Angina

• Unstable Angina = Transient ischemia, normal(-ish) troponins
• NSTEMI = subendocardial ischemia with +Troponins. Partially occluded coronary
• STEMI = Transmural myocardial ischemia, +Troponins. Fully occluded coronary

NSTEMI Types

• Type 1 - Plaque rupture
• Type 2 - Supply-Demand Mismatch
• Type 3 - Cardiac death
• Type 4 - Peri-PCI
• Type 5 - Peri-CABG

RV Infarction

Signs/Symptoms:

• ST-segment elevation in V1 or V4R (right-sided V4)
• hypotension
• clear lung fields
• jugular venous distention

Treat:

• Aggressive volume resuscitation to optimize right ventricular filling (preload)
• intravenous vasopressors if hypotension persists
• urgent coronary revascularization
• AVOID Nitrates, dobutamine

Imaging

• Exercise EKG - initial test in patients with intermediate probability of coronary artery disease and normal findings on baseline ECG. Cannot use if: If there are baseline ECG abnormalities (like LBBB), inability to exercise
• Myocardial perfusion imaging (MPI) (Nuclear medicine stress testing). Looks for differences in blood flow to detect ischemia. Less contrast goes to areas supplied by coronary vessels with stenosis
• Cardiac magnetic resonance (CMR) imaging
• Adenosine myocardial perfusion imaging. UNLESS asthma or reactive airways disease
• Coronary artery calcium (CAC) scoring cannot determine the degree of obstruction. It has no use in patients on a statin

High Sensitivity Trop

• High Sens troponin delta is less than 10-20%, which is less consistent with ACS
• At my institution (Kentucky, USA), call Cardiology for high sensitivity Troponin over 150 or if delta high sensitivity Troponin exceeds 10-20 percent

Misc

• Contraindications to nitroglycerin: Sildenafil or other erectile dysfunction med in past 7 days, Bradycardia (HR below 60), Hypotension, R-side or inferior wall MI
• Do not anticoagulate in a Type-2 NSTEMI caused by Hypertensive Urgency, as it increases risk of hemorrhagic stroke
• ASCVD score http://tools.cardiosource.org/ASCVD-Risk-Estimator/
• Low evidence to hold PPI if on Clopidogrel (Maybe worse with Omeprazole, but still no stong indication to hold)


Sources
• Gulati M, Levy PD, Mukherjee D, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR guideline for the evaluation and diagnosis of chest pain: a report of the American College of Cardiology/American Heart Association. Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2021;78:e187–e285. https://www.ahajournals.org/doi/pdf/10.1161/CIR.0000000000001029

AASLD now classifies some disease as "Advanced chronic liver disease (ACLD)", which does NOT require liver biopsy. So, it is treated the same as Cirrhosis, but can be diagnosed without an invasive procedure Ref. ACLD is diagnosed with Liver Stiffness Measurements over 15kPa. (below 10KPa rules ACLD). If Liver Stiffness Measurements are between 10KPa and 15kPa, then if platelet count is below 110 then this is also ACLD Ref. I will use ACLD and Cirrhosis interchangeably since biopsies are very uncommon.

There are two subtypes of ACLD:

• ACLD without prior decompensation
• Compensated ACLD (cACLD)

This is significant - median survival for compensated is 12 years, while median survival after one decompensating event is 1.5 years or less Ref. Decompensated ACLD has clinical symptoms of Portal Hypertension, which are:

• Overt ascites
• Variceal hemorrhage
• Overt hepatic encephalopathy

These usually present when portal pressure gradients is 10mm Hg or more.

Portal Hypertension is pressure difference between the portal vein and the inferior vena cava over 5mmHg. There are three types of Portal Hypertension

• Prehepatic - resistance in the portal vein
• Intrahepatic - resistance in the liver This can be several types
  • Presinusoidal - Cirrhosis scarring of the sinusoids
  • postsinusoidal - Resistance in the efferent (central) vein
• Posthepatic - resistance in the IVC

References

• Kaplan, David E., Cristina Ripoll, Maja Thiele, Brett E. Fortune, Douglas A. Simonetto, Guadalupe Garcia-Tsao, and Jaime Bosch. "AASLD Practice Guidance on risk stratification and management of portal hypertension and varices in cirrhosis." Hepatology 79, no. 5 (2024): 1180-1211. https://journals.lww.com/hep/fulltext/2024/05000/aasld_practice_guidance_on_risk_stratification_and.22.aspx

Formulae and their required lab value inputs

• MELD - Creatinine, INR, Total Bilirubin, Sodium
  References:

  • Ming Jiang, Fei Liu, Wu-Jun Xiong, Lan Zhong, and Xi-Mei Chen, "Comparison of four models for end-stage liver disease in evaluating the prognosis of cirrhosis" World J Gastroenterol. 2008 Nov 14; 14(42): 6546–6550, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2773344/

• Maddrey Discriminant Function - PT, Creatinine, Total Bilirubin
  References:

  • Maddrey WC, Boitnott JK, Bedine MS, Weber FL, Mezey E, White RI, "Corticosteroid therapy of alcoholic hepatitis" Gastroenterology 75 (2): 193–9. PMID 352788

  • Soultati AS, et. al. "Predicting utility of a model for end stage liver disease in alcoholic liver disease" World J Gastroenterol 2006 July 07;12(25):4020-4025

• Child-Pugh - INR, Total Bilirubin, Albumin, Ascites, Encephalopathy
  References:

  • François Durand, Dominique Valla, "Assessment of the prognosis of cirrhosis: Child–Pugh versus MELD", Journal of hepatology April 2005 Volume 42, Issue 1, Supplement, Pages S100–S107

