Author: Claire

Claire Galea is the Owner and Director of Mariposa Holistic Care, through which she provides holistic care services tailored to her clients' personal needs. She is also in her final year following a Degree in Nursing at the Faculty of Health Sciences, University of Malta. Claire is keen about public education on health-related subjects as well as holistic patient-centered care. She is also passionate about spreading positivity and awareness on various subjects through her blog Student Nurse Life.

Electrical Activity of the Heart

Cardiac muscle cells contract spontaneously, independently, regularly and continuously. Autorhythmic fibres generate action potentials that trigger heart contractions repeatedly, acting as the natural pacemaker of the heart throughout the electrical activity of the heart.

SA Node a.k.a. Sinoatrial Node is the pacemaker of the heart, exactly where cardiac excitation begins. It fires 60-100 electrical impulses per minute (approx. one every 0.8 secs). The SA Node cells DEPOLARISE repeatedly to threshold spontaneously; SPONTANEOUS DEPOLARISATION = PACEMAKER POTENTIAL.

AV Node a.k.a. gatekeeper of the heart acts as an electrical gateway to the ventricles. It fires 40-60 electrical impulses per minute (approx. one every 0.5 secs), evidently having slowed down due to having thinner myocytes with fewer gap junctions over which signals are transmitted. This delay allows the ventricles to fill up with blood before contracting.

The Bundle of His a.k.a. AV Bundle is where action potentials can conduct from the atria to the ventricles, entering both the right and left bundle branches.

Here the Purkinje Fibres conduct the action potential from the apex of the heart up to the rest of they ventricular myocardium, causing the ventricles to contract at the fastest speed of the whole conduction system (4m/s), pushing blood towards the semilunar valves.

Ventricular Myocyte Action Potential

Cardiac myocytes have a stable resting membrane potential of -90mV, depolarising only when stimulated. Ventricular Myocytes’ action potential has 3 phases:

DEPOLARIZATION – a stimulus opens voltage-gated Na+ channels, causing depolarisation as they enter the cells. The threshold voltage opens additional Na+ channels triggering a positive feedback cycle, peaking at almost +30mV. In response the Na+ channels close abruptly, causing the rising phase of the action potential to be very short.

PLATEAU – here is where depolarisation is maintained while the myocytes contract. Voltage-gated slow Ca2+ channels open up allowing small amounts of Ca2+ ions from within the ECF to enter the myocytes. With the binding action of Ca2+ ions to the ligand-gated Ca2+ channels on the sarcoplasmic reticulum, more channels open allowing more Ca2+ ions into the cytoplasm, which then bind to troponin, causing the ventricular myocyte to contract by the stimulus. Finally Ca2+ channels close and K+ channels reopen, causing K+ ions to difuse out of the cell and the Ca2+ ions to return to the ECF.

REPOLARIZATION – The negative resting membrane potential is now restored to -90mV.

Baroreceptors in the Cardiovascular Centre

Baroreceptors are found in the aorta and the internal carotid arteries.

Increase in HR = Increase in CO = Increase in BP = Baroreceptors sense changes & signal to the cardiac centre = cardiac centre Decreases HR.

Decrease in HR = Decrease in CO = Decrease in BP = Baroreceptors sense changes & signal to the cardiac centre = cardiac centre Increases HR & re-stabilises CO & BP.

Chemoreceptors in the Cardiovascular Centre

Chemoreceptors are found in the aortic arch, carotid arteries and the medulla oblongata. These are sensitive to blood pH, Carbon Dioxide and Oxygen.

Chemoreceptors can sense Hypercapnia and Acidosis, which then stimulate the cardiac centre, increasing the HR and restores perfusion of the tissues. Accumulated Carbon Dioxide is then removed.

In response to Hypoxaemia, chemoreceptors lead to a slowing down of the HR.

Below you can find a collection of videos that can help provide a more visual approach to the electrical activity of the heart.

Electrical Activity of the Heart

Ventricular Myocyte Action Potential

Regulation of the Heart Activity Through the ans (autonomic nervous system)

Heart Activity Regulation

role of the cardiovascular centre

baroreceptor reflex

baroreceptor reflex animation

baroreceptors and blood pressure

chemoreceptors

Special thanks to the creators of the featured videos on this post, specifically Youtube Channels Registered Nurse RN, Khan Academy Medicine, DrBruce Forciea, PhysioPathoPharmaco, Khan Academy and Alila Medical Media.

