EXPECTED LEVEL FOR PGY1

CASE BASED PRESENTATIONS: HAVE SPECIFIC CLINICAL QUESTION(S) WHICH

YOU SEEK AND DESIRE TO ANSWER IN YOUR CASE PRESENTATION
CASE BASED PRESENTATION- VEDIKA PANDAY
ALL THAT WHEEZE IS NOT ASTHMA
 Name: D.H

 Age: 58

 Occupation: Housewife (former cook)

 CC: Chest pain x 4/7, SOBx 2/52, Wheezing x 4/7

 HPI: 58 y/o Female patient with PMHx on HTN and

?Asthma diagnosed approx. 5/12 ago when she first
presented to A&E with complains of wheezing and lower
back pain secondary to a fall→hitting her lower back,
thereafter leading to difficulty and limitations to
ambulatory status. Patient refers she has been frequently
visiting the ER since for shortness of breath and wheezing,
and has on multiple encounters been nebulized and given
Inj Hydrocortisone and discharged. She refers 4/7 ago
starting experiencing L sided chest pain, “pressing,” no
radation, Grade 6/10, sudden, lasting approx 10 mins and
associated with SOB and wheezing. Patient refers minimal
relief with inhalers, and a generalized sense of unwell and
weakness and hence presented to GPHC. ROS: No
headaches, dizziness +, SOB+, chest pain, no orthopnea/
PND, exertional dyspnea, no limb edema, no productive
cough, weight loss +, loss of appetite+, post-prandial
vomits(food content, no blood or mucus), no abdominal
pain, lower back pain + (nonradiating, 7/10) & difficulty
with ambulation post fall 5/12 ago.
 PMHx: Asthma (Childhood, No attacks in >20 years,
except over the last 5/12), HTN

 Med Hx: Inhalers, Prednisolone (dose unknown), Ramipril

10mg PO BID

 PSHx: Nil

 Allergic Hx: Dust (sneezing and rhinorrhea when exposed)

 Trauma Hx: Fell 5/12 ago hitting her lower back and has
since been unable to ambulate as normal

 Transfusion Hx: Nil

 Personal and Social Hx: Lives at home with two daughters,

used to lead a very active lifestyle, self-sufficient, would
occasionally used alcoholic wine, no smoking history.
General Inspection:Patient was seen lying comfortably in bed in
no obvious CP/painful distress;acyanotic,afebrile,anicteric
Vitals: BP:124/84mmHg P:82bpm RR:18bpm O2 Sat:99%
T:36.5℃

HEENT: MM: pink and slightly moist, Sclera: Anicteric, PEARL

x2,Ear:Normal external apparatus,Nose:No septal
deviation,Throat:No swollen nor erythematous tonsils,No
enlarged or nodular thyroid on palpation, left supraclavicular
and virchow node present.
Respiratory Exam:No nasal flaring,no tracheal tugging or devition,no
IC/SC retractions,Bilateral and symmetric rise and fall of chest,Chest
expansion approx. 3cm,Tactile fremitus x 2,Resonant x 2,Bilateral air
entry;Bibasal creps and wheezes in both lung fields.

Cardiovascular Exam: No peripheral cyanosis,no finger

clubbing,Pulses:Normal rate and rhythm,no splinter hemorrhages,No
Janeway lesions nor Osler nodes,no central cyanosis,No
hyperdynamic precordium,No palpable heaves nor thrills,S1 and S2
appreciated,no
S3,S4,M+(𝐋𝐞𝐟𝐭 𝟒𝐭𝐡 𝐈𝐂 𝐬𝐩𝐚𝐜𝐞, 𝐬𝐭𝐞𝐫𝐧𝐚𝐥 𝐛𝐨𝐫𝐝𝐞𝐫 𝐓𝐑 𝐦𝐮𝐫𝐦𝐮𝐫 , Systolic in
nature,Grade 2/6,non radiating),JVP not appreciated.
Abdomen Exam:Globular,symmetric,no visible scars or
masses,abdomen rises and falls with respiration,Bowel sounds
+; normal,approximately 6 gurgles/min,Tympanic globally,No
palpable masses,no organomegaly.

Extremities:Normal range of motion x

4,1+𝒑𝒊𝒕𝒕𝒊𝒏𝒈 𝒆𝒅𝒆𝒎𝒂 𝒕𝒐 𝒃𝒐𝒕𝒉 𝒇𝒆𝒆𝒕.

CNS:Conscious,alert,oriented x 3,GCS:15/15
Laboratory findings:
 Hb:9.8↓
 Plts:582
 WBC:11.2
Differentials: POLYS:48.6%
LYMPH:29.5%
EOSIN:15.0%
BASO:0.4%
MONO:6.5%

Blood film:Hypochromasia+, Microcytosis 2+, Eosinophilia

Lytes: Na: 129.2, K.3.92, Cl:97.9,

BUN: 29, Crn: 2.3,

SGOT: 35, SGPT: 44, ALP: 434, GGT: 123, T Bili: 0.6, D Bili: 0.3, I
Bili: 0.3, T Protein: 7.2, Albumin: 2.3, Globulin: 4.5
 58 y/o F patient with PMHx of Asthma and HTN, now with
Anemia, AKI, R.O Multiple myeloma, R/O PTB.

 Reassessed: 58 y/o F patient with PMHx of Asthma and HTN,

with Hypereosinophilic Syndrome R/O Churg Strauss, R/O
Tropical pulmonary eosinophilia
 HOW TO APPROACH A
PATIENT WITH
HYPEREOSINOPHILIA?

ALL THAT WHEEZE ISN’T ASTHMA

  Three levels of severity of eosinophilia have been
defined as follows:
◦ Mild 0.5-1.5 × 109/L,
◦ Moderate 1.5-5 × 109/L
◦ Severe >5 × 109/L.

