Smoking cessation should be regarded as a holistic treatment method, be it with nicotine replacement therapy, electronic nicotine delivery devices and prescription medication.
Tobacco smoking is the most significant cause of premature death, causing almost 700,000 yearly deaths. Smoking causes cancer, heart disease, ischaemia, lung diseases, diabetes, and chronic obstructive pulmonary disease (COPD), which includes emphysema and chronic bronchitis. It also increases risk for tuberculosis, eye diseases, and problems within the immune system, including rheumatoid arthritis.
Behaviour change techniques should be based on providing clear and concise understanding regarding all factors involved in smoking and smoking cessation. According to The National Centre for Smoking Cessation and Training (NCSCT), health practitioners should ask ALL patients whether they smoke or not. If a patient smokes, advice should be given on how to quit, as well as a point of reference on behavioural support and prescription medication.
Smoking is an addiction prone to relapse, with many going through multiple attempts to stop smoking before doing so successfully. Behavioural support should be combined with nicotine replacement therapy and/or medication so as to increase the chance of successfully quitting.
Below you can find a collection of videos that can help provide a more visual approach to smoking cessation nicotine replacement therapy, ENDDs including e-cigarettes and prescription medication.
Smoking Cessation
Nicotine Replacement Therapy
Electronic Nicotine Delivery Devices
Bupropion (Zyban) and Varenicline (Champix)
Special thanks to the creators of the featured videos on this post, specifically Youtube Channel Portico Network.
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Approximately a third of all deaths can be attributed to cardiovascular disease (CVD), making it the leading cause of morbidity and mortality worldwide. 72% of these deaths can be attributed to poor diet, making cardiovascular health nutrition a very important factor to reducing cardiovascular disease.
While low calorie diets can be helpful in improving overall health, long term calorie restriction is usually difficult to adhere to.
Dehydration happens when there is negative fluid balance in the water due to a decrease in water consumption, increased fluid loss or fluid shifts.
Over-Hydration happens when there is an increase in the extracellular fluid in the body (ECF), usually causing oedema.
In cardiovascular health nutrition, fatty acids (for lipoprotein levels), minerals (for blood pressure), vitamins and fiber are the most important nutrients.
Avoid…
Sugar Sweetened Beverages: associated with body weight increase as well as increased effects on fat deposition, lipid metabolism, blood pressure, sensitivity to insulin and lipogenesis.
Added Sugars: sucrose, fructose and such sugars (mostly found in sugar sweetened beverages) have been associated with an increased risk of cardiovascular disease due to lowered high density lipoprotein cholesterol, increased plasma triglyceride concentration and increased blood pressure.
Coffee: more than 8 cups per day may increase blood pressure drastically.
Alcohol: studies show that consuming one to two drinks per day has no negative impact on cardiovascular health. Moderate alcohol intake can be attributed to an increase in high density lipoprotein cholesterol, apolipoprotein A1, adiponectin and decreased fibrinogen levels. Heavy drinkers however show an increased risk of cardiovascular disease when compared to moderate drinkers.
French Fries: associated with an increased risk of hypertension, diabetes (type 2) and coronary heart disease.
High GI Diet: associated with an increase risk of coronary heart disease.
Processed Meat: attributed to an increase in cardiovascular disease risk and mortality.
Red Meat: high consumption may lead to a significant increase in blood pressure, oxidative stress, lipid peroxidation and negative changes within the gut microbiome.
Sodium: high intake is attributed to an increase in blood pressure. Reducing sodium by 1g per day accounts to a reduction in the systolic blood pressure by 3.1mmHg in hypertensive patients.
A = Anthropometric: measuring body composition – weight and height, BMI, circumferences, skinfolds. If further info is required, Bioelectrical Impedance Analysis (BIA), Dynanometry (hand grip), Hydrodensinometry, and DEXA scan.
B = Biochemical Data: help detect early changes in metabolism and nutrition prior to clinical signs onset – blood tests, haemoglobin, urine and stool sample testing, kidney function test, liver function test, cholesterol and lipids (triglycerides), blood sugar, scrapings and biopsy samples.
C = Clinical Exam: patient history, drug history and risk assessment, food intake, conditions affecting digestion, absorption and excretion of nutrients, as well as emotional and mental health.
D = Dietary Assessment: diet history, food frequency questionnaire, and food diary.
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Acute coronary syndrome refers to a range of conditions associated with sudden reduced blood flow to the heart. Such conditions include:
STEMI – a very serious MI during which one of the heart’s major arteries is more than 70% blocked. An ST segment elevation is an abnormality detected on the 12-lead ECG in STEMI. Treat immediately!
