CHRONIC KIDNEY DISEASE

kidney is the site of hormone production and secretion, acid-base homeostasis, fluid and electrolyte regulation, and waste-product elimination.
Baseline cognitive function, time course of present illness, current medications
Differentials Rule IN Rule OUT
CKD Duration ≥3 months, (GFR) <60 mL/min/1.73 m2 Kidney damage, as defined by structural Long-standing DM and HTN
abnormalities or functional abnormalities other than decreased GFR
Bilateral small kidneys (except in DM, HIV)
PE: signs of volume overload/depletion, peripheral neuropathy in DM
Uremia Due to elevated urea
n/v, fatigue - anemia, anorexia, weight loss, muscle cramps, pruritus, mental status changes,
visual disturbances, increased thirst
Skin: Uremic frost (classic finding); sallow discoloration or hyperpigmentation as uremia
worsens Patients may become hyperpigmented as uremia worsens (melanosis).
Eyes: Slightly icteric sclera, or "red eye"
Mouth: A broad range of oral lesions (eg, gingival hyperplasia, enamel hypoplasia, petechiae,
gingival bleeding)
Cardiovascular: Pericardial rub or a pericardial effusion
Pulmonary: Crackles in the lungs, due to pulmonary edema
Encephalopathy: due to imbalances of neurotransmitter amino acids in the brain (GABA,
dopa etc)
- Altered mental status, nystagmus, papilledema, hyperreflexia, altered gait, stupor,
coma
Metabolic hypoNa, hyperNa, hyperglycemia, hypoglycemia
encephalopathy
Medication/Drug abuse Narcotics, benzodiazepine, illicit drugs, alcohol abuse,
Sepsis Infection: UTI, pneumonia
Fever, tachypnea, heart murmur, crackles, meningitis
Hypoxemia, hypotension
Wernicke-Korsakoff’s deficiency of thiamine (vitamin B-1)
encephalopathy chronic alcoholism, bariatric surgery (no intrinsic factor)
triad of confusion – confabulation, hallucination, the inability to coordinate voluntary
movement (ataxia) – gait abnormalities, and eye (ocular) abnormalities – diplopia, painless
vision abnormalities, strabismus, nystagmus,
Strokes RF: HTN, DM< tobacco use, high cholesterol, hx of CAD, trauma

HTN encephalopathy
Stroke should be considered in any patient presenting with an acute neurologic deficit (focal
or global) or altered level of consciousness
Sudden weakness/numbness, confusion, trouble speaking, ataxia, hemisensory deficits,
visual field cuts, facial droop, aphasia
Focal stroke or hemorrhage causing confusion in a patient who has decreased cerebral
reserve
transient migratory neurologic symptoms that are associated with the malignant
hypertensive state in a hypertensive emergency

