MGH Housestaff Manual 2024-2025

The MGH Housestaff Manual serves as a resource for medical residents and clinicians at MGH, reflecting the experiences and contributions of residents in the Internal Medicine Residency Program.

The editors of the 30th Edition are Elizabeth Gay, MD, and Noemie Levy, MD.

The manual emphasizes the diligent work of residents, whose contributions connect them with past generations of house officers and reflect the spirit of growth in their training and profession.

The MGH Housestaff Manual should not be used to provide specific clinical care decisions in individual cases and should not substitute for clinical judgment.

Recommended lifestyle modifications include:

1. Smoking cessation
2. Maintaining blood pressure <140/90 (or <130/80 if DM or CKD)
3. Engaging in cardiac rehabilitation
4. Screening for depression
5. Receiving flu vaccination.

Early Complications (Hours - Days)

1. Cardiogenic Shock

   • Prevalence/Risk Factors: STEMI 6%, NSTEMI ~3%; Anterior MI, LBBB, prior MI, 3VD, age, HTN, DM.
   • Clinical Signs: New CP, cold/wet physiology, HoTN, tachycardia, dyspnea, JVD, rales, new murmur.

2. Myocardial Free Wall Rupture

   • Prevalence/Risk Factors: 0.01% STEMIs & NSTEMIs; Transmural MI, 1-vessel MI, 1st MI, anterior & lateral MI, HTN.
   • Clinical Signs: Tamponade in 85%, electromechanical dissociation, aberrant T wave evolution.

3. Interventricular Septal Rupture (VSD)

   • Prevalence/Risk Factors: 0.21% STEMIs, 0.04% NSTEMIs; 1st MI, 1-vessel MI, CKD.
   • Clinical Signs: New harsh holosystolic murmur, hypotension, BiV failure.

4. Papillary Muscle Rupture

   • Prevalence/Risk Factors: 0.05% STEMIs, 0.01% NSTEMIs; Posteromedial supply issues.
   • Clinical Signs: Abrupt dyspnea, pulmonary edema, hypotension.

5. LV Aneurysm

   • Prevalence/Risk Factors: No reperfusion: 10-30%; Total occlusion of LAD.
   • Clinical Signs: Acute: diffuse PMI, S3/S4, MR murmur; Chronic: HF, VT/VF.

Late Complications (Weeks - Months)

1. LV Thrombus

   • Prevalence/Risk Factors: 5% of AMI patients post-PCI; large infarct size, severe apical akinesis.
   • Clinical Signs: Embolization risk persists for 6 months, most by 3-4 months.

2. Pericarditis

   • Prevalence/Risk Factors: Decreased with reperfusion therapy; friction rub within 2-3 days post-MI.
   • Clinical Signs: 10% at 2-4 days post-transmural MI, may be focal or diffuse.

3. Coronary Artery In-Stent Thrombosis

   • Prevalence/Risk Factors: Highest risk is absence of P2Y12 inhibitor; 1% at 1 year.
   • Clinical Signs: ACS symptomatology, ECG changes, biomarkers elevation.

Users are encouraged to utilize the manual as a quick reference, a teaching tool, a source of relevant publications, and a starting point for personal exploration.

The key components of ACLS related to cardiac arrest include:

1. Cardiac Arrest Management
2. Bradycardia
3. Tachycardia
4. Defibrillation/Cardioversion/Pacing
5. EKG Interpretation
6. Acute Coronary Syndrome
7. MI Complications
8. Cardiac Catheterization
9. Non-Invasive Cardiac Testing
10. Echocardiography

Common conditions addressed in nephrology include:

1. Acute Kidney Injury
2. Chronic Kidney Disease
3. Glomerular Disease
4. Dialysis & Transplant
5. Acid-Base Disorders
6. Electrolyte Disorders (Sodium, Potassium, Magnesium, Phosphorus)
7. Urinalysis & Nephrolithiasis

Major topics covered under Infectious Disease include:

1. Empiric Antibiotics & Antibiogram
2. Multidrug Resistant Organisms
3. Community Acquired Pneumonia
4. HAP/VAP & Aspiration Pneumonia
5. Viral Respiratory/Head & Neck Infections
6. Urinary Tract Infections
7. Skin & Soft Tissue Infections
8. Bloodstream Infections & Endocarditis
9. Meningitis & Encephalitis
10. C. Difficile Infection

Key areas of focus in the Pulmonary & Critical Care section include:

1. Respiratory Distress
2. Hypoxemia & Hypercapnia
3. Noninvasive Oxygenation/Ventilation
4. Interpretation of Chest Imaging
5. PFTs & Asthma
6. COPD
7. VTE Diagnostics & Management
8. Mechanical Ventilation
9. ARDS
10. ECMO

Main topics covered in the Geriatrics & Palliative Care section include:

1. Pain Management
2. Advance Care Planning & Code Status
3. End of Life & Pronouncement
4. Comfort Focused Care & Hospice
5. Geriatric Assessment & Frailty
6. Polypharmacy & Elder Abuse

Primary areas of focus in the Hematology section include:

1. Pancytopenia & Anemia
2. Sickle Cell Disease
3. Thrombocytopenia
4. Eosinophilia
5. Coagulation Disorders
6. Anticoagulation Agents
7. Transfusion Medicine
8. Transfusion Reactions

Key topics covered in the Endocrinology section include:

1. Outpatient Type 2 Diabetes Mellitus
2. Inpatient Diabetes Mellitus Management
3. DKA/HHS
4. Adrenal Insufficiency
5. Pituitary Disorders
6. Calcium Disorders
7. Osteoporosis & Vitamin D
8. Thyroid Disorders & Male Hypogonadism

Check circulation (pulse), airway, and breathing (C-A-B). If no definite pulse is found within 10 seconds, initiate CPR.

The first dose of Amiodarone is 300 mg.

Consider AP pad placement and double sequential defibrillation.

ROSC is indicated by: 1) Pulse + BP, 2) Sustained ETCO2 > 40, 3) Spontaneous waves on a-line.

Compress 2-2.4 inches deep at a rate of 100-120 BPM, minimizing interruptions and allowing full recoil.

The reversible causes include: 1) Hypovolemia, 2) Hemorrhage, 3) Hypoxia, 4) H+ ion (acidosis), 5) Hypokalemia, hyperkalemia, 6) Hypothermia, 7) Thrombosis (coronary and pulmonary), 8) Tension pneumothorax, 9) Tamponade (cardiac), 10) Toxins (drugs, accidents).

Tenecteplase (TNK) is preferred over tPA in PE codes.

Absolute contraindications include: prior intracranial hemorrhage, ischemic stroke, head trauma within 3 months, intracranial neoplasm or AVM, suspected aortic dissection, and active bleeding.

Page 'ECMO Consult MGH' or use the 'MGH STAT' app to call for consult and follow MGH ECMO guidelines ideally within 10 minutes from code initiation.

Norepinephrine is the first line pressor for achieving a mean arterial pressure (MAP) greater than 65 mmHg after return of spontaneous circulation (ROSC).

1. Obtain a 12-lead EKG.
2. Consider other H&Ts (hypoxia and hyper/hypokalemia).
3. If STEMI criteria are met on post-ROSC ECG, activate the Cath Lab.
4. Consider emergent coronary angiography if there are signs of ischemic etiology.

The goal of TTM is to avoid fever for neuroprotection and to aggressively diagnose and treat infections, as fever is associated with worse neurological outcomes following ischemia and reperfusion injury.

• Normothermia (≤37.5°C): Allow passive rewarming until T 37°C, use temperature control devices.
• Mild Hypothermia (T 33-36°C): Individualized selection, maintain for 24 hours, then normothermia for 48 hours, with careful monitoring of blood glucose and electrolytes.

Relative contraindications include:

1. Recent head trauma
2. Active bleeding
3. Major surgery within the last 14 days
4. Refractory hypotension

Propofol is the preferred sedative agent, and dilaudid (or fentanyl) is the preferred analgesic for patients undergoing TTM with mild hypothermia.

1. First line: Acetaminophen 650 mg every 6 hours, Magnesium >3.
2. Second line: Skin counterwarming + dexmedetomidine or propofol or hydromorphone boluses.
3. Third line: Propofol + hydromorphone infusion.
4. Fourth line: Neuromuscular blocking agents (NMBA).

1. Focused exam: Check vitals, mental status, pupils, signs of pulmonary edema, murmurs, and other symptoms.

2. Review: Recent ECG, telemetry, lab results, current medications, and any recent dose changes.

3. Obtain: 12-Lead ECG and have pacing pads available.

4. IV Access: Order BMP, magnesium, lactate, and possibly troponin.

5. Monitor: Blood pressure frequently, maintain oxygen saturation > 92%, and ensure airway is clear.

Transvenous pacing is indicated in the following situations:

1. Need for transcutaneous pacing despite medications.
2. Unstable rhythm with no quickly reversible cause.

Atropine is used as follows:

• Administer 1 mg bolus every 3-5 minutes (maximum 3 mg).
• It is ineffective in cases of complete heart block (CHB) and Mobitz II AV block.
• Avoid use in patients who have had a heart transplant or in cases of Mobitz II or CHB.

Potential causes include:

• Medications, especially in liver or renal disease
• Sick sinus syndrome (SSS)
• Degenerative conduction disease
• Elderly age
• Hypoxia
• Autoimmune or infectious cardiomyopathy
• Post-TAVR
• Increased vagal tone
• Elevated intracranial pressure (ICP)
• Hypothermia
• Carotid disease with recent stenting
• Infiltrative diseases
• Hypothyroidism
• Sleep apnea
• Athlete's heart
• Drugs/toxins
• Ischemia or acute coronary syndrome (ACS)
• Endocarditis
• Lyme carditis, myocarditis, pericarditis
• Hyperkalemia
• Post-septal ablation

Specific antidotes include:

• Beta Blocker: Glucagon 3-10 mg IV (repeat bolus if no response; if response, start infusion at 3-5 mg/h).
• Calcium Channel Blocker: Glucagon as above, calcium gluconate 3-6 g every 10-20 minutes or as a continuous infusion, and insulin 1 U/kg bolus with 0.5 U/kg infusion.

