CARDIOLOGY

Editor: Faria Khimani, MD, Chloe Carr, MD
Faculty Editor: Aniket Rali, MD

Diagnostic Cardiac Tests

Approach to the ECG

Author: Daniela Gomez Zubieta

Method = mastery, approach each EKG the same

Rate

Regular rhythms = "Rule of 300" = 300 ÷ (large boxes between QRS complexes)
1 box = 300 bpm
2 boxes = 150 bpm
3 boxes = 100 bpm
4 boxes = 75 bpm
5 boxes = 60 bpm
6 boxes = 50 bpm
Irregular rhythms or severe bradycardia = (total # of QRS complexes on ECG) x 6

Rhythm

Determine regular vs irregular: calipers or march out QRS complexes on paper
Criteria for Sinus rhythm: P before every QRS; Upright P in Lead I, II; Negative in aVR

Axis

Normal: -30° to +90°
Quick method: Leads I and aVF
Normal Axis: Upright in I and aVF
Left Axis Deviation: Upright in I, down in aVF
- Causes: LVH, LBBB, left anterior fascicular block, prior inferior MI
Right Axis Deviation: Down in I, up in aVF
- Causes: RVH, RBBB, Left posterior fascicular block, prior lateral MI, PE

Intervals

PR Interval: normal 120 – 200 ms
If < 120 ms, consider pre-excitation with accessory pathway (i.e. WPW)
If > 200 ms, first degree AV block
QRS Complex: 60 – 100 ms (normal)
100-120 ms: Incomplete BBB or non-specific intraventricular conduction delay (IVCD)
120ms: complete BBB, ventricular tachycardia, hyperkalemia
QT interval: Normal duration < 450ms in men and < 460ms in women
QT is inversely proportional to HR (QT interval shortens at faster HRs)
Quick estimate: normal QT is less than half the preceding RR interval
QTc estimates the QT interval at a HR of 60 bpm (to allow for comparison across HRs)
A couple of formulas exist to calculate QTc:
- QTcB = most commonly used due to simplicity, most accurate HR of 60
- QTcF = more accurate when HR is outside the range of 60-100
Clinically significant when generally QTc > 500 ms
Causes of Prolonged QTc: hereditary, medication-induced (anti-emetics, ABX, psychiatric meds), hypokalemia, hypomagnesemia, hypocalcemia, ischemia

Morphology

P wave: P waves in limb leads should be ≤2.5 small box high and ≤2.5 small box wide - Right Atrial Enlargement: Peaked P Wave in Lead II that measures >2.5mm - Left Atrial Enlargement: - Lead II: Bifid P Wave (two humps) with total duration > 110 ms - Lead V1: Biphasic P wave, terminal deflection > 1mm wide and deep - If ≥ 3 different P wave morphologies in same lead: wandering atrial pacemaker (HR < 100) or multifocal atrial tachycardia (HR > 100)

QRS complex

Voltage: - Low voltage: QRS amplitude < 5mm in limb leads or < 10mm in precordial - Causes: pericardial effusion, infiltrative cardiomyopathy, obesity - Right Ventricular Hypertrophy: Tall R Waves in V1 (> 7mm) and right axis deviation - Left Ventricular Hypertrophy: multiple criteria exist - Sokolow-Lyon criteria is a common example: S in V1 + R in V5 or V6 >35mm, R in aVL >1.1 mV

Conduction delays: - RBBB: Wide QRS and RSR' in V1 or V2; deep broad S In lateral leads - LBBB: Wide QRS, large S in V1, broad monophasic R wave in lateral leads (I, aVL, V6)

R wave progression: - R wave normally gets progressively larger from V1 to V6 - If the transition does not occur by V4, this is called "poor R wave progression". This is seen in chronic lung disease, LVH, left anterior fascicular block, and anterior MI

Q-wave: Small Q waves are normal in most leads - Never normal in V1-V3 - Pathologic Q waves: > 1 box wide and 2 boxes deep or > 25% height of R wave

ST Segment: - ST Elevation: STEMI, LBBB (ST elevation in leads with deep S waves), LVH, Ventricular paced rhythm, Pericarditis (associated with PR depression), coronary vasospasm, Brugada syndrome - ST Depression: ischemia, reciprocal change in STEMI, posterior myocardial infarction (V1-V3), digoxin, hypokalemia - See ACS section for STEMI criteria, Wellens Syndrome

T wave: - Normal T waves are upright in all leads except aVR and V1 - Inverted T Waves: - Acute ischemia (if present in contiguous leads), LBBB (in lateral leads), RBBB (V1-V3), LVH ('strain' pattern similar to LBBB), RVH (RV 'strain' in V1-V3 or inferior leads), PE (right heart strain or part of S1,Q3,T3), intracranial pathology - Peaked T Waves: - Hyperkalemia vs 'hyperacute' T waves that precede ST elevation and Q waves in STEMI

Bedside Echocardiography

Author: Matthew Gayoso

Additional Resources:

https://www.coreultrasound.com/basiccardiac-function/
http://pie.med.utoronto.ca/tte/
https://www.echocardiographer.org/TTE.html
App: FATE CARD (Focus Assessed Transthoracic Echocardiography)

Finding an Ultrasound

MICU: radiology room behind charge nurse's desk in middle hallway
VA ICU: In front of resident workspace
8N: Behind nurses' station before entering cleaning supply room
8S: In supply closet to left as your walk toward nursing station - (door code is 1-3-5)
6MCE: COVID restricted (ask nurses)
CCU/5N only: supply room on left as entering CCU
Round wing: 5th floor, ask nurses

TTE Standard Views

Parasternal long - Probe position: Rotate probe 180 degrees with right edge of probe/probe marker pointing toward pt's left shoulder - Make sure probe is centered over mitral valve (In right spot if you can see MV and AV)

E Point Septal Separation (EPSS) - Distance separating the anterior MV leaflet from the septal wall as measure of LV systolic function (easy evaluation of systolic function) - Place M mode spike at tip of mitral leaflet and hit M mode (perpendicular to septum) - Identify E point (passive filling of LV) and determine distance from interventricular septum (IVS) - <7mm = Normal - >10mm = HF - Confounders that elevate EPSS: AR, MS

Parasternal short - Probe position: Rotate probe 180 degrees with right edge of probe/probe marker pointing toward pt's left shoulder - Good position to assess EF by visualizing wall thickening

Apical four chamber - Probe position: Slide down and look near pt's left nipple (or in the intermammary fold after lifting up breast tissue if needed - at PMI if able to palpate) - Good to assess EF by visualizing cardiac shortening

Subxiphoid - Probe position: Push probe head into pt's abdomen just below xiphoid and flatten probe to make nearly parallel to pt's position, marker to pt's left - Troubleshooting: shift probe slightly left of midline (toward pt's right) and angle toward heart/right to use liver as acoustic window or ask pt to take big breath (moves heart closer to probe) - Best window to visualize pericardial effusion

IVC - Probe position: subxiphoid area with probe marker facing toward pt's head tilted slightly left of midline, trace IVC into RA to verify correct vessel (vs aorta) - IVC size and collapsibility used as a surrogate for CVP and RAP - <2.1cm and >50% collapse: RAP ~3 mmHg - <2.1cm and < 50% collapse or >2.1cm and >50% collapse: RAP ~8 mmHg - >2.1cm, <50% collapse: RAP ~ >15 mmHg

Right Heart Catheterization

Author: Ahmad Yanis

Pulmonary artery catheter (PAC): Multi-lumen catheter that sits in the right heart to provide invasive measurement of hemodynamic parameters

Indications for PAC placement:

Diagnose undifferentiated shock
Severe cardiogenic shock
Diagnose pulmonary hypertension
Diagnose left -> right shunting
Diagnose valvular and pericardial disease
Titrating medications (specifically inotropes, pulmonary vasodilators, diuresis)

Contraindications to PAC placement

Infection at the insertion site
RA/RV mass or thrombi
Proximal pulmonary artery embolism
Tricuspid or pulmonic valve endocarditis
Mechanical tricuspid or pulmonic valves
Presence of RV assist device

Complications of PAC placement

Arrythmias: VT, RBBB, 3rd degree AV block if preexisting LBBB
Infection (endocarditis of the pulmonary valve)
Bleeding
Pulmonary embolism and pulmonary Infarct
Pneumothorax
Air embolism
Pulmonary artery perforation / rupture
Endocardial/valvular damage

PAC Measurements

Definition	Normal "Rule of 5s"	Interpretation
Central Venous Pressure (CVP) - Pressure in superior vena cava, often an indicator of volume status	0 - 5 mmHg	Elevated CVP: cardiac dysfunction and/or hypervolemia Low CVP: volume depletion or decreased venous tone
Right Atrial Pressure (RAP) - Surrogate for preload, should be same as CVP	0 - 5 mmHg	Elevated RAP: disruption in forward cardiac flow or hypervolemia
Right Ventricle Pressure - Right ventricular systolic* and end diastolic pressures	25/5 mmHg	Elevated RVP**: -PA/PV disorder: pulm HTN, PV stenosis, PE -RV disorder: CM, tamponade, ischemia/infarction
Pulmonary Artery Pressure (PAP) - Measured as systolic, diastolic, and mean pressures. Diagnoses pHTN.	25/10 mmHg Mean: 15 mmHg	Elevated PAP: -Acute: PE, hypoxemia induced pulmonary vasoconstriction -Chronic: PH groups 1-5
Pulmonary Artery Wedge Pressure (PAWP or wedge) - Surrogate for left atrial pressures and LVEDP	10 mmHg	Elevated PAWP (LVEDP): LVHF, mitral and aortic valve disorders, hypervolemia, R to L shunts, constrictive/restrictive CM, HOCM
Thermodilution Cardiac Output & Index - Amount of blood pumped in one min. CI is the cardiac output divided by body surface area (to standardize for body size)	CO: 3.4-15 L/min CI: 2.8-4.2 L/min/m²	Low CI: systolic/diastolic heart failure, severe valvular disorder (MR, AS), RV failure, pHTN, cardiogenic shock. Elevated CI (high-output state): sepsis, anemia, thyrotoxicosis, A-V shunt
Mixed central venous oxyhemoglobin saturation (SvO2) - % of oxygen bound to Hgb in blood returning to the right side of the heart, reflects total body O2 extraction	65-70%	High SvO2 (> 65%): -Decreased O2 demand -High flow states seen in distributive shock (sepsis) Low SvO2 (< 50%): decreased O2 delivery seen in cardiogenic or hypovolemic shock