Hepatic encephalopathy
Ischemic nephropathy
Obstructive uropathy
Nephrotic syndrome
Glomerulonephritis
Heart failure
Diagnostics
CBC
BUN, Crea
Urinalysis
24 hr urine collection
Spot urine crea-protein ratio,
albumin to crea ratio
Urine GSCS
Kidney UTZ
Electrolytes: Na, K, Ca, Phos, Mg
ABG
Lipid Profile
HbA1c, FBS
CBG
Toxicology screen
Serum thiamine levels
CT/MRI
EEG
Sample assessment: CKD St. 5 from chronic GN on chronic HD (3x weekly), s/p AVF creation R (July 2020), with secondary hypertension, anemia,
hyperphosphatemia, hypocalcemia
Management
Goals:
Weight loss of 5%
Glycemic control of HbA1c < 7.0% and FBS 90-130 mg/dL
Smoking cessation
Lipid lowering therapy: Total cholesterol < 200 mg/dL and LDL cholesterol < 100 mg/dL
Avoid and prevent AKI
Diet:
35 kcal/kg/day, low salt (2-4 gm Na/day), low potassium (2-4 gm/day), low phosphate (600-800 mg/day), low protein diet (0.6-0.8 g/kg/day) or supplemented very low protein
diet (0.3 g/kg/day with KAA 600 mg/tab 1 tab per 5-10 kg BW)
IVF: limit OFI to < 1 L/day
Slow progression of CKD
Fluid disturbances/edema
increased cerebral perfusion from the loss of blood-brain barrier integrity, which results in
exudation of fluid into the brain
HTN, headache, confusion, visual disturbances, seizures, n/v
Transient and migratory neurologic nonfocal deficits ranging from nystagmus to weakness
and an altered mental status ranging from confusion to coma.
Papilledema, cotton-wool spots
Jaundice, cirrhosis, asterixis (flapping tremor of extremities)
personality changes, intellectual impairment, and a depressed level of consciousness
Uncontrolled HTN, atherosclerotic dx UTZ: asymmetric kidneys are suggestive of
Uremia, DOB, oliguria, increasing Crea renovascular dx causing hypoperfusion or
obstruction
Decreased UO, increasing Crea, uremiac symptoms Hydronephrosis and obstruction
Hypoalbuminemia, HTN, edema, increasing Crea, Proteinuria HTN is sudden in onset
Need kidney biopsy for diagnosis.
HTN, edema, increasing Crea, proteinuria Suddne onset HTN, UA has casts
Dyspnea, DOB, fatigue, weakness, edema, orthopnea, cough, HTN Cannot be totally rules out, can exist as
CRS
Normocytic (MCV) normochromic (MCHC) anemia by G3
IDA: low ferritin, low serum Fe, high TIBC
anemia, infection, thrombocytopenia
Anemia: less EPO from peritubular cells of the kidney in response to hypoxia, observed when GFR < 50 and serum crea > 2 mg/dL
eGFR
Check for urine sediment abnormalities
- Microscopic hematuria with anisocytosis: GBM disorders
- RBC casts: proliferative glomerulonephritis
- WBC casts: pyelonephritis, interstitial nephritis
- Oval fat bodies / fatty casts: proteinuria
- Granular casts & renal tubular epithelial cells: parenchymal disease
Standard for measuring albuminuria
More practical alternative to check for albuminuria
Albuminuria as a marker of kidney damage
Bilateral small kidneys supports CKD (except DM or HIV nephropathy, polycystic kidney disease, amyloidosis)
hyperNa, hyperK, hypoCa/hyperCa, hyperPhos, hypoMg
hyperCa, hypoPhos, hyperMg and severe hyperPTH: encephalopathy
Metabolic acidosis
High TAG
To check for hyper/hypoglycemia
r/o structural abnormalities: cerebrovascular accident, intracranial mass, subdural hematoma
ACEi or ARB (to reduce intraglomerular HTN and proteinuria) to target:
- Urine protein < 0.5 g/day
- Slow GFR decline to < 1 mL/min/yr
Renoprotective doses: Losartan 100 mg OD, candesartan 16 mg OD, irbesartan 900 mg OD,
valsartan 320-640 mg OD, lisinopril 40 mg OD
May cause reversible hyperK and AKI
Salt restriction
Loop diuretics +/- metolazone to maintain euvolemia
Loop diuretics: tx in dissipating edema, HTN, acidosis and hyperK
Ceiling dose
- GFR 20-50: furosemide 80-160 mg IV or 160 mg PO
 - GFR < 20: furosemide 200 mg IV or PO
Electrolyte HypoNa (Na < 135 mmol/L) Na deficit: (0.6)(kg BW)[desired Na – actual Na]
imbalances n/v, headache, seizure, coma, death Water restriction (<1L/day)
HyperK (K >= 5.5 mmol/L) Dietary K restriction and avoidance of K supplements
Sinus brady, sinus arrest, slow idioventricular rhythms, Cardioprotection: 10 mL of 10% Ca gluconate IV over 2-3 mins with cardiac monitoring or 10
ventricular tachy, ventricular fibrillation, asystole mL of 10% Ca gluconate in 100 mL D5W IV over 20-30 mins
K binding resins (Ca resonium, Na polystyrene sulfonate): promote K loss through GI tract
(exchanges Na for K in the GI tract and increases fecal K excretion)
Kaliuretic diuretics: loop or thiazide diuretics, promote urinary K excretion
Dialysis for intractable K > 6.5
HypoCa (Ca < 2.10 mmol/L) Corrected Ca = actual Ca + (40-actual Alb)(0.20) in mmol/L
Chvostek’s sign, Trousseau’s sign, paresthesia with Asymptomatic (corrected Ca > 1.9 mmol/L):
neuromuscular irritability - Oral Ca in between meals, 1 tab of 500 mg Ca carbonate contains 200 mg
elemental Ca
Symptomatic (corrected Ca <= 1.9 mmol/L):
- IV Ca gluconate to target Ca: 2.1-2.5 mmol/L
- 1 ampule (10 mL) of 10% Ca gluconate = 93 mg elemental Ca
- Diluted in dextrose & H2O or saline, given via SIVP for 10-20 mins
HyperCa (Ca > 2.55 mmol/L) Avoid thiazides, lithium carbonate intake, volume depletion, prolonged inactivity and high Ca
Decrease in sensorium, lethargy, PUD, nephrolithiasis diet (>1000 mg/day)
Volume expansion
- pNSS x 8 hrs
Forced diuresis: loop diuretics to enhance Na and Ca excretion but UO should be > 100 cc/hr
- furosemide 20-40 mg IV q8-12 hrs
Bisphosphonates: onset of action within 1-3 days
- Zoledronic acid 4 mg IV over 15-30 mins
Calcitonin: decreases Ca by 0.3-0.5 mmol/L within 4 hrs
- LD: 4 IU/kg IM/SQ q6-12 hrs
Calcimimetics for hyperCa in hyperPTH and PTH malignancy
Denosumab for refractory hyper Ca, 60-120 mg SQ every week
HypoMg (Mg < 0.70 mmol/L) Mg deficit = desired Mg – actual Mg
Muscular weakness, tremors, seizures, paresthesia, Desired Mg: 1 for cardiac px, 0.8 otherwise
tetany, nystagmus 1g MgSO4 is given per 0.1 mmol/L of Mg deficit
HyperPhos (Phos > 1.5 mmol/L) Low Phos diet
Phosphate binders:
- Calcium based (more common but < 2000 mg/day to prevent hyperCa)
o Ca carbonate 500 mg/tab 1 tab TID with meals = 200 mg elemental
Ca
o Ca acetate 667 mg/cap 2 caps TIB with meals = 169 mg elemental Ca
- Non calcium based
o Sevelamer 800 mg/tab, 1 tab TID with meals
Calcimimetics
- Used in CKD stage 5 w/ hyperPTH and in combination with calcitriol or vit D
analoques
o Cinacalcet 30mg OD
Calcitriol & Vit D analoques
- CKD stage 4-5 with severe hyperPTH
Calcitriol 0.25 mcg OD-BID with monitoring for hyperCa and hyperPhos
Target Phos: 0.81-1.45 mmol/L
Target intact PTH 2-9x the upper normal limit of assay
Metabolic acidosis HCO3 deficit = (desired HCO2 - actual HCO3) x weight in kg x 0.4
- Initial target of 10-12 mEq/l to bring blood pH to 7.20 then increase to 15 mEq/L
over the next 24 hrs
Alkali supplementation (NaHCO3) when HCO3 < 22
- Oral NaHCO3 0.5-1 mEq/kg/day or 1 tab TID for a 60 kg male
Cardiovascular abnormalities HTN
Anemia Oral Iron supplement to provide 200 mg/day of elemental Fe in nondialytic CKD px, to
ensure adequate bone marrow iron stores (avoid when ferritin > 500 mg/mL)
- FeSO4 325 mg/tab (elemental Fe 65 mg/tab) TID
Vit B12 and folate supplementation
IV iron in dialytic and nondialytic CKD pxs
- Fe sucrose 1000 mg IV in 10 doses (100 mg/dose) = Fe content in one bag of
pRBC
Recombinant human EPO: if there are adequate bone marrow iron stores, used when Hb
<100 g/L despite correction
- EPO-alpha/beta 20-50 IU/kg BW 3x/week SC/IV
Target Hb 100-115 g/L, transferrin sat < 30%, serum ferritin < 500 mg/mL