Renal Tubular Acidosis:

• Type I: Distal, Low serum K, High urine pH. Causes: Obstructive uropathy, Sjögren's, Rheumatoid, Lupus, Sickle cell anemia, Hyperthyroid, Hyperparathyroid, Hepatitis, Primary Biliary Cirrhosis, renal medullary cystic disease, chronic UTI
• Type II: Proximal, (usually Fanconi in adults). Low serum K, Glucosuria, Phosphaturia, Proteinuria. Causes: Wilson disease, drugs (Tenofovir, ifosfamide, Acetazolamide), Multiple myeloma
• Type IV: Distal, Low or Normal or High serum K. Causes: Spironolactone or eplerenone, ACE inhibitors or ARBS, Trimethoprim, Pentamidine, NSAIDs, Diabetic nephropathy, HIV/AIDS, Addison's disease, sickle cell disease, urinary tract obstruction, Lupus, Amyloidosis

• Hyperkalemic RTAs include Type 4 (hypoaldosteronism), and voltage-dependent RTA (defects in distal sodium reabsorption)
• HypOkalemic RTAs include Type 1 (Distal - defects in hydrogen ion excretion) and type 2 (Proximal - defects in bicarbonate reabsorption in the proximal tubule)

Types of Heart Failure:

HFrEF	LVEF 40 or lower
HFmrEF	LVEF between 41 and 49
HFpEF	LVEF 50 or higher

Medications for HFrEF (LVEF 40 or lower) ARNI or ACE/ARB SGLT2 MRA Diuretics ICD Hydralazine Ivabradine (HR 170 at rest) ICD No CCB No PPAR and DDP-4

Medications for HFpEF (LVEF over 40) ARB or ARNi SGLT2 MRA (maybe)

LVEF is a spectrum, and among patients with LVEF 41-49, particularly the lower end of this spectrum, seem to respond to HFrEF treatment.

Medications

• ACE/ARB
  In patients with HFrEF and NYHA II-III symptoms, use ARNi (either start or switch ACE/ARB to ARNi) If switching, wait 36 hours between ACEi and ARNi doses. Patients with HFpEF, ARNi or ARB may be considered (decrease hospitalizations). In HFrEF, can use ACEi, or if intolerant to ACEi then can consider ARB. "An ARNi is recommended as de novo treatment in hospitalized patients with acute HF before discharge given improvement in health status, reduction in the prognostic biomarker NT-proBNP, and improvement of LV remodeling parameters compared with ACEi/ARB."
  Angioedema due to ACEi may be due to reduced degradation of vasoactive peptides bradykinin and substance P. Can switch to ARB, see Rasmussen, Eva, et al, "Angiotensin II receptor blockers are safe in patients with prior angioedema related to angiotensin-converting enzyme inhibitors – a nationwide registry-based cohort study". Note that ARNi contains Neprilysin inhibitors, but those inhibitors can cause angioedema when used with ACEi and are contraindicated.

• SGLT2 Inhibitors
  Use for HFrEF and HFpEF, and these reduce hospitalizations and cardiovascular mortality, even in non-Diabetic patients and benefits are independent of the glucose-lowering effects.

• Beta Blockers
  In HFrEF, beta blockers reduce symptoms but in HFrEF patients with history of MI or acute coronary syndrome (ACS) they also reduce mortality Use bisoprolol, carvedilol, metoprolol succinate.

• MRA - Mineralcorticoid Receptor Antagonist
  In HFrEF Spironolactone or eplerenone reduces morbidity and mortality, if eGFR is over 30 and potassium is below 5.0 mEq/L. Stop if K cannot be kept below 5.5. In HFpEF, MRAs may be considered but only decrease hospitalizations not mortality.

• Diuretics
  Other than MRAs, these may not affect mortality, they only improve symptoms. > >

  Diuretic	Oral Bioavailability	Normal Half Life	Half Life in CKD
  Furosemide Oral	50%	1.5-2hrs	2.8hrs
  Bumetanide	80-100%	1hrs	1.6hrs
  Torsemide	68-100%	3-4hrs	4-5hrs
  Hydrochlorothiazide	55-770%	6-15hrs	Longer
  Chlorthalidone	60-70%	40-60hrs	Longer
  Metolazone	70-90%	14-20hrs	Longer

  
  Source: Ellison, CJASN 2019 14:1248-57

• Calcium Channel Blockers (CCB)
  Stop nondihydropyridine CCBs (diltiazem and verapamil) in HFrEF. Dihydropyridine CCBs may be used for hypertension

• PPAR and DDP-4
  Stop Thiazolidinediones (PPAR agonists) and DPP-4 inhibitors (Sitagliptan and others) because they increase hospitalizations.

• Hydralazine
  African American patients with NYHA class III-IV HFrEF on optimal medical therapy, should also get hydralazine and isosorbide dinitrate

• Ivabradine
  Patients with symptomatic (NYHA class II to III) HFrEF and LVEF below 35 and sinus rhythm HR ‡70 bpm at rest, should get ivabradine

• ICD and CRT
  Patients who are at least 40 days post-MI with LVEF below 30 and have reasonable expectation of survival for over 1 year may get an ICD to reduce total mortality. Patients with LVEF below 35%, sinus rhythm, LBBB with QRS over 150ms may also get Cardiac resynchronization therapy (CRT). Many patients who meet the indication for CRT also meet indications for ICD

Some Non-Ischemic Causes of HF, both left and right sided

• Hypertension

• Tachycardia-mediated cardiomyopathy. It may result from either SVT or VT or frequent PVCs. Time to development of cardiomyopathy varies, but it may develop within days to months of tachycardia onset.

