Therapeutic..

I had finished reading these 2 books in a week and a half.. Quite an achievement for me.. hahahah.. Last time I could finish reading a book in a day.. Really enjoyed myself..

So many things.. So little time...

Salam..

The tv is on.. But not watching it.. Something that had been my habit lately.. Switching it on just the sake of not wanting the house being quiet especially when my little princess is asleep.. I am so lucky to have her around.. At least I have someone with me while my life buddy goes to work every night.. Yupp.. My life buddy only works at night.. He will answer he is a "kupu-kupu malam" if anyone asking him.. Working in the music industry, especially with a boss who only works at night as the night brings the best of him so I could do nothing..

Today I had an experience of my life time.. Taking care of 6 kids - 11 years old, 7 years old, 5 years old, 3 years old and 2 one year old babies was a blast.. There are times I could feel my heart beating so fast I could fall any time.. There were times I shut down from hearing all the screaming and crying for the sake of my heart.. Luckily angah came back just on time.. We took the kids to KLCC later today and we had quiet a enjoying time even though it was damn tiring.. The part I enjoyed most was spending time at Kinokuniya..

I love book stores.. Even when I was much younger.. Abah and Mak will swap toys with books.. I am now teaching Rania the same.. Every time I had the chance to visit a book store I will take her too.. Giving her books to hold on (sometimes not even buying it) so she will enjoy the smell of new books (like i do.. hahahahah).. Today I left Rania walking through the isle at Kinokuniya.. Picking up any books of her likings (and again not buying it) but I do buy 2 special books for my life buddy though.. Adding up his books collections..

Actually I had missed few things that I use to love doing.. Reading for example.. Since my sis had pointed out that I might suffering pre-depression so I had looked out for depression signs.. One of the signs are "Loss of interest in daily activities. No interest in former hobbies, pastimes, social activities, or sex. You’ve lost your ability to feel joy and pleasure." Yupp.. I had loss interest in few things that I use to love before.. At first I thought it was because of Rania.. Because of my work load.. But I do think that my loss of interest is also due to depression.. So I am trying to beat it.. I had finished a paperback few days ago.. I frankly could not remember when I last read (and surely finish) reading one.. So I am trying my best doing things I love.. And surely one of it updating this blog.. Well.. So many things to do.. so little time.. But I can do it.. InsyaAllah..

Tachycardia

This is what I am having now. Getting much better but serious observation must be done for the rest of my life. From our wiki..

Tachycardia comes from the Greek words tachys (rapid or accelerated) and kardia (of the heart). Tachycardia typically refers to a heart rate that exceeds the normal range for a resting heartrate (heartrate in an inactive or sleeping individual). It can be very dangerous depending on how hard the heart is working and the activity.

The upper threshold of a normal human heart rate is usually based upon age:^[1]

• 1–2 days: >159 beats per minute (bpm)
• 3–6 days: >166 bpm
• 1–3 weeks: >182 bpm
• 1–2 months: >179 bpm
• 3–5 months: >186 bpm
• 6–11 months: >169 bpm
• 1–2 years: >151 bpm
• 3–4 years: >137 bpm
• 5–7 years: >133 bpm
• 8–11 years: >130 bpm
• 12–15 years: >119 bpm
• >15 years – adult: >100 bpm

When the heart beats rapidly, the heart pumps less efficiently and provides less blood flow to the rest of the body, including the heart itself. The increased heart rate also leads to increased work and oxygen demand for the heart (myocardium), which can lead to rate related Ischemia thus perhaps causing a heart attack (myocardial infarction) if it persists. This occurs because the decreased flow of necessary oxygen to the heart causes myocardial cells to begin to die off. Acutely, this leads to angina; and chronically to ischemic heart disease.^[2]

[edit]Differential diagnosis

12 lead electrocardiogram showing a run of ventricular tachycardia (VT)

An electrocardiogram (ECG) can help distinguish between the various types of tachycardias, generally distinguished by their site of pacemaker origin:

• Sinus tachycardia, which originates from the sino-atrial (SA) node, near the base of the superior vena cava.
• Ventricular tachycardia, any tachycardia which originates in the ventricles.
• Supraventricular tachycardia (SVT), which is a tachycardia paced from the atria or the AV node. SVT rhythms include:
  • Atrial fibrillation
  • AV nodal reentrant tachycardia (AVNRT)
  • AV reentrant tachycardia (AVRT)
  • Junctional tachycardia

Tachycardias may be classified as either narrow complex tachycardias (supraventricular tachycardias) or wide complex tachycardias. "Narrow" and "wide" refer to the width of the QRS complex on the ECG. Narrow complex tachycardias tend to originate in the atria, while wide complex tachycardias tend to originate in the ventricles. Tachycardias can be further classified as either regular or irregular.

[edit]Sinus tachycardia

Main article: Sinus tachycardia

[edit]Ventricular tachycardia

Main article: Ventricular tachycardia

Ventricular tachycardia (VT or V-tach) is a potentially life-threatening cardiac arrhythmia that originates in the ventricles. It is usually a regular, wide complex tachycardia with a rate between 120 and 250 beats per minute. Ventricular tachycardia has the potential of degrading to the more serious ventricular fibrillation. Ventricular tachycardia is a common, and often lethal, complication of a myocardial infarction (heart attack).