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Cardiovascular System – Cardiac Tissue, Valves and Circulation

The Cardiovascular System, also known as the Circulatory System, is an organ system that aims to circulate blood to and from cells in the body, transporting nutrients and removing waste.

Systemic Circuit: The heart pumps blood to the body through arteries that branch off into smaller blood vessels called arterioles.

The capillaries network allow oxygen and other nutrients to diffuse from the blood and into the cells, while metabolic waste diffuses into the venous capillaries from the cells.

Pulmonary Circuit: Blood then returns to the heart through the veins, and the cycle is repeated.

The heart wall consists of 3 layers:

EPICARDIUM (a.k.a. visceral pericardium) – outer layer of the heart
MYOCARDIUM – made up of cardiac muscle
ENDOCARDIUM – lines the chambers of the heart and the heart valves

The boundaries of the 4 heart chambers are marked by 3 grooves known as sulci:

Coronary Sulcus a.k.a. Atrioventricular Sulcus
Anterior Interventricular Sulcus
Posterior Interventricular Sulcus

The atria are separated by a wall-like structure called interatrial septum. The ventricles are separated by the interventricular septum, with both ventricles having internal ridges called trabeculae carnae.

The heart valves ensure a one-way flow:

ATRIOVENTRICULAR VALVES: Right AV (Tricuspid) Valve which has 3 cusps, and Left AV (Bicuspid) Valve a.k.a. Mitral Valve. Chordae Tendinae connect the valve cusps to the conical papillary muscles on the ventricle floor.

The heart has a beat of its own thanks to the electro-chemical circuit system and its 4 relay stations:

SA Node
AV Node
Bundle of HIS
Purjinke Fibres

When the aorta leaves the left ventricle, it gives off to the Right Coronary Artery (RCA) and the Left Coronary Artery (LCA).

The RIGHT CORONARY ARTERY supplies the right atrium and the SA Node and gives off to the Right Marginal Branch and the Posterior Interventricular Branch, as well as a small branch to the AV Node.

The LEFT CORONARY ARTERY travels to the coronary sulcus and divides into the Anterior Interventricular Branch/Left Anterior Descending Branch (LAD), and the Circumflex Branch.

Below you can find a collection of videos that can help provide a more visual approach to the Cardiovascular System.

Cardiac Muscle Tissue

Introduction to the Cardiovascular System – Animation

The 3 Heart Wall Layers

The Pericardium

The Epicardium

The Myocardium

The Heart Valves

Coronary Circulation

branches of the aortic arch

Special thanks to the creators of the featured videos on this post, specifically Youtube Channels Registered Nurse RN, Lecturio Medical, The Noted Anatomist, KenHub, CTE Skills, Dr.G Bhanu Prakash Animated Medical Videos and Catalyst University.

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Hypertension – The Silent Killer

Hypertension is the amount of resistance of blood pumping through the arteries. Organs are susceptible to high blood pressure especially the brain and the kidneys. Cholesterol restricts blood vessels thus affects blood pressure.

Most hypertension cases can be without any visible bodily symptoms, going undiagnosed for a long time.

Hypertension can be classified as Primary (Essential) – originating from an unknown disorder affecting BP regulation mechanisms; or Secondary to other diseases processes. Secondary hypertension could be caused by Renal disease (polycystic kidneys, renal artery stenosis or pyelonephritis), drug-induced (eg. by oral contraceptives or corticosteroids), pregnancy (pre-eclampsia) or hormonal (cushing’s syndrome, phaeochromocytoma, hyper or hypothyroidism, or acromegaly – bone size increase).

Hypertension Risk Factors

Modifiable:

excessive salt diet
obesity
lack of physical exercise
excessive consumption of alcohol
deprivation and socio-economic status
mental health and stress

Non-modifiable:

age
ethnicity
genetics
gender

NICE guidelines suggest that the blood pressure is measured in both arms. In the case of a consistent high blood pressure of 140/90 mmHg or higher, a patient should seek hypertension diagnosis.