NSTEMI – non-ST elevation MI: may progress to STEMI so treat with importance.
MINIMAL MYOCARDIAL NECROSIS – cardiomyocytes cell death related to irreversible myocardial injury.
UNSTABLE ANGINA – experiencing pain even when resting (may progress to STEMI if undiagnosed or not treated in time).
STABLE ANGINA – experiencing pain during exacerbating physical activity.
Vulnerable Plaque – eg. Statin therapy causes plaque to become vulnerable
Inflammatory Cytokines
Emotional Stress – can change the physiological status of the body through high BP, increased heart rate etc.
Physical Stress – strenuous exercise in unfit individuals
Plaque Rupture – thin fibrous cap with lipid beneath makes plaque susceptible to rupture
Myocardial injury extent depends on facturs such as the oxygen demand of the affected tissue, tissue response (younger individuals usually respond better and deal in a better way with an MI than older individuals), rate of flow etc.
Myocardial Infarction Symptoms
pain, pressure and heat sensation usually in the chest area but possibly radiating to the jaw, back, left arm or both arms;
sweating, clammy cold skin, tachycardia
weakness, nausea and vomiting
mild fever
dyspnoea
NOTE: an individual may experience a MI but still be asymptomatic!
Diagnosis of an Acute MI
Obtain information directly from patient; ask questions regarding family history (parents or siblings), degree of pain, how it all started, etc.
Assess symptoms to make sure they are coronary-related
Monitor for ECG changes: check for signs of Ischaemia and MI
Monitor Troponin I & T (absent in healthy individuals, rise 3-4hrs after a MI and peak at 18-36hrs before declining slowly within 10-14 days)
Monitor Creatinine Kinase (CK): injury to the heart is marked as an elevation in CK; CK-MB rises 4-8hrs post MI and peak by 24hrs before returning to normal in 48-72hrs; a 2nd CK-MB indicates a re-infarction (can be noticed easier as CK-MB returns to normal quicker)
Acute Coronary Syndrome Treatment
Morphine: decrease anxiety and pain associated with ACS
Oxygen: monitor SP02 and administer Oxygen on demand
Cardiogenic shock is caused by either a massive Myocardial Infarction or a valve issue. If a patient presents with a prominent jugular vein, low blood pressure and high heart rate consider as emergency…monitor closely!
Below you can find a collection of videos that can help provide a more visual approach to Acute Coronary Syndrome.
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Through cardiac pacing a pacemaker delivers an electrical impulse to a chosen part within the myocardium with the aim of causing depolarisation. This leads to the spreading of the action potential to all parts within the heart.
Pacemakers are able to monitor the natural pacemaker of the heart (SA Node). If this is fully functioning, the pacemaker lets it work uninterrupted, but if or when needed, the pacemaker paces.
Pacemakers are considered to be anti-bradycardia devices. They are individually programmed so as not to fall below a certain heart rate, allowing a low heart rate momentarily so that it is recorded into the patient’s device statistics.
Some pacemakers are also able to defibrillate so as to restart the electrical rhythm of the heart to a sinus rhythm.
RA Appandage = paced P-wave resembling normal activity P-wave
RV Apex = paced QRS complex that is usually prolonged with a following wider looking T-wave
CSL Coronary Sinus Lead = implanted into the LV. A third lead benefits cardiac output by correcting and syncronising both left and right ventricles
Temporary Cardiac Pacing
Temporary pacing is used in emergency settings such as on patients experiencing ventricular bradyarrhythmias, post cardiac surgery (when the patient is susceptible to tachyarrhythmias so temporary pacing can be available immediately on demand with low sensitivity), and whilst undergoing evaluation for a permanent pacemaker.
Pacemakers are able to:
pace – at a fixed rate (asynchronous) independently of intrinsic cardiac rhythm OR on demand – only if intrinsic cardiac rhythm is absent
sense – they are considered to be anti-bradycardia devices since they can sense if the heart rate falls below their programmed lower rate, and in that case, pace
NOTE: a TPM (temporary pacemaker) malfunction, including battery failure, falls under the responsibility of the nurse! Thus, ensure proper checking of equipment, battery, threshold, and that leads and connection points are secured well.
Transcutaneous Cardiac Pacing (Temporary)
Transcutaneous pacing = used in emergency settings as a short term pacing method, easily set up by nurses with an AED device. A spike can be captured to mechanically function the heart temporarily. Although it’s quite a quick pacing method, it is not always tolerated by the patient, and may also be unstable.