Renal Replacement Therapy: kidney transplant, hemodialysis, peritoneal dialysis

Absolute Indications: intractable edema/fluid overload, hypertension, hyperK, hyperCa/hypoCa, hyperPhos, protein energy malnutrition, persistent N/V
Urgent: uremic pericarditis (heparin free), uremic encephalopathy (confusion, asterixis, myoclonus, wrist or foot drop, seizures), significant bleeding diathesis
Relative indications: N/V, impaired nutritional status, increased sleepiness, decreased energy level, attentiveness and cognitive tasking

Therapeutics:
1. Amlodipine 10 mg/tab 1 tab OD CCB
2. Losartan 100 mg/tab 1 tab OD ACEi
3. Carvedilol 25 mg/tab 1 tab BID Beta blocker
4. EPO Alpha, 4000 Units (20-50 IU/kg BW) SC 3x a week post HD
5. Ferrous SO4 325 mg/tab, 1 tab TID or Fe sucrose 1000 mg IV in 10 doses (100 mg/dose)
6. Folic acid 5 mg/tab, 1 tab OD
7. Vit B complex, 1 tab OD
8. Sevelamer 800 mg/tab, 1 tab TID
9. Atorvastatin 20 mg/tab 1 tab ODHS
10. Febuxostat 40 mg/tab, 1 tab ODHS (for uric acid)
11. Paracetamol 300 mg/tab IV q6 PRN for fever
12. Diphenhydramine 50 mg/tab 1 tab OD prior to BT

ACS
Differential Diagnosis

Differentials Rule IN
ACS Gradual pain/discomfort (pressure, heaviness, tightness, fullness or squeezing)
Substernal or in the left chest
Radiation to the ulnar surface of left arm, right arm, both arms shoulder, neck, jaw, abdomen
Precipitated by exertion

Acute aortic dissection
Pulmonary / pleuritic:
Pericarditis, Pulmonary embolism,
tension pneumothorax
Mediastinitis
Pericardial tamponade
GI / Esophageal:
GERD, esophageal spasm, peptic ulcer,
gallbladder disease
Chest wall/ musculoskeletal:
costochondritis (Tietze’s syndrome)
Relieved by rest / nitroglycerin
Stable angina: gradual pain reaching max intensity over a period of minutes before dissipating w/in several minutes with rest
or with nitroglycerin, pain is associated with level of exertion / stress
Unstable angina/NSTEMI: 1) pain that occurs with progressively lower intensity of physical activity or even at rest lasting >
10 min, 2) recent onset (within < 2 wks), 3) crescendo pattern (more severe, prolonged or frequent than previous episodes)
MI: severe, prolonged (> 30 min), not relieved by rest
Associated symptoms: diaphoresis, dyspnea, nausea/vomiting (inferior MI), fatigue, faintness
Pale, cyanotic, diaphoretic, Levine’s sign (clenched fist held against sternum), S3, S4,
Tachycardia, hypotension: acute MI with cardiogenic shock
**papillary muscle rupture may often cause mitral regurgitation
Anginal equivalents (females, elderly, DM): dyspnea, epigastric discomfort, nausea, weakness
Sudden, severe, tearing/ripping pain
Radiates to the back in the middle of the shoulder blades
Absent UE or carotid pulse
Discrepancy in SBP > 20 mmHg between right and left UE
Elderly men
Hypertension and RF for atherosclerosis
Discrepancies in pulses or blood pressure
Ascending aorta: pain in the midline of the anterior chest
Descending aorta: pain in the back
Pleuritic pain
Sudden, severe pain
Sharp/stabbing pain
Worse with inspiration
Pericarditis: worse when lying flat (positional), exacerbated by breathing, coughing or changes in position, pain with deep
inspiration, relieved by sitting up or leaning forward, radiation to trapezius ridge
PE: painless dyspnea, hypoxia, pain that worsens over time, pain with deep inspiration, and may localize to the chest wall,
tachypnea, cough, syncope, hemoptysis
Pneumothorax: ipsilateral chest pain, sharp, pleuritic but may become dull or achy over time
History of forceful vomiting
Sharp anterior chest pain worsened by inspiration or lying supine and relieved by sitting forward
Beck’s triad: hypotension, increased JVP, muffled heart sounds
Nonextertional, relieved by antacids
Upper abdominal and substernal
Associated with regurgitation, nausea, dysphagia
Nocturnal pain
Esophageal spasm: intense, squeezing discomfort that is retrosternal, relived by nitroglycerin or dihydropyridine CCB
GERD: exacerbated by alcohol, spicy foods or by a reclined position, relief can occur with sitting or with antacids or
with food
Persistent & for prolonged pain
Worse with movement or change in position
Often follows repetitive activity

