity),

CTA,

renal arteriography (gold standard for dx)

• Fibromuscular dysplasia → 

  • Multifocal type: “string of beads” d/t alternating stenosis & dilation

  • Focal type: circumferential or tubular stenosis

tx options for RAS

• Antihypertensive therapy (e.g., ACEI or ARB)

• Revascularization in select patients (e.g., those with a short duration of hypertension, intolerance of medical Tx, recurrent flash pulmonary edema/refractory CHF (Percutaneous angioplasty w/ or w/o stent placement)

• secondary CVD prevention (e.g., aspirin, statin, lifestyle modifications)

CAD → atherosclerosis process

Begins w endothelial dysfunction → cause fatty streak formation (initial xanthomas accumulate lipid laden macrophages (foam cells)) → grows in size → a stable fatty plaque with a fibrous cap atheroma → gains O2 supply through intimal neovascularization (originating from vasa visorum) → risk for a plaque rupture thrombosis

CAD RF

family history of premature coronary heart disease, smoking, hypertension, high-density lipoprotein levels below 40 mg/dL, and age ≥ 45 in men or ≥ 55 in women

protective factor CAD

having HDL levels ≥ 60

CAD sx

pattern of chest pain (unstable angina, NSTEMI, STEMI, heart failure)

CAD dx

• 2 lead EKG and exercise stress EKG, stress echocardiography, cardiac catheterization (dx and tx), cardiac enzymes (troponin & creatinine kinase-MB)

  • NSTEMI - same manifestations as unstable angina w/ election in troponin

    • STEMI - elevated troponins, ST segments elevation, and unstable angina symptoms

cardiac enzymes for NSTEMI

same as unstable w/ troponin

cardiac enzymes for STEMI

elevated troponin

ST segment elevation

unstable angina

creatinine kinase-MB and whats it best for determining

rise within 3 hours, peak within 24, normalized within 48-72 → more helpful when determining reinfarction

troponin is best for

initial eval of a possible MI, trop I is the most specific for MI

CAD/atherosclerosis FIRSTLINE and other tx

#1: BB

(alts: CCB, nitrates) + ASA

if recent stent placement → dual antiplt therapy (ASA and P2y12 inhibitor like ticagrelor or clopidogrel)

statins, lifestyle changes, comorbidities

Myocarditis cause

infectious - viral

((e.g., parvovirus B19, coxsackievirus, influenza, adenovirus, coronavirus), autoimmune, toxins, MIS-C))

→ ventricular enlargement, dilated cardiomyopathy

myocarditis sx

• viral prodrome (fatigue, fever, chest discomfort, dyspnea, palpitations)

  • Can present with symptoms of fulminant heart failure

  • S3/S4, abnormal ECG, elevated troponin, unexplained sinus tachycardia, exercise fatigue

myocarditis PE

 tachycardia disproportionate to fever, tachypnea, hepatomegaly, pulmonary edema, jugular venous distention

Triad: fever, new onset/worsening murmur, + culture

myocarditis dx + gold standard

• ECG, inflammatory markers, echocardiogram

  • Echocardiogram will show decreased ventricular ejection fraction with hypokinesis and wall motion abnormalities

  • Cardiac MRI, endomyocardial biopsy (gold standard)

myocarditis tx

• diuretics, ACEI, B-Blocker if EF <40%, afterload reduction, inotropes

  • VADs, ECMO may be required for severe disease

HEART score (for pts with ACS)

• History (slightly, moderately, highly suspicious)

• ECG (normal, nonspecific disturbance, ST depressions)

• Age (< 45 years, 45–65 years, > 65 years)

• Risk factors (none, 1–2, ≥ 3)

• Troponin (≤ normal limit, 1–2x normal limit, > 2x normal limit)

• Results:

