Snake bites

     A nonvenomous (nonpoisonous) snake bite is a bite or puncture wound made by a snake that is incapable of secreting a toxin. This should be distinguished from a dry bite. A dry bite is a bite by a venomous snake that does not inject any toxin. Even bites that are from a nonvenomous snake or are dry need to be evaluated as they can lead to significant tissue damage or infections.A venomous (poisonous) snake bite is a bite or a puncture wound made by a snake that is capable of injecting, secreting, or spitting a toxin into the penetrated skin wound, mucus membranes or the eyes where the toxin can be absorbed.this is is a medical emergency as they can be deadly if not treated quickly.

Diagnostic investigations

1. History -Time and place of definite or possible exposure to a snake.
2. Description of a snake, if seen (colour, size).
3. Number of times bitten (multiple bites are usually more severe
4. Prothrombin time and INR
5. CBC and peripheral blood smear
6. Serum electrolytes
7. Serum BUN and creatinine
8. ABGs
9. Fibrinogen and its products
10. Chest radiograph- to determine pulmonary oedema
11. Urinalysis to monitor for health of kidney and presence of myoglobin

Management 

    There are many aspects to effective treatment of snakebite. They start with a correct approach to managing envenoming cases. There are urgent measures that may be needed. For significant envenoming, anti-venom is generally the treatment of choice.

1. Check the patient's airway for patency, normal breathing and adequate circulation
2. Intubate if the airway begin to become swollen and narrowed
3. Immobilize patient's body part 
4. Monitor vital signs
5. Insert large-bore IV cannula
6. Oxygen therapy
7. Grade the severity of effect of snakebite venom (mild, moderate and severe)
8. Antivenin (CroFab)
• Administered within 4-6 hours after the snakebite
• Can cause either anaphylaxis or serum sickness
• Binds the toxins in the venom to neutralize and reduce its damaging effects
9. Antibiotics (Cephalosporin show benefit in most severe cases)
10. Immunization (Diptheria tetanus toxoids since snakebite can carry different types of bacteria)
11. Fasciotomy is carried out if there is increased compartmental pressure, in order to prevent compartment syndrome.

References

• Gold, Barry S., and R. A. Barish. "Venomous snakebites. Current concepts in diagnosis, treatment, and management." Emergency medicine clinics of North America 10.2 (1992): 249-267.
• Jerry R. Balentine, F. (2015). Snakebite: Learn First Aid Procedures and Treatment. [online] eMedicineHealth. Available at: http://www.emedicinehealth.com/snakebite/article_em.htm [Accessed 27 Apr. 2015].
• Jacob L. Heller, a. (2015). Snake bites: MedlinePlus Medical Encyclopedia. [online] Nlm.nih.gov. Available at: http://www.nlm.nih.gov/medlineplus/ency/article/000031.htm [Accessed 28 Apr. 2015].

CARDIAC ARREST

Cardiac arrest is the sudden loss of cardiac function, when the heart abruptly stops beating. A person whose heart has stopped will lose consciousness and stop normal breathing, and their pulse and blood pressure will be absent. Unless resuscitative efforts are begun immediately, cardiac arrest leads to death within a few minutes. This is often referred to by doctors as "sudden death" or "sudden cardiac death (SCD)."

Differentiating CARDIAC ARREST  and HEART ATTACK

Causes

Adults 

1. Cardiac diseases 
• Ischemic heart disease
• LV impairement
• Electrical abnormalities (Long QT syndrome)
• Congenital heart disease
• Valvular disease  
• Cardiomyopathy
2. Pulmonary embolism
3. Aortic dissection
4. Gastrointestinal hemorrhage
5. Respiratory failure
6. Metabolic disturbance (e.g. drug overdose)

Children 

1. Poisoning
2. Diseases of the respiratory system
3. Trauma

Investigations

1. Cardiac biomarkers (troponin and CK-MB)
2. Serum electrolytes (severe alterations can increse risk of arrythmias)
3. Drug levels above the normal therapeutic values may increase arrythmic effect (e.g. TCAs, quinidine and digoxin)
4. Toxic screening (for toxins that can induce vasospasmic ischemia)
5. Brain natriuretic peptide (BNP)
6. ECG monitoring
7. Coronary angiography (help determine patients who can benefit from revascularisation procedures)
8. TSH (hyperthyroidism can lead to tachycardia)

MANAGEMENT

1.      Remove any possible danger to the patient.

2.      Check whether the client is responsive. Ideally for this the clients shoulders should be held and shake to see the response. Or else can compress xiphoid process to see whether the client is responsive.