Diagnostics
Diagnostics Rationale
12L ECG Obtained within 10 min of presentation
Serial performance of ECGs (every 30-60 mins)
ST elevations -> Q wave
Pulmonary embolism: S1Q3T3 (S-wave in Lead I, Q wave and T wave in Lead III)
Pericarditis: ST elevations which are concave upward, absent Q waves, PR depressions (vs STEMI: ST elevations which are convex
upward, present Q waves)

Most common:
1. Left anterior descending artery (45%): infarction of the anterior wall and anterior septum of the LV
2. Right coronary artery: infarction of the posterior wall, posterior septum, and papillary muscles** of the LV
3. Left circumflex artery: infarction of the lateral wall of the LV
 NSTEMI
ST depression: ST depression >= 0.05 mV (0.5 mm) in two contiguous leads
T wave inversion: T wave inversion >= 0.1 mV (1 mm) in two contiguous leads with a prominent R wave or R/S >1
STEMI
ST elevation: ST segment elevation at J point in two contiguous leads with the ff cut points:
- All leads except V2-V3: >=0.1 mV (1 mm) elevation
- Leads V2-V3: men>=40 yo: >=0.2 mV (0.2mm), men < 40: >=0.25 mV (2.5mm), women: >=0.15 mV (1.5 mm) elevation
- ST e;evation (>=0.5mm) in leads V7-V9 signifies a posterior wall MI
- >= 2 mm in chest leads, >=1 in limb leads
Peaked T waves: >=5 in limb leads, >=10 in chest leads
T wave inversions
Pathologic Q waves: >0.04 sec (1 mm) wide, >0.2 mV (2 mm) deep, > 25% of QRS complex amplitude
Chest x-ray Aortic dissection: wide mediastinum
Pulmonary embolism: Hampton’s hump or Westermark’s sign
Pneumothorax
Cardiac Troponin Superior cardiac tissue-specificity compared with CKMB
Measured within 30 min and repeated in 3-6h
Cardiac troponins: rises within 3-12 hrs, peak at 24 hrs, duration in blood 5-14 days, low sensitivity at early phase of MI (< 8 hrs)
CK rises within 4-8 h, peaks at 24 hrs, then returns to normal by 48-72 hrs, may be elevated in muscle disease, trauma
MI: rising and/or falling pattern with at least one value exceeding the 99 th percentile reference limit (20 to 50x the upper reference limit)
and that is caused by ischemia
Exercise 2D echo / stress STEMI: abnormalities of wall motion are almost universally present
testing Completion of risk stratification for patients who have undergone initial evaluation that has not revealed a specific cause of chest
discomfort
After 8-12 hr of observation
D dimer r/o pulmonary embolism
B-type natriuretic peptide r/o heart failure
CBC Anemia may trigger ischemia
PT/PTT Baseline, to check if px is a candidate for thrombolysis (INR < 2.0)
Electrolytes Baseline
FBP, LP, HbA1c Check risk factors

Sample assessment: NSTEMI (TIMI 2 GRACE 108) or STEMI, anteroseptal wall, Killip I

Therapeutics
Morphine: decreases preload by venodilation, but rarely used
Oxygen: if < 90%
Nitrates: ↓ preload, caution in right ventricular infarction
Aspirin + P2Y12 receptor blocker: ↓ platelet aggregation and rethrombosis of coronary vessels
Beta-blocker: ↓ arrhythmias and oxygen demand and ↓ myocardial damage, contraindicated in bradycardia/cardiogenic shock
ACE-i: ↓ HTN + ↓ remodeling
Statins: ↓ LDL → ↓ plaque formation
Heparin: anticoagulant

PCI
- More effective than fibrinolysis in opening occluded coronary arteries
- Preferred when diagnosis is in doubt, cardiogenic shock is present, high bleeding risk, symptoms present for 2-3 h when the clot is more mature and less easily
lysed by fibrinolytic drugs, Killip III or IV, cardiogenic shock, symptoms < 12 hrs and can be done in <=120 minutes
- Symptoms > 12 hrs and in the presence of schemia, hemodynamic instability, life threatening arrhythmias

Thrombolysis
- Should be initiated within 30 min of presentation, largest benefit if given < 2 hrs
- Tissue plasminogen activator (fibrin specific), streptokinase (non fibrin specific), tenecteplase, reteplase
- Promotes conversion of plasminogen to plasmin which lyses fibrin thrombi
- tPA 15 mg bolus followed by 50 mg IV over the first 30 min, then 35 mg over the next 60 min
- streptokinase 1.5 MU IV over 1 hr
- absolute contraindications: hx of cerebrovascular hemorrhage at any time, nonhemorrhagic stroke w/in the past year, marked HTN (> 180/110), aortic dissection,
active internal bleeding excluding menses
- relative contraindications: current use of anticoagulants (INR>=2), recent (< 2 wks) invasive or surgical procedure, prolonged (>10 min) CPR, known bleeding
diathesis, pregnancy, hemorrhagic ophthalmic condition, active PUD, hx of severe HTN
- done when symptoms < 12 hrs and PCI cannot be done within 120 mins
Cardiac catherization after thrombolysis
- Rescue PCI if there is failure of reperfusion (persistent chest pain and ST segment elevation (<50% ST segment resolution) > 90 mins)
- Urgent PCI if there is coronary artery reocclusion (re-elevation of ST segments / recurrent chest pain) or development of recurrent ischemia/angina or a + exercise
stress test prior to discharge
- Elective PCI

CABG
- Coronary anatomy is unsuited for PCI but whom revascularization appears to be advisable
- L main, 3 vessel, 2 vessel with proximal LAD dx and LV dysfunction, multivessel + DM, > 70% occlusion, pain despite medical treatment, post-infarction angina

