Author: Claire

Claire Galea is the founder and director of Mariposa Holistic Care, providing personalised, holistic care services that prioritise individual needs, dignity and wellbeing. With formal nursing education and extensive clinical training at the University of Malta, Claire brings a strong foundation in healthcare to her work. Passionate about health education, person-centred care and lifelong learning, she uses her blog Student Nurse Life to share knowledge, encourage reflection and inspire a more informed, compassionate and positive approach to health and everyday life.

Cardiac Pacing – Saving Endangered Lives With A Cardiac Pacemaker

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.

Cardiac pacing is used in the case of:

2nd and 3rd degree AV blocks
AV blocks with chronic atrial fibrillation
SA Node disease
Heart failure
Genetic-related long QT syndrome
Anterior Myocardial Infarction with AV block
Drug-induced blocks (eg. digoxin intoxication)
Atrial fibrillation prevention
Hypertrophic Cardiomyopathy (thickened heart muscle)

Cardiac Pacing Sites

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.

The NGB Code

pacemaker nbg codes — Accessed from https://www.ecgmedicaltraining.com/the-basics-of-paced-rhythms-part-1/ on 28th January 2021.

Pacemaker Nursing Management

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 – Indications, Side Effects & Contraindications

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)

CLASS 4 AGENTS: Calcium Channel Blockers (cause cardiac cells conduction to slow down)

OTHER ANTI-ARRHYTHMICS: Digoxin, Adenosine and Magnesium Sulphate

Class 1 Agents are further sub-divided into 3 types of anti-arrhythmics:

1A Quindine, Procainamide, Disopyramide

1B Lidocaine, Mexiletine

1C Flecanide, Propafenone

Below you can find a collection of videos that can help provide a more visual approach to Anti-Arrhythmic Drugs.

Cardiac Action Potential Animation

Anti-Arrhythmic Drugs Animation

Anti-Arrhythmics

Special thanks to the creators of the featured videos on this post, specifically Youtube Channels Alila Medical Media, MedLecturesMadeEasy

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ECG Arrhythmias – Bradycardia, Tachycardia, AV Blocks, VF and Asystole

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)
Irregular Tachycardia: atrial fibrillation (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.

Practice Interpreting ECG Arrhythmias

ECG Simulator: https://skillstat.com/tools/ecg-simulator/

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Interpreting ECG – Echocardiography Principles

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.

interpreting ECG — 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

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
QRS Complex = ventricular depolarisation
T Wave = ventricular repolarisation

The heart’s conductive system functions through the:

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

Accessed from https://aimcardio.com/blog/12-lead-placement-guide-with-diagram/ on 24th January 2021

Accessed from https://slideplayer.com/slide/10943937/ on 24th January 2021

Deflections

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.

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.

NOTE: Some drugs such as antibiotics, anti-psychotic and anti-arrhythmic drugs, prolong depolarisation and repolarisation time.

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Blood Pressure Physiology and Haemodynamics

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

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:

Blood Viscosity
Vessel Length
Vessel Radius

Blood Pressure control can be applied by:

Neural Regulation (Baroreceptors and Chemoreceptors)
Hormonal Regulation (RAAS, Epinephrine and Norepinephrine, AntiDiuretic Hormone ADH and Atrial Natriuretic Peptide ANP)
Auto Regulation (regulation of tissues on their own blood flow eg. in kidneys, mesentery, skeletal muscle, brain, liver and the myocardium)

Below you can find a collection of videos that can help provide a more visual approach to Blood Pressure Physiology.

Cardiac Output, Stroke volume, EDV, ESV and Ejection Fraction

Calculating The Mean Arterial Pressure

Regulation of the Mean Arterial Pressure MAP

Venous Return, Skeletal Muscle Pump and the Respiratory Pump – Animation

Systemic Vascular Resistance (Total Peripheral Resistance)

Regulating Peripheral Resistance (TPR)

Autoregulation of Blood Flow – Animation

Special thanks to the creator of the featured video on this post, specifically Youtube Channel Alila Medical Media, Janux, Registered Nurse RN, Dr Matt & Dr Mike and Interactive Biology.

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Capillary Exchange, Haemodynamics and Blood Flow

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.

Capillary Exchange and Oedema animation

capillary exchange

Special thanks to the creators of the featured videos on this post, specifically Youtube Channels Alila Medical Media and Medicina Didactica.