RVSP can be a surrogate for PASP
*Severe RVP elevations are generally chronic while acute conditions typically have RVSP <40-50

Calculating Hemodynamic Parameters from PAC Pressures

Parameter	Definition	Normal Values	Interpretation
Fick CO and CI	Calculated CO based on Oxygen consumption (VO2), Hbg, and O2 sats of arterial and venous blood	4-7 L/min 2.5-4 L/min/m²	See "Cardiac Index" above.
Systemic Vascular Resistance (SVR)	Measurement of afterload; helpful in delineating the etiology of shock as well as guiding afterload-reduction therapy in HFrEF	700-1200 dynesscm⁻⁵	Elevated SVR: hypovolemic, cardiogenic, and obstructive shock Decreased SVR: distributive shock (sepsis, anaphylaxis, neurogenic)
Transpulmonary gradient (TPG)	Differentiates between pre- and post-capillary pulmonary hypertension. MPAP minus PCWP	< 12 mmHg	A TPG value greater than 12 mmHg indicates that a component of the pHTN is secondary to pulmonary vascular disease
Pulmonary Vascular Resistance (PVR)	Gold standard in the estimation of the severity of pre-capillary pHTN. Reflects the pressure drop across the pulmonary system only and is independent of the LA, mitral valve and the LV. TPG / CO	< 3 Wood Units 30-90 dynesseccm⁵	Elevated PVR (>3 Wood units) suggests pre-capillary pHTN Normal PVR seen in pulmonary venous hypertension (diastolic dysfunction)
Pulmonary artery pulsatility index (PAPi)	Pulmonary pulse pressure relative to preload (RAP), Indicator of RV function. PA Pulse Pressure / CVP	>3.0 = normal 2-3 = mild RV dysfx 1-2 = moderate RV dysfx <1 = severe RV dysfx	PAPi < 0.9 predicts in-hospital mortality and/or need for RVAD in acute MI. Can be decreased in pure RV failure or biventricular failure
Cardiac Power	Cardiac output relative to afterload, a measure of LV contractile reserve. CPO = (Mean Arterial Pressure (MAP) x Cardiac Output (CO)) / 451	Normal > 1	CP< 0.6 strongly suggestive of LV failure. Found to be a strong independent hemodynamic correlate in pts with cardiogenic shock. Predictor of mortality in CCU

Blood Pressure

Inpatient Hypertension

Author: William Lavercombe

Background

Hypertensive urgency: SBP > 180 mmHg/DBP > 120 mmHg
Hypertensive emergency: SBP > 180 mmHg/DBP > 120 mmHg + new or worsening target-organ damage

Evaluation

Are there signs/symptoms of end organ damage? - Neurologic symptoms: agitation, delirium, stupor, seizures, visual disturbances - Focal neurologic deficits - Chest pain - Back pain (consider aortic dissection) - Dyspnea (consider pulmonary edema) - Microvasculature manifestations: high grade-retinopathy, AKI, or microangiopathic hemolytic anemia and thrombocytopenia

Management

Hypertensive Urgency: Goal to gradually lower BP over 24-48 hrs, initial goal 160/110

Hypertensive Emergency

Initial lowering should depend on the end organ damage observed: - Stroke: Initial: 130<SBP<180 mm Hg, MAP decline 15% in 1 hr - Hypertensive Encephalopathy: Immediate MAP decline of 20-25% in first hour - Cerebral Hemorrhage: Decrease SBP to 140-150 within 1 hr if SBP >150-220 - Preeclampsia, HELLP, Eclampsia: Immediate SBP <160 mm Hg and DBP <105 mmHg if severe - Hypertensive Retinopathy BP Target: SBP <180 mmHg, MAP decline of 15% - Acute Kidney Injury: MAP decline 20-25% over several hours - Acute Heart Failure: SBP <140 mmHg - Pulmonary Edema: Immediate SBP <140 mmHg - Acute Coronary Syndrome: SBP <140 mmHg - Exceptions to gradual lowering include: - Acute stroke: call code stroke, lower ONLY if BP > 185/110 in pts under consideration for reperfusion therapy; or BP > 220/120 in pts not candidates for reperfusion therapy - Aortic dissection: Goal = rapidly lower BP in minutes to target of 100-120 systolic to avoid aortic shearing forces; also want to lower heart rate as best as possible.

Pharmacologic therapy: - Ensure their home medicines have been restarted at appropriate doses, formulation (long acting vs. short), and dosing intervals - If pt has a rapid acting anti-HTN med, can consider giving a dose early or an "extra dose" and then up titrating their overall daily dose - Rescue therapies: - Hydralazine PO (10-20mg initial dosing Q6H) - Isosorbide dinitrate PO (5-20mg TID) - Nifedipine XL PO (dose at 30mg initially, max 90mg BID; NOT sublingual) - Labetalol IV (10-40mg initially; dosed up to every 20-30mins) - Hydralazine IV (10-20mg initially; dosed up to every 30 mins). - Nitroglycerin Infusion - Nitropaste 1" (can add/wipe away for titration; dose Q6H until oral meds can be started for better long-acting control) - Dialysis if missed session

Additional Information

Refractory HTN: try additional agents listed above vs. escalation of care for drip (nicardipine, nitroglycerin, nitroprusside, esmolol). Consider secondary workup (urine metanephrines, renal vascular US, renin-aldosterone levels)
Most drips that can be done for this indication are done in stepdown and usually require no-titration of the infusion and occasionally the MD to be bedside to initiate the infusion.
This includes diltiazem, labetalol, nitroglycerin, and verapamil drips. Nicardipine, esmolol, and nitroprusside infusions (ggt) are not allowed on step down.

Autonomics and Orthostatic Hypotension

Author: Faria Khimani

Background

Orthostatic Hypotension (OH): SBP ↓ > 20 mmHg, DBP ↓ > 10 mmHg), or within 3 min of standing up or head-up tilt to 60 degrees on a tilt table
Etiologies: Neurogenic OH (nOH) vs non-neurogenic OH
nOH associated with autonomic failure, often seen in conditions like Parkinson's disease, multiple system atrophy, and pure autonomic failure. Characterized by a blunted heart rate response during hypotension (heart rate rise <15 beats per minute)
Non-neurogenic caused by dehydration, medications, acute blood loss

Evaluation

Orthostatic vitals signs - Perform a bedside simplified Schellong test: Measure blood pressure and heart rate after five minutes in the supine position and three minutes after standing.
Labs: CBC, CMP, EKG, TSH, B12, LFTs
Consider SPEP/UPEP, paraneoplastic panel, autonomic function testing depending on clinical context

Management

Conservative: - TED hose and abdominal binder for ambulation - Drink 16oz of fluid 15 min prior to standing - If they have supine HTN, keep HOB 30-45 degrees at all times - Add 2.3-4.6g of salt per day to diet (if no contraindications) - Avoid high temperatures (which cause peripheral vasodilation)

Drug	Dose	Mechanism	Side effects
Fludrocortisone (Florinef)	0.1mg QD ↑ by 0.1 mg Max: 0.3 mg QD	Mineralocorticoid → increase blood volume. Enhances sensitivity to circulating catecholamines	Edema, HTN, hypoK Do not use in CHF
Midodrine	2.5mg TID ↑ by 2.5mg Up to 10mg TID	Peripheral-selective α1 agonist → constricts both aa & vv	Supine HTN Pilomotor reactions Pruritus GI sx Avoid w/uncontrolled HTN, urinary retention, heart dz
Droxidopa	100mg ↑ by 100mg Max: 600mg TID	NE precursor → carboxylated to NE. Can cross BBB.	Supine HTN, less than midodrine
Atomoxetine	10mg or 18mg	SNRI	Do not use w/ glaucoma or MAOI Supine HTN

Supine HTN treatments: transdermal nitroglycerin (preferred); minoxidil, hydralazine, or clonidine in select pts

Chest Pain

Author: Michael Daw

Chest Pain / Angina:

Symptoms determine likelihood that chest pain has a cardiac etiology
Cardiac > possible cardiac > noncardiac is more useful than typical vs atypical angina

Diagnoses Not to Miss: "The Serious Six" (3 Heart, 2 Lung, 1 Esophagus)

Acute Coronary Syndrome
Aortic Dissection/Aneurysm
Cardiac Tamponade
Pneumothorax
Pulmonary embolism
Mediastinitis (e.g. esophageal perforation)

Other Differential Diagnoses

Skin/subcutaneous: Laceration, herpes zoster, cellulitis, abscess
Musculoskeletal: Costochondritis, rib fracture, myositis, sprain/strain
Pleural space (no pain receptors in the lung): PNA, tumor, pleuritis
Heart: Myocarditis, pericarditis, spontaneous coronary artery dissection (SCAD), coronary vasospasm, hypertensive crisis, aortic stenosis, stress-induced cardiomyopathy (Takotsubo), decompensated heart failure
GI: GERD, esophagitis, rupture, impaction, diaphragmatic hernia
Trachea: Tracheitis, tracheal tear
Nervous system: Thoracic radiculopathy
Hematologic: Acute pain crisis (sickle cell)

Physical Exam

Vitals: BP in both arms (difference in SBP >20 mm Hg is high risk feature for aortic dissection)
Hemodynamic profile: warm/dry, warm/wet, cold/dry, cold/wet
Palpate chest: evaluate costochondral junction, subcutaneous emphysema, examine skin
Cardiac: murmurs, rub for pericarditis, JVD for heart failure, pulsus paradoxus for tamponade
Pulm: absent breath sounds for PTX, crackles for left heart failure, PNA
Abdomen: abdominal pain mistaken or referred as chest pain
Extremities: asymmetric leg swelling (>2 cm difference) for DVT/PE

Diagnostic Studies

EKG: ACS (STEMI, new LBBB, ST depressions, TWI, Wellen's sign), PE (RAD, right precordial or inferior TWI, S1Q3T3), pericarditis, pericardial effusion
Labs: Troponin (ACS, PE, myocarditis), CBC, CMP, BNP, lactate
CXR: PTX, PNA, dissection, esophageal rupture
POCUS: pericardial effusion, R heart strain for PE, wall motion abnormality for infarct/ischemia or stress-induced CM, valvular dx, lung sliding/PTX
CTA: gold standard for PE, versus V/Q scan if CKD or contrast allergy. Dissection can be diagnosed w/ CTA, MRA, or TEE