1. Focused exam: Check vitals, mental status, signs of pulmonary edema, murmurs, temperature (warm/cold), pupils, and other symptoms.

2. Review: Look at the most recent ECG, telemetry, lab results, medications, and events.

3. Obtain: A 12-Lead ECG and prepare defibrillator with pads.

4. IV Access: Administer BMP, magnesium, lactate, and troponin if concerned for ischemia.

5. Monitor BP: Frequently check blood pressure.

6. Oxygen: Supplement to maintain saturation >94% and ensure airway is clear.

A patient is considered unstable if any of the following are present:

• Hypotension / shock
• Altered mental status
• Ischemic chest discomfort / angina
• Acute heart failure / pulmonary edema

• Adenosine: 6mg rapid IV push (followed by normal saline flush) + arm raise. Can repeat with 12mg if required. If using a central line, administer ½ the peripheral dose. Relative contraindication in patients post-heart transplant.

*Biphasic (MGH)

1. Vagal Maneuvers
2. Adenosine
3. IV Beta-Blockers (BB) or Diltiazem
4. Amiodarone / Procainamide

Avoid post orthotopic heart transplant for adenosine and avoid beta-blockers if heart failure with reduced ejection fraction (HFrEF) is present.

• Unilateral Carotid Massage: Supine position with neck extended, apply steady pressure to carotid sinus. Avoid in patients with a history of TIA/CVA in the past 3 months or those with carotid bruits. Success rate: 5%-33%.

• Modified Valsalva Maneuver: Semi-recumbent position, blow forcefully into a 10cc syringe for 10-15 seconds, then reposition to supine and raise legs at 45° for 15 seconds. Success rate: 43% effective in breaking SVTs.

• Cold Ice Face Immersion: More effective in children; success rate: 17%.

The default energy selection for defibrillation is 120 J. The initial dose can be adjusted between 120-200 J depending on the situation.

If there is a failure to capture, consider the following steps:

1. Increase output.
2. Ensure pads are in the correct location, avoiding bony structures.
3. Consider differential diagnoses such as barrel chest, COPD, hypoxia, tamponade, pneumothorax, acidosis, hyperkalemia, obesity, myocardial infarction, or cardiac drug toxicity.

1. Select the desired energy using the up and down arrow keys on the front panel.

   • Narrow, regular: 50-100 J
   • Narrow, irregular: 120-200 J
   • Wide, regular: 100 J
   • Wide, irregular: 150-200 J

2. Press the Sync On/Off button to confirm synchronization.

3. Press the CHARGE button and ensure the patient is clear.

4. Press and hold the illuminated SHOCK button to discharge with the next detected R wave.

5. If additional shocks are needed, increase the energy level as necessary and confirm synchronization.

In case of failure to sense during synchronous pacing, switch to asynchronous pacing and reposition the pads as needed.

For procedural sedation, typically 50 mcg fentanyl followed by 2 mg midazolam is used. In emergent situations, alternatives like Dilaudid 1-2 mg or lorazepam 2 mg can be considered.

Normal heart rate is 60-100 bpm. Bradycardia is defined as a heart rate of <60 bpm, while tachycardia is defined as a heart rate of >100 bpm.

To determine the rhythm of an EKG, check if it is regular or irregular and identify if it is sinus or non-sinus. A sinus rhythm is characterized by a P wave before every QRS and a QRS following every P, with a regular rate of 60-100 bpm and a normal P wave axis.

P waves indicate atrial depolarization. Key characteristics include:

1. Presence of P wave (best visualized in leads II and V1)
2. Atrial rate (e.g., 100-180 bpm for sinus tachycardia)
3. Axis (normal axis shows P wave upright in I/II, biphasic in V1).

A wide QRS complex (>120 ms) suggests aberrant supraventricular conduction or a ventricular origin. It may indicate conditions such as bundle branch block (BBB), ventricular activation, or hyperkalemia.

The Sokolow-Lyon criteria for diagnosing LVH include:

1. S in V1 + R in V5 or V6 ≥ 35 mm
2. R in aVL ≥ 11 mm.
   Additionally, the Cornell criteria can be used: S in V3 + R in aVL > 28 mm (M) or > 20 mm (F).

The QT interval represents ventricular depolarization and repolarization. It is rate-dependent and should be <440 ms (M) and <460 ms (F). A reassuring sign is if the QT interval is less than half the R-R interval with a normal heart rate.

Right Atrial Enlargement (RAE) is characterized by:

• P wave height > 2.5 mm in lead II (often referred to as P-pulmonale)
• Initial positive P wave in V1/V2 ≥ 1.5 mm.

The U wave occurs in the same direction as the T wave and is rate-dependent, typically shorter at faster rates. It may indicate conditions such as bradycardia or hypokalemia/hypomagnesemia/hypocalcemia.

• Hyperacute T waves: Can be found within minutes of ischemia.
• T wave inversions (TWI): ≥1mm in 2 contiguous leads; normal if only in aVR, V1, or III.
• Isolated TWI in aVL: May indicate mid-LAD lesion vs inferior MI.

• Suggests subendocardial injury.
• Measured ≥0.5mm below the baseline (PR segment) in 2 contiguous leads, 80ms after the J point.
• Downsloping or horizontal ST depression is more ominous and does not localize to territories.

• Wellens Syndrome: Indicates critical proximal LM or LAD lesion.
• 75% risk of MI within <2 weeks.
• Often pain-free with a history of angina.
• Normal/slightly elevated troponin levels.
• Type A: 25% biphasic T waves in V2 and V3.
• Type B: 75% symmetric, deeply inverted precordial T waves, with no precordial Q waves.

1. Determine the width of the QRS complex
2. Determine if the rhythm is regular or irregular
3. Assess for the presence of P waves (noting location, axis, and morphology)
4. Compare to baseline ECG
5. Treatment options include synchronized cardioversion for unstable patients and vagal maneuvers for stable patients.

The most common differential diagnosis for Wide Complex Tachycardia is Ventricular Tachycardia (VT), which accounts for approximately 80% of cases.

Features that favor a diagnosis of VT include:

1. Very wide QRS (>160 ms) and rate > 120 bpm.
2. New northwest (extreme) axis (leads I and II negative).
3. AV dissociation (often V rate > A rate).
4. Concordance: all QRS in V1-6 are completely positive or negative.
5. Partial or complete depolarization of His-Purkinje by a competing rhythm.
6. Basel algorithm: VT likely if ≥2 of 3 present (high risk substrate, lead II time to first peak >40ms, aVR time to first peak >40ms).

Management of VT includes:

1. Treat as VT if there is any doubt.
2. Consider underlying processes (active ischemia, CAD, electrolyte derangement).
3. Check and replete electrolytes (K>4, Mg>2).
4. Review baseline ECG for long QT or pre-excitation.

Monomorphic VT is characterized by consistent QRS complexes, while Polymorphic VT is characterized by variable QRS complexes. Monomorphic VT is often associated with ischemia, structural heart disease, or idiopathic causes, whereas Polymorphic VT can be due to ischemia (acute, CAD, ICM) or prolonged QTc.

A VT Storm is defined as ≥3 sustained episodes of unstable VT within 24 hours. Management includes:

1. Lido bolus (preferred if prolonged QTc) and Amio bolus (careful if long QT).
2. Anti-tachycardia pacing (ATP).
3. Treat/minimize ischemia (revascularization, IABP).
4. Reduce autonomic tone (intubation, sedation, stellate ganglion block).
5. Call EP +/- MCS/Shock Team.
6. Consider catheter ablation (VANISH trial).

• Age
• Obesity
• Hypertension (HTN)
• Smoking
• Alcohol (EtOH)
• Diabetes Mellitus (DM)
• Previous Myocardial Infarction (MI)
• Heart Failure (HF)
• Obstructive Sleep Apnea (OSA)

• History & Physical (H&P): Presence & timing of symptoms, history of HTN, DM, valve disease, HF, angina, congenital heart disease, OSA, family history of AF, acute precipitants.
• ECG: Absence of discernible P waves, irregularly irregular R-R intervals.
• Transthoracic Echocardiogram (TTE): Assess LV function, enlarged LA/RA size, valve function, pulmonary HTN, LA thrombus.
• Chest X-Ray (CXR): Evaluate for pulmonary processes.
• Laboratory Tests: TFTs, LFTs, BUN/Cr, CBC, NT-proBNP, BMP (K, Mg).

• Magnesium: 2-4 g IV empirically.
• Beta Blocker: Metoprolol preferred; IV bolus 2.5-5 mg over 2 min, repeat as needed.
• Calcium Channel Blocker: Diltiazem; IV bolus 0.25 mg/kg over 2 min, repeat as needed. |

• Urgent Indications: Ischemia, end-organ hypoperfusion, symptomatic hypotension, severe pulmonary edema.
• Elective Indications: New-onset AF or unacceptable symptoms from persistent AF.

The CHA2DS2-VASc score is used to assess the risk of stroke in patients with atrial fibrillation. It assigns points based on the following criteria:

• 1 point for: CHF, HTN, Age 65-74, DM, female sex, vascular disease.
• 2 points for: Age ≥ 75, history of stroke/TIA.
• Score Interpretation:
  • Score 0: No anticoagulation (AC) or aspirin (ASA).
  • Score 1 (or 2 in women): Clinical judgment for AC initiation.
  • Score ≥ 2 (or 3 in women): Anticoagulation recommended.

The HAS-BLED score is used for risk stratification of bleeding risk in patients receiving oral anticoagulation. It considers factors such as hypertension, abnormal renal function, liver disease, history of stroke, bleeding history, labile INR, age, antiplatelet medications, and alcohol or drug use. A score of ≥3 suggests caution and regular follow-up.