3.      If outside the hospital call the ambulance. If within the hospital inform the cardiac arrest team or the relevant professionals.

4.      Then asses the airway. Check for patency and any obstruction. If there is any obstruction remove.

5.      Then asses breathing. Generally ones in cardiac arrest will show no breathing or will be extremely low. For clients who are not responsive and who are responsive but with abnormal breathing CPR should be given.

6.      If it is outside the hospital and an automated external defibrillator is available deliver one shock as instructed by the device and then start CPR.

7.      Start chest compressions with placing the heel of one hand on the chest of the patient and the other covering it. Keep the elbows straight and compress with the upper body weight at a rate of 100 compressions a minute.

8.      If outside the hospital, do 30 compressions at the above mentioned rate and tilt the head to open the airway and asses the breathing for 10 seconds. If no breathing, give 2 rescue breaths and repeat chest compressions. This cycle, 30 compressions and 2 rescue breaths, should be continued until the patient is taken to the hospital. If within the hospital chest compressions are done continuously as an ambu bag can be used to give rescue breaths continuously with assistance.

9.      CPR should be continued until the victim recovers or the medical emergency personnel take over.

At the emergency department the client should be stabilized, assessed and treated for the cause. Sometimes the clients will require intubation. Usually defibrillation is done right after by giving shocks to get back the heart rhythm normal. Treatments may include antiarrhythmic drugs, implantable cardioverter defibrillation, angioplasty or a CABG depending on the cause.  

 References

• American Heart Association 2014, 'About Cardiac Arrest', retrieved 26 April 2015, <http://www.heart.org/HEARTORG/Conditions/More/CardiacArrest/About-Cardiac-Arrest_UCM_307905_Article.jsp>
• Mayo clinic 2015, ' Sudden cardiac arrest', retrieved 26 April 2015, <http://www.mayoclinic.org/diseases-conditions/sudden-cardiac-arrest/basics/symptoms/con-20042982>
• O'Connor, R.E. 2015, 'Cardiac arrest', retrieved 26 April 2015, <http://www.merckmanuals.com/professional/critical-care-medicine/cardiac-arrest/cardiac-arrest>
• Sovari, A.A. 2014, 'Sudden Cardiac Death', retrieved 26 April 2015, <http://emedicine.medscape.com/article/151907-overview#aw2aab6b2b2aa>
• Jameson, J. N. St C.; Dennis L. Kasper; Harrison, Tinsley Randolph; Braunwald, Eugene; Fauci, Anthony S.; Hauser, Stephen L; Longo, Dan L. (2005). Harrison's principles of internal medicine. New York: McGraw-Hill Medical Publishing Division.

 

Supraventricular tachycardia (SVT)

      Supraventricular tachycardia (SVT) is a cardiac arrhythmia arising from improper electrical activity of the heart. It is a type of tachycardia (rapid heart rhythm) originating at or above the atrioventricular node. It can be contrasted with the potentially more dangerous ventricular tachycardias—rapid rhythms that originate within the ventricular tissue.Its mainly caused by re-entry mechanism.reentry means, "the circular propagation of an impulse around 2 interconnected pathways with different conduction characteristics and refractory periods". In SVT the heart rate goes high by any abnormal electrical impulse originated in the atria. In this the heart beats so rapidly so that the heart muscles does not relax adequately in between each contractions. When the heart chambers do not relax adequately, they may not contract properly or fill with enough blood adequate for the whole body pumped out by the next beat. Especially when the oxygen demand is high when the body is in action or the mind is in stress.

