The document presents a case study of a 53-year-old male patient who presented with difficulty breathing, palpitations, and dyspnea on exertion. Upon examination, the patient was found to have an irregular heart rate and rhythm consistent with atrial fibrillation. Differential diagnoses included hyperthyroidism, CHF, and COPD, but these were ruled out based on the patient's history and examination findings. The working diagnosis was atrial fibrillation in rapid ventricular response.

1. Earl Karyl F. Galvez
PCGH Level 1 Resident
Atrial fibrillation

2. OBJECTIVES
Review the risk factors for atrial fibrillation
Understand the guidelines for anticoagulation
and other pharmacologic drugs where there is
latitude for physician decision making
Be able to determine when patients should be
evaluated for curative ablation versus treatment
with medical therapy

3. Clinical Case

4. General Data
●C.R.B.
●53 years old
●male
●Married
●Filipino
●Pasig City
●Pasig City General Hospital 7/30/2023.

5. Chief Complaint
Difficulty of Breathing

6. History of Present Illness
DOB
Dyspnea on
exertion
Few
hours
Consult
DOB
DYSPNEA ON
EXERTION
PALPITATION
3 day
1 week

7. Past Medical History
UNREMARKABLE
Illness Previous
Hospitalization
s, Accidents,
Surgeries
NONE
Allergies and
Blood
Transfusion
NONE
MEDICATION
UNREMARKABLE

8. Family History
● Both parents: With HISTORY OF DM, HTN, CAD
● No other heredofamilial diseases

9. Personal and Social History
➔ Highschool student
➔ Company employee
➔ Non Smoker
➔ Non-alcoholic beverage drinker.

10. Review of Systems
General
HEENT
(-) weight loss (-) fever (-) chills (-) loss of appetite (-) malaise
(-) Dizziness (-) eye pain (-) blurring of vision (-) diplopia
(-) ear discharge (-) tinnitus (-)epistaxis (-) hoarseness (-) lacrimation
Respiratory
(-) hemoptysis (-) back pain (-) orthopnea (-) difficulty of breathing
(-) cough (-) sputum production
Cardiovascular
(-) edema (-) cyanosis (-) syncope (-) paroxysmal nocturnal dyspnea
(-) palpitation (-) chest pain,
Gastrointestinal
(-) dysphagia (-) diarrhea (-) hematochezia (-) melena (-) dysphagia
(-) hematemesis (-) abdominal enlargement (-) loose stool
(-) abdominal pain

11. Review of Systems
Genitourinary
Musculoskeletal
(-) incontinence (-) discharge
(-) edema (-) swelling of joints (-) stiffness (-) numbness
(-) muscle pain (-) muscle weakness (-) muscular atrophy
Neuropsychiatric
(-) loss of consciousness (-) paralysis (-) numbness (-) paresthesia (-
) speech disorder (-) tremors (-) depression
Endocrine (-) intolerance to heat and cold (-) abnormal growth
Hematopoietic (-) bleeding (-) easy bruising (-) pallor

12. Physical Examination
Findings
General Survey Patient is awake, conscious, coherent and cooperative. The patient is properly groomed, and with no visible gross
deformities. No visible involuntary movements
Vital Signs and
Anthropometric
Measurement
BP=130/80
PR=164
RR=23
Temp=36.6
O2sat = 98% room air
Weight = 50 kg
Height = 5ff
Waist: 34 inches (86.36 cm)
BMI 23 (normal)
HEENT Anicteric Sclerae, (-) Tonsillopharyngeal Congestion, moist lips, moist buccal mucosa, Pale palpebral
conjunctivae
(-) Naso-Aural Discharge, (-) Cervical Lymphadenopathy
Chest & Lungs (-) Retractions, (-) Chest Lag, Clear Breath Sounds
Cardiovascular Adynamic precordium, No Heaves, No Thrills, Irregular Rate and Rhythm,
Abdomen Globular, No striae, No spider angioma, Normoactive Bowel Sounds, Non tender, (-) Shifting dullness test, (-)
Fluid wave test

13. Physical Examination
Findings
Genitourinary N/A
Extremities No Cyanosis, No Bony deformities, No redness, bulging and depression. No Muscular atrophy.
Capillary Refill Time <2s