DOACs (dabigatran, rivaroxaban, apixaban, edoxaban) are recommended over warfarin in all cases except for patients with moderate to severe mitral stenosis, hypertrophic obstructive cardiomyopathy (HOCM), or mechanical valves. Warfarin may be preferred over rivaroxaban in patients with rheumatic heart disease.

Left Atrial Appendage Occlusion (LAAO) is significant as the left atrial appendage is the source of at least 90% of thrombi in patients with cerebrovascular accidents (CVA) and atrial fibrillation. The Watchman device provides stroke prevention comparable to warfarin with a similar bleeding risk and improved mortality, making it a consideration for patients with contraindications to long-term anticoagulation.

Recent guidelines indicate that rhythm control (using antiarrhythmics and ablation) is superior to rate control for patients with recently diagnosed atrial fibrillation and concomitant cardiovascular conditions, as it decreases cardiovascular mortality, stroke, and hospitalization for heart failure or acute coronary syndrome. Rhythm control should be considered if persistent AF symptoms impair quality of life, especially in younger patients or those with heart failure.

In atrial flutter, the risk of thromboembolism is lower than in atrial fibrillation, but anticoagulation management is similar. Rate control strategies (beta-blockers, calcium channel blockers) are also similar, but achieving successful rate control is more challenging. Rhythm control is typically achieved through ablation, which is more effective than antiarrhythmic drugs, particularly for typical flutter.

The QT interval correlates with the repolarization time of the ventricles. Normal values are:

• Normal: ≤460ms
• Borderline (adult): 460-479ms (female), 450-459ms (male)

QTc is the QT interval corrected for heart rate. Recommended formulas by AHA include:

• Framingham: QT + 0.154 * (1 - RR)
• Fridericia: QT / 3 / RR
• Hodges: QT + 1.75 * (60/RR - 60)
• Bazett: QT / √RR
• Rautaharju: QT * (120 + HR) / 180

Symptoms of congenital long-QT syndromes include:

• Presyncope/syncope
• Hemodynamic compromise
• Sudden cardiac death (triggered by exercise or stress)

Treatment options include:

• Beta blockers
• ICD if previous cardiac arrest and expected survival >1 year

Risk factors for TdP in hospitalized patients include:

• Demographics: Elderly, female, congenital LQTS, anorexia/starvation, hypothermia
• Comorbidities: Renal failure, hepatic dysfunction, heart failure, myocardial infarction, left ventricular hypertrophy, hypothyroidism
• Rhythm-related: QTc >500ms, bradycardia, PVCs
• Electrolytes: Hypomagnesemia, hypokalemia, hypocalcemia
• Medication-related: QT-prolonging drugs, diuretic use, beta blocker use

Management of acquired long QT includes:

1. Stop the offending drug if QTc >500ms or increase in QTc of >60ms.
2. Check ECG for bradyarrhythmias and signs of impending TdP.
3. Check electrolytes and consider repleting (K >4, Mg >2).
4. Supratherapeutic repletion may be considered if risk of TdP is present (K: 4.5-5, Mg: 2-2.5).

Characteristics:

• Substernal chest pain
• Worse with exertion
• Relieved by rest or nitrates

Associated Symptoms:

• Chest pain/pressure/tightness
• Discomfort in chest/shoulders/arms/neck/back/upper abdomen/jaw
• Shortness of breath (SOB) and fatigue

Vague Symptoms in Specific Populations:

• Women, elderly, and patients with diabetes may experience palpitations, jaw/neck/back pain, SOB, nausea/vomiting, abdominal pain, (pre-)syncope, altered mental status (AMS).

• Blood pressure variation >20 mmHg between arms
• Pulse deficits
• New diastolic murmur
• Focal neurologic changes

Symptoms:

• Pleuritic, sharp pain that improves upon leaning forward
• May have upper respiratory infection (URI) prodrome; consider bacterial pericarditis if high fevers

Physical Exam Findings:

• Friction rub (distinguish from pleural rub by breath hold)
• Tamponade (pulsus paradoxus >10 mmHg)

Risk Factors:

• History of cancer
• Recent surgery
• Immobility
• Hemoptysis
• Calf/thigh pain/swelling

Symptoms:

• Sudden onset dyspnea/hypoxemia
• Pleuritic chest pain

Pneumonia:

• Sharp, pleuritic chest pain associated with fever and increased white blood cell count
• Productive cough

Physical Exam Findings:

• Bronchial breath sounds
• Crackles
• Dullness

Pneumonitis:

• Similar symptoms but may also include recent radiation exposure or autoimmune conditions.

STEMI Criteria:

• New ST elevation ≥1 mm in any 2 consecutive leads (except V2/V3: M >2 mm, F >1.5 mm) compared to prior ECG
• New left bundle branch block (LBBB) can also indicate STEMI.

• Stress Test: To rule out acute coronary syndrome (ACS) if low to intermediate risk.
• Coronary CTA: 100% negative predictive value (NPV) in patients without coronary artery disease (CAD), especially useful for patients under 65 years old.

• Emergent Angiography: For STEMI patients.
• Early Angiography: For high-risk NSTEMI patients.
• All Patients with Confirmed ACS: Should undergo angiography. Risk stratification can be done using GRACE, TIMI, HEART, and Mayo Clinic scores.

Myocardial injury is defined as any patient with troponin >99th percentile without evidence of myocardial ischemia, which includes symptoms of ischemia, new ischemic ECG changes, new wall-motion abnormalities, and/or acute coronary thrombus on angiography. It can be acute or chronic.

There are two main types of myocardial infarction:

1. Type 1 MI: Caused by spontaneous plaque rupture, erosion, or intraluminal thrombus.
2. Type 2 MI: Results from a supply-demand mismatch that is not due to atherothrombosis, often related to conditions like sepsis, arrhythmias, severe anemia, renal failure, surgery, hypertension, and heart failure. A clear precipitating factor must be identified; otherwise, it is treated as Type 1 MI until further evaluation.

For CP onset ≥3h PTA:

• Rule in ACS: hsTnT ≥52 or Δ ≥5 from baseline.
• Rule out ACS: hsTnT <10 (F) or <12 (M) AND A <3 from baseline.

For CP onset <3h:

• Rule in ACS: hsTnT ≥10 (F) or ≥15 (M) AND 3h ATn ≥7 from baseline AND symptoms or ECG changes or concerning imaging.
• Rule out ACS: No significant A in 3h.

The primary PCI (PPCI) is the recommended revascularization strategy for patients with STEMI if symptoms onset is within 48 hours. The goals are:

• PCI center: Aim for <60 minutes to wire crossing.
• Non-PCI center: Aim for <90 minutes to wire crossing.
• If PPCI is not possible within 120 minutes of FMC and symptoms onset is <24 hours, fibrinolysis is indicated, aiming for <10 minutes to lytic bolus (Tenecteplase preferred).

• LA enlargement
• E/e' >14
• LVH (Left Ventricular Hypertrophy)
  (Note: Diastolic dysfunction is not typically called on MGH TTE reports)

The four subgroups for urgency to revascularization in NSTE-ACS are:

1. Very high risk: Immediate invasive (within 2h) for refractory/recurrent angina, hemodynamic or electrical instability, mechanical complications, or recurrent dynamic ECG changes.
2. High risk: Early invasive (within 24h) for temporal change in troponin, ECG changes, or high-risk patients (GRACE >140).
3. Intermediate risk: Delayed invasive (within 72h) for patients with risk factors at baseline but none of the above conditions.
4. Low risk: No immediate intervention required.

Low-risk patients are defined as those with no risk factors, a GRACE score <109, and a TIMI score of 0-1, or those who are not good candidates for angiography.

The selection of revascularization strategy should be based on:

1. The acuity of the patient's condition
2. The angiographic characteristics of the culprit lesion
3. The complexity of the patient's anatomy
4. Inclusion of a Heart Team discussion when appropriate.

For multivessel disease, CABG is often preferred in cases of:

• 3-vessel disease
• Left main disease
• 2-vessel disease with proximal LAD stenosis or EF <50%
• Diabetes mellitus with 2-vessel disease involving the LAD.

Adjuncts at presentation include:

1. Aspirin (ASA): Immediate loading and maintenance strategy.
2. Peri-Intervention Anticoagulation: Start on diagnosis of ACS, usually stopped after PCI unless indicated.
3. Statin: Atorvastatin 80mg daily regardless of baseline LDL.
4. Nitrates: For chest pain management, with caution in certain conditions.
5. Morphine: Not recommended unless pain is refractory to nitrates.
6. Discontinue NSAIDs: Due to risks of mortality and reinfarction.

The default duration for dual antiplatelet therapy (DAPT) after acute coronary syndrome is 12 months. However, there is an evolving movement to shorten DAPT duration based on recent studies.

Beta blockers should not be started in patients with:

1. Shock
2. Cocaine-induced myocardial infarction
3. PR interval >240ms
4. 2nd or 3rd degree AV block
5. Severe bronchospasm.

• Assess vital signs for hemodynamic instability
• Conduct a focused physical exam for new murmurs, pericardial friction rub, elevated JVP, and crackles
• Perform stat labs including troponin, PT/INR, PTT, T&S, BMP, and lactate
• Ensure adequate vascular access with at least 2 peripheral IVs
• Run telemetry, repeat ECG, and perform a STAT transthoracic echocardiogram (TTE)
• Consider a STAT CT angiography if there is concern for retroperitoneal bleed or aortic dissection
• Notify the interventionalist if necessary

• Bradyarrhythmia/conduction block: May occur due to coronary artery occlusion or baroreceptor reflexes.
• Tachyarrhythmia: Related to re-entrant circuits from scar formation or automaticity from adrenergic surge.
• Sinus bradycardia: Beneficial in reducing myocardial oxygen demand, occurs in up to 40% of acute MIs.
• Atrial fibrillation/flutter: Can be transient or due to atrial stretch; associated with increased mortality if late.
• Ventricular tachycardia: Suggests pre-existing arrhythmogenic scar; requires urgent revascularization if due to ischemia.