Common types of  SVT

Presentation

1. Palpitation    
2. Dizziness
3.  Shortness of breath
4.  Syncope
5. Chest pain
6. Fatigue
7. Diaphoresis
8.  Nausea  

      

       Diagnostic investigations 

              

              

1. ECG- help to determine tachyarrythmic classifications 
• Sinus tachycardia- HR more than 100bpm
• atrial tachycardia- more than 125bpm with long RP wave
• atrial flutter- between 200-300bpm
• atrial fibrillation- irregularly regular and no P waves)
2. Cadiac biomarkers
3. Serum electrolytes
4. Complete blood count
5. Chest X-ray 
6. Transthoracic echocardiography

Management

Short-term
Adenosine (Adenocard)	V: endogenous purine nucleotide	Terminates SVT	6 mg rapid intravenous push, repeat with 12 mg if needed	Can be diagnostic and therapeutic
				Extremely short half-life
				Adverse effects include chest pain and dyspnea during administration
				Contraindicated in patients with Wolff-Parkinson-White syndrome
Diltiazem	IV: calcium channel blocker	Decreases rate	0.25 mg per kg intravenous bolus	Adverse effects include dizziness, heart failure exacerbation
				Avoid in patients with Wolff-Parkinson-White syndrome or wide complex tachycardia
Esmolol (Brevibloc)	II: beta blocker	Decreases rate	500 mcg per kg intravenous loading dose	Can be proarrhythmic; has short half-life
				Avoid in patients with renal disease; use with care in patients with asthma
Verapamil	IV: calcium channel blocker	Decreases rate	5 mg intravenously, up to 15 mg	Avoid in patients with congestive heart failure, Wolff-Parkinson-White syndrome, wide complex tachycardia, or atrioventricular block (second or third degree)
Long-term
Amiodarone(Cordarone)	III: potassium channel blocker*	Prevents SVT	200 to 400 mg orally once daily	Can result in optic neuritis, thyroid dysfunction, pulmonary fibrosis
Disopyramide (Norpace)	Ia: sodium channel blocker*†	Prevents SVT	200 to 400 mg orally twice daily	Adverse effects include urinary retention
Metoprolol	II: beta blocker	Decreases rate	25 to 100 mg orally twice daily	Atrioventricular node suppression possible
Procainamide	Ia: sodium channel blocker	Prevents SVT(long-term use)	250 to 500 mg orally every six hours	Adverse effects include lupus, hypotension, His-Purkinje block
Quinidine	Ia: sodium channel blocker*†	Prevents SVT(long-term use)	324 to 648 mg orally every eight to 12 hours	Avoid in patients with atrial fibrillation because of increased mortality
				Closely monitor QTc interval when initiating therapy
Verapamil	IV: calcium channel blocker	Prevents SVT	80 to 240 mg orally three times daily	Adverse effects include constipation, dizziness
				Avoid in patients with Wolff-Parkinson-White syndrome or wide complex tachycardia

---

Long-term Management of SVT

       References 
       

• Klein, G.J., Sharma, A.D., Yee, R. & Guiraudon, G.M. 1987, 'Classification of supraventricular tachycardias', Am J Cardiol., vol. 60, no.6, pp. 27D-31D.
• Levy, S. & Ricard, P. 1997, 'Using the right drug: a treatment algorithm for regular supraventricular tachycardias', Eur Heart J, vol. 18, Suppl C, pp. C27-32
• Mitchell, L.B. 2015a, 'Reentrant Supraventricular Tachycardias (SVT, PSVT)', retrieved 28 April 2015, <http://www.merckmanuals.com/professional/cardiovascular-disorders/arrhythmias-and-conduction-disorders/reentrant-supraventricular-tachycardias-svt-psvt>
• Mitchell, L.B. 2015b, 'Overview of arrythmias', retrieved 28 April 2015, <http://www.merckmanuals.com/professional/cardiovascular-disorders/arrhythmias-and-conduction-disorders/overview-of-arrhythmias#v936668> 

       

      

Acute Left Heart Failure

Heart failure is defined as an inability of the heart to deliver blood at a rate required by metabolising tissues despite normal filling pressures.