14. Physical Examination
Neurologic Findings
Cerebrum Patient is conscious, coherent, alert, cooperative with intact remote, recent and immediate memory. Oriented to
time, person and place.
Cranial Nerves I
II, III
III, IV, VI
V
VII
VIII
IX, X
XI
XII
Not assessed
Pupils are 2mm wide, equally reactive to direct and consensual lighting
Intact and full extraocular movements. No nystagmus
Intact V1-V3. Can clench both temporalis and masseter muscles. Intact Corneal reflex
Able to demonstrate different facial expressions such as by raising eyebrows, open and closing eyes,
frown, smile, wrinkle forehead, pout, purse lip, and puffing of cheeks.
Able to hear and relay whispered words on both ears.
Uvula in midline. Palate symmetrically rising. Intact Gag reflex
Able to shrug shoulders and rotate the head against resistance.
Tongue at midline moves with ease upon retraction and protrusion, can move from side to side
Cerebellum Able to do finger to nose test. Able to do alternate and supination movement of the hand to thigh.
Sensory
Function
100% on both left and right upper extremities,
Able to distinguish sharp sensation and dull sensation on bilateral lower extremities

15. Physical Examination
Neurologic Findings
Motor Function Muscle strength is 5/5 on lower extremities and 5/5 on upper extremities
Reflexes Biceps = +2
Triceps = +2
Babinski sign: Negative
Meningeal Negative for nuchal rigidity, Negative for Brudzinski sign and Negative for Kernig's sign.
Sensory
100% 100%
100% 100%
Motor
5/5 5/5
5/5 5/5
DTR
++ ++
++ ++

16. Salient Features
DOB
Dyspnea on exertion
Palpitation
CR: 164
RR: 23
Irregular Rate and Rhythm
Diet: Food rich in Oil
and fats / fast food
Both parents: Diabetic
and HTN

17. Primary Working Impression
Atrial Fibrillation In RVR

18. Differential Diagnosis
Reason for ruling in Reason for ruling out
Hyperthyrodism Palpitation
Tachycardia
Tachypnea
FATIGUE
HEAT INTOLERANCE
SEXUAL DYSFUNCTION
PROTRUDING EYES

19. Differential Diagnosis
Reason for ruling in Reason for ruling out
CHF DOB
PALPITATION
DYSPNEA ON
EXERTION
AGE: 53
BIPEDAL EDEMA
CHEST PAIN
COUGH
SOB

20. Differential Diagnosis
Reason for ruling in Reason for ruling out
COPD DOB
ORTHOPNEA ON
EXERTION
NO HISTORY OF
ASTHMA/COPD
NO COUGH
NON SMOKER

21. 21
ER LEVEL

22. 22
SUBJECTIVE OBJECTIVE DIAGNOSTIC
(+) DOB
(+)Palpitation
(+) DYSPNEA ON EXERTION
(-) DOB
(-) Chest pain
(-) Cough
AS Paled Conjuctiva
Irregular Rate and Rhythm
SCE (-) Crackles, (-) rales
Globular abdomen, Non
tender, (-) no direct/indirect
tenderness nor rovsing sign
noted
GNE (-) cyanosis and edema
Vital signs
Bp 130/80
CR 164
RR 23
T 36.6
O2 sat 99 room air
CBC pc, Serum electrolytes
BUN, CREA, ASL, ALT
CBG---143mg/DL
UA
CXR
ECG 12 lead
FBS, lipid profile
Na, k, Mg
Trop I
2decho with DS

23. 23
CBC 7/27/23
HGB 157
HCT 0.47
PLT 154
WBC 7.9
N 0.60
L 0.15
Chemistry 7/27/23
BUN 5.77
CREA 129
Na 132
K 3.9
MG ----
CA ----
Cl ----
ASL 198
ALT 261
U/A
Color yellow
PH TURBID
SG 1.025
PUS 20-30
RBC 3-5
Ketone +3
Albumin +1
Sugar Negative
Trop I 133.5

24. 24
- Cardiomegaly
Chest X-RAY

25. 25
ECG

26. 26
ECG

27. 27
ECG

31. 31
PLAN
IVF: PNSS 1L x 80cc/hr----Heplock
DIET: Low Salt, Low Fat
1. Aspirin 80mg tab OD
2. Clopidogrel 75mg tab OD
3. Enoxaparin 0.6cc Sq BID
4. Lactulose 30cc ODHS
5. Atorvastation 80mg tablet ODHS
6. Carvedilol 6.25mg tablet ½ tablet BID—Metropolol 50g tablet OD
7. Captopril 25mg tablet ¼ tablet BID
8. Spirolactone 25mg tablet OD