 Hypereosinophilic syndrome- AEC >1500/microL/

>1.5 x 109/ L(on two separate occasions > 1 month
apart) plus organ dysfunction attributable to
eosinophilia.

 Classified as:
1)Familial eosinophilia : an autosomal dominant disorder with
stable eosinophil count and a benign clinical course.

2)Acquired eosinophilia : Secondary, Clonal and Idiopathic

Hypereosinophilic Syndrome: Background, Pathophysiology, Epidemiology [Internet]. Emedicine.medscape.com. 2019 [cited 17

November 2019]. Available from: https://emedicine.medscape.com/article/202030-overview#a5
  Predominantly tissue dwelling leukocytes
with function of innate immunity

 Differentiates in the bone marrow in

response to eosinophilopoietic cytokines i.e
IL3, GMCSF and most importantly IL5.

 Special selectins, chemokines, cytokines and

adhesion molecules contribute to eosinophil
homing.

 The exuberant release of granule-derived

proteins, by degranulation or cytolysis, may
contribute to the tissue damage associated
with eosinophil-associated diseases.
Roufosse F, Weller PF. Practical approach to the patient with hypereosinophilia. J Allergy Clin Immunol. 2010;126(1):39-44.
doi:10.1016/j.jaci.2010.04.011
 It is a cytokine derive IL 5 Other common causes include:


reactive phenomenon 1)Malignancies:Metastatic cancer,T cell

lymphoma,colon cancer

 Worldwide: most common 2)Pulmonary eosinophilia:Loffler

cause is Parasitic infections syndrome, EPA, ABPA

3)Connective tissue disorder:Scleroderma,

Developed countries: PAN
Allergic diseases are the
most common symptom. 4)IBD

5)Sarcoidosis

6Addison Disease

Hypereosinophilic Syndrome: Background, Pathophysiology, Epidemiology [Internet]. Emedicine.medscape.com. 2019 [cited 17

November 2019]. Available from: https://emedicine.medscape.com/article/202030-overview#a5
 Diagnosed by:  Causes include:
1. Pre B cell ALL
 bone marrow


2. AML – M4Eo
histology,


 3. Chronic myeloid disorders.

 Molecularly defined:

 cytogenetics,  4. BCR-ABL chronic myeloid

leukemia

 5. PDGFRA, Systemic
mastocytosis
 and molecular chronic eosinophilic leukemia
(SM-CEL)
genetics  6. PDGFRβ-rearranged
eosinophilia

 7. KIT-mutated systemic
mastocytosis

Hypereosinophilic Syndrome: Background, Pathophysiology, Epidemiology [Internet]. Emedicine.medscape.com. 2019 [cited 17

November 2019]. Available from: https://emedicine.medscape.com/article/202030-overview#a5
Diagnosis of exclusion –  Hypereosinophilic
 when secondary and clonal syndrome:
causes of eosinophilia are
excluded.  Subset of idiopathic
eosinophilia

Hypereosinophilic Syndrome: Background, Pathophysiology, Epidemiology [Internet]. Emedicine.medscape.com. 2019 [cited 17

November 2019]. Available from: https://emedicine.medscape.com/article/202030-overview#a5
 Roufosse F, Weller PF. Practical
approach to the patient with
hypereosinophilia. J Allergy Clin
Immunol. 2010;126(1):39-44.
doi:10.1016/j.jaci.2010.04.011
 Although investigations will vary from one patient to
another, the following are recommended in all cases:

 complete blood count and differential,

 peripheral blood smear looking for dysplastic
eosinophils or blasts,
 serum tryptase,
 serum vitamin B12,
 IgE,
 cardiac troponin levels,
 ANCA
 ECG
 ECHO
 PFT
 Thoraco-abdominal computed tomography (CT)-
scan.
Roufosse F, Weller PF. Practical approach to the patient with hypereosinophilia. J Allergy Clin Immunol.
2010;126(1):39-44. doi:10.1016/j.jaci.2010.04.011
 High-dose corticosteroid (1 mg/kg daily,
followed by 15 mg/kg IV on three
consecutive days in the absence of an initial
response).

 If there is any possibility that the patient

may have contracted Strongyloides infection:
ivermectin (200 μg/kg on two consecutive
days) should be given concomitantly, even if
results of serology are not yet available.

 Corticosteroid non-responders: vincristine

(1-2 gr IV) and in selected cases imatinib
mesylate (400 mg/day). J Allergy Clin Immunol
Roufosse F, Weller PF. Practical approach to the patient with hypereosinophilia. .
2010;126(1):39-44. doi:10.1016/j.jaci.2010.04.011
 Roufosse F, Weller PF. Practical approach to the patient with
hypereosinophilia. J Allergy Clin Immunol. 2010;126(1):39-44.
doi:10.1016/j.jaci.2010.04.011

 Hypereosinophilic Syndrome: Background, Pathophysiology,

Epidemiology [Internet]. Emedicine.medscape.com. 2019 [cited
17 November 2019]. Available from:
https://emedicine.medscape.com/article/202030-overview#a5

 Klion, D Amy et.al, Hypereosinophilic syndrome: Clinical

manifestations, pathophysiology and diagnosis, April 6, 2020

 Simon HU, Plötz SG, Dummer R, Blaser K. Abnormal clones of T

cells producing interleukin-5 in idiopathic eosinophilia. N Engl J
Med 1999; 341:1112.