• Sinus tachycardia: Compensatory for left ventricular dysfunction; undesirable as it increases myocardial oxygen demand.
• Atrial fibrillation: Associated with increased mortality, particularly if it occurs late after MI.
• Ventricular fibrillation: Risk factors include age, prior MI, and cardiogenic shock; requires immediate ACLS and defibrillation.
• Accelerated Idioventricular Rhythm (AIVR): Often a reperfusion rhythm; usually does not require treatment unless symptomatic.

Left Heart Catheterization (LHC):

• Arterial access (radial, femoral)
• Assesses coronary anatomy/lesions, left ventricular (LV) and aortic (Ao) pressures, and allows for percutaneous coronary intervention (PCI).

Right Heart Catheterization (RHC):

• Venous access (internal jugular, femoral)
• Assesses hemodynamics and allows for cardiac biopsies (usually from the right ventricle).

1. NPO after midnight.
2. Ensure INR is <2 for radial access and <1.8 for femoral/internal jugular access.
3. Monitor creatinine levels; no prophylactic antibiotics.
4. Continue aspirin and statins; consider loading dose of 324 mg chewed aspirin if not on daily aspirin.
5. Hold anticoagulants based on guidelines (e.g., hold UFH gtt when on call, LMWH 24h prior, DOACs >48h or >72h if CrCl<30).
6. Document pulses and perform Allen's test.
7. Check for contrast allergy and pre-treat if necessary.
8. Assess for respiratory distress and consider intubation if needed.
9. Pre-hydration with crystalloids and NAC/bicarbonate is not shown to prevent contrast-induced nephropathy (CIN) in most patients with moderate CKD.

• Access: Radial access has fewer bleeding/vascular complications compared to femoral access, especially in acute coronary syndrome (ACS).
• Stent Types:
  • Bare Metal Stents (BMS): Risk of stent thrombosis and requires shorter duration of dual antiplatelet therapy (DAPT).
  • Drug-Eluting Stents (DES): Higher risk of late stent restenosis, requiring longer DAPT duration.

Antiplatelet Therapy:

• 81 mg aspirin indefinitely; add P2Y12 inhibitor after catheterization (prasugrel, ticagrelor, or clopidogrel).
• Duration of DAPT varies based on bleeding risk and clinical scenario.

Femoral Access:

1. 4-6 hours of bedrest after the procedure.
2. Perform groin checks immediately, at 6 hours, and at 8 hours post-procedure to assess pulses and check for complications.

Radial Access:

1. Use TR band for 4-6 hours, following RN protocol.
2. Monitor for paresthesias/numbness and check perfusion with finger saturation probe.
3. If hematoma occurs, do not remove the band until assessed by a fellow.

1. Access Site Complications:

   • Hematoma: mass without bruit; apply compression.
   • Pseudoaneurysm: pulsatile mass with bruit; may require thrombin injection or surgery.
   • AV fistula: continuous bruit without mass; surgical repair usually necessary.
   • Limb ischemia: evaluate pulses and limb warmth.
   • Retroperitoneal bleed: presents with hemodynamic instability; requires urgent evaluation.

2. Other Complications:

   • Infection, atheroembolism, contrast-induced nephropathy (CIN), cardiac tamponade, myocardial infarction (MI), cerebrovascular accident (CVA), radiation injury, and delayed hemostasis.

The best approach to testing depends on: 1) the clinical question being asked, 2) symptom acuity (often chest pain), 3) baseline cardiovascular disease (CVD) risk or known coronary artery disease (CAD) history, and 4) patient-specific contraindications.

The classifications are:

• Stage A: High risk for developing CHF with no structural disorder of the heart.
• Stage B: Structural disorder of the heart with no developed symptoms of CHF.
• Stage C: Past or current symptoms of CHF.
• Stage D: End-stage disease with specialized interventions.

Indications for stress/functional testing include:

1. Diagnose CAD: Workup stable angina in patients with intermediate-high risk of CAD.
2. Evaluate new or changing symptoms concerning for ischemia in patients with known CAD.
3. Post-revascularization: Evaluate patients with angina or asymptomatic patients if incomplete revascularization or >2 years post-PCI/5 years post-CABG.
4. Pre-operative risk assessment if indicated.
5. Other: Newly diagnosed heart failure or cardiomyopathy likely secondary to ischemia, functional capacity assessment, viability testing, valvular disorders, and quantifying microvascular disease.

Contraindications for stress/functional testing include:

1. Untreated acute coronary syndrome (ACS)
2. Myocardial infarction (MI) within 2 days
3. High risk or left main CAD
4. Uncontrolled arrhythmia
5. Acute decompensated heart failure (ADHF)
6. Severe aortic stenosis (AS) or hypertrophic obstructive cardiomyopathy (HOCM)
7. Recent deep vein thrombosis (DVT) or pulmonary embolism (PE)
8. Acute myocarditis, pericarditis, or endocarditis
9. Aortic dissection
10. Uncontrolled hypertension.

Exercise testing is preferred over pharmacologic testing if the patient is able to reach goal exertion, as it is more relevant to real-world stress.

If the question is 'Does the patient have CAD?', hold beta-blockers (BB) and nitrates prior to the stress test.

Vasodilation occurs via cAMP, which helps detect ischemia by coronary steal. In stenosed coronary arteries, these arteries cannot further dilate, creating a relative perfusion deficit in diseased vessels.

Side effects include wheezing, bradycardia, and hypotension. Caution is advised in patients with active bronchospasm, high-grade AV block, sick sinus syndrome, or severe aortic stenosis.

Dobutamine acts as a positive inotrope and chronotrope via β-1 receptor agonism, with extremely high doses reaching up to 40 mcg/kg/min.

Nuclear imaging (PET or SPECT) is used to detect areas of perfusion between rest and stress states, measure LV function, assess transient LV dilatation, and evaluate myocardial blood flow reserve.

Key components include:

1. Exercise duration
2. METS
3. BP/HR response
4. HR recovery
5. Double product (HR x SBP)
6. Duke Treadmill Score (estimates CAD risk)

Viability testing aims to determine the viability of ischemic myocardium, assessing for hibernating tissue that may be salvaged with revascularization.

CCTA is indicated to evaluate the presence and extent of coronary artery disease (CAD), offering plaque characterization and CT FFR. It is not recommended for screening asymptomatic patients.

The CAC scan provides a risk-assessment score for ASCVD risk stratification, guiding decision-making for primary prevention and statin therapy in asymptomatic patients aged 40 and older at intermediate risk.

Cardiac MRI is the modality of choice for assessing functional and tissue properties of the heart, including inflammation, scarring, infiltration, cardiac tumors, and pericardial disease, which cannot be adequately assessed with TTE or CCTA.

• LV size, function, wall thickness (septum/posterior wall)
• MV/AoV function/flow (with Doppler)
• LVOT diameter, aortic root size

• Patient: lying flat on back or left decubitus
• Probe: at PMI with probe indicator at 3 o'clock (to the patient's left). For 5-chamber view, fan probe cranially.

• Evaluate hemodynamic instability of suspected cardiac etiology
• Evaluate for early MI complication
• Suspected MI with non-diagnostic biomarkers and EKG
• Identify cause of cardiac arrest

• RV WMA or hypokinesis
• RV dilation (RV:LV ratio >1)
• Interventricular septal bowing
• IVC collapse
• 'D-sign': septal flattening
• 'McConnell's sign': RV free wall akinesia with normal RV apex motion (77% Sn, 94% Sp for acute PE)

Common etiologies include:

• Ischemic (most common cause, 50-75%)
• Hypertension/Left Ventricular Hypertrophy (LVH)
• Valvular disorders (e.g., Mitral Regurgitation)
• Myocarditis
• Stress-induced (Takotsubo)
• Tachyarrhythmia
• Infiltrative diseases (e.g., sarcoidosis)
• Genetic factors
• Substance abuse (e.g., cocaine, alcohol)
• Nutritional deficiencies
• Cirrhosis
• Sepsis
• Peripartum cardiomyopathy

The diagnostic criteria include:

1. Transient dysfunction of LV mid-segments with wall motion abnormalities extending beyond a single coronary distribution.
2. Rule out acute coronary syndrome (ACS) or obstructive coronary artery disease (via catheterization).
3. New ECG changes: either ST elevation or T wave inversion.
4. Absence of pheochromocytoma or myocarditis.

Risk factors for SCD/VT in HCM include:

• Prior VT/SCD or unexplained syncope.
• Family history of SCD in a first-degree relative.
• Massive LVH (greater than 30mm).
• Non-sustained ventricular tachycardia (NSVT) on Holter monitoring.
• Abnormal blood pressure response to exercise.
• Burden of late gadolinium enhancement (LGE) on cardiac MRI.
• History of suspected cardiac syncope.
• Ejection fraction (EF) < 50%.

Presentation and ECG findings for Amyloidosis include:

• Telemetry monitoring
• 2g sodium restricted diet
• Daily standing weights
• Strict intake/output monitoring
• DVT prophylaxis

Black and Latinx patients with heart failure are less likely to be admitted to cardiology services, which contributes to racial inequities in heart failure outcomes.

• Calcium channel blockers (especially non-dihydropyridines)
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Flecainide

• NT-proBNP <300 indicates ADHF is unlikely (NPV 98%)
• NT-proBNP >450 indicates ADHF is likely (>900 if age >50)
• Levels can be difficult to interpret in patients with chronic kidney disease or obesity.

• Ferritin <100 or ferritin <300 with transferrin saturation (TSat) <20% indicates iron deficiency. Some evidence suggests TSat ≤19.8% or serum iron ≤13µmol/L may be more predictive.

1. Identify hemodynamic profile (warm vs cold, dry vs wet)
2. History to identify precipitants (dietary non-adherence, ischemia, arrhythmia, etc.)
3. Early management with diuresis and IV loop diuretics.

The target is the resolution of signs and symptoms of congestion, monitored through daily weights and hemoconcentration.

