VENTRICULAR TACHYCARDIA

VENTRICULAR TACHYCARDIA

An ECG tracing of ventricular tachycardia: Shows

*A very broad QRS complex

*Absence of p wave (Dissociated p wave may seen)

* Heart rate: 140-220 beats/min.

*Occasional sinus capture beat (Normal P, QRS, T complex between ventricular)

*Occasional fusion (Dressler) beat present.

* A bifid, upright QRS with a taller first peak in VI & A deep S wave in V6. * A concordant (same polarity) QRS direction in all chest leads (V1-V6).

Causes of VT:

§Acute MI

§Chronic ischemic heart disease (specially poor left ventricular function) §Myocarditis

§Cardiomyopathy

§Ventricular aneurysm

§Electrolyte imbalance: Hypokalaemia hypomagnesaemia

Mx of ventricular tachycardia:

Clinical feature:

Symptoms:

§History of myocardial infarction,

§Palpitation

§Symptoms of low cardiac output: dizziness, dyspnoea or Syncope.

Signs:

i) Atrioventricutar dissociation (pathognomonic)

ii) Capture/fusion beats (pathognomonic)

iii) Extreme left axis deviation

IV) Very broad ORS complexes (>140ms)

ECG of VT

v) No response to carotid sinus massage or iv adenosine.

Investigation:

 ECG:

Rx:

a) When pt is haemodynamically unstable (systolic BP< 90mm of dinus rhythm is restored by DC cardioversion

b) When pt is haemodynamically stable-sinus rhythm is restored by pharmacological cardioversion such as

- Amiodarone IV 300mg bolus within 30 min. followed 600mg over 24hours

-Lignocaine IV also used

c) To prevent recurrence- Beta-blockers & Amiodarone

d) Corection of Hypokalaenia, hypomagneswemia, acidosis and hypoxaemia e) VT is associated with haemodynamic compromise; the use of an implantable cardiac defibrillator is recommended

f) Rarely surgery of catheter ablation can be used to interrupt the arrhythmia focus or circuit.

Sick Sinus syndrome

Sick Sinus syndrome

ECG OF SICK SINUS SYNDROME

It can occur at young or child age but is most common in older peoples.

Pathology:

- Fibrosis, Degenerative changes and/or, Ischemia of the sinoatrial (sinus) node. 

Features:

§The condition is characterized by a variety of arrhythmias

§May present with palpitation, dizzy spells or syncope, due to intermittent tachycardia bradycardia, or pauses with no atrial or ventricular activity (sinoatrial block of sinus arrest)

Common features of sinoatrial disease:

§ Sinus bradycardia

§ Sinoatrial block (sinus arrest)

§ Paroxysmal suprauentricular tachycardia

§ Paroxysmal atrial fibrillation

§Atriauntricular block

Treatment:

§A permanent pacemaker: May benefit patients with troublesome symptoms due to spontaneous bradycardias or those with symptomatic bradycardias induced by drugs required to prevent tachyarrhythmias.

§Atrial pacing may help to prevent episodes of atrial fibrillation.

§Permanent pacing does not improve prognosis and is not indicated in patients who are asymptomatic.

WPW syndrome

It is syndrome in which there is an accessory pathway that bypasses the AV node & connects the atrium & ventricle.

Types of WPW syndrome: Two types-

1)    Type-A: Accessory pathway on the left side. ECG findings are-tall R waves in V₁ & V_2.

2)    Type-B: Accessory pathway on right side ECG findings are deep a waves in V₁ & V_2.

ECG criteria:

§ Short PR interval (<0.12 second)

§ wide QRS complexes

§ Delta wave: Slurred, thickened initial upstroke of the QRs.

§Presence of Q-wave in leads II, III & a VF (may be confused with inferior MI)

§ Tall R in V₁ & V_2. (In type-A)

§ Deep Q in V₁ & V_2. (In type-B)

Clinical presentation of WPW syndrome:

(a) May be asymptomatic (in 50% cases)

(b) Palpitation.

(c) Paroxysmal attack of atrial or supraventricular tachycardia.