HEART FAILURE
Differential Diagnosis

Differentials Rule IN
Heart failure Framingham Diagnostic Criteria for HF

Major Criteria Minor Criteria

PND or orthopnea Ankle edema

Neck vein distention Night cough
Rales Dyspnea on exertion
Cardiomegaly Hepatomegaly
Acute pulmonary edema Pleural effusion
S3 gallop Vital capacity decreased by 1/3 from maximal capacity
Increased venous pressure >16 cmH2O Tachycardia >120bpm
Hepatojugular reflux

Major or minor criteria: weight loss >4.5kg in 5 days in response to treatment

The diagnosis of HF requires simultaneous presence of at least:

2 Major criteria, or
1 Major criterion + 2 minor criteria*
*use of minor criteria acceptable only if they cannot be attributed to another medical condition, such as pulmonary HTN, chronic lung
disease, cirrhosis, ascites, nephritic syndrome

Clinical classification Typical triggers Signs and symptoms Clinical assessment

Acute decompensation of Patient with chronic compensated Peripheral edema SBP: generally in the normal
chronic HF HF who gradually decompensates Orthopnea range
due to non-compliance to meds, ischemia, Dyspnea on exertion CXR: often clear despite
or infections Usually no/minimal elevated
volume filling pressures
overload Echo: preserved or reduced
EF

Acute Hypertensive HF Patient with no HF suddenly Dyspnea (severe) SBP >140mmHg in most
decompensates Tachypnea CXR: pulmonary edema
Possible causes: HTN emergency, Tachycardia Echo: preserved EF in most
 arrhythmias, or ACS Frank pulmonary edema patients
Hypoxemia common

Cardiogenic shock Progression of advanced HF or End-organ SBP: low or low normal

develops major myocardial insult hypoperfusion Echo: severely depressed EF
(large AMI, acute myocarditis) Oliguria Evidence of end-organ
Confusion dysfunction
Cool extremities (renal, hepatic)

COPD personal history of smoking/exposure to smoking

Chest tightness, chronic persistent dyspnea
Cor pulmonale: edema, ascites
Cardinal symptoms: cough, sputum production, exertional dyspnea
PE: hyperresonant with expiratory wheezing, barrel chest, very distant heart sounds
Blue bloaters / chronic bronchitis: heavy, cyanotic, may have signs of R heart failure (edema, cyanosis)
 may be difficult to distinguish from congestive heart failure: use peak expiratory flow: blow of 150-200ml or less for COPD
pink puffers / emphysema: thin, noncyanotic, pursed lips breathing, tripod sitting position
CXR: hyperinflation

COPD: Post-bronchodilator FEV1/FVC < 0.70 (persistent airflow limitation)

Bronchial Asthma
Past medical/Family history of BA (or atopy/AR)
Possible history of triggers of asthma, worse at night or early morning
Reversibility: rapid improvements in FEV1 after rapid acting bronchodilator
Variability: improvement or deterioration in symptoms and lung function over time
Variable respiratory symptoms (cough, dyspnea, wheezing, chest tightness) AND variable expiratory airflow limitation (excessive
variability in lung function and documented airflow limitation)

Cardiac asthma – more on inspiratory wheeze

BA – expiratory wheeze, episodic/variable, partially reversible

BA: (+) bronchodilator reversibility test: increase in FEV1>12% and > 200 mL from baseline, 10-15 min after albuterol 200-400 mcg, reduced
FEV1/FVC
Pneumonia Exposure history
Past medical history
Character of productive cough, fever
More unilateral pleural effusion
May have normal cardiac findings
CAP
Low risk: stable VS, no altered mental state, no or stable comorbids, CXR: local infiltrates, no pleural effusion
Moderate risk: unstable VS (RR >=30, HR >=125, Temp <=36 or >=40, SBP < 90, DBP <=60), altered mental status, suspected
aspiration, ,unstable/decompensated comorbids (uncontrolled DM, active malignancies, neurologic disease in evolution, CHF class II-IV,
unstable CAD, renal failure on dialysis, uncompensated COPD, decompensated liver dx)
High risk: moderate risk + severe sepsis, septic shock or need for mech vent
TB Cough, fever, night sweats, weight loss
Pericardial dx: restrictive History of possible etiology
pericarditis, cardiac (infection, heart surgery, trauma)
tamponade Chest pain – sharp, center of chest, radiating to trapezius, relived by sitting forward
Pulsus paradoxus, pericardial friction rub
Cardiac tamponade: Beck triad – increased jugular venous pressure, hypotension,
diminished heart sounds
Chest wall dx: Decreased diaphragm excursion, inability to get a deep breath (chest wall movement)
kyphoscoliosis, Normal other lung/cardiac findings
neuromuscular
weakness
ACS Chest pain
Anemia History of possible etiology (nutritional, blood loss, malignancy, etc.)
Pallor, generalized weakness, hypotension, tachycardia, poor perfusion to other organs
(renal failure, confusion/altered mental status)
Anxiety May have normal physical findings
May have identified psychological triggers
Deconditioning Poor fitness

Diagnostics

2D echocardiography with Most useful test for evaluation of ejection fraction or LV function
doppler Semi-quantitative assessment of LV size, function, wall motion abnormalities, valvular defects

Cardiac MRI Gold standard for measurements of volumes, mass, and EF of both RV and LV
High-quality imaging of the heart obtained in tomographic planes
Can characterize myocardial tissue/structure and assess myocardial viability

12 L ECG Cardiac rhythm, LV hypertrophy, prior MI

Normal ECG virtually excludes LV systolic dysfunction
Abnormal ECG increases likelihood of HF, but has low specificity
LV hypertrophy may signify HF but is not diagnostic
 LVH = S in V1 + R in V5 or V6 > 35 mm