Vasodilators can relieve symptoms by decreasing afterload, reducing pulmonary capillary wedge pressure (PCWP), and increasing stroke volume. They are particularly useful in cases of severe hypertension or acute mitral/aortic regurgitation.

• Initiate and uptitrate evidence-based beta blockers (e.g., carvedilol, metoprolol succinate).
• Initiate/titrate ARNI if renal function is stable.
• Initiate spironolactone or eplerenone if creatinine clearance >30.
• Consider SGLT2 inhibitors for cardiovascular mortality reduction.

Treat with diuretics and consider adding GDMT agents for HFrEF (Current Heart Failure Reports 2020;17:1).

The goals include:

1. Toleration of target doses of ACE/ARB/ARNI, B-blocker, aldosterone antagonist, and SGLT-2 inhibitor without symptomatic hypotension or metabolic disarray.
2. For β-blockade, target resting HR < 70 without postural hypotension or unacceptable side effects.
3. Start GDMT immediately on diagnosis, often using 'quad therapy' at lower than target dosing.

ICD is indicated if:

• Ischemic cardiomyopathy with EF ≤ 30% or ≤ 35% with NYHA II-III.

CRT is indicated if:

• EF ≤ 35% & prolonged QRS ± LBBB & some with EF ≤ 50%.

Cardiogenic shock is defined as:

• Hypotension (SBP < 90 for 30 min or pressor requirement) + hypoperfusion (cold extremities, oliguria, lactate) + hemodynamics (CI < 2.2, PCWP > 15).

Immediate management includes:

1. Activate cath lab for PCI if acute MI is suspected (only intervention proven to improve outcomes).
2. Stabilize MAP with norepinephrine as needed prior to obtaining PA catheter for tailored therapy.
3. Consider early SHOCK consult to avoid escalating inotropes/pressors which can worsen myocardial supply/demand imbalance.

The goals of tailored therapy include:

• Tissue perfusion (CO, MAP)
• Decongestion (JCVP, PCWP)
• Ventricular unloading (minimize myocardial O2 demand).

Inotropes such as dobutamine and milrinone are used to improve contractility. Key considerations include:

• Dobutamine: Initial dose 0.5-1 mcg/kg/min; watch for tachycardia and arrhythmias.
• Milrinone: Initial dose 0.125 mcg/kg/min; preferred in patients on β-blockers and with RV failure.

Normal RV function is governed by:

1. Systemic venous return
2. Pulmonary artery (PA) pressure
3. Pericardial compliance
4. Native contractility of the RV free wall and interventricular septum.

Clinical features of acute RV failure include:

• Jugular venous pressure (JVP) elevation
• Peripheral edema
• RV heave
• Pulsatile liver
• Split S2
• New tricuspid regurgitation (TR): holosystolic murmur at left lower sternal border (LLSB) with radiation to right lower sternal border (RLSB).

Imaging techniques for assessing RV function include:

• Chest X-ray (CXR): PA/lateral views
• CT scan: RV/LV ratio >0.9 suggests RV strain
• Echocardiography: measures RV size/function; RVEF based on displacement of base towards apex; TAPSE (normal ≥ 17 mm) reflects RV apex-to-base shortening.

The gold standard for measuring ventricular filling pressures and cardiac output is right heart catheterization (RHC) with placement of a pulmonary artery (PA) line.

Management strategies for acute RV failure include:

1. Treat reversible causes: pericardial disease, RV myocardial infarction (RVMI), pulmonary embolism (PE), hypoxemia, infections.
2. Preload management: maintain CVP goal of 8-12 mmHg.
3. Afterload management: use pressors if hypotensive; consider pulmonary vasodilators if evidence of pulmonary arterial hypertension (PAH).
4. Contractility support: use dobutamine or milrinone.
5. Devices: consider RV mechanical circulatory support (MCS) if refractory RV failure.

Intubation and mechanical ventilation can increase pulmonary vascular resistance (PVR) and RV afterload, leading to:

• Increased RV dilation
• Risk of hemodynamic collapse and cardiac arrest
• Propagation of the 'death spiral' due to decreased venous return and systemic hypotension.

EKG changes associated with RVMI include:

• Right-sided ECG leads: check in patients with inferior STEMI.
• 1 mm ST elevation in V4R: indicates RV involvement with 88% sensitivity and 78% specificity.
• High-grade AV block: seen in approximately 50% of patients with RVMI.

• Refractory heart failure (bridge to durable MCS or transplant, bridge-to-bridge)
• Refractory ischemia
• Cardiogenic shock/massive PE

• Check urine color (hemolysis), LDH
• Check suction events (↓preload, RV failure, position)
• Check for ventricular arrhythmias (device migration)

• Acquired vWF deficiency
• Bleeding
• Hemolysis (possible pump thrombosis)
• Ventricular arrhythmias
• Thromboembolism
• RV failure
• Aortic regurgitation
• Driveline infections

Full bi-ventricular support (4-10 L/min) + oxygenation & CO2 clearance

• Technical/logistical issues
• Patient/family wishes
• Septic shock
• Uncontrolled bleeding
• Aortic regurgitation
• Aortic aneurysm/dissection
• LV/LA thrombus
• Severe PAD or aortic disease

The indications for using a PAC include diagnosing the etiology of shock (e.g., cardiogenic vs. distributive), differentiating between cardiogenic and non-cardiogenic pulmonary edema, assessing left vs. right ventricular failure, determining the etiology of pulmonary hypertension, evaluating left-to-right shunting, valve disease, and pericardial disease.

The ESCAPE trial showed no mortality benefit to the empiric use of PAC in patients with ADHF who were not on inotropes. Despite this, PACs remain standard of care and are guideline-recommended in carefully selected patients, such as those with cardiogenic or mixed shock on inotropes or pressors.

1. Position the patient supine with the head-of-bed between 0-60°.
2. Align the transducer with the mid-axillary line at the 4th intercostal space.
3. Zero the transducer to air and assess the waveform for dampness.
4. Record PA systolic, PA diastolic, PA mean, CVP, and line position.
5. Open the PA catheter balloon port and remove 1.5cc air.
6. Inject 1.5cc air slowly until the PCWP waveform is observed, using the minimum air required to reduce the risk of PA infarction/rupture, and record PCWP (limit balloon inflation to <10 seconds).
7. Release the safety syringe and allow the balloon to deflate passively; verify balloon deflation by visualizing the PA waveform.
8. Troubleshoot as necessary, including checking CXR for position.

The normal hemodynamic parameters are as follows:

• RA: 5 mmHg
• RV: 25/5 mmHg
• PA: 25/10 mmHg
• PCWP: 10 mmHg
• LV: 125/10 mmHg

Clinical considerations for placing a PAC include:

• Placement is usually through the right internal jugular (RIJ) Cordis, advancing only with the balloon inflated.
• Deflate the balloon when withdrawing and at all other times.
• A cardiology or pulmonary fellow must be present to place or advance the catheter.
• Contraindications include insertion site infection, RVAD, RA/RV mass/thrombosis, mechanical TV/PV, and endocarditis.

• Single chamber (RA or RV lead)
• Dual chamber (RA + RV leads)
• Biventricular (RV + coronary sinus ± RA leads)

The ICD is a device with an RV lead capable of terminating re-entrant ventricular tachyarrhythmias via pacing, cardioversion, or defibrillation.

CRT provides simultaneous RV + LV pacing in patients with Heart Failure with Reduced Ejection Fraction (HFrEF) and wide QRS to address dyssynchrony, leading to LV reverse remodeling and increased LVEF.

• Symptomatic sinus bradycardia (± sinus pauses) or chronotropic incompetence
• Recommend DDD for symptomatic SND with extension of AV interval
• Symptomatic medication-induced bradycardia if no alternative medication
• Permanent AF and symptomatic bradycardia

• Ischemic Cardiomyopathy:
  • NYHA Class I: EF ≤30%, >40d s/p MI & ≥90d s/p revascularization
  • NYHA Class II/III: EF ≤35%, >40d s/p MI & ≥90d s/p revascularization
• Non-ischemic Cardiomyopathy: EF ≤35% + NYHA Class II/III
• Other conditions include HoCM, Long QT syndrome, and Arrhythmogenic right ventricular cardiomyopathy after risk modeling.

CRT is indicated for patients with:

• NYHA Class II-III or ambulatory IV
• LVEF ≤35%
• Normal Sinus Rhythm
• QRS >150ms with LBBB

The most common cause of aortic stenosis in patients under 70 years old is a bicuspid valve. Other causes include aortic sclerosis (calcification of the valve), rheumatic heart disease (where leaflets fuse, often with concurrent mitral valve disease), and radiation-induced changes.

The clinical manifestations of severe aortic stenosis include:

1. Angina: Due to increased afterload leading to left ventricular hypertrophy and supply-demand mismatch.
2. Syncope: Exercise-induced vasodilation leads to hypotension due to the inability to augment cardiac output.
3. Heart Failure (dyspnea): Left ventricular hypertrophy leads to diastolic dysfunction, with systolic dysfunction being a late finding.

Prognostic Implications: The most important determinant of prognosis is the presence of symptoms; mortality rates are 50% at 5 years if angina is present, 3 years if syncope, and 2 years if heart failure is present.

The diagnostic criteria for severe aortic stenosis include:

• Physical Exam: Harsh crescendo-decrescendo murmur at the right upper sternal border radiating to the carotids; if severe, the murmur is late-peaking with a delayed carotid upstroke (pulsus parvus et tardus) and a soft S2.
• Echocardiography (TTE): Severe aortic stenosis is indicated by a peak aortic valve velocity ≥4 m/s, mean aortic valve pressure gradient ≥40 mmHg, or aortic valve area (AVA) ≤1 cm².
• ECG: Findings may include left ventricular hypertrophy (LVH), left atrial enlargement (LAE), left anterior fascicular block (LAFB), and left bundle branch block (LBBB).