CARDIAC HAEMODYNAMICS

Cardiac Output (CO) is the volume of blood expelled  by the ventricles in a minute. Its around 5 – 7 litres although in LVF this will be reduced.
Factors determine cardiac output
Preload: the pressure that fills the ventricles during diastole(when the ventriles relax)
Afterload: resistance to flow in the arterial tree against which the heart must work.
Contractility: refers to the muscular pumping ability of the ventricles.


CAUSES OF ACUTE LVF

· Volume overload
· Drugs e.g. beta blockers, cocaine
· Infection e.g. Myocarditis
· Ischaemic Heat Disease / Myocardial Infarction
· Hypertension
· Aortic Stenosis
· Pathophysiology

In LVF the cardiac output is reduced e.g. secondary to an acute Myocardial Infarction. Failure of the ventricles to eject blood results in increased intracardiac pressures and pulmonary capillary pressure.

CLINICAL PRESENTATION
· Cough
· Crepitations - after coughing
· Hypoxia & cyanosis
· Sweating
· Tachycardia
· Fatigue / reduced exercise tolerance
· Dyspnoea
· Frank pulmonary oedema
· Paroxysmal nocturnal dyspnoea

Investigations

Following can be identifeid therough x-ray
· An enlarged heart
· the lungs will appear whiter often with a typical ‘bats wing’ distribution of oedema
· Dilated pulmonary capillaries and upper lobe diversion

Endomyocardial biopsy- recommended test to be carried out if the patient has deteriorating clinical HF despite appropriate treatment
Cardiopulmonary stress test- to test the patient's functional capacity (6 minute walk which evaluate factors such as distance, dyspnea index and the patient's vital sign changes)


Complete blood count (CBC)- to determine cause of HF
Urinalysis
Coronary arteriography
Doppler ultrasound scan
Cardiac MRI
Left-sided cardiac catheterization and coronary angiography- used when the cause of HF cannot be determined using other methods
Serum electrolytes- can be affected due to fluid shifts
BUN and serum creatinine- confirm reduced kidney perfusion
Fasting blood sugar
Liver function test- evaluate the effect of HF on the liver
BNP levels which will rise due to H





MANAGEMENT 

Immediate management consists of :
Morphine IV as required Inoder to relive anxiety but may also reduce preload and afterload Oxygen
Supplemental oxygen- noninvasive positive pressure ventilation (NIPPV)

Drug therapy:

Diuretics: help by reducing circulatory volume and thereby reducing preload. An intravenous loop diuretic such as Frusemide is administered in the first instance
Venodilators: an intravenous infusion of Glceryl Trinitrate may be useful in reducing preload and afterload and may also improve coronary blood flow. Caution must be exercised in patients who are hypotensive
Inotropic drugs: these drugs are used to increase myocardial contractility and output. They are often classified according to their activity at alpha and beta receptors.
Drugs with mainly alpha activity will:
· increase afterload
· increase blood pressure
· slow pulse rate
Drugs with mainly beta activity will:
· reduce afterload
· increase pulse rate and cardiac output
Dobutamine (Dobutrex)
Exerts its effects on beta1 and beta 2 receptors and thereby Increases myocardial contractility and output. It has no renal (dopaminergic) effects.
The standard dose is 2.5 - 20 micrograms per KG per minute by continuous intravenous infusion
Dobutamine does exert chronotropic effects and it may increase myocardial oxygen consumption and aggravate angina
Side effects include:
· ventricular arrhythmias tachycardia
· hypokalaemia
· Angina

Implantation of cardioverterdefibrilators and coronary artery bypass graft.

References

1. American Heart Association. Classes of heart failure. Available athttp://www.heart.org/HEARTORG/Conditions/HeartFailure/AboutHeartFailure/Classes-of-Heart-Failure_UCM_306328_Article.jsp. Accessed September 6, 2011.
2. [Guideline] Hunt SA, for the Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. Sep 20 2005;46(6):e1-82. 
3. [Guideline] Dickstein K, Cohen-Solal A, Filippatos G, et al. for the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). Eur Heart J. Oct 2008;29(19):2388-442. 
4. [Guideline] Lindenfeld J, Albert NM, Boehmer JP, et al, for the Heart Failure Society of America. Executive summary: HFSA 2010 comprehensive heart failure practice guideline. J Card Fail. Jun 2010;16(6):e1-194.