(d) Atrial fibrillation or flutter.

(e) Syncope

(f) Sudden death

(g) Rarely VT or VF.

Treatment of WPW syndrome:

i)                   Asymptomatic-No Rx is needed.

ii)                Symptomatic-

                     Radiofrequency ablation is the treatment for choice for WPW syndromes. If not available-prophylactically anti-arrhythmic drugs such as-

           § Amidarone,

           §Beta blocker,

           § Flecainide 

           §propafenone 

HEART FAILURE

It is also called congestive heart failure. It is an abnormality of cardiac function in which heart is unable to pump blood at an output sufficient to meet the metabolic demands of the tissue or can do so only at an elevated filling pressure .Heart failure is a syndrome that may be result from the end stage of many forms of chronic heart disease and systemic disorders.

TYPES OF HEART FAILURE

§Acute heart failure: Heart failure develops suddenly in this type of heart failure

 §Chronic heart failure: Here heart failure develops suddenly

§ Left sided heart failure: If left ventricular output is decreased and/or left atrial or pulmonary venous pressure increased, left sided heart failure occur.

§Right sided heart failure: In this condition right ventricular output is decreased.

§Biventricular failure: In this condition both sided heart failure occur.

§Compensated heart failure

§Forward failure: Due to inadequate output, forward failure occurs.

§Backward failure: Due to pulmonary and systemic venous pressure congestion backward failure occurs.

§Systolic dysfunction: Due to impaired myocardial contraction this type of heart failure developed.

§ Diastolic dysfunction: Due to poor ventricular failure and high filling pressure, diastolic dysfunction is developed.

heart

CAUSES:

1. Long standing systemic hypertension

2. Coronary hypertension

3. Cardiomyopathy

4. Obstuctive vulver disease

5. Myocardial infarction

6. Shock

7. Intracardiac left to right shunting

8. Extracardiac shunting

9. Infectious agent

10. Metabolic disorders

11. Idiopathic condition

12. Corpulmonale

13. Myocardial ischemia

14. Aging

15. Ischimic fibrosis

16. Endomyocardial disorders

17. Nutritional disorder

18. Thyrotoxicosis

19. Collagen vascular disease

20. Diabetes mellitus

21. Drug abuse: Cocaine

22. Lung disease

23. Nutritional: Beri beri, kwashiorkor, pellagra

Diagnosis:-

1. Signs and symptoms

          a) Dyspnea:-most common symptom of heart failure. Usually exertional dyspnea is present in heart failure

          b) Acute pulmonary edema

          c) Exercise intolarence

          d)Fatigue:-it is a common compliment of patients with heart failure.Usually there any muscular fatigue present

          e) Cough

          f) Third heart sound

          g)rales

          h)elevated jugular venous pressure

          i)Oliguria and nocturia

          j)Weight loss

         k)Infection

         l)Pulmonary embolism

        m)Tender hepatomegaly

        n)Arrhythmia

       o)IV fluid overload

INVESTIGATION:

ECG

Left ventricular hypertrophy

Arrhythmia

X-RAY:

Pulmonary congestion

Cardiomegally

MANAGEMENT:

 Without drug:

   Salt restriction

   Regular exercise

   Stop smoking

  Stop alcoholism

  Vaccination against influenza virus and pneumococcal pneumonia

 Drug treatment
1. Use diuretics drug. Bumetanide 0.5 to 1mg once or twice daily. Furosemide 20 to 40mg once or twice daily.Torsemide 10 to 20mg once or twice daily

2. Use beta blockers drug (Bisoprolol, Carvedilal etc)

3. Use digoxin drug

4. Use low dose of spironolactone

ACUTE PERICARDITIS

If there is an acute inflammation in the pericardium is called acute pericarditis.