Medical Treatment:

• Smoking cessation
• Blood pressure reduction per ACC/AHA guidelines
• Medications: statins, beta-blockers, ACE inhibitors, low-dose ASA

Surgical Treatment:

• Men: >5.5 cm or growing >0.5 cm/6 months or >1.0 cm/year or symptomatic
• Women: >4.5-5 cm (controversial)
• Options: Open repair vs EVAR

Indications for aortic valve replacement (AVR) in aortic stenosis include:

1. Symptomatic, severe AS (Stage D): Prompt AVR is indicated due to the risk of sudden death.
2. Asymptomatic, severe AS (Stage C): AVR is appropriate if left ventricular ejection fraction (LVEF) <50%, if symptoms are provoked with exercise testing, or if the patient is undergoing other cardiac surgery.
3. Very severe AS (AVA ≤0.75 cm²): Early surgery may have a mortality benefit.
4. Low-flow, low-gradient AS: Dobutamine stress echocardiography (DSE) is used to distinguish between low-flow, low-gradient AS and pseudosevere AS.

Anticoagulation recommendations after valve replacement are as follows:

Acute: aortic dissection, valve perforation (usually due to MI or endocarditis), traumatic valve leaflet rupture.
Chronic: leaflet abnormalities (bicuspid valve, endocarditis, RHD) or root dilation (secondary to HTN, CTD, dissection, syphilis).

Diastolic regurgitant flow leads to increased left ventricular end-diastolic pressure (LVEDP), which initially maintains stroke volume (SV) and cardiac output (CO). Over time, this results in progressive ventricular dilatation and eventual heart failure.

Common clinical signs include dyspnea (most common), pulmonary edema, hemoptysis, and venous thromboembolism (VTE) even without atrial fibrillation (AFib).
Auscultation reveals a loud S1, high-pitched opening snap, and a low-pitched diastolic rumble at the apex.

First-line treatment: ACE inhibitors, ARBs, or Entresto.
Second-line treatment: Calcium channel blockers or hydralazine/nitrates to reduce left ventricular afterload.
Surgical intervention: Consider aortic valve replacement (AVR) if symptomatic severe AR or specific left ventricular criteria are met.

Intervention is generally indicated for patients with severe mitral stenosis (MV area ≤1cm²) who are symptomatic.
Rheumatic MS: Consider percutaneous mitral balloon commissurotomy (PMBC) for symptomatic patients with favorable valve morphology.
Nonrheumatic Calcific MS: Consider intervention only after discussing high risk.

Acute treatment options include:

1. Decrease afterload (e.g., nitroprusside)
2. Inotropes (e.g., dobutamine)
3. Diuresis
4. If hemodynamically unstable, consider intra-aortic balloon pump (IABP) and/or urgent surgical repair.

Clinical features include signs of right-sided heart failure such as hepatosplenomegaly, ascites, peripheral edema, and a large V wave in the jugular venous pressure (JVP).
Auscultation reveals a holosystolic murmur at the left mid- or lower sternal border that increases with inspiration, along with an S3 heart sound.

Prophylaxis is reasonable in patients undergoing dental manipulation if they have:

1. Prosthetic heart valves
2. Prosthetic material used in valve repair
3. A history of prior infective endocarditis
4. Unrepaired cyanotic congenital heart disease
5. Cardiac transplant recipients with valve abnormalities.

Cardiac tamponade is a condition characterized by hemodynamic insufficiency due to impaired cardiac filling caused by increased pericardial pressure from effusion. This leads to elevated intracardiac chamber pressures and equalization of diastolic pressure in all four heart chambers. Common etiologies include idiopathic (20%), iatrogenic (16%), malignant (13%), uremic, infectious, heart failure, and autoimmune causes. Tamponade is more likely in cases of malignant, post-viral (including SARS-CoV-2), uremic, and iatrogenic origins.

Beck's Triad is a classic clinical manifestation of cardiac tamponade, consisting of:

• Hypotension (low blood pressure)
• Elevated JVP (jugular venous pressure)
• Muffled heart sounds

Additionally, pulsus paradoxus is noted, which is an exaggerated decrease in systolic blood pressure during inspiration. Other symptoms may include dyspnea and tachycardia. An ECG may show sinus tachycardia, low QRS voltage, and electrical alternans.

Peripheral Artery Disease (PAD) is defined as arterial stenosis or occlusion causing an imbalance of blood flow relative to muscular metabolism, primarily affecting the legs more than the arms.

Treatment for cardiac tamponade includes:

1. Fluid resuscitation: Administer volume urgently to increase intracardiac pressures, starting with a 250-500cc bolus.
2. Inotropes: Consider if intravenous fluids are insufficient, but avoid beta-blockers.
3. Drainage: Options include catheter pericardiocentesis, surgical pericardiectomy, or hemodialysis if uremic.
4. Analysis of pericardial fluid: Conduct tests such as cell count, total protein, LDH, and cultures to determine the cause of effusion.

The following clinical features are associated with cardiac tamponade:

Pericarditis can be classified into the following categories:

• Acute: lasts less than 6 weeks
• Incessant: lasts more than 6 weeks without remission
• Recurrent: returns after a symptom-free interval of 4-6 weeks
• Chronic: lasts more than 3 months

The first-line treatments for pericarditis include:

1. NSAIDs: such as ibuprofen (600-800mg TID) or ASA (650-1000mg TID).
2. Colchicine: 0.6mg BID (or once daily if the patient is less than 70kg).
3. Activity restriction: Avoid strenuous activity until symptoms resolve.
4. Glucocorticoids: Prednisone (0.2-0.5mg/kg/d) if symptoms are refractory to NSAIDs or in cases of recurrent pericarditis.

1. Aortic dissection (AD): Intimal tear resulting in a false lumen.
2. Intramural hematoma (IMH): Rupture of vasa vasorum causing hematoma within aortic wall without tear.
3. Penetrating aortic ulcer (PAU): Ulceration of atherosclerotic plaque that penetrates into intima of aortic wall.

• Male gender
• Hypertension (HTN)
• Age 60-70
• If <40 years, consider:
  • Marfan syndrome
  • Ehlers-Danlos Syndrome type IV
  • Connective tissue disorders (CTD)
  • Bicuspid aortic valve
• Atherosclerosis
• Prior cardiac surgery
• Aortic aneurysm
• Family history of AAS
• Aortitis
• Trauma
• Pregnancy

Clinical Features:

• Chest or back pain (radiates to neck/jaw if ascending; back/abdomen if descending)
• Signs: AI murmur, pulse deficit, upper extremity BP differential (>20mmHg), decompensated heart failure

Complications:

• Syncope
• Shock
• Branch artery occlusion (MI, CVA, paraplegia)
• Cold extremity
• Renal failure
• Aortic valve regurgitation
• Pericardial effusion
• Cardiac tamponade
• Stroke

Goal: Minimize aortic wall stress by reducing left ventricular ejection force (dP/dT) with target heart rate <60 and systolic blood pressure 100-120 mmHg.

Agents:

1. IV beta blockade (e.g., esmolol, labetalol) - except in acute severe aortic insufficiency.
2. If additional BP control is needed, consider:
   • IV nitroprusside
   • TNG
   • Nicardipine
3. NEVER use vasodilators without concomitant beta blockade in aortic dissection without aortic insufficiency to avoid increased wall stress due to reflex tachycardia.

• One-time abdominal ultrasound for all men >60 with family history of AAA.
• Men aged 65-75 who have ever smoked should also be screened.
• Surveillance intervals depend on size:
  1. 3.0-3.9 cm: every 2-3 years
  2. 4.0-4.9 cm: every 12 months
  3. 5.0-5.4 cm: every 6 months

• Rupture: High mortality risk; symptoms include triad of abdominal/back pain, pulsatile abdominal mass, hypotension; requires immediate OR.
• Dissection: Symptoms include chest/abdominal/back pain, occlusion of aortic vessels, thromboembolism, and discrepant blood pressure in upper extremities.

Transient (self-limited) loss of consciousness due to cerebral hypoperfusion, associated with loss of postural tone, followed by complete spontaneous recovery; excludes metabolic causes such as hypoglycemia, hypoxia, and intoxication.

High-risk symptoms include: preceding palpitations, exertional syncope, bleeding, syncope while supine, lack of prodrome, and trauma.

High-risk features include: angina, congestive heart failure (CHF), moderate to severe valvular or structural heart disease, ECG features of ischemia or arrhythmia, family history of sudden cardiac death (SCD), preexcitation syndromes, high-risk occupation (e.g., airline pilot), and facial trauma (lack of warning time).

The San Francisco Syncope Rule (SFSR) is a clinical tool used to assess the need for hospitalization in patients with syncope. It indicates that a patient should be admitted if they have at least one of the following: ECG changes or non-sinus rhythm, dyspnea, hematocrit <30, systolic blood pressure <90, or heart failure.

• Avoid provocative stimuli
• Isometric counterpressure maneuvers of the limbs (e.g., leg crossing, hand grip, arm tensing, Valsalva, squatting)
• Medications for select cases (i.e., midodrine, fludrocortisone, beta-blockers)

Orthostatic vital signs are assessed, looking for a systolic drop of ≥20 mmHg or diastolic drop of ≥10 mmHg within 3 minutes of standing or on a head-up tilt test ≥60°. Additional tests may include hematocrit, A1C, and serum protein electrophoresis if amyloid is suspected.

• Ventricular tachycardia: therapy with ablation and/or an implantable cardioverter-defibrillator (ICD) is indicated in most patients.
• Supraventricular tachycardia: catheter ablation if evidence of accessory pathway is found.
• Bradyarrhythmias: pacemaker therapy may be indicated depending on the etiology of bradycardia.
• Aortic stenosis: aortic valve replacement may be indicated if all other sources of syncope are ruled out and the patient is a surgical candidate.

For seizures, an EEG is used; for stroke, CT or MRI/MRA is performed; for subclavian steal, ultrasound with Dopplers is specified for subclavian steal. Carotid Dopplers are of low clinical utility.

Severe asymptomatic hypertension (HTN urgency) is defined as a systolic blood pressure (SBP) ≥180 or diastolic blood pressure (DBP) ≥120 without evidence of end-organ damage, although patients may experience mild headaches.