Hypertension affects:

cardiovascular system (CHF)
brain (causing a stroke)
kidneys (renal failure)
eyes (retina)

Always assume possible lack of compliance with correct medication intake.

Postural hypotension can be noted as a 20mmHg fall in the systolic reading at a standing position, after another reading in a sitting position.

As for athletic patients, note that athletics have a slower heart rate which is still considered to be healthy.

hypertension nonpharmacologic interventions

Hypertension Pharmacology as listed within the NICE guidelines suggest the following pharmacological steps in the treatment of hypertension:

First line agents for hypertension:

ACEi
ARB
Calcium Channel Blocker

Add-on agents:

Beta Blockers
Alpha Blockers
Thiazide Diuretics
Aldosterone Antagonists / Spironolactone

ACE inhibitors are at times not tolerated by black African or African-Caribbean patients.

If a patient presents with hypertension, check for heart failure and current medication list and review.

Chronic Hypertension Drug Treatment During Pregnancy

Methyldopa: traditionally used drug based on long term data supporting safety
Beta Blockers: although considered generally safe, fetal growth retardation has been reported in the past, especially with the use of Atenolol
Labetalol: contains less side effects than Methyldopa
Clondine: mainly used in the third trimester (limited data)
Calcium Channel Blockers: Nifedipine is used as long acting medication (limited data)
Diuretics: probably safe in low doses if started prior to conception for essential hypertension (still controversial evidence)
ACEi, ARBs, Direct Renin Inhibitors: CONTRAINDICATED.

Ideally, women planning to conceive should be encouraged to discontinue these medications under medical supervision.

Hypertensive Crisis is defined as severely elevated blood pressure associated with new or progressive target organ dysfunction. Although the absolute value of the blood pressure is not as important as the presence of end-organ damage, the systolic blood pressure is usually >180 mmHg and/or the diastolic BP is >120 mmHg. In such crisis, Sodium Nitroprusside is one of the most commonly recommended treatments (contraindicated in patients with chronic kidney disease)

Assessed from https://www.slideshare.net/ParasuramanParasuraman/antihypertensive-drugs-79369508 on 27th January 2021

Hypertension Pathophysiology, Treatment, Nursing Interventions and Pharmacology

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

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Heart Failure Treatment, Management, Nursing Interventions & Drugs

Heart failure happens when the heart is too weak to pump efficiently. This restricts it from providing proper cardiac output to maintain the body’s metabolic needs.

Complex clinical syndrome that results from any structural or functional impairment of ventricular filling (diastole) or ejection of blood (systole)
2013 ACC/AHA

Systolic Heart Failure is attributed to a pumping problem experienced by the heart where it is unable to contract enough to pump blood to supply to the body, thus resulting in contraction and ejection fraction problems. In this case the patient presents with left ventricular failure with reduced ejection fraction of <40% and marked cardiomegaly (where the ventricle becomes enlarged in size).

Diastolic Heart Failure is attributed to a filling problem experienced by the heart where it is unable to relax the left ventricle, leading to a build-up in the lungs, resulting in relaxation and blood filling problems. In this scenario the patient presents with pulmonary congestion and at times with slightly enlarged ventricles, both due to an increased resistance to filling due to increased ejection fraction of >50%.

The ejection fraction is a comparison between the amount of blood in the heart and the amount of blood pumped out of the heart.

Cardiac output is the amount of blood pumped out of each ventricle per minute. Factors affecting cardiac output include the heart rate, blood volume, contractility and venous return.

Stroke volume is the volume of blood pumped out of each ventricle with every beat.

Cardiac Output = Heart Rate X Stroke Volume

Causes of HF include:

Coronary Artery Disease
Hypertension
Cardiomyopathy
Arrhythmias
Valvular and Congenital Heart Disease
Alcohol and Drugs

HF risk factors

Age
Obesity
Smoking
African Descent
Hypertension
High Cholesterol
Diabetes Mellitus
Coronary Artery Disease

Signs and symptoms of heart failure include shortness of breath, coughing, sleep disturbance, feeling overtired, loss of appetite, dizziness, swollen ankles and abdominal bloating.