Evaluation for Coronary Disease

Test	Indications	Benefits	Risks	Considerations
EKG Stress	Low to Intermediate risk pts Do not stress active or suspected ACS	Functional status w/ Bruce treadmill protocol	Exercise tolerance limits use	Must have normal ECG at baseline, nondiagnostic if 85% target HR not achieved
Dobutamine Echo Stress	Serves as screening with high NPV	More sensitive than EKG	Contraindicated: arrhythmias, LVOT obstruction, HTN, AS	Can be useful to eval low grade low flow AS Hold BB
SPECT stress		More sensitive than echo, Assess viability	Adenosine or Regadenoson contraindicated in reactive airway disease	No caffeine or theophylline prior
PET stress		Better PPV than Echo Assess viability		Better for pts with larger abdominal girth (less diaphragmatic attenuation)
Cardiac MRI		Assesses viability		Can assess non-ischemic vs ischemic cardiomyopathy; HR must be < 70, gold standard for structure and function
Coronary CT		Very high NPV for stenosis	Contrast media reactions CIN lower risk than cath	Might have poor lumen visualization if heavy calcium burden Does not assess functional status
Coronary Angiogram	STEMI High risk NSTEMI: Refractory angina, new arrhythmia, cardiogenic shock (HF) Suspected true ACS	Direct visualization of lumen Therapeutic PCI	CIN with contrast Cath site complications Rare: SCAD, cholesterol emboli	Positive Screen (above) necessitates LHC LHC is diagnostic and therapeutic

Acute Coronary Syndromes

Author: Matthew Alonso

Background

Completely or partially occluding thrombus on a disrupted atherothrombotic coronary plaque leading to myocardial ischemia/infarction
STEMI: Elevated troponin & elevation in ST segment or new LBBB with symptoms
0.1 mV in at least 2 contiguous leads
Exception, in V2-V3:
- 0.2 mV in men older than 40 y/o
- 0.25 in men younger than 40 y/o
- 0.15 mV in women
Use Sgarbossa's Criteria for MI with LBBB (≥3 points) or ventricular pacing
- Concordant ST-segment elevation ≥0.1mV in leads with a positive QRS complex (5 points)
- Concordant ST-segment depression ≥0.1mV in leads V1, V2, or V3 (3 points)
- Discordant ST-segment elevation ≥0.5mV in leads with a negative QRS complex (2 points)
NSTEMI: Evidence of myocardial necrosis (elevated troponin) w/o ST segment elevation
ST depression of ≥0.5mV, in two or more contiguous leads
New T-wave inversions of ≥1mV compared to previous ECGs
Normalization of prior T-wave inversions suggestive of dynamic process of ischemia
Unstable Angina: Angina without evidence of myocardial necrosis (normal troponin)
Other causes of myocardial injury: coronary spasm, embolism, imbalance of oxygen demand and supply 2/2 fever, tachycardia, hypo-/hypertension

Presentation

Classic angina: retrosternal with characteristic radiation (e.g., left arm, neck, jaw), pressure or vice-like quality, with associated symptoms (e.g., diaphoresis, dyspnea, nausea, abdominal pain, or syncope)
Change in pt's baseline angina, especially onset at rest
Physical Exam: sinus tachycardia, diaphoresis
If large infarct, can present with symptoms of acute heart failure

High-Sensitivity Troponin (hs-cTnT)

Reference values (sex specific ULN, 99th percentile): 14ng/L for adults assigned female at birth, 22ng/L for adults assigned male at birth, 19ng/L for unknown sex; above these limits are diagnostic of myocardial injury
Acute myocardial injury: absolute delta change of ≥3ng/L for hs-cTNT values below the sex-specific percentile OR changes in hs-cTnT values of ≥20% when at least one of the values is above the 99th percentile
hs-cTnT peaks within 12-48 hours and normalizes in 5-14 days

Obtain ECG and compare to prior if available. Assess for: - New ST elevations → STAT call 1-1111 to activate STEMI alert - New ST depression, T wave inversions (not specific but more concerning if deep; > 0.3mV), Biphasic T waves and deep T wave inversions in leads V2 & V3 (Wellens sign [LAD]) → Obtain hs-cTnT (Order set: Initial + 3hr repeat + 6hr repeat) → Obtain serial ECGs Q2-6h hours to monitor for dynamic changes - Nonischemic ECG → obtain hs-cTnT. Categorize the initial hs-cTnT result: - Low (≤6 ng/L) → Determine timing of symptom onset: - < 3hrs → Obtain 3hr repeat - > 3hrs → May discontinue troponin testing; however, if high suspicion for ACS despite normal initial markers obtain 3hr repeat - Borderline (6-14 ng/L female, 6-22 ng/L male) → Order 3hr repeat - Δ < 3 ng/L → stop trending - Δ > 3 ng/L → obtain 6hr repeat, serial ECG, and monitor patient's symptoms - Elevated (>14 ng/L female, >22 ng/L male) - If clinically, lower concern for ACS → obtain 3hr repeat - If clinically, higher concern for ACS → obtain 3hr repeat, management per NSTEMI

Management:

STEMI

STAT page Cardiology on call via Synergy (whether in VA or Vanderbilt). Rapid PCI within 120 mins is crucial.
ASAP: aspirin 325mg, heparin drip (high nomogram, with bolus)
Hold P2Y12 until discussed with Cardiology fellow

NSTEMI

High risk: Medical management followed by left-heart catheterization within 48h

Anti-thrombotic therapy:

Antiplatelet agents: - ASA 325mg loading dose then 81mg daily after - Do not give P2Y12 receptor blocker until discussed with cardiology fellow - Clopidogrel: prodrug metabolized by CYP219 to active form, irreversible inhibition - Ticagrelor: reversible inhibitor, contraindicated in patients w/ severe hepatic disease, history of ICH, active pathological bleeding - Prasugrel: prodrug but more rapidly metabolized than clopidogrel with less variation, irreversible inhibition, contraindicated if age > 75 or weight < 60 kg or prior TIA/CVA - Cangrelor IV, Integrilin IV

Anti-coagulants: Unfractionated heparin drip - Type this in Epic and select "nursing managed" protocol for "ACS" - VA it can be found under the "Orders" tab along the left-hand column. - Enoxaparin (LMHW) can be used but requires preserved renal function (CrCl > 30) and most interventionalists prefer heparin prior to LHC

Pre-Catheterization Care

New VUMC Policy: patients can have clear liquid diet starting 6 hours before left or right heart cath. Ensure patients have a clear liquid diet after midnight.
Continue anticoagulation with heparin gtt
Cardiac cath request:
VUMC: Place cardiac catheterization request in cardiology context, proceduralist usually "surgeon generic".
VA: Discuss with cardiology fellow cath request and/or call VA cath lab

Post-Catheterization Care

Catheterization Documentation - VUMC: Epic → Cardiac tab → Cardiac Catheterization/Intervention Report - VA: Note tab → Post-Procedure note and Cardiac Catheterization note

Post-Catheterization Heparin - Medical management w/o intervention: stop heparin unless directed in report - If indication for CABG (ex: Left main, proximal LAD), continue heparin gtt until surgery - PCI placed: stop heparin and continue/start DAPT as directed by cardiology - Other medical indication for anticoagulation (DVT/PE, atrial fibrillation): restart ~ six hours after catheterization

Cath Site Checks: - 6-8h post catheterization (typically can be signed out as 0000 cath check), only needed for femoral arterial access: - Look, listen, feel: evaluate for hematoma & pseudoaneurysm; call fellow if concerned. Small amount of bruising and mild tenderness at the site is normal - Listen above and below the site for a bruit; the area should be soft - Hypotension after femoral access is concerning for RP bleed - Apply pressure, STAT page interventional fellow, do NOT take pt to scanner prior to hearing back, order blood if needed, may need FemStop compression system (Call CCU to obtain if needed) - Femoral oozing: Page Cardiology fellow, will need to apply pressure - Radial oozing: instruct nurse to re-inflate the TR band and restart the clock on deflation

Post ACS Care:

TTE prior to discharge
DAPT: Aspirin 81 mg daily and P2Y12 agent
If patient on long term AC for comorbid condition, consider P2Y12 inhibitor plus DOAC, given increased bleeding risk with triple therapy.
Beta blocker in all pts within 24 hours
High intensity statin (ex: rosuvastatin 40 or atorvastatin 80). See outpt lipids section
ACEi/ARB if anterior STEMI, post-MI LV dysfunction
Lifestyle Modification: weight loss, smoking cessation, diabetes control, hypertension management, cardiac rehabilitation

ACS Complications:

VT/VF, sinus bradycardia, third-degree heart block, new VSD, LV perforation, acute mitral regurgitation, pericarditis, and cardiogenic shock

Pericarditis

Author: Michelle Chintanaphol

Background

Inflammation of the pericardial sac
Can be classified as acute (lasting up to 6 weeks), recurrent (symptom-free interval of 4-6 weeks), chronic (lasting more than 3 months)

Etiologies

Idiopathic (most common): thought to be viral or post-viral
Infectious: viral (Coxsackievirus, adenovirus, COVID-19, EBV, parvovirus B19), bacterial (TB, staph, strep), fungal
Malignancy: metastasis from primary cancer (lung, breast, lymphoma), complication of radiation or chemo, immune checkpoint inhibitor-associated
Autoimmune: SLE (most common), RA, hypothyroidism, systemic sclerosis, MCTD, Sjogren's syndrome, myositis, vasculitides, sarcoidosis
Cardiac: Infarction (Dressler syndrome), myocarditis, post pericardiotomy syndrome
Other: Trauma (including procedures), metabolic (uremia), drug-induced

Diagnosis

Chest pain – sharp, substernal, acute, and improved by sitting and leaning forward
Pericardial friction rub at left sternal border
ECG changes: typically diffuse ST elevations and PR depression
Chest pain almost always present. Pericardial rub highly specific.
Even small effusion can help confirm diagnosis, but lack thereof does not rule it out

Evaluation and Management

Always: EKG, chest x-ray, BMP, CBC, troponin, ESR, CRP and TTE - TTE should be performed ASAP if tamponade suspected In select populations if warranted: Blood cultures, ANA, RF, anti-CCP, PPD, chest CT