 World Health Organization classification of tumours of

haematopoietic and lymphoid tissues, Swerdlow SH, Campo E,
Harris NL, et al. (Eds), IARC Press, Lyon 2008
 June 20,2019
Done by: Vedika Latchmi Panday
 History:
 CC: Referred from WDRH for further management of pleural effusion

 HPI: 23 y/o F pt with PMHx of SLE and Subtotal thyroidectomy who was referred
gave a 3/7 history of fever, generalized weakness, joint pains and SOB
(exertional in nature, pleuritic and positional) & non productive cough.

 PMHx: SLE x 3 yrs, Subtotal Thyroidectomy last August for Multinodular thryoid

 Medication Hx: Prenisolone 10mg po od, T hydroxychloroquine

 Family Hx, Trauma Hx, Tranfusion Hx: Nil

 Personal and Social Hx: works as a lab tech, denied any toxic habits, lives with
parents, previously sexually active.
 O.E: F patient in mild to moderate respiratory distress, anicteric, peripheral
cyanosis, febrile, with IV access in situ and Foley’s catheter in situ, with minimal
urine in drainage bag.
 VITALS: T:38, P:130, RR:30, O2sat: 89% R.A, B.P 94/50mmHg
 Head: scarring alopecia, Face: apparent discoid lesions posterior auricular and
malar rash, MM: slightly pale and moist, Eyes: PEARLX 2, sclera anicteric, Oral
cavity: Stage I oral candidiasis, Neck: horizontal scar over lower cricoid region.

 Respiration: decreased resonance and decreased air entry with mild crackles
predominantly to R base, and creps to mid-lower lung field.

 CVS: no appreciable JVD, PMI difficult to localise, muffled distant heart sounds,
SEM loudest at LLSB Grade 3/5

 Abdomen: diffuse abdominal tenderness on light palpation, splenic dullness,

shifting dullness on percussion and vague fluid thrill.

 GU: erythematous lesions on labia majora.

 Extremities: NROMX4, Bilateral pitting edema to both lower limbs up to M/3 leg.

 Skin: petechiae lesions to lower limbs, arms, discoid like lesions to arms, posterior
thorax, nail fold infarcts, peripheral cyanosis.

 CNS: conscious, alert and oriented x 3, Hyporeflexic

Date 7/6/19 8/6/19 9/6/19 10/6/19 11/6/19 12/6/19
Hb 8.4 10.2 8.7
WBC 41(P:95, 46.3 18.9
L:5%
Platelets 465 429 356
ESR 45 35
Blood Hypochr
film omic,
Microcyt
ic,
Macrocy
tic,
Schistoc
ytes
Direct 2+
Coombs
Date 7/6/19 8/6/19 9/6/19 10/6/19 11/6/19 12/6/19
Na 135.6 141.2 143.6 142.6 144.8
K 5.52 4.20 4.79 4.39 4.43
Cl 106.6 112.4 112.2 117.2 118.4
Mg 1.7 2.9 2.3
Ca 5.7 7.5 3.7
P 5.3 2.8 1.9
CKMB 243
CPK 2246 1175
BUN 28 47 59 70 57 25→21
Crn 2.1 2.2 2.1 1.9 1.2 1.4→0.5
Date 7/6/29 8/6/19 9/6/19 10/6/1 11/6/1 12/6/1
9 9 9
SGOT 733 222 143
SGPT 290 160 152
D Bili 1.0 1.0 1.9 1.7 1.3 0.7
T Bili 1.3 1.6 1.0 0.9 0.9 1.0
I bili 0.3 0.6 0.3
GGT 189 118 134
ALP 312 173 121 105
Albumin 2.5
Tprotein 6.7
LDH 1580 620 571 569 545
Urinalysis 3+ 4+prot 3+leuc RBC + 24 hr 466
Blood ein ocytes URINE
 TSH: 33.8, FT4: 0.710

 Abdominal USG: Minimal R pleural effusion, mild ascites, both kidneys normal
size, shape and position with increased echogenicity, but preserved C-M
relations.

 ECG: Sinus tachycardia, ECHO: Sinus tachycardia, Normal LV cavity size and
function, basal inferoseptum appears hypokinetic, LVEF 55-65%, moderate
tricuspid regurgiation into dilated RA and moderate mitral regurgitation into
dilated LA, Circumferential pericardial effusion without hemodynamic
compromise.

 Xray: Cardiomegaly, blunting of costophrenic angles bilaterally with increased

vascular markings and perihilar cuffing, with consolidation over R mid lobe.
 23 y/o F pt with PMHx of SLE, Subtotal thyroidectomy who
presented with a Lupus flare, with SIRS criteria r/o Septic
shock secondary to CAP, R/O pericardial effusion R/O
cardiogenic shock, Electrolyte imbalance, elevated RFTs and
significant proteinuria and hematuria to R/O lupus nephritis,
Hypotensive, hypoglycemia and lyte imbalance R/O adrenal
insufficiency, R/O hemolytic anemia and iatrogenic HypoTSH,
R/O Rhabdomyolysis, R/O Genital HSV in a critical state.
 Admitted to HDU
 V/S +RBS monitoring q 6 hours
 Hydration for possible Rhabdomyolysis with standing Dextrose solution
to correct for Hypoglycemic episodes
 Cardiology review for pericardiocentesis, Vasopressors
 Pulse dose methylprednisolone, after which was switched to oral
prednisolone, one dose Cyclophosphamide after which was switched to
MMF
 Calcium gluconate, Salbutamol,Kayexellate
 Ceftazidime x 1/52
 Acyclovir X 1/52
 Fluconazole x 1/7
 Stomach protection, DVT prophylaxis,
 Levothyroxine, Calcium and Calcitriol
 What is Lupus nephritis?

 Classification of Lupus Nephritis and the role of Renal biopsy

and histology

 What are the indications for immunosuppressive therapy in

lupus nephritis?