32. 32
Discussi
on

33. Atrial fibrillation (AF) is the most common sustained
arrhythmia encountered in clinical practice.
It accounts for 1/3 of hospital admissions for cardiac rhythm
disturbances.
AF is a global epidemic and has adverse effects on long term
morbidity and mortality.
There is a significant difference in the incidence of AF in
various populations.
Studies reported a lower incidence of AF in Indian , Asians and
African Americans as compared with White populations.
8 Jun 2020https://doi.org/10.1161/CIRCRESAHA.120.316340Circulation Research. 2020;127:4–20

34. The worldwide age-adjusted prevalence of AF is estimated at
0.596% in men and 0.373% in women ,a total of 33 million.
Studies from India have shown that the mean age of patients
with AF is nearly a decade younger than the Western cohort.
The commonest underlying etiology in Indian patients with AF
in the IHRS-AF registry was also reported to be RHD in 47.8%.
Studies from India reported that RHD was present in nearly 61%
to 75% of AF patients below 50years of age.
A study by Rao et al further observed that hypertension and
ischemic heart disease was more frequent after 50 years of age.
8 Jun 2020https://doi.org/10.1161/CIRCRESAHA.120.316340Circulation Research. 2020;127:4–20

35. The prevalence of AF varies with the complexity of rheumatic heart disease in Indian
population study :
16% with isolated MR.
29% with MS.
52% with coexisting MR and MS.
70% with mixed mitral and tricuspid valve disease.
8 Jun 2020https://doi.org/10.1161/CIRCRESAHA.120.316340Circulation Research. 2020;127:4–20

38. ESC guidelines 2012 defined VALVULAR AF as rheumatic valvular
disease (predominantly mitral stenosis) or prosthetic heart valves.
2014 AHA/ACC/ HRS guidelines defined non-valvular AF as AF in the absence of rheumatic
mitral stenosis or a mechanical heart valve, but added bioprosthetic heart valves or mitral
valve repair within the “valvular heart disease” group.
LONE and “IDIOPATHIC” AF generally refer to younger AF patients who have no clinical or
echo evidence of cardiopulmonary disease, hypertension, or diabetes mellitus.
LONE/IDIOPATHIC : However, this categorization is being abandoned since the category of
lone AF no longer has mechanistic or clinical utility.
Similarly, the term “chronic AF” has variable definitions and should not
be used to describe populations of patients with AF.

39. Mechanism of Atrial Fibrillation
Two concepts of the underlying mechanism of AF :
• Factors that trigger AF.
• Factors that maintain the arrhythmia.
In general, patients with frequent, self-terminating episodes of AF
are likely to have a predominance of factors that trigger AF.
Whereas patients with AF that does not terminate spontaneously
are more likely to have a predominance of perpetuating factors.

40. TRIGGERS
AF triggering factors include
Sympathetic or parasympathetic stimulation.
Bradycardia
PACs - This may be the most common cause
Atrial flutter
Supraventricular tachycardias
Acute atrial stretch
Catheter ablation of the initiating PACs or SVT can be curative in such patients.

41. PV TRIGGERS Triggering foci of rapidly firing cells within the sleeves of
atrial myocytes extending into the pulmonary veins is the underlying
mechanism in most cases of PAROXYSMAL AF
90% of AF triggering foci that are mapped during EP studies in patients
with PAROXYSMAL AF occur in the PVs
NON-PV TRIGGERS foci within the SVC, small muscle bundles in the
ligament of Marshall, and the musculature of the CS have been identified
The BASIC Concept is that the site of origin is often within a venous
structure that connects to the atrium

42. Mechanism of Maintenance of Atrial Fibrillation
Multiple wave re entry hypothesis : AF is sustained by multiple
randomly wandering wavelets in both atria that collide with each other and
extinguish themselves or create new, daughter wavelets that continually re excite
the atria and perpetuate the arrhythmia.
It has been suggested that at least four to six independent wavelets are required to maintain AF.
Localized source hypothesis : This hypothesis suggests that AF
is intermittently maintained by a small number of localized (spatially
stable) high-frequency sources with periods of self-sustaining
disorganization.Rotors and focal sources exhibit 1 : 1 activation within their
spatial domain, with peripheral disorganization.