CAUSES:

   1. Viral infection: It is the most common causes of acute pericarditis.

   2. Acute myocardial infarction

   3. Other infection: Tubercular, Fungal, Pyogenic etc

   4. Rheumatic fever, Rheumatic arthritis

   5. Post-pericardial syndrome

   6. Post myocardial syndrome

   7. Uraemia

   8. Trauma

   9. Hypothyroidism

   10. Gout

   11. Drugs like Procainamide ,Hydralazine ,Reserpine etc.

   12. Neoplastic invasion

SIGNS AND SYMPTOM:

   1. Central or pericardial chest pain with radiation to neck and shoulder.

   2. Pericardial rub: High pitched, heard in systole and diastole mainly in the time of atrial systole.

   3. Fever

   4. Tachycardia

   5. Pericardial effusion

   6. Pericardial temponade

INVESTIGATION:

   1. ECG:

           §ST segment is elevated and upward concavity present

           §T wave is uprighted

           § PR interval is depressed

  2. X-ray

           Large pericardial effusion

  3. Echocardiography:

           Pericardial effusions are described as small, moderate, or large based on the size of the echo-free space between the parietal and visceral pleura on two-dimensional echocardiography.

  4. Polymorphonuclear leucocytosis

  5. Positive Montaux test in Tubercular pericarditis.

TREATMENT:

   1. Non steroidal anti inflammatory drug (NSAID) can be used to relieve pain

   2. Corticosteroid is given in severe condition

   3. If steroid is non responsive, then colchicines should be given

   4. In case of viral pericarditis Hyperimmunoglobulin(In cytomego viral pericarditis) can be used but in Coxsacike B pericarditis Interferon alpha is used.

   5. In bacterial pericarditis antibiotic should be given.

   6. In tubercular pericarditis treated with a combination of 3 or 4 tuberculostic drug for 9 to 12 months, according to standard protocols.

   7. Uraemic pericarditis—responds within 1 to 2 weeks to dialysis.

CARDIOGENIC SHOCK

Shock may be defined as inadequate tissue perfusion due to absolute or relative decrease of blood volume. It is the final pathway for several lethal clinical events, including severe hemorrhages extensive trauma or burns, large myocardial infarction, pulmonary embolism and myocardial sepsis.

Types of shock:

   1. Cardiogenic shock

   2. Hypovolemic shock

   3. Septic shock

Cardiogenic shock:

It results from low cardiac output due to failure of cardiac muscle (myocardium) to pump. It can be due to intrinsic to myocardial damage (infarction), ventricular arrhythmias, extrinsic compression (cardiac temponade) or outflow obstruction. Shock in acute myocardial infarction occurs when the left ventricle fails to perform its pumping function. However it may also occur due to right ventricular failure and variety of complication including temponade, an acquired ventricular septal defects and acute myocardial regurgitation. Severe systolic dysfunction of heart muscle, cause a fall in cardiac output. We know the equation is that:_

          BLOOD PRESSURE=CO (cardiac output) * TPR (total peripheral resistance)

So when cardiac output decrease there is also fall in blood pressure and thereby coronary perfusion pressure. When diastolic dysfunction occur it cause a rise of left ventricular diastolic pressure, pulmonary congestion, edema and hypoxia which in turn worsen myocardial ischaemia. In cardiac temponade there is also decrease cardiac output and shock occurs.

SIGNS AND SYMPTOM:

   1. Hypotension

   2. Tachycardia

   3. Cold, clammy skin

   4. Rapid shallow breathing

   5. Decrease volume of urine and sometimes anurea

   6. Myocardial depression

   7. Confusion

   8. Intracerebral bleeding

TREATMENT OF SHOCK:

Stage 1: General measure:-

   §Analgesia

   §Oxygen via MC mask or ventilation if necessary

   §Insertion of monitoring lines:-Swan-Gang catheter introduced, redial artery canulation

Stage 2:      Correction of filling pressure:-

As soon as Swan-Gang catheter is in situ, attempts are made to get the LVEDP/PAW PRESSURE TO 16 TO 18 mmHg. This is the optimum filling pressure.

a. Filling pressure too high-

  With normotension (aortic pressure >90 mmHg)_ Vasodilators is used to keeping mean aortic pressure>70mmHg.