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Write A Scientific Paper With WASP

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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The Lymphatic System – Playing a Vital Part In The Immune System

The lymphatic system, which comprises of lymph, lymphatic vessels, and lymphatic tissue, has an important role within the body. It:

drains excess fluid and protein from the interstitial tissue back into the blood
transports fat from the GI tract to the blood
produces and circulates lymphocytes that help in keeping the body protected

Lymph

Lymph is the same as the interstitial fluid. Fluid that bathes the cells is referred to as interstitial fluid, while when it flows through the lymphatic vessels, it is called lymph.

Lymphatic Vessels

The lymphatic vessels are microscopic vessels in between the cells spaces known as lymph capillaries. They are slightly larger than blood capillaries and more permeable. Whilst we can find lymphatic capillaries throughout the whole body, they are not found in the avascular tissue, CNS, splenic pulp and bone marrow.

Lymph capillaries connect through larger lymph vessels known as lymphatics, which converge into two main channels, namely the thoracic duct and the right lymphatic duct. Lymphatics have thinner walls and valves (more valves than veins). Lymph nodes can be found at various intervals.

Drainage of the Lymphatic System

The left side of the head, neck, chest, upper left extremities and the entire body below the ribs all drain into the thoracic duct.

The upper right side of the body drains into the right lymphatic duct.

Lymphatic Tissue

Lymphatic tissue is rich in lymphocytes and accessory cells such as macrophages and reticular cells. It is scattered in the linings of the GI tract, the respiratory tract, the urinary tract, the reproductive tract, and in the stroma a.k.a. core of multiple organs. Lymphatic tissue can also be found surrounded by a capsule within the lymphatic organs a.k.a. lymph nodes, spleen, and the thymus gland.

Lymph nodes

Lymph nodes are oval structures measuring between 1-25mm in length, commonly found in groups, located along the lymph vessels’ pathway.

Afferent Lymphatic Vessels => Sinuses => Efferent Lymphatic Vessels

Lymph passes through the nodes and is filtered from foreign substances by the reticular fibres within the node
Macrophages destroy foreign substances through phagocytosis
T Cells destroy foreign substances through the release of various products
B Cells produce antibodies to destroy them

Lymphatic ORgans: Tonsils

Tonsils are a pair of soft tissue masses located at the pharynx. Their location helps protect against the invasion of foreign substances through the production of lymphocytes and antibodies.

Retrieved from https://www.aboutkidshealth.ca/Article?contentid=1918&language=English on 29th May 2022

Lymphatic Organs: Spleen

The spleen is an oval shaped organ measuring around 12cm in length which is made up of lymphatic tissue. It is located in the upper left side of the abdomen, next to the stomach and behind the left ribs. Functions of the spleen include:

B Lymphocyte Production – eventually develop into antibody-producing plasma cells
Phagocytosis – of bacteria and damaged or worn-out red blood cells and platelets
Blood Storage and Release – in cases such as haemorrhage

NOTE: the spleen does not filter lymph.

Retrieved from https://www.researchgate.net/publication/309457531_A_Brief_Survey_of_Spleen_Segmentation_in_MRI_and_CT_Images/figures?lo=1&utm_source=google&utm_medium=organic on 29th May 2022

Lymphatic Organs – Thymus Gland

The thymus gland is found in the superior mediastinum, between the lungs and behind the sternum. It reaches it’s maximum size during puberty, after which it starts to break down. The main function of the thymus gland is to produce T Lymphocytes.

Retrieved from https://www.thoracic.theclinics.com/article/S1547-4127(10)00194-5/fulltext on 29th May 2022

Body Defences

The human body aims to maintain haemostasis by counteracting pathogens or related toxins in the environment.