Retrieved from https://cardiovascmed.ch/article/doi/cvm.2018.00554 on 9th January 2023
Transvenous Cardiac Pacing (Temporary)
Transvenous pacing = a reliable pacing method that is more tolerated than the transcutaneous method by patients, established within 10-30 minutes by a physician. Transvenous pacing is done via the axillary-subclavian vein or the femoral vein in Endocardial Pacing, or via the axillary-subclavian vein in Epicardial LV Pacing.
may induce ventricular tachycardia
abdominal twitching (voltage should be checked and possibly lowered)
infection may be possible especially if wire is left more than 48 hours in situ (transparent dressings should be used for possible infection monitoring)
perforation of the myocardium whilst advancing wire into the heart
pneumothorax – puncturing of the lungs (may be confirmed by x-ray)
Permanent Cardiac Pacing
Permanent pacing = a fully programmable device implemented through elective surgery.
note pacemaker settings and compare with ECG recordings
ensure that all spikes are followed by a P and/or QRS complex
monitor for pacemaker malfunction – ensure it is both capturing and sensing as it should
monitor route of insertion for bleeding, haematoma formation, and signs of infection – measure the patient’s body temperature every 4 hours
monitor white blood cell count which should be within normal range (5000-10000/mm3)
NOTE: report to cardiologist if malfunction is noted.
Patient Education
When using a temporary pacemaker, patient should remain in bed. Area from where the lead has been inserted should remain immobilised, as if mobilised, lead may become easily displaced. Patients should also restrict activity on the implantation side. Mobile devices should be used on the opposite side of the pacemaker implantation. Patients should keep their 6 monthly or yearly appointments as required. A pacemaker’s battery life is usually between 6-20 years, depending on its use.
Prior to being discharged, ensure that the patient knows how to look for signs and symptoms of infection and when to seek medical attention, and is aware of how to avoid electromagnetic interference.
Whilst nursing a patient with a pacing box, it is important to check the wires for any loose points and to monitor the battery.
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Anti-arrhythmic drugs are used to manipulate how the electrical impulses of the heart are generated and conducted, to restore cardiac rhythm to normal where needed, as well as to effect the cardiac cells’ action potential in changing their impulse initiation and conductivity. Unfortunately, most anti-arrhythmic drugs can aggravate or cause new arrhythmias.
The phrase cardiac action potential (AP) refers to the change in voltage across the cell membrane of cardiac cells caused by the movement of ions between the inside and the outside of the cell through ion channels. An action potential happens when different ions cross the neuron membrane.
There are 5 phases in a Cardiac Action Potential:
Phase 4 – resting phase a.k.a. resting membrane potential (when the heart is into diastole)
Phase 0 – opening of the fast sodium channels causing sodium to move into the cell
Phase 1 – initial rapid repolarisation: when fast sodium channels close
Phase 2 – plateau phase caused by calcium moving in and potassium moving out (ST segment in an ECG)
Phase 3 – repolarisation: potassium channels stay open allowing potassium to move out and repolarise the cell; when membrane potential reaches certain level, potassium channels close (T-wave on ECG)
Anti-Arrhythmics, which are classified according to the Vaughn Williams classification, are organised into 4 major classes:
CLASS 1 AGENTS: Fast sodium channel blockers (affect the depolarisation phase)
CLASS 2 AGENTS: Beta-blockers (affect depolarisation)
CLASS 3 AGENTS: Potassium channel blockers (reduce potassium current during the repolarisation phase)
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ECG Arrhythmias (a.k.a. non-sinus rhythm) can be quite difficult to distinguish. As a starting point it is always ideal to identify the QRS complex and its rate (in relation to the ventricles), identify the P wave and its rate (in relation to the atria), and the relationship between the P wave and the QRS complex.
Identifying ECG Arrhythmias
STEP 1: The Ventricle
is the heartbeat FAST (>100bpm) or SLOW (<60bpm)?
is it REGULAR or IRREGULAR? can you hear any extra beats?
is it NARROW <120ms) or WIDE (>120ms)
STEP 2: The Atrium
focus on the P wave in the II and VI ECG lead reading
note the rate
note the morphology
Step 3: The Relationship between the Ventricle and the Atrium
is there any relationship between the P Wave and the QRS Complex?
is every P Wave followed by a QRS Complex?
is every QRS Complex preceded by a P Wave?
what is the ratio of P:QRS?
can you note an AV dissociation where the atria and ventricles beat independently of each other?
determine the PR interval – does it change?
determine the RR interval – does it change?