HF can be classified in relation to:

CARDIAC OUTPUT: an issue with the ejection fraction (amount of pumped blood to the body). This can be subdivided into High Output Failure and Low Output Failure. High Output Failure occurs due to obesity, anaemia, hyperthyroidism and pregnancy. Usually presents as right sided heart failure followed by left sided heart failure. Low Output Failure happens when the heart fails to generate enough output due to left ventricular systolic or diastolic dysfunction, right ventricular dysfunction caused by changes in the heart rate, preload, afterload and heart contraction.

ANATOMY: issue or defect within the heart muscle

ONSET: acute or chronic

Left Sided HF is characterised by pulmonary oedema. Signs and symptoms include tachypnoea, tachycardia, third heart sound and cardiomegaly.

Right Sided HF is characterised by peripheral oedema, raised jugular venous pressure, hypotension and congestive hepatomegaly (enlarged liver which usually causes an enlarged abdomen).

Accessed from https://www.slideshare.net/raghukishoregalla/inotropic-therapy-for-heart-failure

Below you can find a collection of videos that can help provide a more visual approach to Heart Failure Treatment, Management, Nursing Interventions & Drugs.

Heart Anatomy and Physiology

Congestive Heart Failure (CHF) Treatment, Management, Nursing Interventions & Medications Part 1

Congestive Heart Failure (CHF) Treatment, Management, Nursing Interventions & Medications Part 2

Stroke Volume and Cardiac Output – Preload & Afterload

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

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Learn How To Write A Scientific Paper at WASP

One of the most challenging tasks that student nurses and medical students have to face whilst studying for their future career is undoubtedly the writing of assignments and eventually preparing a thesis. If you are looking to learn how to write a scientific paper, look no further than WASP.

WASP is a three day intensive online course aiming to help you learn how to write a scientific paper through lectures and interactive sessions delivered by highly experienced researchers, lecturers and journal editors. It is a unique course which has been successfully held internationally since 2010 in Europe, the Middle East and Malta.

In just one event, WASP will provide you with everything you need to know in terms of high standard writing skills and academic writing. Additionally it also provides you with information about this writing style’s epistemological and methodological underpinnings. Preparing a thesis, data entry in Excel, structuring a scientific paper, plagiarism and ethical issues, data protection, and RefWorks are only some of the extensive topics that will be covered during this WASP event.

If you are a nursing student, medical student, or you’re into a science-related career and you’re looking to learn how to write a scientific paper with enhanced writing skills and sound competences in academic writing, then this is the course for you!

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.

As student nurses we have so much we still need to learn through this journey, and this learning opportunity can help us increase our potential and excel in our assignment writing skills, as well as prepare us for when the time comes to start writing our dissertation. Nursing is an ongoing learning path, and we can never consider ourselves to be ‘finished’ when it comes to learning.

I will definitely not be missing this event! To be honest, I’ve been wishing to join since the past two events, and now that I finally got the chance to join, I am very much looking forward to it! If you’d like to drop me a message about it, please feel free to do so by clicking here.

If you have any personal queries you’d like to address with regards to this event, please email ITHAMS at info@ithams.com

To register for WASP event please click here.

Reference:

Grech V. WASP – Write a Scientific Paper Course: Why and How. J Vis Commun Med. 2017;40:130-134. Accessed at http://www.ithams.com/wasp/extras/news/WASPpaper.pdf on 16th December 2020

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Anti Hyperlipidaemic Drugs

Here you can find videos related to anti hyperlipidaemic drugs covered within cardiovascular pharmacology that help lower LDL cholesterol…

Cardiovascular pharmacology deals with the study of the effects of drugs upon the heart or circulatory system. Cardiovascular medicines help to prevent and treat cardiovascular disease, slow the progression of it as well as treat its symptoms whilst providing a better quality of life and increasing life expectancy.

Types of Cardiovascular Drugs include:

Anti-Hypertensive Drugs
Anti-Angina Drugs
Anti-Arrhythmic Drugs
Anti-Coagulants
Anti-Hyperlipidaemic Drugs

Below you can find a collection of videos that can help provide a more visual approach to cardiovascular pharmacology, specifically on the AntiHyperlipidaemic Drugs.