Treatment: - Ibuprofen 600-800mg TID (1-2 wks, based on symptom resolution and normalization of CRP) + colchicine 0.6mg BID (3 months for acute, 6 months for recurrent) - If recent MI, aspirin 650-1000mg TID (1-2 wks) + colchicine - If not responding to ibuprofen, indomethacin 50mg TID (1-2 wks) + colchicine - If NSAIDs are contraindicated, prednisone 0.2-0.5mg/kg daily for 2 weeks followed by taper + colchicine - Advise patient to avoid strenuous activity since exercise-induced tachycardia may increase inflammation

Arrhythmias

Acute management of arrhythmias:

12-lead EKG if possible and have defib pads on pt
Is the pt unstable (hypotensive, signs/symptoms of hypoperfusion)?
Is the information real?
Review tele strips if stable: VUMC Web Resources -> VUH PIICiX Philips Web -> pt selection -> alarm review (vuhphilipsweb.app.vumc.org)
Review past EKGs to determine if pt has had this rhythm before
Ensure pt has good IV access
Labs: BMP, Mg, TSH, and +/- troponin, tox screen

Bradyarrhythmia

Author: Benjamin French

Background

Sinus node dysfunction (pacing defect) vs atrioventricular block (conduction defect)
Clinical presentation:
A sinus HR > 50 bpm or a sinus pause < 3 seconds is unlikely to cause symptoms
Symptoms include syncope/presyncope, dyspnea, angina

Potential etiologies: - Older age (most common) - Ischemia (can't miss) - Metabolic: Hypothyroidism, hyper/hypokalemia, hypermagnesemia (generally > 8 mg/dL) - Infection: Perivalvular abscess, Lyme, Toxoplasmosis - Inflammatory/infiltrative: Myocarditis, SLE, cardiac sarcoidosis, amyloidosis, hemochromatosis - Cardiac surgery/valvular procedures - High vagal tone (e.g., pain, nausea, athletes) - Sleep apnea (should be considered in nocturnal sinus bradycardia) - Medications: Beta blockers, verapamil, diltiazem, digoxin, antiarrhythmics, alpha-2 agonists, antiepileptics, propofol, cannabis, etc.

AV Block

Management: - Avoid nodal blocking agents – Adenosine, Beta-blockers, CCBs, Digoxin - Observation if asymptomatic - Treat identified underlying causes - If symptomatic or high-grade block (Mobitz II or complete heart block), EP consult for pacemaker evaluation - If unstable: Call CCU Fellow - IV atropine (1 mg every 3 to 5 minutes; maximum total dose: 3 mg) - Do NOT use in heart transplant - Dopamine (5 to 20 mcg/kg/minute) OR Epi (2 to 10 mcg/min) - Transvenous pacing

Tachyarrhythmias - Narrow Complex

Author: Cesar Campos

Background

Three causes of tachyarrhythmias: - Re-entry: pt with structural heart disease (e.g. post-infarction scar) - Abnormal Automaticity: electrolyte derangement or acute ischemia (Purkinje fibers) - Triggered Activity: early and late after depolarizations. (e.g. Hypokalemia, ischemia, infarcts, excess calcium and drug toxicity)

Evaluation

Unstable tachyarrhythmia: - Start with treatment, determine type later - Synchronized cardioversion: place defibrillator pads, consider 0.5-2mg IV midazolam for sedation, prepare for synchronized cardioversion at 200J (can ↑ to 300-360 J)

Sinus tachycardia

Maximum rate usually (220 - patient age)
Management: Address underlying causes (eg, fever/sepsis, hypo/hypervolemia, anxiety, anemia, PE, ACS, hypoxia, pain, urinary retention, withdrawal)

Atrial Fibrillation/Flutter

See Atrial fibrillation section

Multifocal atrial tachycardia

Mechanism/etiologies: multiple atrial premature beats from hypoxia/increased atrial pressure.
Characteristics: ≥3 p wave morphologies. Irregular rhythm. Gradual onset and termination. Rate 100-150.
Management: BBs and non-DHP CCBs can be effective, address underlying issue

AVNRT/AVRT

Mechanism/etiologies: - AVNRT - reentrant loop that involves the AV node and the atrial tissue causing simultaneous depolarization of the atrium and the ventricle. - AVRT - Involves an accessory pathway that bypasses the normal insulation provided by the atrioventricular valves, allowing conduction between the atria and ventricles

Characteristics: - AVNRT: P wave rarely seen (buried in QRS). - AVRT: in narrow complex (orthodromic), P after QRS; in wide complex (antidromic), P rarely observed (buried in T wave)

Management: - Vagal maneuvers (1st line): Sit pt upright → have them blow into tip of 10cc syringe for 10-15 seconds → rapidly lay supine and raise legs - Adenosine (2nd line): therapeutic (break AVRT/AVNRT and 80% of atrial tachycardias) and diagnostic (allows visualization of underlying rhythm) - Would try and have continuous 12 lead EKG on while pushing adenosine to try and catch the underlying rhythm - Do NOT give in heart transplant, severe COPD, pre-excitation causing wide complex tachycardia (WPW → antidromic AVRT) - Peripheral at AC or above w/ arm elevated: 6mg x1 → 6mg x1 (if not effective after 1-2 min) →12mg x1 (if refractory to 6mg) - Central: cut dose in half to 3mg x1 → 3mg x1 → 6mg

Dosing

Drug	Dosing	Benefits	Side Effects
Metoprolol	5mg IV q5m x3 PO metop tartrate 12.5mg q6h, ↑ every 6h to target	Good 1st line agent Less BP effect than dilt	Hypotension, Negative inotropy
Diltiazem	10-20mg IV over 2m q15m x2 drip = 5-15mg/h	Good 1st line w/ normal EF with drip needed	Hypotension Do NOT use in HFrEF
Esmolol	500mcg/kg bolus drip = 50-200mcg/kg/min	Rapid onset/offset RBC metabolism	Hypotension
Amiodarone	150mg IV over 10-30m, then 1mg/m for 6h, then 0.5mg/m for 18h	Minimal BP effects Long lasting; Relatively fast onset (acute effect is mostly beta blockade)	Pulmonary and thyroid toxicity Cardioversion
Digoxin	500mcg IV x1, then 250mcg IV q6h x2-3	Great for reduced EF, positive inotropy Slow onset	Depends on vagal tone – poor in hyper-adrenergic states
Procainamide	20-50mg/min loading, 1-4mg/min maintenance	Use in pre-excitation syndromes (i.e. WPW), does not inhibit AV nodal conduction	Lupus-like syndrome Hypotension

Tachyarrhythmias - Wide Complex and PVCs

Author: Cesar Campos

Definitions

Premature Ventricular Complex (PVC): early ventricular depol +/- mechanical contraction
PVCs are common: Up to 80% of apparently healthy people have PVCs
PVC induced cardiomyopathy may be present with PVC burden >10-20%
Inpt Eval: Order 12 lead EKG to look for conduction disease (Long QT, brugada), K, Mg, TSH, Drug screen (EtOH, nicotine, stimulants, caffeine), med rec for QT prolonging agents, tele to assess PVC burden
Inpt management: consult to EP for PVCs rarely warranted unless significant PVC burden (>5 PVC/min, consistently) in setting of reduced LVEF.
For pts with >5 PVC/min or pts with symptoms, discharge with Ziopatch (VA) or mobile cardiac telemetry (VU) and obtain TTE if not done in past 3 months.
Ventricular tachycardia: a run of 3+ PVCs
Sustained VT: VT for >30 seconds or shorter if it requires intervention
Nonsustained VT (NSVT): VT for < 30 seconds
VT storm: 3+ separate episodes of sustained VT within 24 hrs.

VT Morphologies

Monomorphic VT: similar QRS configuration from beat to beat
Usually 2/2 scar-mediated VT from prior infarction
Polymorphic VT: a continuously changing QRS configuration from beat to beat
Ischemia until proven otherwise
Torsades de Pointes: a form of polymorphic VT with a continually varying QRS that appears to spiral around the baseline of the ECG in a sinusoidal pattern
Ventricular fibrillation (VF): chaotic rhythm characterized by undulations that are irregular in timing and morphology, without discrete QRS complexes
Wide-complex tachycardia (WCT): QRS >0.12 seconds and HR >100 beats/min

Wide-complex tachycardia evaluation

WC-caused by ventricular arrhythmias (ventricular tachycardia or ventricular fibrillation) or supraventricular tachycardias with aberrant conduction resulting from one of the following: disease in the His–Purkinje system, such as left or right bundle-branch block; a bypass tract (i.e., Wolff–Parkinson–White syndrome), with depolarization of the ventricle from the bypass tract; or a ventricular paced rhythm from a pacemaker.
Of note, a bundle branch block may appear with faster or slower heart rates and disappear with normal heart rates (ie, rate dependent).

To differentiate between WCTs: - Regular WCT: monomorphic VT or SVT with aberrant conduction - Look at baseline rhythm: If QRS morphology identical to those seen in sinus rhythm, likely SVT with aberrant conduction; if not, likely monomorphic VT - If AV dissociation present and ventricular rate faster than, atrial rate, then it is likely VT. - If an escape beat or fusion beat is seen, this would also support VT - If AV dissociation present and ventricular rate faster than atrial rate, likely VT - Positively or negatively concordant QRS complexes in precordial leads suggest VT. - Irregular WCT: atrial fibrillation with aberrant conduction (if same QRS morphologies) or polymorphic VT (if different QRS morphologies)

Management

Unstable: - Sedate with midazolam 1-2mg - Cardioversion for monomorphic VT. Synchronized shock at 100-200J - Defibrillation if VF/polymorphic VT

Stable:

Drug Name (Antiarrhythmic class)	Dosing	Side Effects
Amiodarone (class III)	150mg IV over 10 min, then 1mg/min for 6 hours; repeat bolus if VT recurs	Bradycardia, hypotension (acutely)
Lidocaine (class IIB)	1-1.5mg/kg (usually 75-100mg) at a rate of 25-50mg/min; lower doses of .5-.75mg/kg can be repeated every 5-10min as needed	Slurred speech, AMS, seizures, bradycardia
Procainamide (class IA)	20-50mg/min until arrhythmia terminates or max dose 17mg/kg is reached	Bradycardia, hypotension, torsades, drug-induced lupus Avoid in HF pts, prolonged QT

Cardioversion if refractory to medical management
Treatment of underlying cause if identifiable: Ischemia, electrolyte disturbances, heart failure, drugs

Atrial Fibrillation and Flutter

Author: Michael Daw

Background

AF: 12-lead EKG with absence of p-waves and irregularly irregular QRS complexes
Flutter: sawtooth atrial F waves (300 BPM) with regular or regularly irregular QRS complexes
Ventricular rate ratio of F waves: V waves ~150 (2:1), ~100 (3:1), or ~75 (4:1)
4 classifications:
Paroxysmal (intermittent and terminates <7 days)
Persistent (continuous >7 days)
Longstanding persistent (continuous for >12 months)
Permanent (normal rhythm cannot be restored or no further attempts to restore it)
Rapid ventricular response (RVR) is HR > 100 (i.e. AF/Flutter w/ tachycardia)
AF/RVR is far more often a consequence of hypotension than the cause of it.

