Dr Barnabo

Dr Barnabo MEDECINE,MALADIES CARDIOVASCULAIRES.

03/01/2023

Happy new year 2023 to you all.

21/02/2022

After several hours of surgery all we wish is to patient back on his feet and smile on family’s face.

Happy and prosperous year 2022.Wish you and your family good health.
03/01/2022

Happy and prosperous year 2022.
Wish you and your family good health.

Mission accomplie!I did my best God accomplish wonderful ending.Dr BARNABO 🎉🎉🎉
22/05/2021

Mission accomplie!
I did my best God accomplish wonderful ending.
Dr BARNABO 🎉🎉🎉

19/01/2021

ATRIAL FIBRILLATION

ATRIAL FIBRILLATION

A. DESCRIPTION

Atrial Fibrillation describes a state whereby multiple areas of chaotic electrical impulses occur in the atrium of the heart,.

The synchronous harmonious rhythm governed by the Sino Atrial (SA) node is totally absent.

This is reflected by an erratic baseline tracing with no P waves on the ECG.

There is sporadic Atrio Ventricular (AV) conduction which manifests as an irregularly irregular heart beat.

The AV node conducts less well in elderly patients hence the heart rate tends to be slower in this age group.

B. CLINICAL CLASSIFICATION

1. PAROXYSMAL
- Stops spontaneously within 7 days
Occurs more in the young to middle aged population

2. PERSISTENT
- Requires Pharmacological/Electrical Cardioversion to stop

3. PERMANENT
- No Resumption of sinus rhythym despite efforts to induce cardioversion

C. PROFILE
With a prevalence of 0.5% of the general population, atrial fibrillation is the commonest arrhythmia. It occurs in greater than 5%-10% of those over the age of 75 years. It is the commonest post operative arrhythmia, 33% of patients get it after cardiac surgery within the first 4 days. This results in an increase in morbidity, hospital stay and readmissions.

D. CONSEQUENCES
1. CARDIAC
Atrial contraction contributes to 30% of normal cardiac filling.The loss of this 'Atrial Kick' with AF decreases diastolic filling thereby reducing cardiac output. This can have serious effects in patients with diastolic dysfunction ie Aortic Stenosis or hypertensives with Left ventricular hypertrophy, ischemic heart disease etc. In fact long term atrial fibrillation increases an individual's risk of heart failure.

2. THROMBOSIS
Loss of coordinated atrial contracton promotes stasis of blood within the left atrium and this leads to the formation of atrial thrombi, these can subsequently dislodge and cause infarction in the systemic circulation. The consequence of mural thrombosis is a serious clinical danger of atrial fibrillation hence prophylactic anticoagulation is thus mandatory.

The Risk of Thromboembolism is highest if there is return to sinus rhythm after 48 hours of AF

With AF the risk of CVE is 4% at 75years of Age
This is halved by anticoagulation

E. CAUSES OF ATRIAL FIBRILLATION

This is due to a SUBSTRATE & A TRIGGER

SUBSTRATE
Diseased Atrial Muscle
When the muscle is diseased it becomes more excitable and thus becomes a substrate for foci to depolarize.
Tne substrate is formed by the following factors;
Increased atrial pressure
Increased atrial mass
Atrial Inflammation
Atrial Infiltration
Atrial Fibrosis

TRIGGER
A Rapidly discharging atrial focus

LOCATION OF TRIGGER
It can arise from anywhere
It is mainly in the left atrium occuring at the entry point of the pulmonary vein or***ce
Multiple reentry circuits are formed
This then leads to ELECTRICAL REMODELING
The refractory period of the myocytes gets shorter
This MALADAPTION then establishes the chronicity of Atrial Fibrillation

The increased left atrial size and mass are positive predictors of atrial. Fibrillation.

F. PREDOSPOSIMG FACTORS
Rheumatic Heart Disease
Hyperthyroidism - it can be an early feature of thyrotoxicosis
COAD
Sepsis
Alcohol Intake (especially binge drinking ie Holiday Heart Syndrome)
Pericarditis
Pulmonary Embolus
ASD
Hpokalemia, hypomagnesemia

G. INDEPENDANT RISK FACTORS
Hypertension
Ischemic Heart Disease
Valvular Heart Disease
Congestive Cardiac Failure
Diabetes Mellitus

H. CLINICAL FEATURES
Atrial Fibrillation presents with an irregularly irregular pulse and pulse deficit.
This irregularity in pulse is maintained with exersize.
There may be signs of background cardiac dysfunction.