 What is the optimal induction and maintenance therapy in

lupus nephritis?
 35% of patients have clinical evidence of nephritis at the time of
diagnosis

 Estimated 50-60% develop nephritis during the first 10 years of

disease onset

 Higher in African Americans and Hispanics than in whites,

Men>Women

 10% of patients with lupus nephritis develop ESRD

 Associated with a higher mortality

Hahn, B. H., McMahon, M. A., Wilkinson, A., Wallace, W. D., Daikh, D. I., Fitzgerald, J. D., … American
College of Rheumatology (2012). American College of Rheumatology guidelines for screening,
treatment, and management of lupus nephritis. Arthritis care
 Clinical & laboratory manifestations that meet ACR criteria:
◦ Persistent proteinuria > 0.5gm/d
◦ >3+ by dipstick
◦ &/ cellular casts including RBCs, Hb, granular, tubular or mixed.

 ACR recommended that a spot urine protein/creatinine ratio of

>0.5 can be substituted for 24-hour protein measurement & active
urine sediments.

 Additonal & optimal criteria is renal biopsy sample demonstrating

immune complex-mediated glomerulonephritis compatible with
LN.

Hahn, B. H., McMahon, M. A., Wilkinson, A., Wallace, W. D., Daikh, D. I., Fitzgerald, J. D., …
American College of Rheumatology (2012). American College of Rheumatology guidelines for
screening, treatment, and management of lupus nephritis. Arthritis care
Clinical Manifestation Approximate Prevalence
Proteinuria 100%
Nephrotic range 50%
proteinuria/nephrotic syndrome
Microscopic hematuria 80%
Macroscopic hematuria <5%
Urinary RBC cast 30%
Other urinary cellular cast 30%
Renal insufficiency 60%
Rapid decline in kidney function 15%
Hypertension 30%
Tubular abnormalities 70%

Salem Almani et.al. Update on Lupus Nephritis, CJASN, May 2017

 Indications for Renal Biopsy in Patients with
SLE:
◦ Increasing serum creatinine without compelling
alternative causes (such as sepsis, hypovolemia or
meds)

◦ Confirmed proteinuria of ≥ 1.0gm per 24 hours

◦ Combinations of the following assuming the

findings are confirmed in at least 2 tests done
within a short period of time and in the absence of
alternative causes:
 Proteinuria ≥0.5gm per 24 hours plus hematuria,
defined as ≥ 5 RBCs per hpf
 Proteinuria ≥0.5gm per 24 hours plus cellular casts
Hahn, B. H., McMahon, M. A., Wilkinson, A., Wallace, W. D., Daikh, D. I., Fitzgerald, J. D., …
American College of Rheumatology (2012). American College of Rheumatology guidelines for
screening, treatment, and management of lupus nephritis. Arthritis care
  International Society of Nephrology/Renal
Pathology Society 2003 Classification of LN
CLASS CLASSIFICATION
I Minimal Mesangial LN
II Mesangial proliferative LN
III Focal LN (<50% of glomeruli)
III A: Active lesions
III A/C: Active and chronic lesions
III C: Chronic lesions
IV Diffuse LN (>50% glomeruli);
Segmental or Global
IV A, IV A/C, IV C
V Membranous LN
VI Advanced sclerosing LN (≥90%
globally sclerosed glomeruli without
residual activity)
ISN/RPS, International Society of Nephrology/Renal Pathology Society.
CLASS USUAL CLINICAL FINDINGS
I None relevant to the kidneys so rarely
diagnosed or biopsied
II Hematuria, low grade proteinuria, renal
insufficiency, nephrotic syndrome not
expected
III Hematuria, proteinuria seen in most
patients, renal insufficiency, nephrotic
syndrome not unusual
IV Hematuria, proteinuria seen in most
patients, renal insufficiency, nephrotic
syndrome not unusual
V Proteinuria, often nephrotic range;
hematuria possible; usually no renal
insufficiency
VI Renal insufficiency; proteinuria,
hematuria often absent
ISN/RPS, International Society of Nephrology/Renal Pathology Society.
 A proposed algorithm for when to perform a kidney biopsy in patients with lupus nephritis
(LN).

Salem Almaani et al. CJASN 2017;12:825-835

©2017 by American Society of Nephrology

 Aggressive immunosuppressive therapy is indicated in
patients with active proliferative LN.

 This includes virtually all patients with focal or diffuse

proliferative glomerulonephritis (Class III/IV)

 Immunosuppressive therapy is usually not indicated for

minimal mesangial and mesangial proliferative LN.

Falk, J Ronald et.al., Treatment and prognosis of Diffuse or focal

proliferative lupus nephritis, March 26, 2019
Hahn, B. H., McMahon, M. A., Wilkinson, A., Wallace, W. D., Daikh, D. I., Fitzgerald, J. D., … American College of Rheumatology (2012).
American College of Rheumatology guidelines for screening, treatment, and management of lupus nephritis. Arthritis care
 The ultimate goals of treatment in lupus nephritis are:
 long-term preservation of renal function
 prevention of disease flares
 avoidance of treatment-related harms
 improved quality of life and survival

 Treatment should aim for

 Complete renal response with UPCR <50mg/mol and normal or near-normal (±10% of
normal GFR if previously abnormal) renal function

 Partial renal response defined as ≥50% reduction in proteinuria to sub-nephrotic levels and
normal or near-normal renal function, should be achieved preferably by 6 but no later than
12 months following initiation of treatment.