Evaluation

Causes: Mnemonic "H PIRATES": - Hypertension - Pneumonia - Pericarditis - Post-op - Ischemia (rare) - Rheumatic Valve - Atrial Myxoma or Accessory Pathway - Thyrotoxicosis - Ethanol, Electrolytes, or Excess Volume - Sick sinus, Sepsis - Additional causes: Lung disease (COPD, asthma, smoking), OSA, obesity

Management

Treatment goals: - Rate control, Goal HR < 110 (RACE II) - Rhythm control (if indicated) - Stroke prevention (CHADS2VASc)

Rate control: - RVR ~ sinus tach of AF; Always work to address the underlying cause (infection, volume overload, etc.). Rate control is rarely an emergency unless the pt is unstable - Unstable (SBP <80): Cardioversion - Stable (SBP >90): IV AV nodal blockers if HR > 130 or symptomatic (metop 5mg IV or dilt 15-20mg IV, every 15 minutes up to 3x), otherwise opt for PO

B-blockers: Start with metop tartrate (titratable) → consolidate to succinate. Avoid in decompensated or borderline HF
Calcium channel blockers (diltiazem): DO NOT give in HFrEF
Peri stable (SBPs 80-90s w/ preserved perfusion):
Amiodarone: Consider if decompensated HF, anti-coagulated. Caution that you may cardiovert pt (stroke risk)
Digoxin: consider if decompensated HF, will require IV loading dose prior to transition to PO. Will need to monitor digoxin levels
Avoid AV nodal blockers and amiodarone in AF with preexcitation (WPW) as these can trigger Vfib, consider procainamide in consultation with cardiology

Rhythm Control: - Consider in new onset AF (first time diagnosis), symptomatic AF, younger patients, high cardiovascular risk, or heart failure not acutely decompensated (EAST-AFNET 4) - If onset clearly within 48h, can proceed without TEE. Often TEE is done anyway (pt may have had intermittent asymp AF) - If onset >48h or unclear, will need TEE to rule out LAA thrombus; you can also anti-coagulate for 3 weeks prior to TEE if unable to get TEE. - Pharmacologic options include class 1C: flecainide, propafenone (avoid in structural heart disease) and class 3: Amiodarone, dronedarone, sotalol, ibutilide, dofetilide (some require loading inpt) - Caution using antiarrhythmics in any pt you wouldn't cardiovert without TEE - Consider EP consult for ablation in symptomatic paroxysmal or persistent AF refractory to anti-arrhythmic drugs, AF in HFrEF, or flutter in outpt setting

Stroke Prevention (for AF and flutter): - If cardioversion planned for new onset AF, start AC as soon as possible - Post-cardioversion, must be on anticoagulation for at least 4 weeks d/t atrial stunning and stroke risk - CHA2DS2-VASc risk score >2 in M or >3 in F should prompt long term AC in AF persisting >48 hours, even after successful rhythm control - DOACs (apixaban, dabigatran, edoxaban, rivaroxaban) are preferred to warfarin except in moderate to severe MS or mechanical valve - For apixaban, consider reduced dose 2.5 mg BID if age >80, body weight <60 kg, or serum Cr >1.5 mg/dL - Typically, do not need to bridge AC for AF in the setting of procedures unless mechanical valve is present. Decide on a case by-case basis - Left atrial appendage closure (WATCHMAN, Amulet) can be considered in those with increased risk of bleeding, but post-operative oral AC plus aspirin is typically required for 45 days, followed by DAPT for 6 months.

Heart Failure

Author: Matthew Alonso

Background

ACC/AHA Stages of HF

Stage A: At risk but without structural heart disease, symptoms, or cardiac biomarkers
Stage B: no symptoms/signs of HF; presence of structural heart disease, incr filling pressures, or incr cardiac biomarkers
Stage C: + structural HD, + prior or current symptoms
Stage D: end stage/refractory HF, symptoms interfered with daily life and recurrent hospitalizations

NY Heart Association (NYHA) Functional Classes of HF

Class I: Ordinary physical activity does not cause symptoms of HF. No limitation of physical activity.
Class II: Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF.
Class III: Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF (such as walking short distances).
Class IV: Unable to perform any physical activity without symptoms of HF, or symptoms of HF at rest.

Nomenclature

HF with reduced EF (HFrEF): HF with an LVEF of ≤40%
HF with mildly reduced EF (HFmrEF): HF with an LVEF of 41% to 49%
HF with preserved EF (HFpEF): HF with an LVEF of ≥50%
HF with recovered EF (HFrecEF): HF with a baseline LVEF of ≤40%, a ≥ 10-point increase from baseline LVEF, and a second measurement of LVEF of >40%

Etiologies

HFrEF (clinical diagnosis + LVEF < 40%)

Ischemic (approx. 2/3): Obstructive CAD, previous/current myocardial infarction

Non-ischemic: - Load: HTN, valvulopathy - Arrhythmia: tachyarrhythmia, pacemaker induced - Myocardium: - Toxins (EtOH, drugs, chemo, radiation) - Inflammatory (autoimmune, peripartum CM, infectious, eosinophilic, giant cell, hypersensitivity) - Metabolic (thyroid, thiamine deficiency, DM) - Infiltrative (amyloid, sarcoid, hemochromatosis) - Stress-induced/Takotsubo CM - Genetic - Idiopathic

HFpEF: HTN, CAD, obesity, DM, CKD, infiltrative, hypertrophic cardiomyopathy

Causes of Heart Failure Exacerbations (FAILURES)

Forgetting medications or taking drugs that can worsen HF (e.g. BB, CCB, NSAIDs, TZDs), chemo (anthracyclines, trastuzumab)
Arrhythmia/Anemia: AF, VT, PVCs; Increased arrhythmia burden on device check?
Ischemia/Infarction/Infection: myocarditis; Acute vascular dysfunction (e.g. endocarditis), especially mitral or aortic regurgitation.
Lifestyle choices: Dietary indiscretions - high salt, EtOH, excessive fluid intake. Obesity.
Upregulation (of CO): pregnancy and hyperthyroidism
Renal failure: acute, progression of CKD, or insufficient dialysis
Embolus (pulmonary) or COPD
Stenosis (worsening AS, RAS)

Presentation

Volume overload: shortness of breath, dyspnea on exertion, Orthopnea, PND
Nausea/poor PO intake (hepatic and gut congestion)
Confusion (decreased CO)
Exam: Edema (legs, sacrum), rales, S3, S4, murmur (AS, MR), elevated JVD, + hepatojugular reflux, ascites

Evaluation

CBC, CMP, Magnesium, Lactate, TSH, iron studies
Troponin, ECG
BNP (Pro-BNP if on Entresto) – high negative predictive value for HF (false negative can occur in obese pts)
CXR – differentiate other causes of dyspnea
TTE
Determine hemodynamic and volume profile:

Volume Status	Euvolemia	Hypervolemia
Cardiac Index	Low	Normal
Warm Extremities Adequate UOP Nl Pulse Pressure	Warm and Dry Forrester Class I Tx: GDMT as tolerated	Warm and Wet Forrester Class II Tx: Diuresis, Vasodilators
Cardiogenic Shock Cool Extremities Renal Failure Narrow Pulse Pressure	Cold and Dry Forrester Class III Tx: Inotropes	Cold and Wet Forrester Class IV Tx: Diuresis +Tailored therapy (+/- vasodilators, inotropes)

Management of exacerbations

Tele, Daily STANDING weights, 2L fluid restriction, 2g sodium diet, strict I/Os
Diuresis: Place on 2.5 x home dose of IV diuretic, dose BID-TID
Goal is to be net negative (generally 1-2L per day but patient dependent)
Check BMP BID and Mg QD, keep K>4 and Mg>2
Low threshold for substantial increase (double) in loop vs transition to drip if not diuresing adequately vs augment with sequential nephron blockade (thiazides, acetazolamide)
Continuation/optimization of GDMT (below)

Advanced Diuretic Management

Diuretic Conversion: - Bumetanide 1mg IV = Furosemide 40mg IV (Torsemide not available IV) - Bumetanide 1mg PO = Torsemide 20mg PO = Furosemide 80mg PO

Diuretic Resistance & Augmentation strategies: - Can switch to lasix drip after bolus - Consider secondary diuretics: Thiazide (most effective option), Metolazone 2.5-10mg PO (distal tubule) OR Chlorothiazide (Diuril) 250-500mg IV (if IV option needed), Acetazolamide (Diamox) 250-500mg IV (proximal tubule)

Use of SGLT2i in Acute HF: - Dapagliflozin/Empagliflozin can be initiated in hospitalized patients on the first day even if they are not diabetic.