  • Low risk 0-3: low risk of major cardiovascular event (MACE) in next 6 wks

  • Moderate risk 4-6: moderate risk of MACE in next 6 wks

  • High risk 7-10: high risk of MACE in next 6 weeks

MI RF

advanced age, HTN, hyperlipidemia, DM, obesity, smoking, prior CV disease

MI sx and what pop can have atypical presentatoin

• chest pain (MC) tightness/pressure and worse with exertion, dyspnea, N/V, weakness, palpitation, syncopes

  • Women, pts with diabetes, older pts are more likely to have an atypical presentation w/o chest pain

MI dx (short)

•  ECG (new ST elevation at the J point in two contiguous leads), troponin w/in 10 mins of first contact (cardiac injury biomarker)

MI tx

 1. supplemental O2 if <90% sat or in respiratory ditress

2. aspirin (if no contra.),

3. anticoagulation therapy,

4. nitroglycerin to alleviate chest pain (contra. if taken a phosphodiesterase inhibitor (sildenafil/viagra) w/in 24 hours or if hypotensive),

5. B-Blocker and statins (if not contra.

6. reperfusion,

7. thrombolysis (If PCI not available), medical therapy

MI most important part of tx

reperfusion -

• Fibrinolytics 

• PCI (percutaneous coronary intervention): more direct effect (preferred), increased survival, decreased ICH and recurrent MI

  • If have PCI center (cath lab): < 90 minutes door-to-device time

  • Non-PCI center: transfer for PCI if door-to-device time can be < 120 minutes

if >120 mins → thrombolysis has to be given in 30 mins and 12 hours within sx onset but CI in ICH, intracranial malignancy, stroke within 3 months, aortic dissection

medical therapy for MI (pt 1)

• Oxygen: indicated for saturations < 90%, dyspnea, heart failure

• Nitroglycerin: relieves ongoing chest pain, lowers BP

• Morphine: relieves pain, reduces work of breathing in setting of pulmonary edema

  • Only used if nitroglycerin fails to relieve the pain

  • Can be associated with negative outcome

• Beta-blockers: prevent recurrent ischemia and dysrhythmia

  • Metoprolol or esmolol

medical therapy for MI (pt 2 - anticoags/antiplts)

• Antiplatelet agents: reduce recurrent coronary artery thrombosis, stent thrombosis, and death

  • Aspirin: given before PCI and continued indefinitely

  • P2Y12 inhibitor (clopidogrel, prasugrel, ticagrelor): continue for 1 year if stent placed

  • GPIIb/IIIa antagonists for patients undergoing PCI

• Anticoagulation: if LV thrombus or Afib present and for all patients receiving thrombolytic therapy

• ACE inhibitors: reduce cardiovascular events, prevent LV remodeling

• High-dose statin: lipid lowering, and lowers risk of death, recurrent MI, and stroke

• Pt with hx of MI and current dx of HTN → B-Blockers and ACEI’s are 1st line

troponin (long)

• Highest sensitivity and specificity

• Time detectable from onset: 3–12 hours

• Peak: 24–48 hours

• returns to baseline in 5-14 days

CK-MB

• Time detectable from onset: 3–12 hours

• Peak: 24 hours

• Return to baseline: 48–72 hrs

• Useful for Dx of reinfarction

myoglobin

First to appear, first to peak, first to decline. But lacks specificity

Cardiac Electrical Conduction System

SA node → AV node → bundle of His → bundle branches → Purkinje fibers

ST Elevation Myocardial Infarction (STEMI) presentation

Patient presents with substernal chest pain that radiates to the neck and arm so severe that nitro or even opioids give no relief

STEMI dx

• elevated troponin I or troponin T and CK, ST segment elevations > 1 mm in two or more contiguous leads

• ECG: should be performed within 10 minutes of medical contact

  • Hyperacute T waves, ST elevation, Q wave development, T wave inversion, NEW LBBB

STEMI tx

• <12 hours since sx = PCI (if 90 mins) or fibrinolysis

• thrombolytic therapy in 3 hrs (CI if hemorrhage, stroke, brain cancer, internal bleeding, AD)