Normal Sinus Rhythm
A normal sinus rhythm features a good relationship between the ventricles and the atria, with a heart rate between 60-100bpm.
Bradycardia
Bradycardia presents with a heart rate of less than 60bpm.
Tachycardia
Tachycardia presents with a heart rate of over 100bpm; may present as:
NARROW COMPLEX, REGULAR OR IRREGULAR:
Regular Tachycardia: sinus tachycardia OR atrial flutter
Irregular Tachycardia: atrial fibrillation with no P Waves OR atrial flutter with variable AV conduction
WIDE COMPLEX, REGULAR OR IRREGULAR:
Regular Tachycardia: sinus tachycardia (VT with aberrant conduction)
Atrial Fibrillation presents with absent, very hard to identify P wave, indicating issues within the atrial chambers functionality.
Ventricular Tachycardia presents with an absent P wave, high heart rate, and with a wide and somewhat weird-looking QRS complex.
Retrieved from https://www.grepmed.com/images/12601/tachycardia-narrow-differential-cardiology-diagnosis on 9th January 2023
AV Block
1° AV Block = Delayed Block – PROLONGED but CONSTANT PR interval (>200ms) + P wave with every QRS complex.
2° AV Block Mobitz Type 1 a.k.a. Wenchenbach = Intermittently Blocked – PROGRESSIVELY LENGTHENING PR intervals until a P Wave fails to conduct, leading to a DROPPED QRS complex (missed beat); next cycle restarts with a normal PR.
2° AV Block Mobitz Type 2 = Intermittently Blocked – P waves NOT ALWAYS FOLLOWED by QRS complex + CONSTANT NORMAL or PROLONGED PR interval.
High Grade AV Block = Intermittently Blocked – consecutive P Waves are not followed by QRS complex + CONSTANT NORMAL or PROLONGED PR interval.
High Grade AV Block (right) – Retrieved from https://www.youtube.com/watch?v=uzMdL2HFEZY on 9th January 2023
3° AV Block = Completely Blocked – NO RELATIONSHIP a.k.a. dissociation BETWEEN P wave and QRS complex; PR interval is different with each beat and P Waves are usually faster than QRS complexes.
The Escape Rhythm
In complete heart block (3° AV Block), the heart functions through the:
Junctional escape beating @ 40-50bpm indicating block in the AV node;
Ventricular escape beating @ 20-40bpm indicating block in the His-Purkinje site. This is unreliable and results in asystole.
Ventricular Fibrillation happens when the ventricles fibrillate without prefilling, pushing no blood volume out to circulation = no cardiac output. This is a SHOCKABLE RHYTHM.
Asystole presents with an absence of electrical impulses as an almost flat line on an ECG. Prior to this rhythm, the patient may present with agonal breathing. CPR should be performed. Asystole is NOT A SHOCKABLE RHYTHM.
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An ECG is a ‘snapshot’ of the electrical activity of the heart presented on a graph. When interpreting ECG one can note the heart rate and rhythm, normal/abnormal conduction of both the atria or ventricles, structural changes within the heart such as atrial or ventricular enlargement, as well as an indication of a past Myocardial Infarction.
ECG Principles
The ECG’s value is magnified when recorded during a stress test eg. when the patient is running on a treadmill, or when recorded for a long period of time as in with a Holter.
The pumping action of the heart:
DEPOLARISATION – is initiated by an electrical activation of the myocardium
AUTOMATICITY – causes heart action
EXCITABILITY – responds to the electrical impulse
CONDUCTIVITY – conducts an electrical impulse
CONTRACTILITY – initiates contraction
Repolarisation in an ECG acts as an indication for diagnosis of ischaemia, myocardial stretch, pharmacological effects, electrolyte imbalance, and congenital ionic diseases able to cause a sudden cardiac arrest and imminent death.
Motor Unit Action Potential showing Depolarization, Repolarization and Resting Potential – Retrieved from https://www.researchgate.net/figure/Motor-Unit-Action-Potential-showing-Depolarization-Repolarization-and-Resting-Potential_fig2_340126449 on 8th January 2023
In both depolarisation and repolarisation, cardiac myocytes act like electric generators that cause electric currents to flow out into the body and back again into the heart. This produces various electrical potentials on the body’s surface, which are then recorded and represented on an ECG.