• Obesity hypoventilation syndrome (OHS). Daytime hypercapnia with PCO2 greater than 45mm Hg

• Stress cardiomyopathy (Takotsubo)

• Cardiac amyloidosis. Increased wall thickness on echo with low voltage on the ECG. Cardiac magnetic resonance (CMR) imaging for diagnosis. There are several causes: light-chain amyloid (AL) amyloidosis and transthyretin amyloid (ATTR) amyloidosis.

• Peripartum cardiomyopathy. LV dysfunction toward the end of pregnancy or in the months after delivery. Following delivery, add ACE/ARB/ARNi.

• Sarcoidosis. Cardiac magnetic resonance (CMR) imaging for diagnosis.

• Infection - HIV, COVID-19, Chagas

• Drug toxicity - Chemotherapy, Alcohol, Cocaine, Amphetamines

• Chronic thromboembolic pulmonary hypertension. Diagnose with ventilation-perfusion scan (Chest CTA is less sensitive)

• Hypertrophic cardiomyopathy (HCM). Autosomal dominant, causes LV Hypertrophy. Avoid beta-blockers, verapamil and refer to ICD

• Others: hemochromatosis, hypothyroidism, hyperthyroidism, acromegaly, Familial cardiomyopathy

NYHA Classes I - No limitation of physical activity II - Slight limitation of physical activity. Comfortable at rest. III - Marked limitation of physical activity. Comfortable at rest. IV - Unable to carry on any physical activity without discomfort.

ACC Stages A At risk B Asymptomatic Risks (HTN, CVD, DM, Obese) or signs (Elevated BNP or Trop) C Symptomatic heart failure D Symptoms interfere with daily life

Notes on Diuresis (from an old ASN Kidney Week presentation)

• Adding Acetazolamide helps diuresis by reducing Proximal tubule Na reabsorption and downregulates Pendrin (Cl/HCO23).
• Diuretic are excreted in PCT by OAT
• Hypochloremia reduces diuretic response due to less Cl for the NKCC2 to work (the CC2 is 2 Chloride atoms). You can fix this with PO KCl, or Amiloride or Spirono
• During diuresis, If K remains low add spironolactone at 25 mg PO daily. Also can add Amiloride or Triamterene to blocks K losses. However, Spironolactone does NOT help K losses (ATHENA-HF Trial)
• SGLT2 DOES help. It blocks PCT reabsorption of Na
• No evidence coadmin of Albumin helps, and it can cause HTN and Pulm Edema
• Only add an MRA (spironolactone or eplerenone) if eGFR is over 30 and serum potassium is below 5
• Loop diuretics may stilumate Renin and so reduce eGFR. Increased urine NaCl loss causes renal pelvic chomoreceptors to activate renal nerve stimulation and reduce GFR. Despite its effects on decreasing Na sensing in Macula Densa, it blunts tubuloglomerular feedback. Loop Diuretics also stimulate vasopressin, so cause free water retention and hyponatremia. However, that also may be outweighed by the free water effects of loop diuretics on the interstitial osmolar gradient.
• Torsemide may cause Aldo receptor blockade, and maybe decrease Aldo synthesis, decrease myocardial fibrosis, decrease RAAS activation
• d/c NSAIDs (which blunt sodium excretion)

NT-proBNP Cutoffs (from ICON trial)

• 450 - Patients under 50 years old
• 900 - Patients 50-75 years old
• 1800 - Patients over 75 years old

BNP cutoff is 100 (from "Breathing Not Properly" Trial)

Diagnosing Cardiogenic shock

• Hypotension (e.g., SBP below 90 mm Hg) Or requirement of vasopressors to maintain systolic BP over 90 mm Hg
• End-organ hypoperfusion should be present (Decreased mentation, Cold extremities, livedo reticularis, Urine output below 30 mL/h, Lactate over 2 mmol/L)

Misc

• H2FPEF estimates the liklihood of HFpEF. The E/e ratio is peak early mitral inflow velocity (E) over early diastolic mitral annular velocity (e′). This can estimate LV filling pressure.

• In women with HF who are pregnant or currently planning for pregnancy, ACEi, ARB, ARNi, MRA, SGLT2i, ivabradine, and vericiguat should not be administered

• First-line therapy for acute idiopathic pericarditis is aspirin or NSAIDs and colchicine. In patients with recurrent pericarditis initially treated with both colchicine and an NSAID, the addition of a glucocorticoid should be considered.

• Compression therapy is an essential component of the treatment of venous stasis ulcers Must check ABI since an absolute contraindication to compression therapy is an ABI of 0.5 or less, although cautioun for any patient with an ABI less than 0.9

Sources

• Heidenreich PA, Bozkurt B, Aguilar D, et al, "ACC/AHA Joint Committee Members. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines", Circulation. 2022 May 3;145(18):e895-e1032. https://www.ahajournals.org/doi/10.1161/CIR.0000000000001063

Stages

• Stage I (below 160/100)
• Stage II (over 160/100)
• Resistant (on 3 agents including a diuretic)

Daily salt-intake is approximately (23 x 24-hour urine Na in mEq)
If resistant, check Renin/Aldosterone ratio. If over 25 then possible primary hyper-aldo