43. VAGALLY MEDIATED AF : In some patients with structurally normal hearts, AF is precipitated
during conditions of high-parasympathetic tone, such as during sleep and following meals.
Avoidance of drugs, such as digoxin, that enhance parasympathetic tone has been suggested in
these patients.
ADRENERGIC MEDIATED AF : Adrenergic stimulation, such as that during exercise, can also
provoke AF in some patients by causing Triggered activity.
Adrenergic system causes excess intracellular Ca+2 and trigger automaticity.

44. The Pathophysiological Triangle in Atrial Fibrillation

45. Unmodifiable Risk Factors
Age : The prevalence of AF increases with advancing age.
AF occurs in less than 1% of individuals younger than 60 years
6% of those older than 65 years
In more than 10% of those older than 80 years.

46. Unmodifiable Risk Factors
• Gender. The age-adjusted annual incidence of AF is higher in men
compared with women (3.8 vs. 1.6 per 1000 person-years).
• Race. The age-adjusted risk of developing AF is higher in whites as
compared to blacks, Asians, and Hispanics.

47. RISK
FACTORS
FOR AF

48. RISK
FACTORS
FOR AF

49. RISK
FACTORS
FOR AF

50. CLINICAL
SYMPTOMS
OF AF

51. CLINICAL
SYMPTOMS
OF AF

52. TREATMENT

87. 87
Ward Level

88. 88
SUBJECTIVE OBJECTIVE DIAGNOSTIC
(+) PALPITATION
(-) DOB
(-) ORTHOPNEA
(-) chest pain
(-) Fever
AS Pale Palpebral Conjunctiva
(+) IRREGULARR RATE AND
RHYTHM
SCE (-) Crackles, (-) rales
Globular abdomen, no Epigastric
tenderness, (-) no direct/indirect
tenderness nor rovsing sign noted
GNE (-) cyanosis and edema
Vital signs
Bp 110/70
CR 122
RR 22
T 36.6
O2 sat 97 room air
PT PTT INR
2DECHO WITH DS
SERUM NA K AND MG
ECG 12 LEAD MONITORING Q6

89. 89
Problems:
1.AF in RVR
2.ACS NSTEMI

90. 90
PLAN
Diet: LSLF
IVF: HEPLOCK
ECG 12 LEAD MONITORING Q6
VS q 4
I&O Q shift
Medication:
1. ASA 80MG TAB OD
2. CLOPIDOGREL 75MG TAB OD
3. ENOXAPARIN 0.6CC SQ TO COMPLETE 5 DAYS
4. ATORVASTATIN 40MG TAB ODHS
5. LACTULOSE 30CC ODHS
6. OMEPRAZOLE 40MG CAP OD
7. METROPOLOL 25MG TABLET OD

97. 97
DISCHARGE PLANNING
Home Medication:
1. METROPOLOL 25MG TABLET OD
2. CLOPIDOGREL 75MG TABLET OD
3. ATORVASTATIN 40MG
FOR CONSULTATION TO PHC FOR ASSESSMENT AND FUTHER
WORKUP
FF UP AT IM OPD AFTER 2 WEEKS

98. 98
MGH

99. Final Diagnosis
ATRIAL FIBRILLATION IN CVR
99

100. 22/Female + Type I DM
100
Epigastric tenderness
Vomiting
Dizzines
tachycardic
Tachypneic
Dry lips
Pale conjuctiva
History of DM since 9 yrs
old
History of Hospitalization
Both parents: Diabetic
On keto diet
Glucose Utilization(muscle
Gluconeogenesis
Glycogenolysis
Ketogenesis Free fatty Acids
Hyperglycemia Metabolic Acidosis

101. 101
Hyperglycemia Ketogenesis
Glucosuria
Ketoacidosis
Ketonuria
Dehydration
Admission

102. Take Home Message
• DKA is a life-threatening complication of diabetes mellitus
• Fluid therapy and insulin remains the key factors for
managing DKA and frequent monitoring is essential
• DKA can be prevented through patient education and
adherence to medication

103. References:
1.https://www.ahajournals.org/doi/10.1161/CIRCRESA
HA.120.316340
103

104. THANK YOU