Joint European League Against Rheumatism and European Renal Association–European Dialysis
and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult
and paediatric lupus nephritis
 Active lupus nephritis should be regularly monitored by determining at each visit:
 Body weight

 Blood pressure

 Serum creatinine and eGFR

 Serum albumin

 Proteinuria

 Urinary sediment (microscopic evaluation)

 Serum C3 and C4

 Serum anti-dsDNA antibody levels

 Complete blood cell count

 Anti-phospholipid antibodies and lipid profile should be measured at baseline

and monitored intermittently.

Joint European League Against Rheumatism and European Renal Association–European

Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the
management of adult and paediatric lupus nephritis
 Hahn, B. H., McMahon, M. A., Wilkinson, A., Wallace, W. D., Daikh, D. I.,
Fitzgerald, J. D., … American College of Rheumatology (2012). American
College of Rheumatology guidelines for screening, treatment, and management
of lupus nephritis. Arthritis care

 Salem Almani et.al. Update on Lupus Nephritis, CJASN, May 2017

 ISN/RPS, International Society of Nephrology/Renal Pathology Society.

 Falk, J Ronald et.al., Treatment and prognosis of Diffuse or focal proliferative

lupus nephritis, March 26, 2019

 Joint European League Against Rheumatism and European Renal Association–

European Dialysis and Transplant Association (EULAR/ERA-EDTA)
recommendations for the management of adult and paediatric lupus nephritis
 EXPECTED LEVEL FOR PGY2 CASE BASED PRESENTATIONS: EMPLOY USE
OF THE PICO FORMATTING AND PEER-REVIEWED
JOURNALS/GUIDELINES/ARTICLES TO ANSWER THE CLINICAL QUESTION
CASE BASE PRESENTATION

Ravin R. Sooklall
CASE
• History
• c/o: sob x 1/12
• Hpi: pt is a 52 y/0 f with a pmhx of afib and hfref who presented
to AE with co of chronic sob, recent pnd, orthopnea and dyspnea
at rest.
• She also reported swelling to both lower limbs.
• Chest pain0, fever0, productive cough0
• Medications: metaprolol 25mg po bd, Asa, atorvastatin, lasix
20mg po od
PHYSICAL EXAMINATION

• Vitals: Bp: 150/90, Hr: 150/min, T: 97 RR: 26/min

• General Exam: mild to moderate tachypnea
• Resp: BAE, mild basal creps
• Cvs: S1S2 M0, Jvp: ~8cm at 90 degrees, Pulse: irregularly
irregular tachycardia
• Abd: ? Mild ascites
• Ext: edema x 2
• Cns: alert and oriented x 2
ECG
IMPRESSION
• 56 y/o female with a pmhx of afib and hfref with afib with rvr 2 Adhf
• Plan:
• Ecg- done
• Cbc
• Biochm: kft, lft, SE, ESE
• Cxr
• Inj Gtn infusion at 25mcg/min
• Inj Lasix 40mg iv stat
• Urine Output charting
• To repeat Ecg and Vitals after Gtn and lasix
MANAGEMENT OF ATRIAL FIBRILLATION
CLINICAL QUESTION
• P: patients with Afib
• I: Rhythm control
• C: Rate vs Rhythm control
• O: cardiovascular morbidity and mortality
MANAGEMENT OF AFIB
HOLTER MONITOR AND CARDIAC TELEMETRY
 Figure 1 Diagnosis of
AHRE/subclinical atrial
fibrillation
CIEDs with an atrial lead can monitor atrial rhythm and store
the tracings. ICM have no intra-cardiac leads but
continuously monitor cardiac electrical activity by recording
and analysing a single-lead bipolar surface ECG based on
specific algorithm.
Left-bottom image: pacemaker with a right atrial lead, and a
ventricular lead in the right ventricular apex. In addition
to pacing at either site, these leads can sense activity in the
respective cardiac chamber. The device can also detect
pre-programmed events, such as AHRE.
Right-bottom image: subcutaneous ICM: these devices have
no intra-cardiac leads and essentially record a single, bipolar,

©ESC
surface ECG with inbuilt algorithms for detection of AHRE or
©ESC AF.

www.escardio.org/guidelines 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation
(European Heart Journal 2020-doi/10.1093/eurheartj/ehaa612)
Figure 8 Diagnostic work-up and follow-up in AF patients

All AF patients Selected AF patients Structured follow-up

Ambulatory ECG monitoring:

Medical history: • Adequacy of rate control • To ensure continued optimal
• AF-related symptoms • Relate symptoms to AF recurrences management
• AF pattern Transoesophageal echocardiography: • A cardiologist / AF specialist
• Concomitant conditions • Valvular heart disease coordinates the follow-up in
• CHA2DS2-VASc score • LAA thrombus collaboration with specially
cTnT-hs, CRP, BNP/NT-ProBNP trained nurses and primary
12-lead ECG Cognitive function assessment care physicians
Thyroid and kidney function,
electrolytes and full blood Coronary CTA or ischaemia imaging:
count • Patients with suspected CAD
Brain CT and MRI:
Transthoracic • Patients with suspected stroke
echocardiography LGE-CMR of the LA:
• To help decision-making in AF

©ESC
treatment

www.escardio.org/guidelines 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation
(European Heart Journal 2020-doi/10.1093/eurheartj/ehaa612)
AFIB- ANTICOAGULATION
 Including
Hfpef
Recommendation
Bp <120/80
Table 11 Dose selection criteria for NOACs

Dabigatran Rivaroxaban Apixaban Edoxaban

Standard dose 150 mg b.i.d. 20 mg o.d. 5 mg b.i.d. 60 mg o.d.
Lower dose 110 mg b.i.d.
Reduced dose 15 mg o.d. 2.5 mg b.i.d. 30 mg o.d.
Dose- Dabigatran CrCl 15−49 mL/min At least 2 of 3 If any of the following:
reduction 110 mg b.i.d. in criteria: • CrCl 15−50 mL/min,
criteria patients with: • Age ≥80 years, • Body weight ≤60 kg,
• Age ≥80 years • Body weight • Concomitant use of
• Concomitant ≤60 kg, or dronedarone,
use of • Serum creatinine ciclosporin,
verapamil, or ≥1.5 mg/dL erythromycin, or
• Increased (133 μmol/L) ketoconazole
bleeding risk

