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A. Fib Presentation

Advance Physiology and Pathophysiology II

Leslie Fernandez

on 23 April 2013

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Transcript of A. Fib Presentation

Pathophysiology Atrial Fibrillation is known as the most common arrhythmia. It is characterized by disorganized, rapid and irregular atrial activation. The ventricular response is also irregular and rapid depending on the conduction properties of the AV junction. That is why patients may experience a heart rate of 120-160 bpm or even greater than 200 bpm. Case Study Presenting problem: Shortness of breath, Palpitations

History of Present Illness: Mr. H.M. is a 66-year old African American male who reports 3 days of generalized weakness, dizziness and fatigue. He reports having palpitations, diaphoresis and dyspnea this morning. Otherwise: (-) fever, (-) chest pain, (+) non-productive cough, (-) hemotypsis, (-) GI bleeding, (-) travel. Patient is also reporting high blood pressure. It is unclear how long this has been going on and if he is compliant with his medications. Diagnostic Evaluation Common and less severe symptoms include the following:
•Fatigue or poor exercise tolerance
•Presyncope or syncope
•Generalized weakness, dizziness, fatigue

Consider unstable when patients present with:
•Decompensated congestive heart failure (CHF)
•Uncontrolled angina/ischemia Intervention Goals:
1.Prevention of thromboembolism,
2. Hemodynamic stabilization
3. Symptom relief Follow-up 1. Patient needs to have weekly PT/INR drawn in the beginning and then blood work will be done monthly. If there are any questions or concerns he should contact the doctor immediately. In the future there are other ways of monitoring the PT/INR such as self monitoring or going to a Coumadin clinic. This can be discussed at the next doctor’s visit. by Leslie Fernandez and Kerry McCann Advanced Physiology and Pathophysiology II Atrial Fibrillation Review of Systems: Other than symptoms associated with the present events, the following is reported with regard to recent health: General: (-) prior fever. HENT: (-) congestion. Respiratory: (-) prior cough. Cardiovascular: (-) prior chest pain. GI: (-) abdominal pain. GU: (-) urinary complaints. Musculoskeletal: (-) ached and pains. Endocrine: (-) prior generalized weakness. Neurological: (-) localized weakness. Psychiatric: (-) emotional stress. Past Medical History: (-) DM, (+) HTN, (-) asthma, (-) COPD, (-) heart disease.

Family History: (-) known inherited disease

Social History: (-) smoking, (-) alcohol abuse

Medications: Lasix PO daily

Allergies: NKDA Physical Examination

Generalized Appearance: Patient is alert and in moderate distress.

Vital Signs: BP 180/105, Pulse: 120, Respirations: 25, Temperature: 98.5 deg F

Skin: pale, cool, diaphoretic, (-) cyanosis

Eyes: (-) conjunctival pallor

ENMT: Mucous membranes moist. Airway patent: (-) stridor, (-) hoarseness

Neck: (-) tenderness, (-) stiffness, (-) lymphadenopathy, (-) JVD Chest and Respiratory: (-) rales, (-) rhonchi, (-) wheezes, (-) rub, breath sounds decreased in lower bases bilaterally

Heart and Cardiovascular: (+) irregularity, (+) palpitations, (-) murmur, (-) gallop, (-) rub

Abdomen and GI: soft, (-) tenderness

Extremities: (-) deformity, (-) edema, (-) calf tenderness

Neuro and Psych: AAOx3, anxious, (-) focal findings Hematology

WBC 11.0
RBC 4.63
HGB 14.4
HCT 44.7
PLT 180 Chemistry

GLUC 128
BUN 17
NA 143
K 4.1
CL 107

BNP 449 Coagulation

PTT 25.5
PT 12
INR 1.09 Cardiac Enzymes

TNI (baseline) 0.26
CPK 110 Chest X-ray: Infiltrates in bilateral lung bases. No pleural effusion. Cardiomegaly. No pneumothorax.

Pulse Oximetry: 91% on RA

EKG: A. Fib with ventricular response at 120. No acute changes.

Cardiac Monitor: A-fib, (-) significant ventricular ectopy Clinical Impression: New-onset A. Fib, Accelerated HTN, CHF.