• Usually give IV Furosemide when urine Osm is over 500
• A loop diuretic will wash out the interstitial gradient and so free water is not reabsorbed even when Aquaporins are open. As a result, a loop diuretic will waste free water (loop diuretic urine is approx 1/2 NS) and so will raise sodium concentration in blood. A Thiazide preserves interstitial gradient so aquaporins reabsorb free water, so Thiazides preserve free water reabsorption and lower sodium concentration.
• If cirrhotic, then just restrict fluids and diuretics - vaptans are contraindicated
• Free water clearance = (1 - (urine Osm / serum Osm)) x DailyUrineVolume
• ElectrolyteFreeWaterClearance = Urine Volume x (1 - ( ( UruneSodium + UrinePotassium ) / SerumSodium ))
  • If FreeWaterClearance over 0 then pt is losing free water and Na will rise
  • If FreeWaterClearance below 0 then pt is retaining free water and Na will drop

NEWS Score

Add up scores for each finding

Heart Rate	Below 40=3	41-50=1	51-90=0	91-110=1	111-130=2	Over 131=3
Systolic BP	Below 91=3	91-100=2	101-110=1	111-219=0	Over 220=3
Respiratory Rate	Below 8=3	9-11=1	12-20=0	21-24=2	Over 24=3
Temp (F)	Below 95=3	95.1-96.8=1	96.9-100.4=0	100.5-102.2=1	Over 102.3=2
Alert?	Alert=0	Voice or pain or unresponsive=3
SpO2	Below 92=3	92-93=2	94-95=1	Over 95=0
Supplemental O2	Yes=1	No=0

Interpretation:

• Low (NEWS 1–4) Monitor
• Medium (NEWS 5–6 or any score 3) Urgent review
• High (NEWS over 6) Emergency assessment, usually transfer to MICU

MEWS Score

Add up scores for each finding.

Heart rate	below 40=2	41-50=1	51-100=0	101-110=1	11-129=2	Over 130=3
Systolic BP	Below 70=3	71-80=2	81-100=1	101-199=0	Over 200=2
Respiratory rate	Below 9=2	9-14=0	15-20=1	21-29=2	Over 30=3
Temp (F)	Below 95=2	95–101.12=0	Over 101.3=2
Alert?	Alert=0	Voice=1	Pain=2	Unresponsive=3

Interpretation: A total score of 5 or greater statistically correlates with increased risk of death or admission to ICU.

DSM 5 Criteria for Dependence (Mild: 2-3, Moderate 4-5, Severe 6 or more)

• Hazardous use
• Social/interpersonal problems related to use
• Neglected major roles to use
• Withdrawal
• Tolerance
• Used larger amounts/longer
• Repeated attempts to quit/control use
• Much time spent using
• Physical/psychological problems related to use
• Activities given up to use
• Craving

Duration of different substances in Urine Drug Screen:

Alcohol	7-12hrs
Amphetamine	2 days
Buprenorphine	4-10 days
Cocaine	2-4 days
Diazepam	30 days
Heroin	1-3 days
Lorazepam	2 days
Opioids	2-4 days
THC (chronic use)	30 or more days

Note, Alprazolam, Fentanyl and synthetics are often not detected in a routine urine tox.

Hemorrhage Class

• Class I - No tachycardia and blood pressure is normal, blood loss less than 750mL or 15% total blood volume
• Class II - Tachycardia (HR over 100) but blood pressure is normal, blood loss 750mL to 1500mL or 15 to 30% total blood volume
• Class III - Tachycardia (HR over 120) and blood pressure is low, and urine output is decreased, blood loss 1500mL to 2000mL or 30% to 40% total blood volume
• Class IV - Tachycardia (HR over 120) and blood pressure is low, and urine output is low, blood loss over 2000mL or over 40% total blood volume

Anemia chronic disease and Iron deficiency anemia both have low serum iron and low Iron saturation. How do we tell them apart?

• Anemia of Chronic Inflammation has Normal/High Ferritin, normal/Low Transferrin
• Iron-Deficiency Anemia has Low Ferritin, High Transferrin

ITP

Generally a diagnosis of exclusion, no megakaryocytes on peripheral smear however MPV elevated indicating larger platelets.

Primary bone marrow disorder

HIT

If normal prior to admit then the timing could fit with low platelet count.

DIC

Expect high INR, low fibrinogen and fever

Hemolytic anemia or TMA

Expect hemolysis labs (hapto, LDH), schistocytes

RBC production issues

Low folate, B12, TSH

Infectious causes

EBV, HIV, and hep C normal

SGLT2 Criteria

• Everyone with DM2 and CKD (KDIGO Rec 4.2.1) regardless of UACR. Must have DM2 and GFR over 30
• Everyone with HFrEF. Empa, Cana, Dapa to reduce CV events, but Empa is only that reduces death
• Everyone with CKD and UACR over 200 ug/mg but NO DM. Only 1 trial with non-diabetic pts, but, EMPA-Kidney is coming
• Not for DM-1, Transplant, Dialysis, PKD, SLE, ANCA, imunosuppressed, past DKA, GFR below 30. May continue SGLT2 if GFR drops below 30 while on SGLT2.

SGLT2 Criteria

• Everyone with DM2 and CKD (KDIGO Rec 4.2.1) regardless of UACR. Must have DM2 and GFR over 30
• Everyone with HFrEF. Empa, Cana, Dapa to reduce CV events, but Empa is only that reduces death
• Everyone with CKD and UACR over 200 ug/mg but NO DM. Only 1 trial with non-diabetic pts, but, EMPA-Kidney is coming
• Not for DM-1, Transplant, Dialysis, PKD, SLE, ANCA, imunosuppressed, past DKA, GFR below 30. May continue SGLT2 if GFR drops below 30 while on SGLT2.