The ECG graph is usually set up at a speed of 25mm/s:
1 small square = 0.04 sec
1 large square = 0.2 sec
5 large squares = 1 sec
15 large squares = 3 sec
Retrieved from https://www.practicalclinicalskills.com/ekg-course-contents?courseid=301 on 8th January 2023
Each ECG lead used represents the heart from a different point of view on an ECG strip. The horizontal base line recorded is referred to as the iso-electric line, and a deflection from it signals electrical activity of the heart.
A normal ECG strip features the following:
P Wave = electrical activity within the atrial chamber
SA Node (Sinus Node a.k.a. sino-atrial node) – The pacemaker of the heart, firing about 60-100 times per minute;
AV Node (Atrio-Ventricular Junction) – Fires at a rate of 40-60 times per minute. The AV node takes charge whenever the SA node experiences impulse issues;
AV Bundle (Bundle of His), Left Bundle and Right Bundle Branches, and the Purkinje Fibres – Fire at 20-40 times per minute if both the AV and the SA node experience impulse issues.
Interpreting ECG
Heart Rate
The Rule of 300: when the rhythm is regular = 300 / (number of boxes between R to R wave)
Six Second Method: when the rhythm is irregular = number of R waves per 6 seconds X 10
ECG Recording
Limb Connection Points – Retrieved from https://www.pngegg.com/en/search?q=ecg+Monitor on 8th January 2023
The direction of the electrical current determines the upward or downward deflection of an ECG waveform.
Major deflections include:
P Wave – atrial depolarisation
QRS Complex – ventricular depolarisation
T Wave – ventricular repolarisation
Retrieved from https://ijdr.in/article.asp?issn=0970-9290;year=2014;volume=25;issue=3;spage=386;epage=389;aulast=Anoop;type=3 on 8th January 2023
Retrieved from https://aneskey.com/ecg-basics/ on 8th January 2023
P Wave should be small, rounded, and positive, visible through leads I, II, aVF, and V2-V6, with an amplitude of 0.5-2.5mm and duration of <120ms; there should be only 1 P Wave preceding the QRS Complex.
QRS Normal Interval should be less than 3 small squares on the ECG graph.
ST Segment is normally isoelectric and gently upsloping.
Retrieved from https://www.aclsmedicaltraining.com/basics-of-ecg/ on 8th January 2023
QT Prolonged could be indicating Hypokalaemia, Hypocalcaemia, Bradycardia, Drugs, issues with the CNS, Left Ventricular Hypertrophy and Pericarditis.
ST Elevation could be indicating MI or Myocardial Injury, Coronary Vasospasm or Pericarditis.
ST Depression could be indicating Ischaemia, Digitalis Glycocides use (eg. Digoxin), block in the left or right Bundle Branch, or left or right ventricular hypertrophy. ST Depression is a sign of a narrowed blood vessel.
Retrieved from https://www.cvphysiology.com/CAD/CAD012 on 8th January 2023
Retrieved from https://www.cvphysiology.com/CAD/CAD012 on 8th January 2023
Retrieved from https://www.washingtonhra.com/arrhythmias/long-qt-syndrome.php on 8th January 2023
NOTE: Some drugs such as antibiotics, anti-psychotic and anti-arrhythmic drugs, prolong depolarisation and repolarisation time.
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Blood pressure is the force that the blood exerts against a blood vessel wall. When measuring BP, both the systolic and the diastolic blood pressure are recorded. The systolic blood pressure records the peak arterial blood pressure reached in the arteries during ventricular contraction, while the diastolic blood pressure records the minimum arterial blood pressure reached in the arteries during ventricular relaxation…
Normal Blood Pressure = 120/80 mmHg
PULSE PRESSURE is the difference between systolic and diastolic blood pressure…
Normal Pulse Pressure = 40 mmHg
MEAN ARTERIAL PRESSURE (MAP) is the average pressure in the arteries within a cardiac cycle…
MAP = (Diastolic X2) + Systolic = Answer / 3
or
MAP = CO X TPR
A stroke volume increase or a heart rate increase result in an increase in cardiac output. Total Blood Volume affects MAP as well.
Blood Pressure is determined by 3 main principles:
Cardiac Output (CO)
Blood Volume (BV)
Total Peripheral Resistance (TPR)
Venous Return, which is the volume of blood flowing towards the heart through systemic veins, affects BV resulting in a change in CO and stroke volume. Venous return is affected by the pressure difference between the pressure in the venules and the pressure within the right ventricle.