Plan: Patient to be admitted to CCU for further evaluation and treatment. Diagnostics Evidenced-Based Study Implications for APNs The cause of atrial fibrillation is still being debated but it is believed to occur as a complex interaction between the drivers responsible for its initiation and the anatomical substrates sustaining multiple wavelets of micro-reentry. The pulmonary vein has similar electrical properties as those of atrial myocytes. Thus, the pulmonary vein can be a common source of these drivers, which have automatic foci of origin. Meanwhile sustaining the cardiac rhythm of atrial fibrillation, all depends on the number of wavelets. Increased number of wavelets is yielded by an increased in atrial mass, shortened atrial refractory period, and delayed intra-atrial conduction. Atrial fibrillation has three major consequences namely: loss of atrial contractility, inappropriate fast ventricular response and loss of atrial contractility and emptying, making a patient susceptible to clot formation and be at high risk for subsequent thromboembolic events. Risk factors include the following:

Hemodynamic stress – mitral or tricuspid valve diseases that increase atrial pressure

Atrial ischemia – CAD

Inflammation – myocarditis, pericarditis

Non-cardiovascular respiratory causes – pneumonia, pulmonary embolism, lung cancer, hypothermia

Alcohol and drug use – “holiday or Saturday night heart,” also known as alcohol-related cardiomyopathy

Endocrine disorders – hyperthyroidism, diabetes, pheochromocytoma

Neurologic disorders – subarachnoid hemorrhage, stroke

Genetic factors

Advancing age Of all risk factors, atrial fibrillation has strong associations with other cardiovascular diseases, such as heart failure, coronary artery disease (CAD), valvular heart disease, diabetes, and hypertension. Differential diagnoses:

Atrial Flutter
Atrial Tachycardia
Atrioventricular Nodal Reentry Tachycardia (AVNRT)
Multifocal Atrial Tachycardia
Paroxysmal Supraventricular Tachycardia
Wolff-Parkinson-White Syndrome Electrocardiography (ECG) – findings include: •Irregular ventricular rate
•P waves absent, replaced by irregular, chaotic F waves
•Heart rate (typically in the 110-140 range)
•Left ventricular hypertrophy
•Bundle-branch block
•Acute or prior MI Diagnosis of atrial fibrillation can be confirmed by: Labs

•CBC (anemia, infection)
•Serum electrolytes and BUN/creatinine (electrolyte disturbances or renal failure)
•Cardiac enzymes - CK and/or troponin level (myocardial infarction)
•D-dimer (pulmonary embolism)
•Thyroid function studies (thyrotoxicosis)
•Digoxin level (sub-therapeutic levels and/or toxicity; generally considered safe to give digoxin to patient with AF on digoxin for rate control without waiting for lab values if patient presents with AF with rapid ventricular response)
•Toxicology testing or ethanol level Echocardiography - evaluate for valvular heart disease, left and right atrial size, left ventricular (LV) size and function, left ventricular hypertrophy (LVH), and pericardial disease

CT and MRI - rule out pulmonary embolus; evaluate atrial anatomy if AF ablation is indicated

Chest radiography – evidence of CHF, lung or vascular pathology

Six-Minute Walk Test or Exercise Test - assess the adequacy of rate control

Holter Monitoring or Event Recording – establish a diagnosis not evident in presentation, evaluate rate control

Electrophysiology Study - identify the mechanism of a wide-QRS tachycardia or sites for curative ablation or AV node ablation References Longo, D. L., Fauci, A. S., Kasper, D. L., Hauser, S. L., Jameson, J. L., & Loscalzo, J. (2012). Harrison’s Principles of Internal Medicine (18 ed.). USA: McGraw Hill Companies. Start IV line and give a Diltiazem Hydrochloride 20mg IV bolus, and then hang a Diltiazem Hydrochloride drip at 5mg/hr IV. Place patient on continuous electrocardiographic monitoring. Use CHADS score to decide if patient is in need of anticoagulation therapy. According to two recent clinical trials AFFIRM and RACE ventricular rate control should be the first choice toward A.fib management. These trials found that it is cheaper and problems related to treatment such as death, stroke, hospitalizations, and new arrhythmias were less common.“Ventricular rate control is achieved by depression of atrioventicular nodal conduction” (Wakai and O’Neil, 2003). When picking the drug of choice for VRC, (ventricular rate control) Calcium Channel Blockers such as Verapamil and Diltiazem, Beta blockers, and Amiodarone are found to be the most common used in the ER. C- Congestive Heart Failure

H- Hypertension- 140/90 mmHg (or treated hypertension on medication)