• ASA OR p2y12 receptor blocker (ticagrelor)

• BB

• anticoag (UFH, LMWH, fondaparinux)

MI walls + arteries

• Anterior wall ST elevation in leads V1 through V4 → LAD artery

• Inferior wall ST elevation in leads II, III, and aVF → R coronary artery or L circumflex

• Lateral wall ST elevation in leads I, aVL, V5, and V6 → L circumflex

• Posterior wall ST depressions in leads V1 through V3 and elevations in leads V8 and V9 (posterior lead placement)

Right Ventricular Infarction ECG and sx

assoc with anterior STEMI

hypotension, JVD, clear lungs

ECG

• ST elevation in lead V1

• ST elevation in lead III > lead II

• ST elevation in V4R–V6R

right ventricular infarction tx and what to avoid

patient is preload-dependent and has impaired filing of left ventricle

• Reperfusion, IVF

• Avoid nitrates (decreases preload which a R Vent. infarction is dependent on)

Non-ST Elevation Myocardial Infarction (NSTEMI) sx

• Sx: substernal chest pain that often radiates to left arm or jaw, dyspnea, nausea

• Commonly presents with T wave inversions or ST segment depressions on ECG and elevated troponin

NSTEMI medical therapy

• Oxygen: indicated for SpO2 < 90%, dyspnea, heart failure

• Nitroglycerin: relieves ongoing chest pain, lowers BP

• Morphine: relieves pain and anxiety, reduces work of breathing in setting of pulmonary edema

• Beta-blockers: prevent recurrent ischemia and dysrhythmia

• Antiplatelet agents: aspirin and P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor)

  • GPIIb/IIIa antagonists may be considered in certain patients (e.g., high-risk patients undergoing PCI)

• Anticoagulation: while hospitalized or until PCI is performed

• High-intensity statin: lowers lipids, risk of death, recurrent MI, and stroke

• ACE inhibitor: indicated for patients with LVEF < 40%, DM, heart failure, CKD

• Treat underlying condition if NSTEMI is type 2

NSTEMI revascularization strategy

• Within 2 hours: heart failure, hemodynamic instability, angina at rest, mechanical complications, sustained VT or VF

• Risk scores (e.g., TIMI, GRACE) stratify risk of further cardiovascular events and may aid in determining need for or timing of revascularization

• PCI or CABG

Dressler Syndrome (aka postmyocardial infarction syndrome) hx

• History of MI → pericarditis occurring 1-2 weeks after an acute MI or cardiac procedure

  • Most likely d/t autoimmune inflammatory response following necrosis

dressler syndrome sx (short)

pleuritic chest pain that is improved when leaning forward

dressler syndrome PE

pericardial friction rub, tachycardia, fever, leukocytosis, CRP, ESR

dressler syndrome ECG

• PR depression, PR elevation (aVR), diffuse ST segment elevation (concave)

dressler syndrome tx

• NSAIDs, colchicine

  • First line → Aspirin and Colchicine

  • Glucocorticoids may be considered in refractory cases

pericarditis causes

idiopathic, viral (mc after an acute viral illness in US i.e. URI), neoplastic, uremic, rheumatologic

pericarditis sx

•  pleuritic chest pain radiating to the back that is worse when lying back and improved when leaning forward

  • 3Ps of Chest Pain in Pericarditis: Pleuritic, Persistent, and Postural

pericarditis PE

 tachycardia and pericardial friction rub (sensitive and specific), distant heart sounds

pericarditis dx

• ECG: PR depression, PR elevation (aVR), diffuse ST segment elevation (concave)

  • 1 week after onset → ECG is isoelectronic, diffuse T wave inversions

  • Resolution of abnormal ECG findings in 2-6 weeks

pericarditis tx

• NSAIDs (ASA) + colchicine

• corticosteroids in refractory cases, NSAID contraindication, or certain rheumatologic disease

constrictive pericarditis cause and RF

• Caused by thickening and scarring of the pericardium → resulting in loss of elasticity of pericardial sac