The recommended blood pressure goal for a patient with acute pulmonary edema in a hypertensive emergency is to achieve a systolic blood pressure (SBP) of less than 140 mmHg within 1 hour.

For managing aortic dissection in a hypertensive emergency, the suggested medications include:

1. IV beta-blockers (labetalol, esmolol) to rapidly lower SBP to <120 mmHg and HR to <60 bpm within 20 minutes.
2. Followed by a vasodilator (nicardipine or clevidipine).

Esmolol is administered as a 500 µg/kg load given over 1 minute, followed by an infusion of 25-50 µg/kg/min, which can be adjusted by 25 µg/kg/min every 10-20 minutes up to a maximum of 300 µg/kg/min. Its onset is <1 minute, and the duration of action is 10-20 minutes.

Common symptoms of Peripheral Artery Disease include:

1. Classic claudication (10-35%): Reproducible exertional pain in the buttock, thigh, calf, or ankle, relieved by rest.
2. Atypical leg pain (40-50%): Pain that does not fit the classic claudication pattern.
3. Asymptomatic (20-50%): No symptoms present.
4. Threatened limb (1-2%): Pain at rest, ulcers at pressure points, or dry gangrene.

An Ankle-Brachial Index (ABI) of ≤0.9 is considered abnormal and indicates a high likelihood of arteriogram-positive lesions with ≥50% stenosis, suggesting the presence of Peripheral Artery Disease.

Treatment options for Peripheral Artery Disease include:

1. Optimize cardiovascular risk factors: Manage hypertension, diabetes, hyperlipidemia, and promote weight loss.
2. High-intensity statin therapy.
3. Smoking cessation.
4. Formal exercise program: Supervised exercise therapy is effective.
5. Anti-platelet therapy: Aspirin or clopidogrel for secondary prevention.
6. Cilostazol: For symptom relief in patients refractory to exercise therapy.
7. Endovascular repair: Angioplasty or stenting for severe symptoms or threatened limb.

Signs of acute limb ischemia include the 6Ps:

1. Pain: Sudden onset of severe pain.
2. Poikilothermia: Coldness of the limb.
3. Pallor: Pale appearance of the limb.
4. Pulselessness: Absence of pulse in the affected limb.
5. Paresthesia: Loss of sensation or tingling.
6. Paralysis: Inability to move the limb.

Chemotherapy cardiovascular toxicity includes:

• Cardiomyopathy
• Ischemia
• Vasospasm (e.g., 5-FU)
• Atherosclerosis
• Hypertension (HTN)
• Myocarditis (associated with immune checkpoint inhibitors)
• Pericardial disease (due to chemotherapy or radiation therapy)
• Thromboembolism
• QT prolongation
• Arrhythmias

Risk factors include:

• Pre-existing cardiovascular disease
• Known cardiovascular risk factors (e.g., diabetes mellitus, hyperlipidemia)
• Extremes of age
• Female sex

Diagnostic methods include:

• Transthoracic echocardiogram (TTE) compared to baseline
• Electrocardiogram (ECG)
• Troponin T (TnT) levels (elevated correlates with adverse cardiac events post-chemotherapy)
• MRI/PET/biopsy if immune checkpoint inhibitor myocarditis is suspected

Prevention strategies include:

• Consider beta-blockers (BB) or ACE inhibitors (ACEi) if:
  1. Ejection fraction (EF) < 50%
  2. EF drop > 10%
  3. Abnormal TnT levels
• Angiotensin receptor blockers (ARB) may provide better protection against EF decline in early breast cancer with adjuvant treatment
• Consider pre-emptive vasodilators and serial ECGs in patients receiving 5-FU and capecitabine

Screening and monitoring recommendations include:

• TTE surveillance schedule based on therapy and baseline cardiac risk, typically every 3-6 months for long-term risk >10 years.
• Additional imaging for patients with cardiac risk factors.
• Monitor blood pressure weekly during the first cycle, then every 2-3 weeks during therapy.
• Follow guidelines for therapies with known cardiovascular risks (e.g., anthracyclines, Trastuzumab) for CV monitoring.

Treatment options include:

• Optimize preventative cardiovascular health (e.g., manage lipids, diabetes, blood pressure)
• Standard heart failure and ischemic workup/management (e.g., aspirin if platelets > 10k, dual antiplatelet therapy if platelets > 30k)
• Cessation of chemotherapy may be considered as a last resort after a multi-disciplinary discussion

Common cardiotoxic therapies include:

• Anthracyclines (e.g., Doxorubicin): Dose-dependent heart failure, LV dysfunction
• Taxanes (e.g., Paclitaxel): Conduction abnormalities
• Alkylating agents (e.g., Cyclophosphamide): Cardiomyopathy with high-dose protocols
• Monoclonal antibodies (e.g., Trastuzumab): Risk of LV dysfunction
• Protein kinase inhibitors (e.g., Osimertinib): Cardiomyopathy, QTc prolongation
• Proteasome inhibitors (e.g., Carfilzomib): Heart failure, pulmonary hypertension

• Age: Each decade increases risk by 2x.
• Sex: Females have ~20% lower risk than males, but risk increases 3x post-menopause.
• Family History: Premature ASCVD in 1st degree relatives (before 55y for males, 65y for females).
• Elevated lipoprotein(a): A genetic risk factor for CVD.

• No routine prescription of low-dose ASA for primary prevention.
• Consider low-dose ASA for select patients aged 40-70 years at increased ASCVD risk who are not at increased bleeding risk.
• Avoid ASA for primary prevention in patients over 70 years.

• Clinical Clues:

  • 50% rise in creatinine after ACE/ARB initiation.

  • Lateralizing abdominal bruit.
  • Severe hypertension in patients with atrophic/asymmetric kidneys or diffuse atherosclerosis/FMD.

• Work-up:

  • Begin with Duplex Doppler ultrasound if intervention is likely; consider angiography if stenosis is >50% or results are ambiguous.

Stage I hypertension should be treated if there is clinical cardiovascular disease (CVD), diabetes mellitus type 2 (DM2), chronic kidney disease (CKD), or atherosclerotic cardiovascular disease (ASCVD) risk of 10% or greater.

The target blood pressure for hypertension management is less than 130/80 mmHg.

First-line agents for treating hypertension include thiazides (such as chlorthalidone or HCTZ), ACE inhibitors (ACEi), angiotensin receptor blockers (ARB), and calcium channel blockers (CCB).

Compelling indications for using beta-blockers in hypertension management include coronary artery disease (CAD) and pregnancy.

Follow-up evaluations for blood pressure response and adherence should occur at monthly intervals until blood pressure is controlled. Additionally, check BMP/Mg if starting ACEi/ARB or diuretic, 2-4 weeks after initiation, then yearly or with dose adjustments.

The SPRINT trial found that a systolic blood pressure goal of less than 120 mmHg compared to 135-139 mmHg resulted in a reduction of cardiovascular events and all-cause mortality in high-risk patients, although it also noted risks of non-orthostatic hypotension, syncope, electrolyte abnormalities, and acute kidney injury.

Adults aged 20 years and older should have a lipid panel checked to establish baseline LDL-C and estimate ASCVD risk. Measurement of apoB and Lp(a) may also be beneficial for risk estimation.

Recommended lifestyle interventions include:

1. Diet: Emphasize vegetables, fruits, whole grains, legumes, healthy protein sources, and limit sweets, refined carbs, and trans/saturated fats.
2. Weight control: Encourage weight loss in overweight/obese patients.
3. Exercise: Aim for aerobic activity 3-4 times a week for about 40 minutes per session.
4. Tobacco: Screen for tobacco use at every visit and assist with cessation efforts.

Indications for statin therapy include:

• Clinical ASCVD in patients under 75 years: maximally tolerated statin to reduce LDL-C by ≥50%.
• LDL-C ≥190 in ages 20-75: maximally tolerated statin to reduce LDL-C by ≥50%.
• Diabetes in ages 40-75: moderate-intensity statin; consider high-intensity if ASCVD risk >20%.
• Age 40-75 without above: lifestyle changes for low risk, consider moderate-intensity statin for borderline risk, and statin therapy for intermediate to high risk.

Statins are indicated as 1st-line therapy for primary and secondary prevention of cardiovascular events.

Ezetimibe works by decreasing intestinal cholesterol absorption and is indicated for statin-intolerant patients or those with LDL-C >70 mg/dL with cardiovascular disease.

PCSK9 inhibitors, when used with statins, have been shown to reduce cardiovascular events, with an ARR of 1.5% for evolocumab and 1.6% for alirocumab.

Recommended medications include:

1. Lipid Lowering: Goal of ≥50% LDL reduction and/or LDL ≤ 70mg/dL.
2. Anti-platelet: ASA 81mg for all patients.
3. Beta-blocker: Long-term use indicated for individuals with prior MI <1 year or LVEF ≤40%.
4. Anti-Hypertension: Goal BP <130/<80.
5. Anti-anginal: Beta blocker or calcium channel blocker as first-line agents.

Lifestyle modifications include dietary changes, physical activity, smoking cessation, and weight management, as part of comprehensive cardiovascular care.

Procainamide works by Na channel blockade, leading to conduction slowing and an increase in action potential. It is primarily used for ventricular tachycardia (VT) and atrial fibrillation (AF), especially in accessory bypass tracts like Wolff-Parkinson-White (WPW) syndrome.

For Lidocaine, the dosing guidelines are as follows:

1. Loading dose: 1.0-1.5 mg/kg.
2. May give an additional 0.5-0.75 mg/kg IV push as needed every 5-10 minutes.
3. Total dose should not exceed 3 mg/kg.
4. Maintenance: 1-4 mg/min (30-50 mcg/kg/min).