Anti Hyperlipidaemic Drugs include:

HMG-CoA Inhibitors – Simvastatin, Atrovastatin and Rosuvastatin

Lower elevated LCD Cholesterol.
Causes a large reduction in coronary events and death from heart disease.
Considered as 1st line treatment for patients with elevated coronary artery syndromes and ischaemic heart disease.
Simvastatin is highly effective at night; others may be taken during the day as well.
ADVERSE EFFECTS: liver damage, myopathy, rhambdomyolysis.
CONTRAINDICATIONS: chronic liver disease, pregnancy and lactation.
MONITOR: liver function tests (4-6wks initially, then yearly); muscle enzyme levels if patient complains of muscle pain.

Lipoprotein Lipase Activators – Fenofibrate, Gemfibrozil, Clofibrate and Bezofibrate

Lowers serum TGs and increase HDL cholesterol levels.
ADVERSE EFFECTS: GI disturbances, gall stone formation, myositis, myopathy and rhambdomyolysis.

Bile Acid Sequestrans

Sequestrants bind to bile acids in the intestine, preventing them from being reabsorbed into the blood.
SIDE EFFECTS: constipation, diarrhoea, bloating, flatulence.
PATIENT EDUCATION: take before a meal or at bedtime. Leave at least 1 hour before or 4 hours after taking cholestyramine since it interferes with their absorption.

Hyperlipidaemic Drugs

HMG-CoA Inhibitors a.k.a. Statins

Special thanks to the creators of the featured videos on this post, specifically Youtube Channels Speed Pharmacology and Registered Nurse RN

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Drugs Affecting Coagulation: Anti Platelets, Anti Coagulants, Thrombolytics

Here you can find videos related to drugs affecting coagulation, including anti-coagulants, anti-platelets and thrombolytics…

Types of Cardiovascular Drugs include:

Anti-Hypertensive Drugs
Anti-Angina Drugs
Anti-Arrhythmic Drugs
Anti-Coagulants
Anti-Hyperlipidaemic Drugs

Below you can find a collection of videos that can help provide a more visual approach to cardiovascular pharmacology, specifically on the Anti-Platelet drugs, Anti-Coagulant Drugs and Thrombolytic Drugs.

Drugs affecting coagulation include:

Anti Platelet Drugs – alter formation of platelet plug

Aspirin:

Effect lasts for up to 10 days, which is approximately the platelets lifespan.
INDICATED FOR: transient ischaemic attack, prevention of ischaemic stroke and MI, acute MI, Angina (chronic stable and unstable).
ADVERSE EFFECTS: GI bleeding, haemorrhagic stroke.
DOSE: 75mg-150mg daily.
MAJOR DRAWBACKS: allergic reactions, lack of effectiveness as an anti-thrombotic drug, lack of response in some patients, irreversible platelet inhibition.

Clopidogrel:

INDICATIONS: prevents blocakage of coronary artery stents, reduces thrombotic events in patients with acute coronary syndrome, prevents stenosis of coronary stents.
ADVERSE EFFECTS: easy bruising, dyspepsia, increased risk of bleeding.
MAJOR DRAWBACKS: increased risk of bleeding (attention when used in combination to other drugs that promote bleeding), limited bioavailability, must be broken down to be activated, patients respond differently to it due to metabolic differences.

Abciximab / Eptifibatide (Glycoprotein IIb/IIIa receptor antagonists):

Most effective anti platelet drugs which can be reversed.
INDICATIONS: acute coronary syndrome, percutaneous coronary interventions.
ADVERSE EFFECTS: bleeding.

Anti Coagulant Drugs – interfere in the clotting cascade and thrombin formation

Warfarin & Coumarins – Vitamin K Antagonists (reduce blood clotting by reducing Vitamin K).

Warfarin:

Stops coagulation by decreasing the production of 4 clotting factors that are dependent on Vitamin K.
Administered orally at the same time each day with or without food.
Initial onset 6-12 hours, with the peak effect developing after several days.
Effect persists for 2-5 days after discontinuation.
INDICATION: long term prophylaxis of thrombosis, prevention of thromboembolism and venous thrombosis, prevention of thrombosis in atrial fibrillation, reduction of recurrent ischaemic attacks and MI.
CONTRAINDICATED: in pregnant and lactating women as it passes through the placenta and breast milk.
ADVERSE EFFECTS: bleeding signs & symptoms, haemorrhage.
DOSE: 2-5mg depending on INR results.
PATIENT EDUCATION: will need ongoing monitoring through INR testing (International Normalised Ratio). Normal INR is usually less or equal to 1, but for patients on Warfarin, INR should range between 2-3, and rechecked every 4 weeks after stabilisation. Should be stopped 5 days before elective surgery. Check for food interactions. Must inform all healthcare providers of Warfarin use. Wear medication bracelet at all times.