Definition of Very High-Risk

• History of multiple major ASCVD events
• OR One major ASCVD event AND two or more high-risk conditions

Major ASCVD Events

• Recent ACS (within the past 12 mo)
• History of MI (other than recent ACS events listed above)
• History of ischemic stroke
• Symptomatic peripheral artery disease (history of claudication with ABI below 0.85, or previous revascularization or amputation)

High-Risk Conditions

• Age over 65yo
• Diabetes
• Hypertension
• Chronic kidney disease (any eGFR below 60)
• Current tobacco smoking
• History of CABG or PCI
• LDL-C over 100 mg/dL despite maximal statin
• Familial hypercholesterolemia
• History of congestive heart failure

Lipid Treatment

High-intensity statin goal is 50 percent reduction in LDL-C levels. Measure fasting lipids in 4 to 12 weeks after statin initiation or dose adjustment and Q3-12 months thereafter.

• Statin
• Ezetimibe - if very high risk max statin with LDL over 70 mg/dL
• PCSK9 monoclonal antibodies may be used if Statin+Exetimibe are not enough. It binds to PCSK9, a liver enzyme that degrades hepatocyte LDL receptors. Uncertain economic value at US prices
• Icosapent ethyl may be considered
• Niacin, or fenofibrate or Omega-3 diet supplements are not beneficial

High intensity

Use these:

• Atorvastatin 40mg, 80mg
• Rosuvastatin 20mg

Moderate Intensity

Do not use these for CCD/CAD, but they may be useful for diabetes

• Atorvastatin 10mg (20mg)
• Rosuvastatin (5mg) 10mg
• Simvastatin 20-40mg
• Pravastatin 40mg (80mg)
• Lovastatin 40mg (80mg)
• Fluvastatin XL 80mg
• Fluvastatin 40mg BID
• Pitavastatin 1-4mg

Hypertension

BP target of below 130/80 mm Hg is recommended. May use ACE/ARB, Beta Blockers, CCB, Thiazine, MRA

Anticoag

If DOAC are Tolerated (no major bleeding)

• +/- ACS, No PCI: then use DOAC
• +ACS, +PCI then use one of these:
  • Low/mod bleed risk -> DOAC+DAPT x1mo then DOAC+Plavix x6mo then DOAC
  • High bleed risk -> DOAC+DAPT x1mo then DOAC+Plavix x1-6mo then DOAC

Prasugrel is contraindicated in patients with a history of stroke or TIA. Ticagrelor is preferred for patients with PCI

No DOAC (Bleeding Risks)

• No ACS, No PCI then Asa
• +ACS, No PCI then DAPT for 12+ months
• +ACS, +PCI then:
  • Low/mod bleed risk -> DAPT x6mo then SAPT
  • High bleed risk -> DAPT x1-3mo then P2Y12 x9mos

If no indication for DOAC, then rivaroxaban 2.5mg BID and Asa 81

Beta Blockers

Long-term beta-blocker therapy is not recommended to improve outcomes in patients with CCD in the absence of myocardial infarction in the past year, left ventricular ejection fraction below 50%, or another primary indication for beta-blocker therapy Either a calcium channel blocker or beta blocker is recommended as first-line antianginal

Misc

• Colchicine for secondary prevention may be considered to reduce recurrent ASCVD events
• Ivabradine is potentially harmful in patients with CAD
• Nitrates improve myocardial oxygen delivery through coronary vasodilation and decrease oxygen consumption by reducing preload. nitrate-free interval of 8 to 12 hours daily is required to avoid nitrate tolerance,
• Breast cancer is often perceived as the principal threat to a woman's life, but cardiovascular disease is the leading cause of mortality in women. Breast cancer survivors are also at increased risk for CAD

AntiAnginal

• Beta Blocker
• CCB
• Long Acting Nitrate

PAD Treatment

Diagnose:

• ABI 0.90 or less is diagnostic for PAD
• ABI 1.40 or more means calcified arteries and is uninterpretable.
• Toe-brachial index 0.70 or less is diagnostic for PAD.

Treat:

• Statin
• Two antiplatelet agents
• Beta-blocker
• ACE inhibitor
• Cilostazol - PDE inhibitor with antiplatelet and vasodilator activity. Contraindicated in patients with heart failure.
• Smoking cessation
• Exercise

Aortic dissection

Findings

• Irregular Pulsatile JVD (cannon waves)

Treat:

• Intravenous Beta-blockers are the initial drugs of choice (labetalol and esmolol)
• SBP below 120
• CTA
• Echo (for acute Aortic Regirg - a surgical emergency)
• Emergent surgery
• Do not start with CCB or Nitroprusside. May cause reflex tachycardia

Sources

• Virani SS, Newby LK, Arnold SV, Bittner V, Brewer LC, Demeter SH, Dixon DL, Fearon WF, Hess B, Johnson HM, Kazi DS, Kolte D, Kumbhani DJ, LoFaso J, Mahtta D, Mark DB, Minissian M, Navar AM, Patel AR, Piano MR, Rodriguez F, Talbot AW, Taqueti VR, Thomas RJ, van Diepen S, Wiggins B, Williams MS; Peer Review Committee Members. 2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With Chronic Coronary Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation. 2023 Aug 29;148(9):e9-e119. doi: 10.1161/CIR.0000000000001168. Epub 2023 Jul 20. Erratum in: Circulation. 2023 Sep 26;148(13):e148. doi: 10.1161/CIR.0000000000001183. Erratum in: Circulation. 2023 Dec 5;148(23):e186. doi: 10.1161/CIR.0000000000001195. PMID: 37471501. https://www.ahajournals.org/doi/10.1161/CIR.0000000000001168
• Gulati M, Levy PD, Mukherjee D, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR guideline for the evaluation and diagnosis of chest pain: a report of the American College of Cardiology/American Heart Association. Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2021;78:e187–e285. https://www.ahajournals.org/doi/pdf/10.1161/CIR.0000000000001029

COPD is about more than smoking:

• Tobacco only causes 30-40 percent of all COPD worldwide. Burning wood/dung/coal/crop residues in open stoved cause most.
• Less than 50 percent of heavy smokers develop COPD.
• Mow/Middle Income Countries have 85 percent of total COPD burden worldwide
• Asthma is also a risk for COPD, and asthmatics have 12x higher risk of COPD

Chronic Bronchitis is a condition within COPD, not a form of COPD. It is chronic cough and sputum production for 3 months/year for 2 years, and it affects ~27-35 percent of COPD pts.