Amiodarone is contraindicated in patients with:

• Increased QTc interval
• Sick sinus syndrome (SSS)
• 2°/3° AV block
• Symptomatic bradycardia
• Cardiogenic shock

Sotalol can cause the following side effects:

• Increased QT interval
• Typical effects of beta-blockade

Contraindications include:

• CrCl < 40
• Left ventricular hypertrophy (LVH)
• Heart failure with reduced ejection fraction (HFrEF)
• Increased QTc
• Hypokalemia

Digoxin inhibits the Na/K ATPase, leading to increased calcium influx, suppression of AV node conduction, and increased vagal tone, acting as a positive inotrope. It is primarily used for AFib, Aflutter, heart failure with reduced ejection fraction (HFrEF), and SVT.

The dosing recommendations for Dofetilide are:

• Initial dose: 500 mcg twice daily.
• Max dose: Decrease by 50% if CrCl < 60 or if QT interval is prolonged.

JVD (Jugular Venous Distension) indicates elevated right atrial pressure. It is associated with conditions such as heart failure, tension pneumothorax, cardiac tamponade, superior vena cava syndrome, tricuspid stenosis, and large CV waves in tricuspid regurgitation.

The S3 heart sound is characterized as a 'sloshing' of blood hitting a compliant ventricular wall, occurring after S2. It is associated with heart failure and can be physiological in younger patients. It is best heard with the bell at the apex in the left lateral decubitus position.

The S4 heart sound indicates blood flow from the atrial kick into a stiff ventricular wall, occurring right before S1. It is associated with left ventricular hypertrophy, acute myocardial infarction, and cardiomyopathy. It can be normal in older adults but cannot be present in atrial fibrillation (AF) due to the absence of an atrial kick.

Peripheral edema occurs when capillary hydrostatic pressure overwhelms the lymphatic drainage ability, indicating volume overload. It is assessed by measuring the depth of the depression left by pressing on the skin, with varying degrees indicating severity.

An RV heave indicates right ventricular enlargement and is felt best over the left parasternal region. If the heel of the hand rises with systole, it suggests a heave. It is associated with conditions like pulmonary hypertension and right ventricular volume overload.

The AS murmur is characterized by turbulent flow across a stenotic aortic valve, becoming later and diminishing S2 as severity increases. It is loudest at the right 2nd intercostal space and radiates to the right carotid. It is associated with aortic stenosis and can be differentiated from increased aortic flow without obstruction.

Key steps in measuring JVP include:

1. Position the patient at a 30°-45° angle.
2. Identify the external jugular vein (EJV) as a proxy for the internal jugular vein (IJV).
3. Measure the height of the JVP above the sternal angle, adding 5 cm to approximate right atrial pressure.
4. Interpret the JVP in the clinical context and trend while managing volume status.

Steps to run telemetry include:

1. Locate the patient's name on the telemetry monitor and select their telemetry strip.
2. Select 'Patient Data' on the telemetry strip.
3. Click 'Event Review' to see any abnormal events since telemetry placement.
4. Choose the desired episode from the event list.
5. Review the options available for further analysis, including events, FD strip, graphic trends, and calipers.

• Tachypnea: Respiratory rate ≥20
• Cyanosis: SpO2 typically <80%
• Increased Work of Breathing (WOB): Signs include nasal flaring, retractions, grunting, tripod position, diaphoresis
• Obstruction: Symptoms include wheezing and stridor

1. Confirm code status
2. Call Rapid Response for assistance if needed
3. Assess airway, breathing, circulation & confirm access:
   • Place on supplemental O2 (NRB to start)
   • Identify red flags for immediate intervention
4. Initial workup: CXR, ABG, labs, and additional studies based on clinical suspicion

• Inability to protect airway due to altered mental status
• Pooling secretions or hemoptysis
• Life-threatening hypoxemia despite supplemental O2 (SpO2 <80%, PaO2 <55mmHg)
• Severe hypercapnia despite BiPAP
• Signs of tiring out (increased WOB, progressive hypercapnia)
• Respiratory rate >35

• Do not delay intubation in patients with impending respiratory failure.
• Have the following information ready prior to intubation:
  • Code status & urgency of decline
  • Hemodynamics: LV, RV, valves, volume status
  • Aspiration risk: NPO status, last meal, risk factors
  • Difficult airway history
  • Allergies
• Prepare sedation and paralytic agents as needed.

Respiratory failure can be classified as:

1. Hypoxemic Respiratory Failure: Inability to oxygenate, characterized by PaO2 < 60 mmHg.
2. Hypercapnic Respiratory Failure: Inability to ventilate, characterized by PaCO2 > 45 mmHg.

The P:F ratio (P=PaO2/F=FiO2) serves as a quick surrogate for the A-a gradient. A P:F ratio < 300 suggests the presence of ARDS (Acute Respiratory Distress Syndrome).

Causes of hypoxemic respiratory failure include:

1. Hypoventilation & Low FiO2: Decreased O2 delivery to lungs.
2. V/Q Mismatch: Imbalance in delivery of oxygenated air and blood flow, which can be due to:
   • Focal alveolar infiltrates (e.g., pneumonia, edema, cancer)
   • Airway issues (e.g., asthma, COPD)
   • Vascular problems (e.g., pulmonary hypertension, pulmonary embolism)
3. Shunt: Blood flow through the lung without encountering oxygenated air, which does not improve with supplemental oxygen. Causes include:
   • Diffuse alveolar infiltrates (e.g., ARDS)
   • Alveolar collapse (e.g., pneumothorax, atelectasis)
   • Intra-cardiac/pulmonary shunts (e.g., PFO, ASD, VSD).

Hypercapnic respiratory failure can be categorized into two main types:

1. 'Won't Breathe' (IRR): Conditions that prevent the patient from initiating breath, such as sedatives, obesity hypoventilation, brainstem issues, and central sleep apnea.
2. 'Can't Breathe' (VA): Conditions that impair the ability to breathe effectively, including:
   • Increased dead space due to conditions like emphysema or severe pulmonary embolism.
   • Chest wall or pleural constraints affecting lung volume, such as obesity or pleural effusion.

Hypercapnia leads to respiratory acidosis, characterized by an increase in pCO2. The bicarbonate (HCO3) levels change as follows:

• Acute: HCO3 increases by 1 for every 10 mmHg increase in pCO2.
• Chronic: HCO3 increases by 3-4 for every 10 mmHg increase in pCO2.

Target SpO2 levels are recommended to be 91-96%. Recent trials found no benefit to higher or lower targets in critical illness.

Flow rates for a Non-Rebreather mask are 10-15 LPM, providing an FiO2 of 60-100%. It is considered first for acute hypoxemia due to its easy accessibility.

Contraindications for NIPPV include:

1. Risk of delay for intubation in emergent situations.
2. Risk of aspiration due to gastric insufflation.
3. Risk of injury from conditions like pneumothorax or recent facial trauma/surgery.

The ROX index is a tool for predicting HFNC failure and monitoring the need for intubation in patients with pneumonia.

The physiological effects of HFNC include:

• Oxygenation: delivery of O2 and some PEEP.
• Ventilation: increased ventilation due to dead space during expiration.
• Other: Humidification enhances mucociliary clearance of secretions.

The ABCDEF approach includes:

1. (A)ssess technical quality and (A)irways: Check rotation, lung volumes, penetration, and airways for abnormalities.
2. (B)ones/soft tissue: Look for subcutaneous air, rib fractures, and cervical ribs.
3. (C)ardiac Silhouette: Evaluate the cardiac silhouette and mediastinum for signs of cardiomegaly.
4. (D)iaphragm: Assess diaphragm position and shape, noting that the left hemidiaphragm is usually lower.
5. (E)ffusions: Identify blunting of the costophrenic angle and differentiate between free-flowing and loculated effusions.
6. (F)ields & (F)oreign bodies: Examine lung fields for focal or diffuse processes and check for lines or drains.

Honeycombing refers to the clustering of cystic airspace disease, with microcystic <4mm and macrocystic >4mm. It is commonly associated with Interstitial Lung Disease (ILD), specifically Non-Specific Interstitial Pneumonia (NSIP) for microcystic and Idiopathic Pulmonary Fibrosis (IPF) for macrocystic changes.

CT chest is used to characterize abnormal findings seen on CXR and to investigate suspected pathology that may not be visible on CXR. It involves:

• HRCT (High-Resolution CT): Thin-section CT (<2mm) for diagnosing diffuse lung pathology.
• Approach to interpretation: Review scout imaging for anatomic overview, assess lines/tubes, and evaluate mediastinum, heart, vessels, and airways in both soft tissue and lung windows.

Asthma is a heterogeneous condition characterized by respiratory symptoms such as wheeze, shortness of breath (SOB), chest tightness, and cough, along with variable expiratory airflow limitation.

Common triggers for asthma symptoms include:

• Exercise
• Cold air
• Allergens
• Irritants (e.g., smoke, perfume)
• Viral respiratory infections
• Drugs (e.g., ASA, NSAIDs, ß-blockers)

Key components of asthma management in outpatient care include:

1. Controller and reliever medications: Stepwise approach based on severity.
2. Non-pharmacological interventions: Smoking cessation, regular physical activity, vaccines, breathing exercises, and weight loss if obese.
3. Monitoring and adjusting treatment: Step up if not controlled; step down if well controlled for 2-3 months.

Outpatient Exacerbations:

• Short course of prednisone (40-50mg for 5-7 days) + controller/reliever regimen.

Inpatient Exacerbations:

• Assess severity (vital signs, mental status, SpO2, work of breathing).
• Treatment may include bronchodilators, steroids, and oxygen therapy, with consideration for mechanical ventilation in severe cases.

The FEV1/FVC ratio is crucial in pulmonary function testing:

• A ratio of less than 0.7 indicates obstructive lung disease, which may suggest asthma if there is a significant response to bronchodilators.
• A normal ratio suggests other conditions may be present, and further testing (e.g., DLCO, methacholine challenge) is needed to evaluate for asthma.

In asthma/COPD overlap (ACO), treatment includes:

• ICS-containing treatment is essential.
• Addition of LABA and/or LAMA is necessary.
• Escalation to triple therapy or biologics may be required for management.