Dabigatran, Rivaroxaban, Apixaban: NOAC (Novel Oral Anticoagulants)

Dabigatran:

Directly inhibits thrombin production which then prevents formation of fibrin and clots.
DOSE: 150BD orally every 12hrs at the same time each day.
INDICATION: atrial fibrillation, hip replacement, knee replacement.
ADVERSE EFFECTS: bleeding which could be fatal, GI disturbance, dyspepsia.
ANTIDOTE: Idarucizumab countaracts bleeding caused by Dabigatran.
CONTRAINDICATION: not to be used in patients being administered medications with increased bleeding risk.
PATIENT EDUCATION: should not be discontinued prematurely as it causes increased risk of thrombolitic events; must be stopped 2-5 days before elective surgery.

Rivarobaxan and Apixaban:

Reduce thrombin production by inhibiting selectively factor Xa and prothrombinase activity.
Does not require ongoing lab testing.
INDICATION: prevention of DVT and PE after hip and knee surgery, treatment of DVT and PE unrelated to surgery, prevention of stroke in patients with atrial fibrillation.
DOSE: same time each day once or twice daily.
ADVERSE EFFECTS: dyspepsia, increase risk of bleeding which could be fatal.
CONTRAINDICATION: not to be used in patients being administered medications with increased bleeding risk.
PATIENT EDUCATION: should not be discontinued prematurely as it causes increased risk of thrombolitic events; must be stopped 2-5 days before elective surgery.

Heparin:

Used when rapid anticoagulation is required or quick reversal due to its rapid onset.
May be used in pregnant or lactating women.
DOSE: in units, administered IV or SC, with preferred administration site being the abdominal area 2″ away from the umbilical cord, thighs or buttocks. Rotate injection site to avoid skin damage. Stop 6-12 hours prior to elective surgery.
INDICATIONS: DVT (deep vein thrombosis), Pulmonary Embolism, Arterial Thromboembolism, MI, unstable Angina.
ADVERSE EFFECTS: haemorrhage, heparin-induced thrombocytopenia, hypersensitivity reactions.
CONTRAINDICATIONS: Thrombocytopenia (low platelet level), uncontrollable bleeding. DO NOT ADMINISTER during or immediately after eye, brain or spinal cord surgery.
UNFRACTIONED HEPARIN: APTT monitoring essential, higher risk, antidote Protamine Sulphate used to reverse effects.
LOW MOLECULAR WEIGHT HEPARIN: no APTT monitoring needed, lowers risk of bleeding, osteoporosis and Heparin-induced Thrombocytopenia, no antidote.

Thrombolytic Drugs – stimulate the plasmin system to break down the formed clot

Streptokinase, Anistreplase and Urokinase (Non-Fibrin Specific)

Alteplase, Reteplase and Tenecteplase (Fibrin Specific Tissue Plasminogen)

CONTRAINDICATIONS OF THROMBOLYTICS: active internal bleeding, intracranial trauma, cerebral haemorrhagic stroke, cerebrovascular disease, major surgery in the past 2 weeks, active peptic ulcer, diabetic retinopathy, pregnancy.

Drugs Affecting Coagulation: Blood Thinners

Heparin

Warfarin

PT/INR vs aPTT

Thrombolytics

Special thanks to the creators of the featured videos on this post, specifically Youtube Channels Simple Nursing and Registered Nurse RN

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Direct Vasodilators – Anti-Hypertensives in Cardiovascular Pharmacology

Here you can find videos related to direct vasodilators which are anti-hypertensive drugs covered within cardiovascular pharmacology…

Types of Cardiovascular Drugs include:

Anti-Hypertensive Drugs
Anti-Angina Drugs
Anti-Arrhythmic Drugs
Anti-Coagulants
Anti-Hyperlipidaemic Drugs

Anti-Hypertensive Drugs are further sub-divided into 4 categories, namely:

Renin-Angiotensin Aldosterone Inhibitors

Adrenergic System Inhibitors

Diuretics

Direct Vasodilators

Below you can find a collection of videos that can help provide a more visual approach to cardiovascular pharmacology, specifically on the Anti-Hypertensive Drugs – Direct Vasodilators.