• Risk factors: history of viral or idiopathic pericarditis, prior radiation therapy or cardiac surgery, prior infection (e.g., tuberculosis), autoimmune conditions, malignancy

constrictive pericarditis sx

• sx of RHF (edema), INC JVD

• pericardial knock

• kussmaul sign

• pulsus paradoxicus (BP drops when you breathe in)

pericardial knock definition

extra heart sounds heard just prior to S3 and is sometimes palpable - caused by sudden cessation of ventricular filling d/t thickened and noncompliant pericardium

constrictive pericarditis echo

thickened pericardium, abnormal septal motion, dilated IVC and hepatic veins

pericarditis tx

depending on whether early or chronic disease) include anti-inflammatory agents (NSAID and colchicine), Tx of the underlying cause, pericardiectomy (is hemodynamically unstable or persistent symptoms)

Pericardial Tamponade cause

penetrating trauma, pericarditis, iatrogenesis (central line placement, pericardiocentesis, pacemaker placement), post MI with free wall rupture, recent viral illness

pericardial tamponade sx

dyspnea and chest pain

pericardial tamponade PE

•  muffled heart sounds, JVD, hypotension (Beck’s triad), pulsus paradoxus (an abnormal drop in systolic BP ≥10 mmHg on inspiration), tachypnea, tachycardia, 

pericardial tamponade ECG

low-voltage QRS

electrical alternans (beat to beat change in amplitude of QRS or t wave)

pericardial tamponade CXR

• enlarged cardiac silhouette (water bottle sign) if effusion > 200mL

• Echocardiography (sensitive and specific)

  • Diastolic collapse of RV (less sensitive but very specific)

  • Early systolic collapse of RA (sensitive and specific)

  • Plethoric IVC (sensitive)

pericardial tamponade tx

pericardiocentesis or pericardial window

angina definition

• Chest pain or pressure with exertion or stress that is relieved by rest

  • Duration of pain → typically < 30 minutes (if > 30 mins suggestive of acute coronary syndrome (MI or unstable angina))

stable: caused by activity, stops when activity stops

unstable: CP >10 mins, less responsive to nitro, ST segment depression, normal troponin

angina diagnosis is made by

exercise ECG

• Angiogram needed to confirm and assess degree of CAD

• ECG: horizontal or downsloping ST segment depression or T wave flattening/inversion that resolve after sx of angina disappear → a/w stable angina

angina tx

• lifestyle modifications, statins, antiplt (ASA or clopidogrel), BB, nitrates, CCB, ranolazine, surgery

  • Acute 1st: sublingual nitroglycerine** (TOC) for stable angina for immediate sx relief & 325 mg aspirin (unstable)

  • Chronic 1st: B-Blockers → decrease recurrence of MI

    • If not tolerated then try CCB, long acting nitrate, or ranolazine

    • AVOID B-Blockers in a cocaine induced MI

    • ASA and B-Blockers are only known meds to lower mortality in patients with stable angina

vasospastic angina (variant or prinzmetal) cause

• coronary (MC right coronary) artery spasm with minimal fixed coronary lesions (often late PM - midnight or early AM)

  • Vasospasm at rest with preservation of exercise capacity

  • Associated with other vasospastic disorders, i.e. raynaud’s

vasospastic angina RF

•  smoking/cocaine, female, < 50 years, HTN, DM, obesity, emotional stress, medications (B-blockers and -triptans)

  • Triggers: sympathomimetic use, migraine therapies, ergot derivatives, hyperventilation, extreme cold

vasospastic angina sx

• squeezing, pressure-like chest discomfort at rest but have preservation of exercise capacity

  • Episodes commonly occur from midnight to early AM (overnight)

vasospastic angina ECG and dx

transient ST segment elevations

dx - cannot differentiate from STEMI but cardiac enzymes normal, angiographic evidence of spasm, no lesions

vasospastic angina - tx ; absence vs presence of stenosis

• NO coronary stenosis = CCB and nitrates, and ACEI NO BB!!!