Exercise-induced ventricular tachycardia is a phenomenon related to sudden deaths, especially in patients with severe heart disease (ischemia, acquired valvular heartand congenital heart disease) accompanied with left ventricular dysfunction.^[3] A case of a death from exercise-induced VT was the death on a basketball court of Hank Gathers, the Loyola Marymount basketball star, in March 1990.^[4]

Both of these rhythms normally last for only a few seconds to minutes (paroxysmal tachycardia), but if VT persists it is extremely dangerous, often leading to ventricular fibrillation.

[edit]Supraventricular tachycardia

This is a type tachycardia that originates from above the ventricles, such as the atria. It is sometimes known as paroxysmal atrial tachycardia (PAT). Several types of supraventricular tachycardia are known to exist.

Main article: Supraventricular tachycardia

[edit]Atrial fibrillation

Atrial fibrillation is one of the most common cardiac arrhythmias. It is generally an irregular, narrow complex rhythm. However, it may show wide QRS complexes on the ECG if a bundle branch block is present. At high rates, the QRS complex may also become wide due to the Ashman phenomenon. It may be difficult to determine the rhythm's regularity when the rate exceeds 150 beats per minute. Depending on the patient's health and other variables such as medications taken for rate control, atrial fibrillation may cause heart rates that span from 50 to 250 beats per minute (or even higher if an accessory pathway is present). However, new onset atrial fibrillation tends to present with rates between 100 and 150 beats per minute.

[edit]AV nodal reentrant tachycardia (AVNRT)

AV nodal reentrant tachycardia is the most common reentrant tachycardia. It is a regular narrow complex tachycardia that usually responds well to the Valsalva maneuver or the drug adenosine. However, unstable patients sometimes require synchronized cardioversion. Definitive care may include catheter ablation.

[edit]AV reentrant tachycardia

AV reentrant tachycardia (AVRT) requires an accessory pathway for its maintenance. AVRT may involve orthodromic conduction (where the impulse travels down the AV node to the ventricles and back up to the atria through the accessory pathway) or antidromic conduction (which the impulse travels down the accessory pathway and back up to the atria through the AV node). Orthodromic conduction usually results in a narrow complex tachycardia, and antidromic conduction usually results in a wide complex tachycardia that often mimics ventricular tachycardia. Most antiarrhythmics are contraindicated in the emergency treatment of AVRT, because they may paradoxically increase conduction across the accessory pathway.

[edit]Junctional tachycardia

Junctional tachycardia is an automatic tachycardia originating in the AV junction. It tends to be a regular, narrow complex tachycardia and may be a sign of digitalis toxicity.

[edit]Hemodynamic responses

The body has several feedback mechanisms to maintain adequate blood flow and blood pressure. If blood pressure decreases, the heart beats faster in an attempt to raise it. This is called reflex tachycardia. This can happen in response to a decrease in blood volume (through dehydration or bleeding), or an unexpected change in blood flow. The most common cause of the latter is orthostatic hypotension (also called postural hypotension). Fever, hyperventilation and severe infections can also cause tachycardia, primarily due to increase in metabolic demands.

[edit]Autonomic and endocrine

An increase in sympathetic nervous system stimulation causes the heart rate to increase, both by the direct action of sympathetic nerve fibers on the heart and by causing the endocrine system to release hormones such as epinephrine (adrenaline), which have a similar effect. Increased sympathetic stimulation is usually due to physical or psychological stress. This is the basis for the so-called "Fight or Flight" response, but such stimulation can also be induced by stimulants such as ephedrine, amphetaminesor cocaine. Certain endocrine disorders such as pheochromocytoma can also cause epinephrine release and can result in tachycardia independent nervous system stimulation. Hyperthyroidism can also cause tachycardia.^[5]

[edit]Management

The management of tachycardia depends on the underlying cause.

If it is due to an underlying cardiac conduction abnormality chemical conversion (with antiarrhythmics), electrical conversion (giving external shocks to convert the heart to a normal rhythm) or use of drugs to simply control heart rate may be used.

If the tachycardia originates from the sinus node (sinus tachycardia), treatment of the underlying cause of sinus tachycardia is usually sufficient. On the other hand, if the tachycardia is of a potentially lethal origin (i.e.: ventricular tachycardia) treatment with anti arrhythmic agents or with electrical cardioversion may be required. Below is a brief discussion of some of the main tachyarrhythmias and their treatments.

The electrocardiac management of atrial fibrillation and atrial flutter is either through medications or electrical cardioversion. Pharmacologic management of these arrhythmias typically involves diltiazem or verapamil as well as beta-blocking agents such as atenolol. The decision to use electrical cardioversion depends heavily on the hemodynamic stability of the presenting patient; in general those patients who are unable to sustain their systemic functions are electrically converted although conversion to a normal sinus rhythm can be performed with amiodarone. An interesting type of atrial fibrillation which must be carefully managed is when it appears in combination withWolff-Parkinson-White syndrome. In this case, calcium channel blockers, beta-blockers and digoxin must be avoided to prevent precipitation of ventricular tachycardia. Here,procainamide or quinidine are often used. Of note: patients who have been in atrial fibrillation for more than 48 hours should not be converted to normal sinus rhythm unless they have been anti-coagulated to an INR of 2-3 for at least 4 weeks. This is to help prevent blood clots embolizing from the heart chambers to the rest of the body where they can cause adverse events like a stroke.