The Skeletal Muscle Pump and the Respiratory Pump are responsible for pumping blood from the lower body back to the heart through the inferior vena cava thanks to the valves present within the veins.
At rest, the proximal and distal valves within the calf are open, allowing blood flow to move upwards towards the heart. In leg muscle contraction, veins are compressed, pushing blood through the proximal valve, leading to the distal valve to close due to blood pushing against it.
Within the respiratory pump, the diaphragm moves downwards during inhalation, leading to a decrease in the intrathoracic pressure and an increase in the intrabdominal pressure. This creates compression within the abdominal veins.
Total Peripheral Resistance (TPR) refers to the resistance to flow due to friction of blood against the vessel walls. TPR depends on:
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The term haemodynamics refers to the physical principles of blood flow, with ‘flow’ being the amount of blood flow in a given time (mL/min). The cardiovascular system’s main aim is to keep blood flowing throughout the capillaries so that capillary exchange can happen.
Capillary exchange is a two-way traffic type movement of substances that occurs between the blood plasma and the interstitial fluid.
It is important to note that tissue perfusion occurs through capillary exchange, making the blood within the capillaries (which is usually around 250-300ml at a given time) the most important blood within the body.
Chemicals pass through capillary walls through 3 possible routes:
endothelial cell cytoplasm
intercellular clefts
filtration pores of the fenestrated capillaries
Movement through the capillary walls happen by:
Diffusion: allows exchange through the use of the concentration gradient across a permeable membrane (eg. glucose, oxygen, carbon dioxide and waste);
Transcytosis: through pinocytosis, fluid droplets are picked up by endothelial cells. Vesicles move across the cell and releases fluid through exocytosis (eg. fatty acids, albumin and hormones);
Filtration: fluids and solutes from blood capillaries move into the interstitial fluid due to blood hydrostatic pressure (BHP), which is the pressure that water within the blood plasma exerts against blood vessel walls, and interstitial fluid osmotic pressure (IFOP), which is the opposing pressure of the interstitial fluid;
Reabsorption: fluids and solutes from the interstitial fluid move into the blood capillaries due to blood colloid osmotic pressure (BCOP).
Starling’s Law of the Capillaries refers to the near equilibrium existing between the volume of liquid reabsorbed and the volume filtered. The discrepancy in filtration and re-absorption is normally absorbed back into circulation through the lymphatic system.
If filtration exceeds re-absorption in an excessive way, oedema becomes present due to the abnormal increase in interstitial fluid volume. Excessive filtration can be caused by an increase in capillary blood pressure and capillary permeability, while inadequate re-absorption can be caused by a decrease in the concentration of plasma proteins which in turn lowers the blood colloid osmotic pressure (BCOP).
Below you can find a collection of videos that can help provide a more visual approach to Capillary Exchange.
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If you are interested in learning how to write a scientific paper look no further than WASP. The next WASP is to be held between 12 and 14 April 2021 throughout an online course with faculty comprised of experienced researchers and journal editors.
WASPs are intensive, three day events with formal lectures & interactive sessions delivered by highly experienced researchers and journal editors. All aspects of paper writing are covered, from proposals, to presenting to dealing with journal editors. Statistical analysis is demonstrated within Excel® and includes hands on sessions on attendees’ own laptops. Excel modules used for analysis are given to attendees along with soft copies of the presentations.
WASP is suitable for all individuals in the sciences who wish to enhance their paper writing skills by acquiring sound competences in academic writing. WASP is not only intended for the medical profession: engineers, architects, pharmacists, nurses etc. have all joined, enjoyed and benefited from WASP.
At the end of the WASP event, attendees are also presented with a certificate of attendance attesting to the 18 EACCME (CME) points that are allotted to this event via the Medical Association of Malta (MAM).
The course is endorsed by several international and local bodies. More details about the WASP Faculty can be found here.
We practice what we preach in WASP – all of the talks (as well as related topics) have been published in the peer-reviewed journal (impact factor 2.2) Early Human Development in a series of medical education sections in consecutive issues of the journal. See PubMed link.
Prof. Victor Grech, creator and director of WASP.
There is now a Malta Cross Foundation partial (50%) scholarship for this course. The scholarship is open to all local and International students or young graduates. If interested send an email to info@maltacross.org copied to info@ithams.com. Subject: WASP Scholarship. For further information contact info@maltacross.org. The Foundation reserves the right to refuse any application. Details from here.
Now is your chance to learn how to write a scientific paper in the proper way. An early bird registration and discount are currently available. You may register at http://www.ithams.com/wasp/
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