Nitrates

Available as sublingual spray, oral tablets, transdermal patch, and IV preparation.
Oral medication can be taken up to 3 times within 5 minute intervals; burning sensation may be experienced (harmless).
Sustained release formulas: do not crush and swallow whole; Injection sites should be switched continuously; taper dose over 4-6 weeks to prevent MI.
Transdermal patches can lead to patient tolerance. To avoid, remove patch for 4-8 hours, ideally during the night.
Nitrates are sensitive to light. Protect from sunlight.
INDICATIONS: angina, acute coronary syndrome, for reduction of chest pain and infarct size in MI.
ADVERSE EFFECTS: CNS – throbbing headache, dizziness, weakness; CV – hypotension, reflex tachycardia, syncope; GI – nausea, vomiting, incontinence; EENT – pallor, flushing, sweating; methemoglobinemia and cyanosis if administered in high doses.

Calcium Channel Blockers

Nifedipine, Amiodipine, Nicardipine – Dihyropyridines (Anti Hypertensive properties).

Diltaziem, Verapamil – Non-Dihydropyridines (Anti-Arrhythmic properties).

Causes a decrease in peripheral resistance, blood pressure and cardiac workload, as well as vasodilation.
INDICATIONS: angina pectoris, effort-associated angina, chronic stable angina, unstable crescendo preinfarction angina, essential hypertension.
Parenteral administration for treatment of supraventricular tachyarrhythmia, and temporary control of rapid ventricular rate in atrial flutter or atrial fibrillation.
ADVERSE EFFECTS: dizziness, light-headedness, headache, fatigue, hypotension, heart block, peripheral oedema, bradycardia, nausea, skin flushing, rash.

Direct Vasodilators: Nitroglycerin and Angina

Direct Vasodilators: Administering Nitroglycerin Sublingual Tablets and Translingual Spray

Calcium Channel Blockers

Special thanks to the creators of the featured videos on this post, specifically Youtube Channels Simple Nursing and Registered Nurse RN

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Diuretics – Anti-Hypertensives in Cardiovascular Pharmacology

Here you can find videos featuring Diuretics through a visual approach to anti-hypertensive drugs for Cardiovascular Pharmacology use

Types of Cardiovascular Drugs include:

Anti-Hypertensive Drugs
Anti-Angina Drugs
Anti-Arrhythmic Drugs
Anti-Coagulants
Anti-Hyperlipidaemic Drugs

Anti-Hypertensive Drugs are further sub-divided into 4 categories, namely:

Renin-Angiotensin Aldosterone Inhibitors

Adrenergic System Inhibitors

Diuretics

Direct Vasodilators

Below you can find a collection of videos that can help provide a more visual approach to cardiovascular pharmacology, specifically on the Anti-Hypertensive Drugs – Diuretics

Diuretics: Promote the production of urine, thus increasing urine volume and the excretion of water from the body.

Before starting patient on diuretics, take baseline data of fluid and electrolyte disturbances, hepatorenal diseases, glucose tolerance abnormalities; Assess skin for oedema and skin tugor status; Assess cardiopulmonary status (blood pressure, pulse, heart and lung sounds); Measure body weight to monitor fluid loss or retention.

Monitor intake and output of voiding; monitor lab tests especially K+, Ca+ uric acid and glucose levels; monitor LFTs and renal function.

ADVERSE EFFECTS: electrolyte imbalance, hyperglycaemia, hyperuricemia, acid base disturbances.

Thiazide Diuretics: Bendroflumethazide, Hydrochlorthiazide, Indapamide

Most commonly used diuretic.
Milder effect when compared to loop diuretics.
Causes lower peripheral vascular resistance as well as the excretion of sodium, water, chloride and potassium.
INDICATIONS: pulmonary oedema, forced diuresis.