Guideline-Directed Medical Therapy for HFrEF

General Principles: - Starting pts on low dose of multiple agents preferred to max dose of single agent - D/C summary should have discharge weight, GDMT and diuretic regimen, and renal function - Daily home weights w/ rescue diuretic plan (pm dose for 3lbs in 1 day, 5lbs in 1 week)

Common Drugs	Indication	Mechanism/Benefits	Precautions
Beta Blockers Carvedilol Metoprolol succinate Bisoprolol	HFrEF <40 % Stage C HF (NYHA class I – IV)	Blocks catecholamines. Decreased HR/myocardial oxygen demand Less adverse remodeling.	Avoid if pt is decompensated (cold); "start low and go slow" Can continue during exacerbation if pt compensated
ARNIs Sacubitril/valsartan	HFrEF < 40% NYHA class II – IV Used in place of ACE/ARB	Prevents vasoactive natriuretic peptide degradation involved in pathogenesis of HF (+ action of ARB)	Need 36h wash-out period if transitioning from ACEi to ARNI. Hypotension Risk of angioedema
ACEIs/ARBs Lisinopril Enalapril Losartan Valsartan	HFrEF <40 % Stage C HF (NYHA class I – IV)	Blocks RAAS activation Reduces adverse cardiac and vascular remodeling	Risk of angioedema Monitor renal function and K Preference for ARB > ACEi if plans to start ARNI
MRAs Eplerenone Spironolactone	NYHA class II-IV and GFR >30 and K <5	Diuretic and blood pressure lowering effects and blocks deleterious effects of aldosterone on the heart (including hypertrophy and fibrosis)	Hyperkalemia
SGLT2i Dapagliflozin Empagliflozin	HFrEF <40% with and without DM NYHA class II-IV	Osmotic diuresis and natriuresis, improve myocardial metabolism, inhibit sodium-hydrogen exchange in myocardium, reduce cardiac fibrosis	UTI/ GU infections Risk of ketoacidosis (both DKA and euglycemic)
Vasodilators Hydralazine Isosorbide Dinitrate	Persistently symptomatic black pts despite ARNI/BB/MRA/SGLT2i NYHA class III-IV	Reduces cardiac afterload and preload and may also enhance nitric oxide bioavailability Reduction in mortality for African American pts	Hypotension
Ivabradine	HFrEF <35%, on maximally tolerated BB, sinus rhythm with HR > 70 NYHA class II or III	I(f) current inhibitor involved in SA node activity Decr HR associated with improved outcomes	Need sinus rhythm Caution in sinus node disease and conduction defects
Iron Repletion (IV) Iron sucrose Ferric carboxymaltose Iron dextran	Ferritin <100 µg/L or ferritin 100-299 µg/L AND transferrin saturation <20%	Decreases HF hospitalizations Improves exercise function and QOL	Risk of anaphylaxis higher in iron dextran

Device therapies (after optimization of medical GDMT for 3 months):

Cardiac resynchronization therapy (CRT) - Class I indication: NYHA class II–IV, LVEF ≤35% with QRS ≥150 ms and left bundle branch block (LBBB)

ICD - Class I indication: primary prevention for ischemic or non-ischemic CM, NYHA class II–III with LVEF ≤35% (must have >1yr expected survival and 40+ days from MI) - Secondary prevention for patients who have survived cardiac arrest due to ventricular fibrillation or hemodynamically unstable ventricular tachycardia

Mitra Clip - Criteria: moderate-to-severe or severe secondary mitral regurgitation, on maximally tolerated GDMT, an EF >20% and <50%, and a left ventricle end-systolic dimension < 7cm

CardioMEMS - NYHA II-III symptoms who have had a hospitalization for HF in the past year or with elevated BNP to reduce risk of subsequent HF hospitalizations

Guideline-Directed Medical Therapy for HFpEF

Medications overlap with HFrEF treatment (above) but outcomes are less significant - SGLT2 inhibitors can decrease HF hospitalizations and CV mortality - MRAs can decrease HF hospitalizations - ARBs and ARNis can be used to decrease hospitalizations - Diuretics as needed for congestion (no morbidity or mortality benefit)

Consider GLP1-agonists patients with concomitant obesity.

Cardiogenic Shock

Author: Matthew Alonso

Definition

Impairment of CO due to primary cardiac disorder that results in end-organ hypoperfusion and hypoxia
Mortality up to 40-50%

Etiology

Cardiomyopathic: acute myocardial infarction with LV dysfunction (most common cause), exacerbation of heart failure, PHTN exacerbation, myocarditis, myocardial contusion, drug-induced
Arrhythmogenic: atrial tachycardias (atrial fibrillation/flutter, AVRT, AVNRT), VT/VF, complete heart block, 2nd degree heart block
Mechanical: valvular insufficiency, valvular rupture, papillary muscle rupture, critical valvular stenosis, ventricular septal wall defect, ruptured ventricular wall aneurysm, atrial myxoma, HOCM

Presentation and diagnostic criteria

Signs of end-organ hypoperfusion - AMS, cold and clammy skin, decreased UOP (<30cc/hr), and elevated lactate (>2).
SBP < 90 mmHg for >30min or needing vasopressors to achieve this goal
Drop in MAP >30mmHg below baseline or MAP <60mmHg
Cardiac index <1.8L/min/m² without hemodynamic support or <2.2L/min/m² with support
PCWP >15mmHg

SCAI Classification

Stage A: At Risk – Normotensive with normal perfusion
Stage B: Beginning (Pre-shock) - Hypotension without hypoperfusion. CI >2.2
Stage C: Classic Cardiogenic Shock – Hypotension and hypoperfusion. Clinical signs cold, clammy skin, altered mentation, and decreased urine output, elevated lactate. CI <2.2, PCWP >15
Stage D: Deteriorating – Worsening hemodynamics despite initial interventions, requiring escalating use of pressors or MCS to maintain SBP and end-organ perfusion.
Stage E: Extremis – Refractory hypotension and hypoperfusion requiring multiple simultaneous acute interventions, often experiencing cardiac arrest requiring CPR and/or ECMO.

Evaluation

EKG, CBC, CMP, BNP, troponin, lactate
Echocardiogram: assess EF and valves
LHC if ischemic (see ACS)
Hemodynamic monitoring via Swan-Ganz or PA catheter:
No benefit for general shock but does improve in-hospital mortality for those with cardiogenic shock
PA catheter hemodynamic profile:
- Cardiac index < 2.2 with support or <1.8 without support, cardiac power <0.6, SVR >1200 initially, then may drop <800 as systemic inflammation causes vasodilation, SVO2 (mixed venous O2 sat) <60%, RVEDP >10
- LV-dominant: PCWP >RA (CVP), PAPi >1.5 (pulmonary artery pulsatility index = (Pulmonary Artery Systolic Pressure - Pulmonary Artery Diastolic Pressure) / Right Atrial Pressure)
- RV-dominant: RA >15, PCWP <15, PAPi <1.5
- Bi-V-dominant: RA >15, PCWP >15, PAPi <1.5
- PAPi < 0.9 predicts RV failure and that pt will likely need RV support. PAPi <1.85 predicts RV failure in pts with LVADs
- CPO < 0.6 strongest independent hemodynamic correlate of mortality in CS
- See right heart cath section for interpreting PA catheter profiles
- While on CCU rotation, CCU swan sheet provided by Chiefs prior to start. Equation is built into the spreadsheet, although you will need to make sure to input patient specific height and weight metrics in top right corner of sheet.
- On CCU, update swan sheet Q4H for patients with active Swan-Ganz or PA catheters. Utilize hemodynamics/filling pressures that correlate with timing of draw of MVO2 as this is the value that was zeroed by nursing staff.
- Thermodilution: uses temperature gradient between two points along PA catheter.
- Clinical conditions that compromise accuracy of thermodilution measurements due to underestimation or overestimation of cardiac output: valvular regurgitation, intracardiac shunts, and very low flow states

Management (medical & mechanical circulatory support)

Medical management: focus on optimizing preload, afterload, and contractility - Preload: IV diuresis – hypotension IMPROVES with diuresis in cardiogenic shock - Afterload: IV – nitroglycerine, nitroprusside; PO – captopril, hydralazine, isosorbide dinitrate; vasoconstricting pressors (norepinephrine, vasopressin, phenylephrine) if needing BP support - Contractility - Inodilators (increase contractility, decrease afterload – milrinone, dobutamine) or inoconstrictors (increase contractility and afterload – epinephrine, norepinephrine)

Mechanical circulatory support indications: - Shock refractory to >1 pressor - Shock 2/2 MI (physiology: unloads LV, increases systemic perfusion, increases myocardial perfusion, and provides hemodynamic support during PCI)

Types of mechanical circulatory support (MCS):

	Intra-aortic Balloon Pump	V-A ECMO	Tandem Heart	Impella
Mechanics of Support	Balloon pump placed in the proximal aorta that inflates during diastole (increasing coronary perfusion) and deflates during systole (LV afterload reduction)	Blood from femoral vein is oxygenated and pumped to femoral artery	LV: blood aspirated from LA to femoral artery RV: blood aspirated from RA to PA	Impella 5.5 & CP: Blood aspirated from LV and ejected to aortic root Impella RP: Blood aspirated from IVC and delivered to PA
Flow	0.5-1 L/min	4-6 L/min	4-5 L/min	2.5-5 L/min
Support	LV	BiV	LV, RV, or BiV	LV or RV (RP)
Hemodynamics	Reduces afterload and LVEDP → decr cardiac work, O2 consumption Increases SV Increases coronary perfusion	Increases afterload Reduces SV Reduces LV preload and PCWP Improves tissue perfusion	Increases afterload Reduces SV Reduces LV preload and PCWP Improves tissue perfusion	Reduces SV Reduces preload and PCWP Improves tissue perfusion
Complications	Infection, stroke, thrombocytopenia, balloon malpositioning leading to ischemia, aortic rupture, air embolism	Circuit thrombosis, LV dilation. Hypothermia, air embolism, bleeding, thrombocytopenia	Tamponade d/t perforation, bleeding, femoral AV fistula, thromboembolism, ASD, limb ischemia	Pump migration, bleeding, hemolysis, thrombocytopenia, aortic regurg, stroke, perforation, VT/VF, vascular injury

Possible contraindications to mechanical circulatory support (right or left sided support): - Severe aortic regurgitation, intracardiac shunt via ASD, VSD, or PFO, severe RV dysfunction, LA or ventricular thrombus, aortic dissection, severe peripheral arterial disease/inability to achieve adequate vascular access, uncontrolled sepsis, severe coagulopathy or bleeding diathesis

Daily management of MCS devices: - Ensure optimal placement of device with daily CXR (IABP) / Echo (Impella) - Anticoagulation (based on device) - Hematoma monitoring at device site - Check distal pulses to monitor for limb ischemia - Check urine color to monitor for hemolysis (Impella) - IABP: Ensure that the balloon inflation and deflation are synchronized with the cardiac cycle. Inflation should occur at the onset of diastole (middle of the T-wave on ECG) and deflation at the onset of systole (peak of the R-wave on ECG).

Cardiac Devices

Author: Daniela Gomez Zubieta

1. Pacemakers

A device that maintains or restores a normal heart rhythm by stimulating the myocardium.