©ESC
www.escardio.org/guidelines 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation
(European Heart Journal 2020-doi/10.1093/eurheartj/ehaa612)
Table 12 Antithrombotic therapy after left atrial appendage
occlusion
Device/patient Aspirin OAC Clopidogrel Comments
Watchman 75−325 mg/day Start warfarin after Start 75 mg/day when Some centres do not
/low bleeding risk indefinitely procedure (target INR 2−3) OAC stopped, continue withhold OAC at the time
until 45 days or continue until 6 months after the of procedure (no data to
until adequate LAA sealing procedure support/deny this
is confirmeda by TOE. approach)
NOAC is a possible
alternative
Watchman 75−325 mg/day None 75 mg/day for 1−6 Clopidogrel often given for
/high bleeding indefinitely months while ensuring shorter time in very
risk adequate LAA sealinga high-risk situations

ACP/Amulet 75−325 mg/day None 75 mg/day for 1−6 Clopidogrel may replace
indefinitely months while ensuring long-term aspirin if better
adequate LAA sealinga tolerated

Note: Load aspirin or clopidogrel before procedure if untreated. Heparin with activated clotting time >250 seconds before or immediately after trans-septal punctures for al
patients, followed by low-molecular-weight heparin when warfarin needed.
aLess than 5 mm leak.
AFIB- RATE CONTROL
UNSTABLE ATRIAL FIBRILLATION
HEMODYNAMIC UNSTABLE CHRONIC ATRIAL
FIBRILLATION
• Rate Control and Hemodynamic Support
Table 14 Antiarrhythmic drugs used for restoration of sinus
rhythm (1)
Antiarrhythmic drugs for restoration of sinus rhythm (pharmacological cardioversion)
Drug Administration Initial dose Further dosing Acute success rate Contraindications/
route For For and expected time to Precautions/
cardioversion cardioversion sinus rhythm comments
Flecainidea Oralb 200−300 mg - Overall: 59−78% • Should not be used in
i.v. 2 mg/kg over (51% at 3 h, ischaemic heart disease
10 min 72% at 8 h) and/or significant structural
Propafenonea Oralb 450−600 mg - Oral: 45−55% at 3 h, heart disease
i.v. 1.5−2 mg/kg 69−78% at 8 h; • May induce hypotension, AFL
over 10 min i.v.: 43−89% with 1:1 conduction (in
Up to 6 h 3.5−5.0% of patients)
• Flecainide may induce mild
QRS complex widening
• Do NOT use for
pharmacological
cardioversion of AFL

©ESC
aMost frequently used for cardioversion of AF, available in most countries. bMay be self-administered by selected outpatients as a ‘pill-in-the-pocket’ treatment
strategy. For more details regarding pharmacokinetic or pharmacodynamic properties refer to EHRA AADs–clinical use and clinical decision making: a consensus
Table 14 Antiarrhythmic drugs used for restoration of sinus
rhythm (2)
Antiarrhythmic drugs for restoration of sinus rhythm (pharmacological cardioversion)
Drug Administration Initial dose Further dosing Acute success rate Contraindications/
route For For and expected time to Precautions/
cardioversion cardioversion sinus rhythm comments
Vernakalantc i.v. 3 mg/kg over 2 mg/kg over <1 h (50% conversion • Should not be used in
10 min 10 min within 10 min) patients with arterial
(10−15 min hypotension (SBP
after the initial <100 mmHg), recent ACS
dose) (within 1 month), NYHA III or
IV HF, prolonged QT, or
severe aortic stenosis
• May cause arterial
hypotension, QT
prolongation, QRS widening,
or non-sustained ventricular
tachycardia

©ESC
cNotavailable in some countries. For more details regarding pharmacokinetic or pharmacodynamic properties refer to EHRA AADs–clinical use and clinical decision
making: a consensus document.

www.escardio.org/guidelines 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation
(European Heart Journal 2020-doi/10.1093/eurheartj/ehaa612)
Table 14 Antiarrhythmic drugs used for restoration of sinus
rhythm (4)
Antiarrhythmic drugs for restoration of sinus rhythm (pharmacological cardioversion)
Drug Administration Initial dose Further dosing Acute success rate Contraindications/
route For For and expected time to Precautions/
cardioversion cardioversion sinus rhythm comments
Ibutilidec i.v. 1 mg over 1 mg over 31−51% (AF) • Effective for conversion of
10 min 10 min 63−73% (AFL) AFL
0.01 mg/kg if (10−20 min ≈1 h • Should not be used in
body weight after the initial patients with prolonged QT,
<60 kg dose) severe LVH, or low LVEF
• Should be used in the setting
of a cardiac care unit as it
may cause QT prolongation,
polymorphic ventricular
tachycardia (torsades de
pointes)
• ECG monitoring for at least 4
hours after administration to

©ESC
detect a proarrhythmic event
cNot available in some countries.
For more details regarding pharmacokinetic or pharmacodynamic properties refer to EHRA AADs–clinical use and clinical decision making: a consensus document.