Loop: Bumetanide, Furosemide

Causes greatest possible amount of diuresis.
Bumetanide is 40% more potent in producing rapid diuresis.
Available in oral, IV and IM formulation.
INDICATIONS: hypertension, heart failure, oedema.

Potassium Sparing: Spironolactone, Amiloride.

Stops sodium reabsorption by interfering with the sodium potassium pump in the distal convoluted tubule.
Used along with Thiazides or Loops when increased diuretic effect is desired.
INDICATIONS: ideal for patients with low potassium level (hypokalaemia).

Thiazide Diuretics

Loop Diuretics

Potassium Sparing Diuretics

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

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Adrenergic System Inhibitors – Anti-Hypertensives in CV Pharmacology

Adrenergic System Inhibitors features videos that provide a visual approach to alpha and beta blockers in cardiovascular pharmacology.

Types of Cardiovascular Drugs include:

Anti-Hypertensive Drugs
Anti-Angina Drugs
Anti-Arrhythmic Drugs
Anti-Coagulants
Anti-Hyperlipidaemic Drugs

Anti-Hypertensive Drugs are further sub-divided into 4 categories, namely:

Renin-Angiotensin Aldosterone Inhibitors

Adrenergic System Inhibitors

Diuretics

Direct Vasodilators

The Adrenergic System:

The main neurotransmitter of the Adrenergic system is Nonepinephrine. Nonepinephrine acts on all adrenergic receptors to generate a response.

When the sympathetic system is stimulated, there is an increase in heart rate and contractility, and blood vessels constrict. When the sympathetic system is blocked, the heart rate slows down and the blood vessels dilate.

Drugs that STIMULATE the adrenergic system = alpha or beta agonists (sympathomimetics).

Drugs that BLOCK the adrenergic system = alpha or beta blockers (sympatholytics).

Beta Blockers:

Beta Blockers block action of Epinephrine and Nonepinephrine and act as antagonists, blocking beta1 (heart) and beta2 (lungs) adrenergic receptors.

First Generation Nonselective Beta Blockers – Act on B1 (Heart) & B2 (Lungs) eg. Nadolol, Oxprenolol, Penbotalol, Pindolol, Propanolol, Sotalol, Timolol.

Second Generation B1 Selective Beta Blockers – Act on B1 (Heart) eg. Acebutolol, Atenolol, Bisoprolol, Esmolol, Metoprolol. Ideal for asthmatics!

Third Generation Vasodilatory: Nonselective eg. Carteolol, Carvedilol, Labetalol; B1 Selective eg. Betaxolol, Nebivolol.

INDICATIONS: angina, arrhythmias, heart failure, hypertension, MI.
ADVERSE EFFECTS: bradycardia, hypotension, increase in lipidemia, decrease in libido, bronchospasm causing shortness of breath, chronic heart failure due to abnormalities in conductivity, kinks peripheral vessels, exhaustion, emotional depression, masks hyperglycaemia.
CONTRAINDICATIONS: bradycardia, heart block, asthma (do not administer 1st Gen Beta Blockers especially Propanolol), CHF, diabetes, COPD. Avoid concurrent administration of BB with CCBs and Diuretics.
NURSING INTERVENTION: check pulse and do not administer if patient is bradycardic. Be extremely careful with HF patients. Monitor side effects.
PATIENT EDUCATION: advise not to stop medication abruptly. Take with food to reduce or prevent GI disturbances. Whilst body adjusts to medication, side effects such as dizziness, light headedness, drowsiness and blurred vision may occur. Cold extremities may be due to the reduction of blood circulation to the extremities.

Alpha Blockers:

Alpha Blockers eg. Doxasozin, Prasozin.

Alpha 1 causes blood vessels to dilate = reduction in the peripheral resistance = fall in BP = postural hypotension. Decreases contraction force of the heart.

Alpha 2 causes vascular smooth muscles to dilate = decrease in BP.

The Sympathetic vs Parasympathetic Nervous System: Inhibiting and Stimulating Drugs

Beta Blockers

Alpha Blockers

Special thanks to the creators of the featured videos on this post, specifically Youtube Channels Registered Nurse RN and Drugs in Motion.

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