Chest x-ray Cardiac size, shape, and pulmonary vasculature

Kerley B-lines: thin, horizontal linear opacities extending to the pleural surface due to fluid in the interstitial space
Other findings: peribronchial cuffing, prominent upper lobe vasculature (cephalization), bilateral pleural effusion, cardiomegaly, bat
wing’s sign (pulmonary edema)
COPD: hyperinflation

Cardiac biomarkers Markers of cardiac myocyte strain: B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP)
· Upper limits in chronic HF: BNP 35 and NT-proBNP 125
· Upper limits in acute HF: BNP 100 and NT-proBNP 300
Increase with age and renal impairment
Falsely low in obese

ABG Assess lung function, oxygenation status esp. in dyspneic patients

CBC Anemia, signs of infection, bleeding - contribute to HF

Electrolytes, BUN, Crea, AST, ALT Electrolyte disturbances or beginning cardiorenal syndrome, ischemic hepatitis or chronic passive congestion of liver, severity of HF
is proportionate to degree of hypoNa

FBS<OGTT Diabetes

Lipid profile Dyslipidemia

FT4, TSH Thyroid hormone abnormalities

Blood culture Search for focus of infection

Urine culture, urinalysis Search for focus of infection

Troponin I Index event - suspicious for MI

Blood typing Streamline transfusion if needed in high output states (anemia)

Spirometry BA: (+) bronchodilator reversibility test: increase in FEV1>12% and > 200 mL from baseline, 10-15 min after albuterol 200-400 mcg,
reduced FEV1/FVC
COPD: Post-bronchodilator FEV1/FVC < 0.70 (persistent airflow limitation)

Sample assessment: HF FC III from 1) MAP cardiomyopathy 2) IHD in SR

Therapeutics
Goals:
 Institute prevention
o Prevention and/or controlling of diseases leading to cardiac dysfunction and heart failure
o Prevention of progression to heart failure once cardiac dysfunction is established
 Reduce morbidity
o Maintenance or improvement in quality of life
 Decrease mortality
o Increased duration of life

Admitting Orders
Admit to Intensive Care Unit
Secure consent for admission and management
Diet: NPO if dyspneic, tachypneic, or with decreased sensorium
High caloric, high protein diet if with cardiac cachexia
Sodium restriction: 2-3 g/day for all patients with HF
Sodium restriction: <2g/day in patients with moderate to severe HF
IVF: heplock
Fluid restriction: unnecessary unless with hyponatremia (<130mEq/L and volume overload)
D5W 500ml x KVO or 10cc/hr

Acute Decompensated Heart Failure (ADHF) Heart Failure with Reduced Heart Failure with Preserved Ejection Fraction
Ejection Fraction (HFrEF) (HFpEF)

Furosemide 20-240 mg/day Captopril 6.25-50 mg TID Evidence is lacking for the management
 First line therapy in volume overload  Cornerstone of HF treatment No treatment has been shown to reduce
morbidity or mortality
Nitroglycerine 10-20 mcg/min Losartan 25-100mg OD Approach:
Isosorbide dinitrate 1mg/hr  If ACE inhibitor intolerant  Manage individual risk factors
 Initial therapy for hypertensive AHF  Reduce symptoms
 Used for patients with pulmonary congestion for rapid Carvedilol 3.125-25mg BID o Diuretics for FO
relief of dyspnea  Cornerstone of HF treatment  Prevent acute decompensation

Dobutamine 2-20 mcg/kg/min Spironolactone 25-50mg OD

 Improve exercise tolerance

Dopamine 5-20 mcg/kg/min Digoxin 0.125-0.375mg OD

 If hypotensive however DO NOT GIVE Ivabradine 5.0-7.5 mg BID
Sacubitril/Valsartan 49/51 –
 IF SBP IS ≤ 70 mmHg, start with NE first
97/103 mg BID

Norepinephrine 0.2-1.0 mcg/kg/min If with fluid retention:

Furosemide 40-240 mg
DO NOT GIVE BETA BLOCKERS TO ADHF Hydrochlorothiazide 12.5-100 mg
Tolvaptan 15mg OD
Satavaptan 25mg OD

Referrals
CVS
1. Cardiac Resynchronization Therapy or Biventricular Pacing
a. if patient has ECG findings of sinus rhythm and a widened QRS complex (most helpful if with LBBB) [normal QRS ≤ 110 to 120 msec (≤ 3 small squares)
NOTE: Bazetts Formula is for abnormal heart rates hence no need to compute for possible CRT patients as they need to be in sinus rhythm]
2. Implantable Cardioverter-Defibrillator (ICD)
a. to threat tachyarrhythmias (VF or VT) for primary/secondary prophylaxis against sudden cardiac death (SCD)

Long Term Plan

 Manage contributing and associated conditions
 Exercise (exercise testing first)
 Cessation of smoking
 Restriction or abstinence from alcohol consumption
 Avoid illicit drug use
 Sodium restriction to 3g/day
 Fluid restriction (1.5 to 2L per day) in patients with refractory HF or symptomatic or severe hyponatremia (serum sodium <120meq/L)
 Avoidance of obesity
 Daily weight monitoring is recommended to detect fluid accumulation before it becomes symptomatic
 Daily check for edema and symptom severity (exercise tolerance, breathing at night, dizziness/lightheadedness)
 Adherence to medications
 Prevent infections
o Pneumococcal vaccination
o Annual influenza vaccination

THYROTOXICOSIS
History and PE

Signs and Symptoms of Thyrotoxicosis (Descending Order of Frequency)