• YES: PCI

rheumatic fever hx*

hx of GAS infx (ie strep throat, 5-15 yo)

rheumatic fever - sx and MC affected valve

• fever, red skin lesions on the trunk and proximal extremities, and small nontender lumps located over the joints, migratory arthritis of large joints

  • MC affected valve is the mitral valve

rheumatic fever PE

• Jones criteria: joints, oh no—carditis!, nodules, erythema marginatum, Sydenham chorea

  • Initial Dx: 2 major OR 1 major and 2 minor 

  • Recurrent dx: 2 major OR 1 major and 2 minor OR 3 minor

rheumatic fever labs

• antistreptolysin O, anti-DNase B, positive throat culture, or positive rapid antigen test

rheumatic fever tx

• antibiotics, NSAIDs

  • Secondary prophylaxis against GAS

    • Penicillin G benzathine → administer IM q21-28 days

      • If have rheumatic fever with carditis and echocardiographic evidence of persistent valvular disease → continue prophylaxis for 10 years or until age 40 (whichever is longer)

jones major criteria

• Joints (Polyarthritis)

• ♥- Carditis (Pancarditis - MC mitral regurgitation)

• Nodules (subcutaneous)

• Erythema Marginatum (nonpruritic rash, central clearing, face is spared)

• Sydenham’s Chorea

jones minor criteria

fever, poly or monoarthralgia, elevated ESR or CRP, prolonged PR interval on ECG

Most common cyanotic congenital heart disease in childhood

tetralogy of fallot

tetralogy of fallot hx

• episodes of cyanosis (tet spells) and squatting for relief (decreases R ➔ L shunt, increases oxygenation)

  • Test spells are preceded with irritability/crying or feeding - sudden onset, deepening of dyspnea, irritation, alteration in consciousness, decrease/disappearance of systolic murmur (d/t increased obstruction to the point of no flow through valve and increased VSD R → L shunt)

    • Spells frequently occur between 4-6 months and may resolve spontaneously

    • “Pink tet” → mild to moderate RV outflow obstruction

tetralogy of fallot sx

easy fatigue, dyspnea on exertion, cyanotic episodes

tetralogy of fallot PE

palpable Right ventricular lift, nail clubbing

tetralogy of fallot dx

• TOC - Echocardiogram: pulmonic stenosis, right ventricular hypertrophy, overriding aorta, and VSD

• CXR: boot-shaped heart, RVH

• ECG: RVH and right axis deviation

tetralogy of fallot - tx

• Tet spell → supplemental O2, place in knee to hest position to reduce shunting across VSD

• Corrective surgery → for infants w/ severe obstruction

  • If less severe can delay operation until up to 2 years old

• Palliative surgery (stent placement to maintain PDA or to creat a shunt with similar effect) → Neonates that cannot yet undergo corrective surgery 

tetralogy of fallot - PROVe

• Pulmonic stenosis (RV outflow tract obstruction)

  • Rough, crescendo-decrescendo systolic ejection murmur heard best at the LSB in the 3rd ICS with radiation to the back

• Right ventricular hypertrophy

• Overriding aorta 

• VSD (ventricular septal defect)

pathologic murmurs

• Grade ≥ 3 intensity

• Holosystolic timing, diastolic, friction rub (pericarditis), gallop rhythm (S3 or S4), systolic click

• Harsh or blowing quality, maximum intensity along Left upper sternal border

• Increased intensity with upright positions (sitting or standing from supine)

innocent murmurs

• Grade ≤ 2 intensity (Still or flow murmur)

• Short systolic duration (not holosystolic and not diastolic)

• Minimal radiation

• Musical or vibratory quality

• Soften in intensity when patient is sitting/standing compared to supine 

  • Exception is venous hum murmur (louder when sitting)