One must also look for underlying features of predisposing factors such as
COAD,
Mitral Stenosis,
thyrotoxocosis,
Alcohol excess etc
If the patient has Rhematic Mitral Stenosis, the onset of Atrial Fibrillation will result in worsening of Cardiac Function.

As an isolated feature Atrial Fibrillation often has vague symptoms
AF is an incidental finding in 30% of patients with some getting generalized weakness and fatigue.

However some may present to Hospital with
Angina,Shortness of Breath, Orthopnoea or Hypotension.

ECG
The ECG shows an irregular baseline with no P waves
The baseline is replaced by fine oscillatory waves called f waves.

CHEST X-ray
Often reflects the cause ie COAD, Mitral Stenosis

I. MANAGEMENT

A large proportion of patients with new onset Atrial fibrillation will experience spontaneous conversion to sinus rhythym by 24-48hours.

In some cases treating the underlying condition eliminates atrial fibrillation

As far as Lone AF is concerned ->

A. ACUTE LESS THAN 48hr onset
Synchronised DC Cardioversion, with 200J, is indicated.

B. MORE than 48hrs after onset
Cardioversion more than 48 hours after established Atrial Fibrillation is risky, it will push out a thrombus into the systemic circulation
These patients need to be anticoagulated 3 weeeks prior to cardioversion and for 4 weeks after.

THERAPY For Established Atrial Fibrillation
- keep the heart rate below 100 and provide anti coagulation

There are 2 options

1. Rate Control
This is done with Digoxin, Beta blockers or Calcium channel blockers

2. Rhythm Control
Amiodarone or Class 1 antiarrhythmia drugs
Radiofrequency Ablation - Quite helpful for the younger population.

The AFFIRM Study has shown Rate Control to be better, however it is best to treat the patient from a case to case perspective and do a risk benefit analysis.

If there is new onset atrial fibrillatiion before induction of anesthesia
Surgery should be postponed until ventricular rate control or sinus rythym has been achieved

J. ANTICOAGULATION - CHADS2VASC

There is a significant risk of thromboembolism and all patients in Atrial Fibrillation with Rheumatic Heart Disease or Prosthetic Valves must be anti coagulated

Anticoagulation with Warfarin should occur to keep the INR between 2-3

Those in AF without Rheumatic Heart disease or prosthetic valves are scored using the CHAD2VASC score for anticoagulation. See previous posts.

K. ATRIAL FIBRILLATION IN PATIENTS HAVING SURGERY

1. Patients in Fast Atrial Fibrillation are slowed with either
Digoxin
Beta blocker

2. Warfarin is stopped and the patient is commenced on Clexane or Heparin until before the operation.
3. The INR is allowed to drift down to 1.5 upon stopping Warfarin as long as there is Clexane/heparin cover

4. The last dose of Clexaneand must administered 12 hours prior to surgery whereas that of heparin 6 hours.

5. An emergency operation will require Fresh Fozen Plasma, Cryoprecipitate or Hemosolvex.

6. Intraoperative management depends on the hemodynamic stability of the patient. It is important to prevent a tachycardia as fast AF is not good since it impairs diastolic filling.

7. If vital signs are stable than rate control is advised with a beta blocker or calcium channel blocker
An electrical accessory pathway will need Amiodarone instead.

8. Atrial fibrillation is the most common postoperative arrhythmia and it can cause signifiant morbidity.
These complications are mainly increased in those with
1. Pre existing Cardiac Risk Factors
2. Hypotension
3. Oxygen Desaturation
4. Positive Fluid Balance
5. Electrolyte Imbalance - esp K+ and MG++

Courtesy
1. Miller's Anesthesia 7th Edition
2. Kumar & Clark's Clinical Medicine 8th Edition
3. Cardiology An Illustrated Textbook by Newby & Grubb
4. Oxford Handbook of Anaesthesia 3rd Ed

02/01/2021

HAPPY AND PROSPEROUS NEW YEAR 2021

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Dr BARNABO

Spécialiste de maladies cardio-vasculaires.

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