Symptoms Signs

Hyperactivity, irritability, dysphoria Tachycardia, Atrial fibrillation in the elderly >50 years old
Heat intolerance and sweating (sinus tachy often assoc. with palpitations)
Palpitations Tremor (Fine)
Fatigue and weakness Goiter
Weight loss with increased appetite Warm, moist skin
Diarrhea (sec. to decreased GI transit time) Muscle weakness, proximal myopathy without fasciculation
Polyuria Lid retraction or lag
Oligomenorrhea, loss of libido Gynecomastia

Symptoms
General Hyperpyrexia, profuse sweating, poor feeding, fatigue
 Cardiac Cardiac arrhythmia (MC: supraventricular), CHF/high output failure signs
Respiratory Distress
Abdominal Severe nausea, vomiting, diarrhea, abdominal pain, hepatic failure with jaundice
Neurologic Altered mentation: agitation, anxiety, psychosis, stupor, coma
Pyramidal signs, hyperreflexia
Seizures

Objective
Thyroid - Diffusely enlarged / nodular
exam - If the lower border is not felt, the goiter may be restrosternal. Large retrosternal goiters can cause venous distention over the neck and DOB
especially when the arms are raised (Pemberton’s sign)
- (+) bruit or thrill – indicated increased vascularity, associated with turbulent flow
HEENT - Ophthalmopathy (in Grave’s)
- Lid lag
Cardiac - Tachycardia > 140 bpm disproportionate to fever
- Hypertension with wide pulse pressure -> hypotension
- CHF / high output failure signs
- Hyperdynamic precordium
Respiratory - Tachypnea
- Congestion / crackles
Extremities - Hand tremor
- Warm, moist skin
Neurologic - Altered sensorium
- Hyperreflexia
- Pyramidal signs
- Proximal muscle weakness

Differential Diagnosis

Primary Hyperthyroidism Thyrotoxicosis without Hyperthyroidism Secondary Hyperthyroidism

Graves’ Disease Subacute Thyroiditis TSH-secreting pituitary adenoma

Toxic Multinodular Goiter Silent Thyroiditis Thyroid hormone resistance syndrome
Toxic Adenoma Other causes of thyroid destruction: amiodarone, radiation, infarction of Chorionic Gonadotropin-secreting
Functioning Thyroid Carcinoma adenoma Tumors
Metastases Ingestion of excess thyroid hormone (thyrotoxicosis factitia) or thyroid Gestational Thyrotoxicosis
Activating mutation of the TSH receptor tissue
Activating Mutation of Gsa (McCuneAlbright
Syndrome)
Struma Ovarii
Drugs: iodine excess (Jod-Basedow phenomenon)

Differentials Rule IN Rule OUT

Grave’s disease Smooth diffuse, (+) eye bulging, pretibial myxedema
RAI: diffuse increased uptake
 60-80% of thyrotoxicosis
 Autoimmune hyperthyroidism caused by thyroid-stimulating immunoglobulin
which chronically stimulates the TSH receptor
 Rarely begins before adolescence, between 20-50 years old, also occurs in

Thyroid storm
Thyroglossal duct cyst
Toxic adenoma
Toxic multinodular goiter /
Plummer’s dx
Silent thyroiditis
Subacute thyroiditis
Exogenous thyroidism or
struma ovarii
Septic shock
Hypertensive Emergency
Heart Failure
Pheochromocytoma (VMA and
normetanephrine)
Panic Disorder
Malignant Hyperthermia
elderly
 Graves’ disease specific signs
o Graves’ ophthalmopathy
 Assessed by the NO SPECS scoring system
 0 = No signs or symptoms
 1 = Only signs (lid retraction or lag), no
symptoms
 2 = Soft tissue involvement (periorbital
edema)
 3 = Proptosis (>22mm)
 4 = Extraocular muscle involvement
(Diplopia)
 5 = Corneal involvement
 6 = Sight loss
 Thyroid dermopathy (<5%)
 In the presence of moderate or severe ophthalmopathy
 Anterior and lateral aspects of lower leg (pretibial
myxedema)
 Noninflamed, indurated plaque with deep pink or
purple color and orange skin
 Thyroid acropachy (<1%)
Clubbing
Exaggeration of the usual symptoms block
Fever and atrial fibrillation
Leukocytosis, mild hyperCA, LFT abnormality, mild hyperglycemia
Midline mass in anterior neck, asymptomatic, moves with deglutition and tongue
protrusion
Solitary nodule
RAI: focal increased uptake
Nodular diffuse, (-) eye bulging
RAI: multiple areas of focal increased and suppressed uptake
No to minimal thyroid enlargement
Painful and tender thyroid
(-) thyroid enlargement
Altered sensorium, Hypotension, Tachycardia, hyperpyrexia Decreased temperature, little to no urine
output, must have a source of infection
Altered sensorium, dizziness, seizures, nausea, hypertension History of hypertension, persistently
elevated BP
Altered sensorium, dizziness, nausea, DOB, signs of congestion Long standing heart disease, edema
Classic triad: episodic headache, sweating, tachycardia Persistently high BP, postural
Paroxysmal/sustained hypertension hypotension
Headache, diaphoresis, palpitations, tremor, weakness, anxiety, abdominal pain,
tachyarrhythmia, fever, congestion
Diaphoresis, shortness of breath, nausea, abdominal pain, dizziness, tachycardia Psychiatric symptoms: derealization, fear
of dying/losing control
Hyperpyrexia, tachycardia Use of medications (anesthetic meds),
muscle rigidity
Diagnostics
Diagnostics Rationale Expected Findings
Sensitive TSH analysis Single best screening test for Low in primary
hyperthyroidism thyrotoxicosis
-should be taken with free T4 and total T3