In the case of narrow complex tachycardias (junctional, atrial or paroxysmal), the treatment in general is to first give the patient adenosine (to slow conduction through the AV node) and then perform Valsalva maneuvers to slow the rhythm. If this does not convert the patient, amiodarone, calcium channel blockers or beta-blockers are commonly employed to stabilize the patient. Again as in atrial fibrillation, if a patient is unstable, the decision to electrically cardiovert him/her should be made.

With wide complex tachyarrhythmias or ventricular tachyarrhythmias, in general most are highly unstable and cause the patient significant distress and would be electrically converted. However one notable exception is monomorphic ventricular tachycardia which patients may tolerate but can be treated pharmacologically with amiodarone orlidocaine.

Above all, the treatment modality is tailored to the individual, and varies based on the mechanism of the tachycardia (where it is originating from within the heart), on the duration of the tachycardia, how well the individual is tolerating the fast heart rate, the likelihood of recurrence once the rhythm is terminated, and any co-morbid conditionsthe individual is suffering from.

Kecewa..

Dalam hidup ini seringkali kita kecewa. Bermacam jenis kecewa yang pernah kita lalui. Kecewa dalam percintaan, kecewa dalam kehidupan, kecewa segala macam jenis kecewa. Malam ini saya kecewa. Kecewa dengan persekitaran yang menyesakkan.

Sudah hampir dua tahun saya mengajar di sekolah itu. Tahun lepas saya betul-betul kurang sihat. 9 bulan mengandungkan Rania bukan perkara yang senang. Mungkin ada yang mengandung tiada masalah. Tapi saya tidak, boleh dikatakan setiap hari saya akan muntah. Lembik. Lesu. Sudah tentu saya tidak dapat mempamerkan prestasi sebenar saya. Dalam hati ini membuak-buak perasaan kurang senang. Saya tahu saya boleh beri lebih lagi tapi badan saya tidak mampu melakukannya. Kalaulah mereka boleh tahu (atau mahu ambil tahu) bagaimana prestasi saya semasa di sekolah lama, sudah tentu mereka akan faham. Tapi mereka tidak mahu faham (ada yang mengatakan mereka faham - tapi saya ragu)

Dalam masa seminggu ini saya kurang sihat lagi. Digagahi jua badan ini melakukan yang termampu. Dipaksa diri ini menyiapkan apa yang diminta walaupun hanya diri ini tahu betapa peritnya setiap saat yang berlalu. Semuanya kerana tugas. Semuanya dengan niat mahu halalkan setiap sen rezeki yang diterima setiap bulan untuk membesarkan anak. Dan yang penting semuanya Lillahitaala. Berapa kali dirasakan badan ini mahu tumbang. Berapa kali dirasakan kepala ini terlalu berat untuk berbuat apa-apa. Tapi masih digagahi juga.

Malam semalam akhirnya saya tumbang juga. Dalam kepenatan yang mencengkam, dalam kesakitan yang amat sangat, saya terjatuh dalam longkang. Untuk lindungi Rania, badan ini yang sakit-sakit. Kaki ini yang terseliuh. Kaki ini berdarah. Ditahan kesakitan yang amat sangat sepanjang 15 minit perjalanan. Mengalir juga air mata menahan kesakitan.

Pagi ini kepala makin berpusing. Hati ini memberontak ini ke sekolah menjalankan tugas. Kesian rakan sekumpulan sekiranya saya tidak hadir. Namun saya betul-betul tidak mampu. Kaki sudah semakin berkurangan sakitnya jadi saya ke klinik. Bercerita kepada tuan doktor masalah saya. Diambilnya tekanan darah dan kadar denyutan jantung. Terasa ada sesuatu yang tidak kena kerana doktor mengambil masa yang lama mencari kadar denyutan jantung. Muka tuan doktor semakin berkerut. Akhirnya dikhabarkan satu berita yang kurang baik. Kadar denyutan jantung saya terlalu laju. Tidak sekata dan ada disesetengah tempat kurang kedengaran. Aduh. Terus ditulis surat rujukan, diminta ke hospital segera. Tapi rasanya tidak mampu terus ke hospital. Siapa yang akan menemani Rania. Makan minumnya. Banyak yang perlu diuruskan.

Dalam menahan kesakitan ini, hati ini terluka. Bukan diminta jadi begini. Bukan dipinta untuk rasa begini. Semuanya ketentuanNya. Namun ada yang meragui, ada yang mempersoalkan, ada yang memperkatakan. Aduhai hati.. kuatlah hati.. tabahlah hati. Mereka tak mampu mengerti. Semoga mereka diberi petunjuk. Tapi hati ini tetap KECEWA.