www.escardio.org/guidelines 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation
(European Heart Journal 2020-doi/10.1093/eurheartj/ehaa612)
Table 14 Antiarrhythmic drugs used for restoration of sinus
rhythm (3)
Antiarrhythmic drugs for restoration of sinus rhythm (pharmacological cardioversion)
Drug Administration Initial dose Further dosing Acute success rate Contraindications/
route For For and expected time to Precautions/
cardioversion cardioversion sinus rhythm comments
Amiodaronea i.v. 5−7 mg/kg 50 mg/h 44% • May cause phlebitis (use a
over 1−2 h (maximum 8−12 h to several large peripheral vein, avoid
1.2 g for 24 h) days i.v. administration >24 hours
and use preferably
volumetric pump)
• May cause hypotension,
bradycardia/atrioventricular
block, QT prolongation
• Only if no other options in
patients with
hyperthyroidism (risk of
thyrotoxicosis)

©ESC
aMostfrequently used for cardioversion of AF, available in most countries. For more details regarding pharmacokinetic or pharmacodynamic properties refer to EHRA
AADs–clinical use and clinical decision making: a consensus document.
REFERENCES
• ESC Guidelines on Atrial Fibrillation (Management of)
(escardio.org)
• Atrial Fibrillation | NEJM
 EXPECTED LEVEL FOR PGY3
CASE BASED PRESENTATIONS:EMPLOY PICO FORMAT AND BRIEF SUMMARY OF
THE LITERATURE REVIEW AS PART OF THE CASE DISCUSSION
Serena Ogbeiwi

31-05-2021
• Sex: Male
• Age: 34
• Initials: J.J
• Race: AG
C/O: Pt referred from spirometry
clinic HPI:
Worsening SOB, abdominal swelling and bilateral pittingedema.
Patient stated that he was diagnosed with HTN 2 yrs ago when he started
with leg swelling and exertion SOB. His SOBE has progressively worsened
over the last 2/52 and for this reason sought medical attention. He denies
CP, Orthopnea, PNA, no cough/cold like symptoms, no fever, no N/V/D
PMHx: HTN
PFHx: Nil
Surg Hx: Nil
Social Hx: Quit smoking and drinking 2yrs ago. Prior occasional
use of alcohol and marijuana 2 joints per
day Trauma: Nil
Transfusion: Nil
DH: Amlodipine, Ramipril,Lasix
Allergies: Nil
Vs: P 105 R:20 BP: 150/70 T 35.4 C Spo2 95% on 4L/O2, 80% RA

O/E: Pt obese, in decubitus supine, no obvious CP distress, receiving O2 via

FM PE+ve
RS: Decreased BS globally due to body habits and poor resp. Effort by
patient. CVS: S1S2Mo, no obvious JVD
ABD: Globulous, distended but soft, non
tender EXT: 2+ bilateral pitting edema
CNS: Pt conscious and oriented x3
 Work up
• Covid Gene Xpert Negat i ve
• Troponin: 0 . 6 ABG

• H b 18.4 g / d l
• Cr 1.2
• WBC 10.4
• SGOT 2 7
• Plts 2 0 5
• SGPT 2 3
• LDH 3 4 5
• ALp 3 . 2
• Ca 10.3
• N a 135.9
• M g 1.8
• K 4.18
• Phos 3 . 4
• Cl 97.4
• Bun 19
Ass: 34y/O M with PMHX HTN who presented with 2/52 worsening SOBE 2 CAP, R/
O RHF, R/O PHTN 2 OSA, reactive polycythemia
 Definition and Epidemiology
• Apnea is lack of airflow for a minimum of 10 sec or longer, resulting in a
drop in oxyhemoglobin and or an electroencephalographic arousal.
• Subtypes include central and obstructive.
• Sleep apnea is associated with the incidence and morbidity of
Hypertension, CAD, HF, Arrythmia, Sudden Cardiac Death, PHTN, VTE and
Stroke,
• Accounts for >800,000 deaths in theUS
• It is 2-4 times more common in men than in women.
• OSA is a modifiable CVS risk factor.
 Pathophysiological Consequence

PNA: parasympathetic nervous system activity; PO2: partial pressure of oxygen; PCO2: partial pressure of carbon dioxide; SNA: sympathetic nervous system activity; HR: heart rate; BP:
blood pressure; LV: left ventricular.
Reproduced from: Bradley TD, Floras JS. Obstructive sleep apnoea and its cardiovascular consequences. Lancet 2009; 373:83. Illustration used with the permission of Elsevier Inc. All rights
reserved.
Graphic 93834 Version 1.0
© 2021 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
• Hypertension • A. Fibrillation

• 50% of persons with OSA have coexistent HTN • Autonomic dysfunction and hypoxia ,
• One study showed increase incident with >5-15 hypercapnia and exaggerated negative
AHI and beyond. intrathoracic pressures leading to increased
juxtacardiac and transmural pressures affecting
the thin-walled atria all contribute to A.Fib in
• PHTN
patients with OSA.