TSH FT4
Low High Primary thyrotoxicosis: graves, multinodular goiter, toxic adenoma
Destructive thyroiditis, xs iodine intake, xs thyroid hormone
Low Normal Subclinical hyperthyroidism (if normal FT3)
T3 toxicosis (if High T3)
Normal/high High Secondary thyrotoxicosis: TSH secreting pituitary adenoma or thyroid
hormone resistance syndrome
Free T4 RIA To assess circulating levels of free T4 Elevated
Free T3 RIA To assess circulating levels of free T3 Elevated
Thyroid Stimulating Antibodies Especially used when Graves’ Disease is of primary consideration, not routinely used Elevated in grave’s
Blood sugar Catecholamine-induced inhibition of insulin release and increased glycogenolysis Mild to moderate
hyperglycemia
Calcium Hemoconcentration and enhanced bone Mild hypercalcemia
resorption
CBC To evaluate blood parameters critical for management Leukocytosis (shift to L if
with infection)
Leukopenia
Signs of infection
 Liver function test
Thyroid UTZ
Radioactive iodine uptake and
thyroid scan
Urinary and plasma fractionated
metanephrines and catecholamines
Thyroid dysfunction noted Elevated
Determine compressive symptoms, suspicious sonographic findings, tracheal narrowing
Measures radioactive iodine trapped into
thyroid tissues
Thyrotoxicosis with elevated RAI uptake:
- Graves’ disease: increased uptake distributed homogenously
- Toxic adenoma: focal areas of increased uptake with suppressed tracer uptake in the rest of the gland
- Toxic MNG: gland enlarged with distorted architecture & multiple areas of relatively increased or
decreased tracer uptake
- TSH producing pituitary adenoma
- BhCG
Thyrotoxicosis with low RAI uptake:
- Painless thyroiditis
- Amiodarone induced thyroiditis
- Subacute thyroiditis
- exogenous intake
- ectopic: struma ovarii
r/o pheochromocytoma
24 hr urine fractionated metanephrines and catecholamines:
- normetanephrine > 900 mcg/24 hrs or metanephrine > 400 mcg/24 hrs
- NE > 170 mcg/24 hrs
- Epi > 35 mcg/24 hrs
- Dopa > 700 mcg/24 hrs
Plasma fractionated metanephrine
- indwelling cannula: metanephrine < 0.3 nmol/L and/or normetanephrine < 0.66 nmol/L
- venipuncture: metanephrine < 0.5 nmol/L and/or normetanephrine < 0.9 nmol/L

Management
Admitting Orders
 Admit to ICU
 Secure IV line. Insert foley catheter.
 Diet: as tolerated, no added salt, SAP
 Monitor NVSQ1, strict I/O qshift
 IVF: D5NM x 8-12 hours
 Diagnostics: CBG, Sensitive TSH analysis, FT4, CBC, Na, K, Crea, AST, ALT, Chest Xray, ECG, Urinalysis, ABG when indicated
 Therapeutics:
o PTU 500-1000 mg LD and 250 mg q4h PO or per rectum/ per NGT
o SSKI 5 drops q6h 1 hr after 1st dose of PTU
o Propranolol 60-80 mg PO q4hrs or 2mg IV q4hrs
o Hydrocortisone 300 mg IV bolus load, then 100 mg IV q8hrs
o Cholestyramine 4 g PO q6hrs
o Paracetamol 600 mg IV q4-6hrs PRN for fever
 If with frank seizure, Diazepam 5 mg IV PRN
 If with atrial fibrillation, Digoxin 0.5 mg IV then PO PRN
 When indicated, hook to O2 via NC @ 2 lpm PRN.
 Hook to cardiac monitor at all times.
 Refer to Endocrinology, ORL (if with enlarged mass and obstructive symptoms), CVS (if with profound cardiovascular problem), MSS (for financial aid).
 RAI: lifelong thyroid hormone replacement therapy (levothyroxine), carbimazole/methimazole must be stopped at least 2 days prior while PTU must be stopped
several weeks prior
o Contraindications: pregnancy, breastfeeding, coexisting thyroid cancer
 Surgery: pregnant who are intolerant to medications, non pregnant who refuse RAI, very large goiters, pediatric px

Long term Plan

 Discontinue iodine therapy, taper glucocorticoids when with clinical improvement (defervescence, resolution of central
 nervous system and CVS manifestations)
 Withdraw beta-blockers when thyroid function tests return to normal
 Switch PTU to Methimazole
 Titrate thionamides to maintain euthyroidism
 Definitive therapy for Graves’ disease: radioactive iodine, or thyroidectomy

Thyroid storm
Goals of management: Stop synthesis of new thyroid hormones, halt release of preformed thyroid hormones, prevent conversion of T4 to T3, control adrenergic symptoms
associated with thyrotoxicosis, control systemic decompensation, treat underlying cause

PTU 50mg/tab 4 tabs every 6 hours (inhibition of new hormone production + inhibits peripheral conversion)
Supersaturated solution of potassium iodide, 5 drops every 6 hours, administer 1 hour AFTER giving propylthiouracil (inhibit release of pre-formed hormones)
Hydrocortisone 100mg IV every 8 hours (supportive management + inhibits peripheral conversion)
Propranolol 20mg/tab 1 tab every 8 hours (control adrenergic symptoms + inhibits peripheral conversion)
Cholestyramine 4 g PO QID (alternative, hastens removal of T4 and T3 from serum)

Hyperthyroidism
Methimazole 20mg/tab, 1 tab twice a day
Propranolol 20mg/tab to 1 tab every 6 hours (80mg/day)

CAP MR
Ceftriaxone 2g IV once a day
Azithromycin 500mg/tab 1 tab once a day for 5 days