With hypertension:-Dopamine 5 to 10 microgram/Kg/min

b.Filling pressure too low_

Often caused by combination of right ventricular infarction and hypovolaemia due to a reduced oral intake of fluids, vomiting and inappropriate diuretic therapy. These patients are managed by IV fluid therapy.

Stage 3: Improvement of stroke volume:-

Inotropes are usually required. Dopamine should be initiated promptly to raise mean arterial blood pressure and be maintained at the minimum dose required. Dobutamine may be combined with Dopamine at moderate dose or used alone for a low output state without frank hypertension. Both Dopamine and Dobutamine have their advocate.

Stage 4: Early definition of coronary anatomy:-

   Coronary angiography

Stage 5: Further measures:-

  Support by Intra aortic ballon pumping (IABP) while arrangements are being made for further measures. IABP can now be inserted precutaneously. The R wave of the ECG triggers balloon deflation. The balloon is timed to inflate just after the dicrotic notch of aortic valve closure. Inflation increase coronary cerebral flow. Hilium is used as inflation gas.

Tetralogy of Fallot

Tetralogy of Fallot described by Fallot in 1988.It has four feature:-

   1. Pulmonary stenosis

   2. VSD (ventricular disease)

   3. Overriding of aorta

   4. Right ventricular hypertrophy

There is a failure of the bulbus cordis to rotate properly so that the aorta lies more anterior to the right (dextroposed) than normal. The aorta moves nearer to the tricuspid valve and overrides the septum with a “malignment” VSD beneath the aortic valve. Infundibular stenosis develops ,with hypertrophy of the septal  and parietal bands of infundibular muscle that form part of crista.Obs6truction of  right ventricular outflow is usually due to combination of infundibular  and valve stenosis, but may be either alone.

This is the most common cyanotic congenital heart disease presenting after 1 year

Diagnosis

History/Symptom:

§ Increased cyanozed after crying or feeding

§  Dyspnoea on exertion

§ Paroxysmal hypercyanotic attacks(Fallot’s spellor bluve spell)-Patient goes on squatting position (knee elbow position) during crying, playing & after feeding to relieve Fallot’s spell is called Fallot’s sign’s.

§ Growth and development failure

§Patient may become apnoeic of unconscious

§ Delayed puberty

On examination:

a.     On general exam: Short of stature

§ cyanosis

§ Congested red eyes

HEART

§ Polycythaemia

§ Clubbing

b.     Systemic examination:

Precordial Examination:

§ Right ventricular heave/ left parasternal heave-present

§ Systolic thrill felt along the left sternal edge in 3^rd on 4^th intercojfal space.

§ First heart sound is normal

§ Second heart sound is either soft or single

§ Loud ejection systolic murmur in the pulmonary area (Due to pulmonary stenosis)

(iii) Investigation:

(a)   Blood (Routinely):

§ Hb%: Increased

§ PCV-Increased (Polycythaemia)

§ Full Blood count (FBC)

§ ESR-Reduced

§ Peripheral Blood film: Immature RBC

(b)Diagnostic

X-ray chest:

§ Boot shaped heart with normal transverse diameter

§ Small pulmonary artery

ECG:

§ Evidence of RVH

§ Evidence of right axis deviation

Echocardiography-diagnostic (To find 4 components of Fallot’s teratology) § Cardiac cheterization

B. Treatment:

i) Medical treatment:

(a) Treatment of cyanotic attack

§ Patient should be propped up position on patient goes on squatting position (knee elbow position)

§ 02 should be given

§ Propranolol is given

§ Decreased agitation by giving pathediane injection 1-2 mg/kg 1M

§ Correction of acidosis by NaHCO₃ (8.5%) IV

b.Maintenance of hydratias: Intake of large amount of fluid

c. Iron & vit-B complex supplementation.

d. Prophylaetic antibiotic for infective endocarditic.

(ii) Surgical treatment: Correction should be done before 5 years.

(a) Palliative shunt procedure: Anastomosis between pulmonary & systemic circulation.

§ Black Taussing’s shunt

§ Warson’s shunt

§ Pot’s shunt

(b)Total corrective surgery:

Total correction of the defect by surgical relief of pulmonary stenosis & closure of the VSD.