COPD seems to be an altered inflammatory response.

• Both COPD and Asthma are the result of inflammation, but asthma seems to cause more immediate muscle response to an allergen while COPD causes tissue destruction and long term structural changes.
• COPD starts with macrophages, which bring in other inflammatory cells, then proteases cause destruction of elastin, and eventually leads to peribronchial fibrosis.
• Airflow obstruction is caused by a mix of small airway disease (increase airway resistance) and parenchymal destruction (reduce elasticity of lung). It also causes loss of alveolar attachments to airways, decrease elastic recoil, which both cause reduced ability to keep the lung open. All of these limit lung emptying during expiration, and so decrease FEV1. This leads to air trapping and hyperinflation.
• Parenchymal destruction in emphysema also leads to decreased lung diffusing capacity (DLco).
• In Exacerbations, there is increased inflammation, hich causes worse air trapping, hyperinflation, and reduced expiratory flow.

Diagnosing

• Symptome: dyspnea, chronic cough, incrreased sputum
• Spirometry should be repeated if the FEV1/FVC is between 0.6 and 0.8

In spirometry, a Z-score is the number of standard deviations that the raw score is above/below the median score.

Exacerbation Criteria (ROME Criteria)

• Mild: RR below 24, HR below 95, SaO2 over 92 percent on RA or baseline home O2, CRP below 10
• Moderate: Must meet at least 3 of these
  • RR over 24
  • HR over 95
  • SaO2 below 92 percent on RA or baseline O2
  • CRP over 10
  • If you get an ABG, then PaO2 must be <= 60 and/or PaCO2 must be >= 45
• Severe: Must meet at least 3 of these
  • RR over 24
  • HR over 95
  • SaO2 below 92 percent on RA or baseline O2
  • CRP over 10
  • Must have ABG, PaCO2 must be > 45 and pH < 7.35

Severity of Airflow Obstruction - GOLD Staging

• GOLD1 FEV1 over 0.8
• GOLD2 FEV1 0.5 - 0.8
• GOLD3 FEV1 0.3 - 0.5
• GOLD4 FEV1 below 0.3

Current Symptoms - Modified Medical Research Council Dyspnea Questionaire

• mMRC0 = dyspnea only with strenuous exercise
• mMRC1 = dyspnea with rapid walking
• mMRC2 = dyspnea with normal walking, must walk slowly
• mMRC3 = Must stop for breath when walking 100 meters
• mMRC4 = Breathless when dressing or undressing

Other factors for staging COPD

• Previous Exacerbations - 2 or more exacerbations annually or at least one hospitalization annually
• Eos Count - This predicts the efficacy of ICS for preventing exacerbations
• DLco - This measures gast transfer
• Alpha-1 Antitryptsin

PFT Results:

• Obstructive Disease ha FEV1/FVC below 70 percent. Air trapping will cause TLC over Upper limit normal.
• Restrictive Disease has FEV1/FVC is normal or high, and TLC below 80 percent predicted

DLCO measures alveolar surface area, and it distinguishes between disease within alveolar tissue and disease outside the lung.

• Obstructive Lung Disease:
  Asthma - Normal DLCO COPD - Low DLCO
• Restrictive Lung Disease:
  • Neuromuscular disorder - Normal DLCO
  • Interstitial Lung Disease - Low DLCO

Lung disease with normal DLCO is like a crumpled up paper sac. The surface area is still there, but it cannot expand.

Treat Stable COPD (Note, there are NO rapid meds)

• If 0 or 1 exacerbations and no hospitalizations
  • Just a bronchodilator or LABA + LAMA
• If 2 or more exacerbations or 1 exacerbation leading to hospitalization in the past year:
  • LABA+LAMA - like Vilanterol/Umeclidinium, Formoterol/aclidinuium, Formoterol/glycopyrronium
  • Or LAMA+LABA+ICS if Eos over 300 or if the patient has asthma. Note, do NOT prescribe LABA-ICS alone. You MAY convert LABA+ICS to LABA+LAMA in stable patients
  • If not controlled with LABA + LAMA and Eos > 100 then LAMA+LABA+ICS
• If not controlled with LABA + LAMA
  • Roflumilast (a PDE4 inhibitor) if FEV1 < 50 percent predicted and chronic bronchitis
  • Azithromycin (in former smokers) 250 to 500 mg 3 times weekly (Ref) or 250 mg once daily

Treat Exacerbations

• Short Acting Bronchodilators. Start with SABA+SAMA Q1h x2 then Q2-4h.
• May add LABA+LAMA
• Steroids (5 days) - Pred 40 x5 days
• Antibiotics (5 days). Do not use a negative Procal to limit antibiotics as they also have anti-inflammatory effects.
• BiPAP O2 or Intubation
  • If pH below 7.35 or else PaO2 below 45, then BiPAP
  • If pH below 7.25 or else PaO2 below 40, then Intubation

Prior to Hospital Discharge:

• Smoking Cessation - Nicotine Gum/patch/lozenge, Varencycline, Buproprion SR,
• Give O2 if SaO2 < 88 percent or PaO2 < 55mmHg or < 60mmHg AND HCT >= 55 or Pulm HTN)
• Annual Low Dose CT is recommended in all patients 50-80yo with >20 pack years smoking
• α1-antitrypsin level should be obtained once in all patients with COPD.
• Vaccines:
  • Pneumococcal (65yo and up, 19-64 if COPD, Asthma, Smoker, Transplant). Give PCV15 then PPSV23 or else 1 dose of PCV20
  • Covid
  • Flu
  • RSV (age 60yo up)
  • Tdap (if not vaccinated as child)

Things that reduce mortality:
LABA+LAMA+ICS, Stop smoking, Pulm Rehab, O2 therapy, NIVPP, Lung Reduction

Bronchiectasis

• Symptoms: chronic cough, mucopurulent sputum, frequent respiratory infections
• Diagnose: High-resolution chest CT (airway diameter that is greater than that of its accompanying vessel and lack of distal airway tapering)
• Workup: immunoglobulin levels, connective tissue disease

References:

• Global Initiative for Chronic Obstructive Lung Disease. 2024 GOLD report: global strategy for prevention, diagnosis and management of COPD: 2024 report. Accessed October 11, 2024.
  GOLD Guidelines

Typical Dialysis Bath

• F-160, Blood Flow Rate 400, Dialysate flow rate 600
• Temp=37 Use lower temps if the patient becomes hypotensive on dialysis or you want to UF a lot. Typical values are 36
• Ca=2.5
• K=3 patient K on BMP was x, and serumK + bathK = 7
• HCO3=30 (patient HCO3 on BMP was x)
• Na=138 (patient Na on BMP was x, target total Na change less than 6mEq)
• Ultrafiltration: x L (patient weight x kg, EDW = x, max 10-13 mL/kg/hr)

PD Hints

• If the patient is on Icodextran at home, then check all sliding scale glucose measurements with a test insensitive to Icodextran, such as serum Glucose, not fingetstick
• If slow draining, add 500 units Heparin to each bag

• Note that HHS may have small urine and serum ketones, those alone do not define DKA
• DKA should have Glucose over 250, ABG pH below 7.3, serum bicarb below 18, urine and serum ketones and anion gap over 10.
• See
  http://care.diabetesjournals.org/content/27/suppl_1/s94
• See also
  http://care.diabetesjournals.org/content/32/7/1335

• HAP, started after the patient had been in a hospital for 48 hours
• HCAP, patient had been hospitalized within 90 days, or lives in a long-term care facility, or has received chemotherapy or IV antibiotics
• VAP - started after the patient had been intubated for 48 hours

AHA/ASA 2013 Guidelines
tPA within 3-4.5 hours of onset unless:

• Age over 80yo
• Oral anticoagulants (regardless of INR), or any dose within the past 2 days
• NIHSS score over 25
• Past history of stroke and diabetes
• Imaging shows infarct covering more than 1/3 of the MCA territory

No keppra ppx unless symptoms of seizure
NIHSS Stroke Scale (https://www.aan.com/Guidelines/Home/GetGuidelineContent/581)

• Level of conciousness: 0 - 3
  • 0 = Alert
  • 1 = Arousable
  • 2 = Repeated stimulation
  • 3 = Motor reflexes only
• Ask month and age: 0 - 2
  • 0 = Both correct
  • 1 = One correct
  • 2 = Neither
• Blink eyes and squeeze hands: 0 - 2
  • 0 = Both correct
  • 1 = One correct
  • 2 = Neither
• Horizontal Extraocular movements: 0 - 2
  • 0 = Normal
  • 1 = Partial gaze palsy
  • 2 = Forced deviation
• Visual Fields: 0 - 3
  • 0 = No visual loss
  • 1 = Partial hemianopia
  • 2 = Complete hemianopia
  • 3 = Blind
• Facial Palsy: 0 - 3
  • 0 = Normal
  • 1 = Minor paralysis (asymmetry on smiling)
  • 2 = Partial paralysis (lower face)
  • 3 = Complete paralysis of one or both sides
• Left arm motor drift: 0 - 4
  • xxx
• Right arm motor drift: 0 - 4
  • xxx
• Left leg motor drift: 0 - 4
  • xxx
• Right leg motor drift: 0 - 4
  • xxx
• Limb ataxia (FNF and Heel/shin) 0 - 2
  • xxx
• Sensation: 0 - 2
  • xxx
• Language/aphasia: 0 - 3
  • xxx
• Dysarthria: 0 - 2
  • xxx
• Inattention: 0 - 2
  • xxx

• Do not anticoagulate in a Type-2 AFib caused by Hypertensive Urgency, as it increases risk of hemorrhagic stroke

HAS-BLED risks

• 0 - 0.9 percent annual risk
• 1 - 3.4 percent annual risk
• 2 - 4.1 percent annual risk
• 3 - 5.8 percent annual risk
• 4 - 8.9 percent annual risk
• 5 or more - 9.1 percent annual risk

CHADSVaSC risks

• 0 - 0.2 percent annual risk
• 1 - 0.6 percent annual risk
• 2 - 2.2 percent annual risk
• 3 - 3.2 percent annual risk
• 4 - 4.8 percent annual risk
• 5 - 7.2 percent annual risk
• 6 - 9.7 percent annual risk
• 7 - 11.2 percent annual risk
• 8 - 10.8 percent annual risk

References:

• Global Initiative for Asthma. 2024 GINA Main Report. Global strategy for asthma management and prevention. Available from: https://ginasthma.org/2024-report/