Peripheral permanent pacemakers (PPMs) - SubQ generator, transvenous leads - Single chamber: RV (most common) or RA lead - Dual chamber: RV and RA leads - BiV (CRT- cardiac resynchronization therapy): RV, RA, and LV (coronary sinus) leads

Leadless pacemaker (Micra) - Implanted generator in RV

Indication: (class 1 indications below, refer to ACC/AHA guidelines for class 2 and 3) - Sinus node dysfunction (sinoatrial exit block, sinus pause, sinus bradycardia, tachy-brady syndrome) - AV block (Mobitz II, 3rd degree, 2nd degree of any kind w/ symptomatic bradycardia, chronic bifasicular block - Persistent symptomatic 2nd or 3rd degree block after acute MI - Neurocardiogenic syncope

2. Implantable Cardioverter/Defibrillators (ICDs):

Transvenous: defibrillation coil +/- pacing lead - Detect and treat VT/VF - Anti-tachycardic pacing (ATP)- attempts to pace out of VT to prevent a shock - Defibrillation if ATP unsuccessful

Subcutaneous: defibrillation only, all extravascular

Indications:

Primary prevention: - HFrEF - EF <35% and NYHA II-III or EF <30% and NYHA I - Must be >90d from revasc, >40d from MI, and on GDMT >90d if non-ischemic - Arrhythmogenic syndromes - Arrhythmogenic RV cardiomyopathy, Brugada syndrome, HCM and cardiac sarcoid with specific risk factors

Secondary prevention: - Sudden cardiac death - Sustained VT/VF (spontaneous sustained, cardiac arrest 2/2 VT/VF) - Inducible VT on EP study with history of syncope

3. Cardiac Resynchronization Therapy (CRT)

BiV pacer that coordinates LV/RV contraction through synchronized activation of each ventricle following atrial contraction.
P: CRT pacing only
D: ICD function

4. LVADs

Augment cardiac output for end-stage heart failure

Examples of Common Pacing Modes on PPM:

VVI: Single RV lead that delivers a beat if no beat sensed. Often used with chronic AF with bradycardia
DDDR: Senses and paces both the atria and ventricle. If beat not sensed within a predefined interval, beat delivered. R indicates rate responsivity (changes rate based on changes in pt activity)
Magnet: Paces at a fixed rate without respect to native electrical activity (AOO,VOO,DOO). Deactivates ICD shock. Often used in surgery or at end of life to avoid ICD shocks

Peri-Procedural Anticoagulation:

NOAC: hold 24-72h before procedure and 24-72h following procedure
Warfarin: continue through procedure
Antiplatelet: continue through procedure
Heparin and heparin related products to be avoided peri-implantation due to higher rates of pocket hematoma

Placement Complications

Pocket hematoma
Pneumothorax
Myocardial Perforation
Lead Displacement
Lead Disconnection
Cardiac Tamponade
Infection

Long term Complications

Secondary device Infection
Lead fracture (lead lifetime 10-15 years)
Insulation failure

The Pacemaker ID app is free and is useful for identifying device brand for interrogation

When differentiating PPM vs. ICD, look for a coil and charge generator to identify the ICD.

Pulmonary Embolism

Author: Matthew Alonso

Background

A thrombus originating in a deep vein (LE > UE) embolizing to the pulmonary arterial circulation
Risk Factors = Virchow's Triad:
Stasis: immobilization, hospitalization, spinal cord injury, or long travel
Hypercoagulable state: cancer, prothrombotic genetic conditions, OCPs, nephrotic syndrome, peri-partum, infection, autoimmune disease, etc.
Endothelial Injury: surgery, trauma, CVC, recent major infection/sepsis
Most originate from a DVT in the iliac, femoral, and popliteal veins

Presentation

Dyspnea and tachypnea
Respiratory alkalosis on blood gas from hyperventilation
Hypoxemia
Sinus tachycardia or atrial arrhythmias
Hypotension
Hemoptysis
Lower extremity pain, swelling, and redness – occurs in 50% of pts with DVT
RV Failure (large PE) – elevated JVP, hypotension, syncope, R parasternal heave, accentuated P2, hepatomegaly
Other: S3/S4, pleural friction rub, decreased breath sounds, wheezing, fever

Evaluation

If hemodynamically unstable and PE suspected, provide hemodynamic support (ie. O2, pressors, etc.) and perform emergent bedside TTE - If no RV strain evident on TTE, low likelihood of hemodynamically significant PE. Consider other causes of shock. - Signs of RV strain: D-sign (flattened interventricular septum during systolic) and McConnell's sign (hypokinetic mid-free wall of RV with preserved contractility of RV apex)

Hemodynamically stable:

EKG: - Most commonly sinus tachycardia, but could see a fib vs flutter - Less commonly and indicative of large PE: Right axis deviation, RVH, RBBB, RA enlargement, S1Q3T3 (deep S in lead I, deep Q and inverted T in lead III), TWI in V1-V3

CXR: Typically normal

Labs: ABG, troponin, BNP, lactate, coags

May consider lower extremity dopplers

Imaging vs d-dimer based on pre-test probability: - Low pre-test probability (use Wells Criteria) → d-dimer - For moderate to high pre-test probability → CTA Chest PE protocol - If high pre-test probability or moderate pre-test probability with >4h delay in workup, start empiric anticoagulation if bleeding risk is acceptable while work-up is ongoing

TTE

Risk stratification: PE Severity Index (PESI): Predicts 30-day outcome of patients with pulmonary embolism

Management

Categorization of PE	Low Risk	Intermediate-Low Risk	Intermediate-High Risk	High Risk
Definition	Hemodynamic stability No evidence of right heart strain on TTE or CT or myocardial necrosis (hs-TnT) or ventricular stretch and pressure overload (BNP) on labs	Hemodynamic stability Either elevated cardiac biomarkers (hs-TnT & BNP) or evidence of RV strain on imaging (TTE or CT)	Hemodynamic stability. Both elevated cardiac biomarkers and imaging evidence of RV dysfunction	Hemodynamically unstable (ex: SBP<90) Elevated cardiac biomarkers (hs-TnT & BNP) Imaging evidence of RV dysfunction (TTE or CT)
Management	Start AC: LMWH or heparin gtt (if renal impairment) Rivaroxaban & apixaban can be used as initial management. Edoxaban & dabigatran can be used after 5-10d of parenteral therapy	Provide hemodynamic support (cautious IVF, O2: HFNC), monitor for decompensation Start AC w/ unfractionated heparin gtt Consult cardiology for consideration of catheter directed thrombolysis (EKOS) or embolectomy Transition to LMWH when clinically appropriate if renal function allows	Provide hemodynamic support (cautious IVF, O2: HFNC), monitor for decompensation Start AC w/ unfractionated heparin gtt. Consult Cardiology for consideration of catheter directed thrombolysis (EKOS) or embolectomy Transition to LMWH when clinically appropriate if renal function allows	Provide hemodynamic support (cautious IVF, vasopressors, inotropes, O2: HFNC) STAT page CCU fellow Discuss with PERT team systemic thrombolytic therapy vs catheter-based thrombolysis, thrombectomy and/or surgical embolectomy If impending circulatory collapse, discuss ECMO AC: LMWH vs UFH (w/ bolus)

tPA Considerations

Most effective within 24 hours but effective up to 14d
Contraindications:
Absolute:
- CNS Pathology: hemorrhagic or ischemic CVA within 3mo, AVM, CNS neoplasm, recent surgery
- Trauma: Recent head trauma w/ fx or injury
Relative:
- Surgery: surgery w/in 3wks
- Heme: active bleeding, bleeding diathesis, plt < 100, oral AC
- Age: >75yo, dementia

Long-term management

Anticoagulation: - NOAC - Remember to give initial loading dose (duration of load varies with each agent) - Warfarin (Coumadin): Goal INR 2-3, requires frequent monitoring - Need to bridge with heparin or lovenox - Pharmacy consult, and will need to be set up with coumadin clinic at the time of discharge

IVC filter: only if AC is contraindicated, bleeding risk unacceptably high, recurrent VTE despite optimal AC, patients undergoing major surgery with recent VTE and require temporary interruption in AC - Placed by IR or Interventional cards

Duration of Anticoagulation:

Major reversible/transient risk factors (surgery, trauma): 3-6 months
Idiopathic, unprovoked, or with less compelling risk factors: 12 months
Major permanent risk factors (cancer, homozygote F5L or prothrombin gene mutation, APLS, protein C/S deficiencies, AT III deficiency): At least 1 year, preferably lifelong.
Recurrent DVT/PE: lifelong (consider etiology)
Chronic Thromboembolic Pulmonary Hypertension (CTEPH): lifelong

Syncope

Author: Michelle Chintanaphol

Background

Definition: abrupt, transient loss of consciousness with rapid & spontaneous recovery

Classification

Cardiac syncope - can have sudden onset with little or no prodrome - Tachyarrhythmias: VT, SVT - Brady-arrhythmias: sinus node dysfunction, AV blocks (high grade) - Structural: Aortic Stenosis, HCM, cardiac tamponade, congenital anomalies, masses/tumors, ICM or NICM causing low cardiac index - Obstruction: Pulmonary embolism, severe pHTN - Aortic dissection

Noncardiac syncope: - Orthostatic hypotension - Autonomic dysfunction - Medication-induced (diuretics, nitrates/CCB/alpha blockers, TCAs) - Volume depletion (hemorrhage, dehydration) - Vasovagal (stress-mediated with prodromal symptoms) - Situational (micturition/defecation/coughing/laughing) - Carotid sinus sensitivity syndrome (pause for >3 sec and/or decrease in systolic pressure >50 mmHg after stimulation of carotid sinus) - Postural orthostatic tachycardia syndrome

Differential diagnosis: - Seizure, stroke/TIA, subclavian steal, metabolic derangements, Intoxication/withdrawal, hypoglycemia, head trauma/concussion - With rare exceptions, these do not result in complete LOC with spontaneous recovery

Evaluation

Characteristics associated with cardiac syncope: - Male, >60, known structural/ischemic heart disease, brief/no prodrome, palpitations, syncope while supine/at rest or during exercise, family hx of SCD/premature death, abnormal exam, abnormal baseline ECG

Characteristics associated with noncardiac syncope: - Younger age, syncope with positional changes, prodrome (nausea, vomiting, warmth), triggers, normal baseline ECG