Resistance = the body’s ability to keep off disease

Susceptibility = the body’s inability to resist disease

Body defences can be divided in two groups: Non-Specific Defence and Specific Defence a.k.a. Immunity

Non-Specific Defences

The non-specific defence mechanism provides an immediate response to protect the body from foreign substances. Components of the non-specific defence mechanisms include:

SKIN & MUCOUS MEMBRANES – MECHANICAL FACTORS include the epidermis‘ anatomy i.e. made up of closely packed cells, continuous layering and the presence of keratin; mucous membranes that secrete mucus to prevent cavities from drying up whilst trapping microbes at the same time (eg. in nose through hairs and in the upper respiratory tract through cilia); lacrimal apparatus; saliva which helps prevent microbe colonisation; epiglottis which helps prevent microbes from entering the lower respiratory tract; CHEMICAL FACTORS include sebum which forms a protective film over the skin’s surface and inhibits bacterial growth; perspiration which flushes microbes from the skin; gastric juice produced by the stomach glands which is highly acidic due to being made of hydrochloric acid, enzymes and mucus, all of which help preserve the stomach’s sterility whilst destroying bacteria and most bacterial toxins; lyzozyme (found in perspiration, tears, saliva, nasal secretions and tissue fluids) which is an enzyme that can break down cell walls of various bacteria;
ANTI-MICROBIAL SUBSTANCES – INTERFERON (IFN) (alpha, beta & gamma) which are produced by lymphocytes and other leucocytes and fibroblasts; COMPLEMENT – a group of 11 proteins found in normal blood serum which complements immune and allergic reactions involving antibodies – once activated, destroys microbes; PROPERDIN – a protein found in the serum which together with COMPLEMENT causes the destruction of several types of bacteria, enhances phagocytosis, and triggers inflammatory responses;
PHAGOCYTOSIS– the ingestion and destruction of microbes or other foreign particulate matter by phagocytes through the Adherence process and the Ingestion process;
INFLAMMATORY PROCESS – when cells are damaged by microbes, inflammation is triggered, characterised by redness, pain, heat, swelling, and loss of function; during inflammation, vasodilation increases permeability of blood vessels, neutrophils migrate to the injured area within one hour, nutrients are released to help support defensive cells and increased metabolic reactions of the affected cells, fibrin formation, and pus formation;
FEVER – inhibits microbial growth and speeds up body reactions which help the body to heal

HIGH FEVER => HIGH BODY TEMPERATURE => INCREASED RATE WITH WHICH THE BODY WORKS TO FIGHT OFF INFECTION, BACTERIA OR VIRUSES.

Specific Defences a.k.a. immunity

Immunity involves the production of a specificy cell type or molecule a.k.a. antibody that can destroy a particular antigen.

An antigen is a chemical substance which causes the body to produce specific antibodies which can react with the antigen. Antigens have immunogenicity (can stimulate the formation of specific antibodies) and reactivity (can react specifically with the produced antibodies). Antigens with both immunogenicity and reactivity are called complete antigens eg. proteins, nucleoproteins, lipoproteins, glycoproteins, and some polysaccharides. Non-microbial antigens include pollen, egg white, incompatible blood cells, and transplanted tissues and organs.

An antibody is a protein produced by the body in response to antigen presence. An antibody can combine with the antigen.

Antibodies belong to a group of proteins called globulins, hence the name immunoglobulins.

Cellular immunity & Humoral Immunity

The body can defend itself against bacteria, toxins, viruses and foreign tissues thanks to 2 components:

CELLULAR IMMUNITY A.K.A. CELL-MEDIATED IMMUNITY – includes the formation of specially sentisised lymphocytes which can attach to the foreign agent and destroy it; T cells are responsible for cellular immunity
HUMORAL IMMUNITY A.K.A. ANTIBODY-MEDIATED IMMUNITY – includes the formation of circulating antibodies able to attack an invading agent; B cells are specialised plasma cells which produce antibodies and provide humoral immunity

Retrieved from https://www.pinterest.com/pin/729442470871870835/ on 30th May 2022

The Immune Response

The immune response of the body, be it cellular or humoral, is more intense after a second or subsequent exposure to an antigen than after initial exposure, as illustrated below…

Retrieved from https://www.elevise.co.uk/gab3q5.html on 3th May 2022

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Blood Vessels – Arteries, Veins and Capillaries

Blood vessels can be divided into 3 principal categories:

ARTERIES are the efferent blood vessels of the CVS which carry blood away from the heart;

VEINS are the afferent blood vessels that carry deoxygenated blood back to the heart;

CAPILLARIES are microscopic thin-walled vessels that connect the smallest arteries to the smallest veins.