Types of Asthma

• Mild asthma - well controlled with low-intensity treatment such as PRN low-dose ICS-formoterol
• Moderate asthma - well controlled with Step 3 or Step 4 treatment
• Severe asthma - remains uncontrolled despite optimized treatment with high-dose ICS-LABA, or that requires high-dose ICS-LABA to prevent it from becoming uncontrolled. This does not include difficulties due inappropriate treatment or non-compliance or obesity

There are many clinical phenotypes of asthma:

• Allergic asthma: Patients with this asthma phenotype usually respond well to ICS treatment
• Non-allergic asthma: Patients with non-allergic asthma often demonstrate a lesser short-term response to ICS
• Cough variant asthma and cough predominant asthma
• Adult-onset (late-onset) asthma
• Asthma with persistent airflow limitation: This is thought to be due to airway wall remodeling
• Asthma with obesity: some obese patients with asthma have prominent respiratory symptoms

Diagnose in adults with positive bronchodilator (BD) responsiveness (reversibility) if FEV1 increases 12-15 percent or more from baseline or FVC increases 200-400 mL with bronchodilator, or if Peak expiratory flow (PEF) increases 20 percent or more. Note that PEF is less reliable than spirometry, but it is better than nothing.

Eosinophils

• Anti-IgE - Omalizumab - Blood eos over 260/uL

Diagnosing Allergic bronchopulmonary aspergillosis (ABPA) ABPA is a hypersensitivity response to Aspergillus fumigatus, a common indoor and outdoor mold. Diagnostic creiteria include:

• Asthma or cystic fibrosis
• CT or XRays show bronchiectasis
• Total serum IgE
• IgG to A. fumigatus
• Blood eosinophils

• For CNI-induced diabetes use Metformin (assuming eGFR is ok) and DDP4 blockers like Sitagliptan
• For CNI-induced dyslipidemia use Fluvastatin or Pravastatin. Simvastatin is contraindicated becasue of P450 interactions
• For CNI-induced Hypertension, use CCB or ACE/ARB

USPSTF recommends annual screening for lung cancer with low-dose computed tomography (LDCT) in adults aged 55 to 80 years who have a 30 pack-year smoking history and currently smoke or have quit within the past 15 years

Clinical Frailty Scale
This is a 9-point scale to describe a patients baseline status. It is not a questionnaire, but rather is based on clinical observations.

• Level 1 - Very Fit - daily vigorous activity. This may include patients on chronic BP meds.
• Level 2 - Fit - less frequent or less vigorous activity.
• Level 3 - Managing Well. less frequent or less vigorous activity but some medical symptoms although these do not limit activity.
• Level 4 – Living with Very Mild Frailty. Some symptoms with activity, such as fatigue. Incomplete symptom control. May require help with heavy housework, or difficulty climbing stairs.
• Level 5 – Living with Mild Frailty. Does not attempt heavy housework or climbing stairs
• Level 6 – Living with Moderate Frailty. Dependence for intermediate ADLs, including dependence in bathing.
• Level 7 – Living with Severe Frailty. Dependence in some ADLs.
• Level 8 – Living with Very Severe Frailty. Bed-ridden for periods, such as acute illness.
• Level 9 – Terminally Ill. Independant of activity status

Get a Bone density screening (DEXA) every 2 years if female and between the ages of 65 and 75

Chemotherapy Side Effects: Tenofovir - Monitor for Fanconi (daily K, CO2, Phos, Cr) Cisplatin - Monitor for AKI, Fanconi, RTA-1 (daily K, CO2, Phos, Cr) Surveillance: Monitor for PE or Fanconi

The patient has xxx pulmonary risk factors (COPD, OSA, tobacco)
Elevated risk elective surgery may be reasonable if there is severe but asymptomatic Aortic stenosis (valve area less than 1.0cm**2) or severe mitral stenosis (if cannot balloon commissurotomy) or asymptomatic severe mitral or aortic regurg. 2014 ACC/AHA Pre-op guidelines
If bare-metal stent, may need to postpone elective surgery for 1 month while on Clopidogrel
If drug-eluting-metal stent, may need to postpone elective surgery for 12 months while on Clopidogrel
If balloon angioplasty, may need to postpone elective surgery for 14 days
Smoking cessation 6-8 weeks before elective surgery
If coronary stents, consider continuing Asa and Clopidogrel if BMS or DES placement within 6 weeks of urgent surgery (weigh risks of bleed vs stent thrombosis). Otherwise, try to continue Aspirin alone, and then retsart Clopidogrel soon after surgery
If on Coumadin, hold for surgery and resume with bridge if mechanical mitral valves
Continue statins day of surgery
Continue Pulm-HTN meds day of surgery (PDE inhibitors, endothelin antagonists, prostanoids, ets)

Post-operatively monitor for A-Flutter (peak incidence 1-3 days post-op, with incidence 1 to 30 percent)
If A-Flutter, rate control with betablockers or Calcium channel Blockers (such as Diltiazem, but avoid if reduced EF). Cardioversion is usually not required
If SVT, break with Adenosine and then rate control with beta blockers or Calcium channel Blockers (such as Diltiazem, but avoid if reduced EF or AF)

Pre-operative colonization with Staphylococcus aureus increases SSI risk. Screening and decolonization with intra-nasal mupirocin and pre-operative chlorhexidine bathing remains the most common and effective strategy, especially for orthopedic and cardiovascular surgery. Intra-nasal povidone-iodine immediately before surgery appears effective in preliminary studies, is less expensive, and may be easier to implement in the clinical setting.

• Axis I (clinical syndromes like mood, anxiety, eating disorders): None
• Axis II (personality disorders): None
• Axis IIII (medical conditions): None
• Axis IV (social and environmental problems): None