A- Age equal or more than 75

D- Diabetes mellitus

S- Prior Stroke or TIA or Thromboembolism Each of these risks count as a point:
0 - low risk no anticoagulation or Aspirin daily
1 -Moderate risk Asprin daily or Coumadin- must raise INR to 2-3; depending on doctor’s decision
2 or greater - moderate or high risk for stroke- Coumadin- raise INR to 2-3; unless contraindicated The patient scores a CHADS2 of 2. This means he needs anti-coagulation therapy with Coumadin. Heparin with begin immediately since this is a fast acting anti-coagulant. A first dose of Coumadin 2mg PO will also be started. Another IV needs to be started and a bolus 4,000 units of Heparin is to be given. Heparin drip is to start (12 units/kg/hr) at 1350units/hr (based on 75kg weight of the patient). However, the starting rate is 9ml/hr. A PTT is to be drawn 6 hours from the time the bolus was given and then the Heparin protocol should be followed going forward. CBC and PT/INR is to be drawn daily. Patient is to be observed for any signs of bleeding especially in the stool. HR decreased to 100s but remains in A. Fib. Patient reports feeling somewhat improved. Blood cultures were drawn however antibiotic treatment are not indicated at this time. On re-evaluation, somewhat patient approved: HR 90s-100s, Pulse Ox: 95% on 3L NC, BP 145/98. Patient to be admitted to CCU for further evaluation and treatment. The patient will remain in the CCU for further testing and until patient is switched to oral Diltiazem. Patient is to continue on Heparin drip until he has a therapeutic INR between 2 and 3. A cardiac monitor will be placed on patient and will remain until patient is discharged from the hospital. Vital signs will be hourly until patient is transferred to level of less acuity or discharged. Common symptoms to look for with A. Fib :

Racing heartbeat- Afib will typically vary between 120-160 beats however in some patients it can be >200

Shortness of breath- worse with exertion or while lying flat in bed

Lightheadedness and/or fatigue

Swelling of the shins

Irregular heartbeat/palpatations


Pulmonary congestion

Patients can be asymptomatic with A.Fib. There are double the amount of elderly that are asymptomatic versus symptomatic.

There are over one hundred medications that are associated with an increase and decrease in INR response. Be aware when prescribing new medications to patients on Coumadin.

The incidence of A.Fib increases with the adult population over the age of 70

A.Fib is common during acute or early recovery phase of major vascular, abdominal, and thoracic surgery 2. If the patient has any of the feelings he was having that brought him to the ER, he needs to call 911 and come to the ER again. If the patient is not feeling well such as nausea or vomiting, he must come to the office. These may be signs that the A.Fib is back again. 3. Notify healthcare provider if you are having any of these symptoms since they may be side effects of the Coumadin:

•Severe prolonged headaches
•Urine that is pink, red or brown
•Bleeding that doesn’t stop
•Stools that are loose and read or black in color
•Nose bleeds
•Severe pains anywhere in your body
•Excessive bruising or swelling for no obvious reason
•Vomiting that looks like coffee grounds ***IF PATIENT CANNOT REACH THE DR. HE MUST GO TO ER WITH ANY OF THESE SYMPTOMS*** 4. Patient and Family education regarding Coumadin:

Contact your doctor before having any procedures such as dental work, mole removal, surgery, etc.

Try to take the medicine at the same time every day. If a dose is missed, DO NOT double up on a dose.

AVOID injuries that can cause you to bleed.

Patient is to use a soft toothbrush when brushing.

Use an electric razor instead of a razor blade to avoid cutting yourself.

Be careful when you handle any sharp instruments such as kitchen knives.

Don’t blow your nose too hard. This may cause a nose bleed.

Maintain a normal eating pattern Avoid eating EXTRA or large quantities of leafy green vegetables. Contact your doctor first if thinking about losing weight or want to change your diet.

Keep a record o the test results and your daily dose of Coumadin.

Wear an identification bracelet such as a MedicAlert bracelet that states that you are on Coumadin or carry a card in your wallet with this information.

DO NOT miss your blood test appointment. Reschedule and notify your doctor as soon as you know if you are unable to keep an appointment.

Avoid drinking alcohol. Check with your doctor if you have a small amount of alcohol on occasion. Alcohol can increase your risk of bleeding.

ALL doctors treating you must know you are on Coumadin. A Wakai & J O’Neil. (2003). Post Grad Medical Journal. Emergency management of atrial fibrillation. 79: 313-319. Retrieved on March 24, 2013 from svnnet.org/uploads/File/PatientED/Coumadin07.pdf Medscape Reference: http://emedicine.medscape.com/article/151066-overview#showall

Medscape Reference: http://emedicine.medscape.com/article/151066-clinical#showall

Medscape Reference: http://emedicine.medscape.com/article/151066-differential

Medscape Reference: http://emedicine.medscape.com/article/151066-workup#showall LFTs

ALT 35
AST 28
ALP 80
Albumin 4 Thyroid Levels

T3 110
T4 7 ABGs (on RA)

pH 7.33
pCO2 47
pO2 78
HCO3 24
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