Workup

EKG on all pts with syncope, monitor those who are admitted on telemetry
CBC, CMP, troponin, BNP (If cardiac cause suspected), POC glucose, UDS, orthostatic VS
TTE and consider stress testing particularly in exertional syncope
EEG and neuroimaging if high concern for seizure activity or focal neuro deficit (neuro testing comes at high cost and low diagnostic yield)
Consider based on clinical suspicion: A1C, Vitamin B12, iron studies, TSH, free light chains/SPEP/UPEP if concerned for amyloidosis

Management - dependent on suspected cause of syncope

Cardiac: - If arrhythmia is suspected but not captured on admission, consider discharge with event monitor - Monitoring duration should be equal to or greater than the frequency of events (e.g. If the symptoms occur roughly once a month, monitoring duration should be at least a month)

Noncardiac:

Reflex: - Vasovagal - consider tilt table testing if recurrent or diagnosis not clear - Situational - mainly avoiding triggers - Carotid sinus syndrome- may require PPM

Orthostasis: - Medication related: - Appropriate to hold potentially offending medications (diuretics, vasodilators, anti-hypertensives) during evaluation - Monitor for worsening supine hypertension, arrhythmias, or heart failure when holding - Volume depletion; resuscitate as appropriate and re-measure orthostatic vitals - Autonomic dysfunction: see autonomics section

Driving: TN law does not require any MD to inform the state of TLOC

Valvular Heart Disease

Aortic Stenosis

Author: Michelle Chintanaphol

Etiology

Fibrosis and degenerative calcification of the aortic cusps
Congenital bicuspid aortic valve
Chronic deterioration (calcific) of tricuspid aortic valve
Prior rheumatic fever
Less common causes: SLE, Fabry disease, radiation, inflammation

Presentation

Usually asymptomatic, though could have exertional dyspnea, decreased exercise tolerance, exertional dizziness/lightheadedness, syncope, exercise-induced angina, heart failure (worse prognosis) when severe
Typically, aged 70–80 yo; if bicuspid aortic valve expect 10-20 yrs earlier

Physical exam: - Loud, late-peaking systolic crescendo-decrescendo murmur in right intercostal space that radiates towards the carotids - Signs of severe AS: late peaking murmur, faint or absent S2, or "parvus et tardus" (delayed and reduced/low volume carotid upstroke)

Evaluation

TTE with doppler is test of choice for diagnosis and evaluation

Severity	Valve Area (cm²)	Mean Gradient (mmHg)	Velocity (m/s)	Indexed Valve Area (cm²/m²)
Mild	>1.5	<20	2.0-2.9	>0.85
Moderate	1.0-1.5	20-39	3.0-3.9	0.60-0.85
Severe	<1.0	>40	>4.0	<0.6
Critical	<0.5	--	--	--

Management

No proven effective medical therapy. Definitive treatment is valve replacement for:
Stage D (symptomatic AS)
Stage C (asymptomatic with inducible symptoms on stress testing, low EF, or undergoing other cardiac procedure)
Rapid progression (increase in velocity >0.3m/sec per year)
Consult cardiac surgery for determination of SAVR vs TAVR
In general, high risk surgical pts benefit most from TAVR
At VUMC: If determined to be intermediate to high operative risk by Cardiac Surgery, they will often recommend contacting the TAVR team for evaluation
Avoid rapid hemodynamic shifts and aggressive changes in preload or afterload
Aim for normotension: avoid preferential vasodilators such as hydralazine, nitroglycerin, or peripheral alpha blockers
Significant vasodilation may → coronary filling pressures -> myocardial ischemia

Monitoring:

Severe AS: TTE q 6-12 months
Moderate AS: TTE q 1-2 years
Mild AS: TTE q 3-5 years

Post AVR anticoagulation

All pts will get 3-6 months of AC s/p AVR depending on bleeding risk
Continued duration based on type of AVR
- TAVR: Aspirin 75-100mg daily following initial AC
- SAVR: Aspirin 75-100mg daily following initial AC (usually warfarin)
- Mechanical: lifelong AC with warfarin only

Aortic Regurgitation

Author: Faria Khimani

Etiology

Primary valve disease (rheumatic disease, bicuspid aortic valve, infective endocarditis, syphilis)
Primary aortic root disease (medial degeneration, aortic dissection, Marfan's syndrome, bicuspid aortic valve, syphilis, non-syndromic familial)

Presentation

Acute AR: LV cannot respond to increased volume to maintain stroke volume, leading to pulmonary edema and cardiogenic shock
Chronic AR: indolent presentation, often pt will develop symptoms of heart failure including DoE, orthopnea, PND
Physical exam: "Water-hammer" pulses, wide pulse pressure, laterally displaced PMI, high pitched "blowing" decrescendo murmur best heard at third intercostal space at left sternal border, S3

Management

Acute severe AR: - Page cardiac surgery for urgent surgical repair, do not delay - Vasodilators such as nitroprusside and diuretics can be used to stabilize pt - Use beta blockers with caution with concomitant severe AR and dissection and may block compensatory tachycardia leading to marked hypotension.

Chronic severe AR: - Surgical management: Aortic valve replacement (AVR) in severe AR (Stage D), asymptomatic severe AR with LV ejection fraction (LVEF) ≤55% (Stage C2), and severe AR in patients undergoing other cardiac surgery - Medical management: - For patients with severe AR or LV systolic dysfunction with prohibitive surgical risk, optimize GDMT for HFrEF - Systolic BP should also be controlled with goal SBP < 140 in chronic AR

Imaging and Monitoring: - Echo primary modality for monitoring AR severity. CMR used with echo data inconclusive - Regular follow-up every 3-6 months to monitor LV function and dimensions

Mitral Regurgitation

Author: Faria Khimani

Etiology:

Primary MR – caused by direct involvement of the valve apparatus (leaflets or chordae tendineae) - Most common cause: Degenerative/myxomatous mitral valve disease (mitral valve prolapse with flail leaflet, mitral annular calcification, chordal rupture) - Rheumatic fever - Infective endocarditis - Papillary muscle rupture following acute (inferior) MI

Secondary MR (also called functional MR) - caused by changes of the LV that lead to valvular incompetence - Dilated Cardiomyopathy - HOCM

Presentation

Acute MR - Sudden onset reduction in forward cardiac flow, dyspnea with flash pulmonary edema, left-sided heart failure.
Chronic MR - Progressive symptoms due to cardiac remodeling, worsening heart failure, left ventricular dilation, left atrial remodeling leading to atrial fibrillation.

Auscultation

Holosystolic murmur best heard at apex with radiation to the axilla. Associated S3 filling sound. Murmur may be absent in acute MR due to large regurgitant orifice/low velocity regurgitant jet

Evaluation

CXR: assess for pulmonary edema, typically normal cardiac silhouette in acute MR. Cardiomegaly and LA enlargement in chronic MR.
ECG: often non-specific if chronic LA enlargement notable on p wave morphology (p-mitrale). Chronic MR often c/b development of atrial fibrillation.
Echocardiography needed for confirming diagnosis
TEE, CMR, or cardiac catheterization performed when insufficient or discordant information from TTE. TEE used to guide MV interventions

Chronic MR stages

A: At risk for MR due to risk factors (i.e. mild valve thickening or leaflet restriction)
B: Progressive MR w/o hemodynamic changes or symptoms
C: Asymptomatic severe MR
C1: preserved EF and normal LV size
C2: reduced EF (<60%), dilated LV (LVESD > 40mm)
D: Symptomatic severe MR

Management

Asymptomatic severe MR (stage C): - Follow-up echo every 6-12 months to monitor LV function/size and pulmonary pressure

Acute hemodynamically significant MR: - Urgent surgical repair or replacement - Medical stabilization as a bridge to surgery: - Afterload reduction with vasodilation (nitroprusside, nitroglycerine) is key to promote forward flow - Diuresis to reduce preload and improve pulmonary edema

Chronic severe primary MR: - Surgical repair favored over valve replacement

2020 ACC/AHA Heart Valve Disease Guidelines: Mitral Regurgitation Management Algorithm

Mitral Stenosis

Author: Faria Khimani

Etiology

Characterized by thickened mitral valve leaflets and fused leaflet tips - Rheumatic Fever (leading cause worldwide) - Calcification of the mitral valve annulus (common in high-income countries) - Autoimmune Diseases: SLE, Rheumatoid arthritis

Presentation

Progressive symptoms: Asymptomatic to Heart Failure - Orthopnea/PND - Hoarseness/Dysphagia (compression of recurrent laryngeal nerve/esophagus by enlarged left atrium from pressure overload) - Symptoms of right heart failure - Acute symptoms may present in settings of increased cardiac output (pregnancy, sepsis, or exercise).

Physical exam: - Diastolic murmur, best heard at apex, opening snap following s2

Evaluation

CXR: increased pulmonary vasculature, left atrial enlargement; typically normal cardiac silhouette in acute MS.
ECG: Often non-specific; chronic left atrial enlargement notable on P wave morphology (P-mitrale). Chronic MS often complicated by atrial fibrillation.
Echocardiography: thickening of mitral valve leaflets, decreased area of valve leaflets, left atrial enlargement

Stages of Chronic MS

A: At risk for MS due to risk factors (e.g., mild valve thickening or leaflet restriction)
B: Progressive MS, characterized by commissural fusion, increased transmitral flow velocities, asymptomatic
C: Asymptomatic severe MS, characterized by above + mitral valve area <1.5cm²
D: Symptomatic severe MS, characterized by above criteria + decreased exercise tolerance

Management

Varies between rheumatic MS and calcific MS (in general, intervention of calcific MS is challenging and high risk)
Severe, symptomatic rheumatic MS:
Percutaneous mitral balloon commissurotomy (PMBC)
Surgical repair/replacement if pt failed PMBC or undergoing other cardiac surgery
Calcific MS has a poor prognosis with 5-year survival <50%, Intervention is higher risk and should be reserved for severely symptomatic pts
No role for commissurotomy with calcific MS
Surgical valve replacement may be considered for severely symptomatic pts (technically challenging)

Anti-Coagulation

Anti-coagulation is indicated if: - Mechanical prosthetic mitral valve: - Warfarin, goal INR 2.5-3.5 lifelong - Bioprosthetic mitral valve replacement: - Warfarin, goal INR 2-3 for first 3-6 months - Atrial Fibrillation regardless of CHADS2VASC score

2020 ACC/AHA Heart Valve Disease Guidelines: Mitral Stenosis Management Algorithm