The artery and vein walls are composed by 3 layers called tunics. The tunica intima lines the inside of the vessel and acts as a selectively permeable barrier to materials entering or leaving the blood stream. The tunica media is the middle layer of the vessel (usually the thickest layer) which consists of smooth muscle, collagen and elastic tissue that help strengthen the vessels and prevent them from rupturing due to the blood pressure, and allows vasoconstriction or vasodilation of the vessels. The tunica adventitia, which is the outermost layer, consists of loose connective tissue that merges with neighbouring blood vessels, nerves or organs.

Arteries are resistance vessels of the cardiovascular system. Their muscular built allows them to retain their round shape even when they are empty. Due to the left ventricle pressure surge, arteries need to be able to resist the blood pressure surge, otherwise they would burst.

There are 3 types of capillaries:

Continuous capillaries: present in most tissues;
Fenestrated capillaries: found in kidneys, endocrine glands and small intestine;
Sinusoids a.k.a. Discontinued capillary: found in the liver, bone marrow and spleen.

Veins are the capacitance vessels of the cardiovascular system. They are relatively thin and flaccid, and collapse when empty. However they are able to expand easily to accomodate blood volume increase. Different type of veins include:

large veins (such as the vena cava)
venous sinuses
medium veins (containing venous valves, usually found in lower limbs)
muscular venules
post-vapillary venules

Below you can find a collection of videos that can help provide a more visual approach to Blood Vessels including Arteries, Veins and Capillaries.

blood vessel layers

3 types of capillaries

arteries vs veins

Post-capillary venules

Special thanks to the creators of the featured videos on this post, specifically Youtube Channels Khan Academy Medicine and Khan Academy.

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Electrolyte Imbalance Affecting The Heart

Electrolyte imbalance is a frequent and potentially hazardous complication in patients with heart failure.

Potassium keeps blood pressure levels stable, regulates heart contractions and helps with muscle functions…

HYPOKALAEMIA: HR slow and irregular, weak pulse, orthostatic hypotension, diminished breathing sounds. The heart may also arrest in diastole. ECG shows a depressed ST segment, flat or inverted T wave, and a U wave.

HYPERKALAEMIA: muscle weakness, low or absent urine production due to renal failure, respiratory failure, seizures, decreased cardiac contractility, low BP. ECG shows tall peaked T wave, flat P wave, wide QRS complex or prolonged QR interval.

Calcium helps with muscle contractions, nerve signaling, blood clotting, cell division, and the formation or maintenance of bones and teeth…

HYPOCALCAEMIA: heart beats slower due to the effect of calcium on heart contractility. Muscle spasms, arrhythmias. ECG shows prolonged QT interval or prolonged ST interval.

HYPERCALCAEMIA: heart beats faster due to the effect of calcium on heart contractility. Muscle weakness, absent reflexes, constipation, kidney stone formation. ECG shows shortened QT interval.

Magnesium is needed for muscle contractions, proper heart rhythms, nerve functioning, bone building, bone strength, reducing anxiety, digestion, and keeping a stable protein-fluid balance.

HYPOMAGNESEMIA: muscle twitching, positive Trusseau sign, weak respirations, irritability, high BP, involuntary movements, low bowel mobility. ECG shows tall T waves and depressed ST segment. Prolonged PR and QT intervals with wide QRS complex in case of severe hypomagnesemia.

HYPERMAGNESEMIA: Signs are showing only in severe cases: lethargy, ECG shows PR and QT prolonged intervals and wide QRS complex, hypotension, bradycardia, GI issues, impaired breathing, cardiac arrest.

Sodium helps maintain fluid balance, and is needed for muscle contractions and nerve signaling.

HYPONATREMIA: seizures, lethargy, abdominal cramping, orthostatic hypotension, muscle spasms, trouble concentration, lack of urine, lack of appetite, shallow respirations.

HYPERNATREMIA: fever, flushed skin, restlessness, agitation, increased fluid retention, oedema, confusion, dry mouth, dry skin, decreased urine output.

Below you can find a collection of videos that can help provide a more visual approach to electrolyte imbalance affecting the heart.

Hypokalaemia

Hyperkalaemia

Hypocalcaemia

hypercalcaemia

hypomagnesemia

hypermagnesemia

hyponatremia

hypernatremia

Special thanks to the creator of the featured videos on this post, specifically Youtube Channel Registered Nurse RN.

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