• The prevalence of PHTN in persons with mod to

• CAD and Cardiovascular events.
severe OSA is approximately 20%
• Risk factors for PHTN include comorbid lung
Severe OSA pose greater risk factor for CAD.
disease, daytime hypoxemia, increasing apnea
• Hypertension,
hypopnea index (AHI), and comorbid obesity
• Decreased HDL
hypoventilation syndrome.
• Increased C-reactive protein
• Increased homocysteine
• Elevated blood glucose
• And insulin resistance/diabetes mellitus
• Surgical Therapies Other treatment options in
• Medical therapies study include:
• Oral appliances Atrial optimised pacing
• Gold standard of care in CPAP Surgical such as upper airway
stimulation system implants,
CPAP reduces daytime: (UPPP)uvulopalatopharyngoplasty and
1. Sleepiness Less invasive treatment modalities that
2. Normalizes sleep architecture also target tongue-based
3. Improves morbidity and mortality obstruction include
associated with OSA but outcomes mandibular advancement
have been only modest splints and tongue stabilizing devices
Optimal treatment is described as 4 to
6 hours per night.
• The SAVE study was an international, multicenter, randomized, parallel-group, open-label trial, with blinded
end-point assessment.
• 2717 patients with moderate to severe OSA and established CVD randomised.
• The primary composite end point was death from cardiovascular causes, myocardial infarction, stroke, or
hospitalization for unstable angina, heart failure, or transient ischemic attack.
• Secondary end points included other cardiovascular outcomes, health-related quality of life, snoring
symptoms, daytime sleepiness, and mood.
• Results showed a reduction in the apnea-hypopnea index from 29 to 3.7 events per hour per night. However,
CPAP was not associated with a significant reduction in cardiovascular events (cardiovascular deaths,
myocardial infarction, stroke or hospitalizations for heart failure, unstable angina or transient ischemic
attack; 17 percent [CPAP] versus 15.4 percent
 In conclusion, in a large group of adults with both
cardiovascular disease and moderate-to-severe
obstructive sleep apnea, the use of CPAP therapy
had no significant effect on the prevention of
recurrent serious cardiovascular events, despite
significantly reduced sleepiness and other
symptoms of obstructive sleep apnea and improved
quality-of-life measures.
Carr, G. E., Mokhlesi, B., & Gehlbach, B. K. (2012). Acute cardiopulmonary failure from sleep-disordered breathing. Chest, 141(3), 798–808. https://
doi.org/10.1378/chest.11-1389
 Recommendation Rationale

Consider comorbid OSA, OHS, or the overlap Many patients with SDB have not received a diagnosis at the time of acute
syndrome in patients with cardiopulmonary
ventilatory failure. failure.
Failure to diagnose SDB may lead to increased morbidity or mortality.

Look for and treat OSA in CHF. NIV may improve left ventricular ejection fraction and outcomes.

Consider OSA in patients who survive cardiac arrest. Untreated OSA may represent a potentially reversible cause of sudden death.

Consider early empiric NIV for ventilatory SDB is treated directly and complications of endotracheal intubation and
failure in sedation are
appropriate avoided.
candidates.
Consider extubation to NIV as a liberation strategy NIV may reduce postextubation respiratory failure.
when patients require endotracheal
intubation. Some obese patients are capable of spontaneous breathing even though they do not
meet the traditional success criteria on spontaneous breathing
trials.
Consider performing spontaneous breathing Higher levels of end-expiratory pressure may be necessary to offset increased
trials on higher CPAP or chest wall elastic load even when lung compliance is
PEEP levels. acceptable.
Use sedation and analgesia judiciously. Opiates and benzodiazepines promote pharyngeal collapsibility, blunt respiratory drive,
and impair thearousal mechanism.
Table 1 Limit sleep disruption at night. SDB is worsened by sleep deprivation.
—Critical Care Considerations in the Patient With Suspected Sleep-Disordered Breathing
Arrange close
CHF=congestive heart follow-up with
failure; CPAP sleep specialist.
=continuous Chronic SDBventilation;
positive airway pressure; NIV= noninvasive should be formally diagnosed
OHS= obesity and treated.
hypoventilation syndrome; OSA=
obstructive sleep apnea; PEEP=positive end-expiratory pressure; SDB=sleep-disordered breathing.

Carr, G. E., Mokhlesi, B., & Gehlbach, B. K. (2012). Acute cardiopulmonary failure from sleep-disordered breathing. Chest, 141(3), 798–808. https://
doi.org/10.1378/chest.11-1389
“Obesity in critically ill patients is not associated with excess mortality
but is significantly related to prolonged duration of mechanical
ventilation and intensive care unit length of stay.”
•OSA has a strong association with overall cardiovascular disease.
•It is a modifiable risk factor.
•Obese patients may be asymptomatic due to their sedentary lifestyle.
•Physicans should have a high index of suspicion for PHTN is persons with OSA.
•Patients should be screened, although there is no clear guideline for screening.
•CPAP is the gold standard of treatment in persons with OSA.
•According to the SAVE trial there are no significant reduction in cardiovascular
events for persons treatment with CPAP
•Obesity in critically ill patients is not associated with increase mortality.
 Reference
Shah, Farhan A et al. “Obstructive Sleep Apnea and Pulmonary Hypertension: A Review of
Literature.” Cureus vol. 13,4 e14575. 20 Apr. 2021, doi:10.7759/cureus.14575
Antic NA, Heeley E, Anderson CS, et al. The Sleep Apnea cardioVascular Endpoints (SAVE)
Trial: Rationale, Ethics, Design, and Progress. Sleep. 2015;38(8):1247-1257. Published 2015
Aug 1. doi:10.5665/sleep.4902
Javaheri S, Barbe F, Campos-Rodriguez F, Dempsey JA, Khayat R, Javaheri S, Malhotra A,
Martinez-Garcia MA, Mehra R, Pack AI, Polotsky VY, Redline S, Somers VK. Sleep Apnea: Types,
Mechanisms, and Clinical Cardiovascular Consequences. J Am Coll Cardiol. 2017 Feb
21;69(7):841-858. doi: 10.1016/j.jacc.2016.11.069. PMID: 28209226; PMCID: PMC5393905.
Obstructive sleep apnea and cardiovascular disease in adults, Uptodate, edited by Reena
Mehra, MD, MS, FCCP, FAASM, published by UpToDate in Waltham, MA.
•Akinnusi, Morohunfolu E. MD; Pineda, Lilibeth A. MD; El Solh, Ali A. MD, MPH Effect of obesity
on intensive care morbidity and mortality: A meta-analysis*, Critical Care Medicine: January
2008 - Volume 36 - Issue 1- p 151-158