Nursing The Individual Archives - Student Nurse Life

Cardioprotective Drugs – Increasing Survival & Decreasing Symptoms

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Cardioprotective drugs aim to increase survival and decrease symptoms of cardio-related issues through primary and secondary risk factor prevention. Blood pressure, lipid management, diabetes mellitus and metabolic syndrome are among the targeted concerns. Apart from pharmaceutical therapy, weight management, an increase in physical activity as well as smoking cessation help in providing a total holistic approach for the patient.

Cardioprotective Drugs – Anti-Platelet Therapy

Aspirin 75mg

provides an irriversible anti-thrombotic effect that lasts throughout the whole platelet life, which is between 9-10 days
provides secondary prevention of cardiovascular events (not to be used as primary prevention due to its increased risk of bleeding

Clopidogrel

provides an anti-thrombotic effect which is similar to Aspirin
should be given to patients who are allergic to aspirin
may be combined with Aspirin and administered post coronary stenting or acute coronary syndrome for a year

Prasugrel

should be given to patients unresponsive to Clopidogrel

Cardioprotective Drugs – Beta-Blockers

beta-blockers names end with _lol
reduce blood pressure and oxygen demand by reducing the heart rate and contractility of the heart
reduce symptoms of angina – unless contraindicated, patients with angina requiring regular symptomatic treatment should be prescribed beta blockers
possible side effects include bradycardia, worsening of respiratory symptoms such as in asthma and COPD (switching to beta 1 selective agents may help reduce this)
erectile dysfunction
rebound angina and an increase in cardiac events may be possible if medication is discontinued abruptly

Cardioprotective Drugs – Calcium Channel Blockers

improves angina
non-dihydropyridines such as Verapamil and Diltiazem help lower the heart rate, reducing contractility, heart rate and AV node conduction, but they may worsen heart failure; may cause side-effects such as bradycardia, conduction disturbances and constipation; can be used with beta-blockers in symptomatic patients (but be careful about possible severe bradycardia)
dihydropyridines, including Nifedipine and Amlodipine, may cause side effects such as headaches, flushing and ankle oedema

Cardioprotective Drugs – ACE Inhibitors

helps in treating stable angina pectoris as well as related hypertension, diabetes, heart failure, asymptomatic left ventricular dysfunction or MI injury
may cause a persistent dry cough, causing some patients to have to switch to an ARB instead
rarely causes angioedema

Cardioprotective Drugs – Nitrates

Short-Acting Nitro Glyceral Spray

results in vasodilation
provides pain relief and anti-ischaemia effects
sublingual Nitro Glyceral spray reduces angina pectoris attacks and may also be used in prophylaxis
side effects include headache and flushing, as well as possible orthostatic hypotension
angina unresponsive to nitroglycerin should be assessed as a possible MI or non-cardiac pain

Long-Acting Nitrates

provides relief for symptomatic angina
patient tolerance to oral or transdermal nitrates happens fast, thus, nitrate-free intervals are recommended (eg. nitrate patch should be reduced during the night)
side effects include headache and orthostatic hypotension

Trimatazidine

anti-angina properties
side effects include fatigue and drowsiness

Ivabridine

preserves AV and intraventricular conduction of the myocardium
slows heart rate

Statins

used as primary and secondary preventative measures along with healthy lifestyle changes
lowers lipid levels, inhibiting cellular cholesterol production, reducing LDL cholesterol by up to 40%, thus accounting to a reduction in coronary events
may increase HDL (the ‘good’ cholesterol)
reverses endothelial dysfunction, decreases thrombogenicity and reduces inflammation
stabilise lipid-rich atherosclerotic plaques, making them less vulnerable to become unstable and possible rupture
should be prescribed for all patients with Ischaemic Heart Disease due to their long-term benefits
patients with acute coronary syndrome taking statins are less likely to experience a MI or acute arrhythmias
patients admitted to hospital with acute coronary syndrome should be prescribed statins independently of their LDL level
side effects may include skeletal muscle damage which may be indicated by symptoms, Creatine Kinase level elevation and possibly rhabdomyolysis
OTHER LIPID LOWERING DRUGS include Bile Acid Binding Resins, Fibric Acid derivatives, Nicotinic Acid and Ezetimibe

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Cardiac Catheterisation To Diagnose and Treat Cardiovascular Conditions

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Cardiac catheterisation is an invasive diagnostic procedure where a catheter is inserted through a peripheral blood vessel to acquire important information about the structure and function of the heart. Through angiography, x-ray images are produced, showing the coronary arteries supplying blood to the myocardium. Treatment of cardiovascular conditions are also possible through cardiac catheterisation.

Cardiac Catheterisation Indications

Emergency situation eg. STEMI or NSTEMI presenting with chest pain;
Urgent situation eg. STEMI treated with fibrinolysis or NSTEMI;
Elective situation eg. in stable coronary artery disease (patient experiences pain during exercise or climbing a flight of steps which goes away after rest – non-urgent situation where planning is possible).

Cardiac Catheterisation Contraindications

anaemia
electrolyte imbalance
uncontrolled hypertension
arrhythmias
renal impairment
allergy to radiographic contrast used in procedure (in which case a different technique may be used)
peripheral vascular disease (in this case the best route to be used to advance catheter should be sought)
recent cerebrovascular accident
severe cardiac failure (in which case patients should NOT be put in supine position due to dyspnoea)
coagulopathy (patient could bleed excessively)
uncontrolled diabetes mellitus (blood glucose should be controlled prior to the procedure)
pregnancy (dye used in procedure could be toxic for the foetus)

Nurse Responsibilities

know about the patient’s comorbidities that may increase complication rate
allergy history especially to drugs and iodine/seafood
know patient haemoglobin level before patient reaches operating table so as to know how to manage bleeding if needed
acquire patient signature on consent form
explain frequently experienced sensations such as hot flush or metallic taste that comes with the procedure when dye is injected
keep patient monitored on ECG with remote defibrillation pads available especially with unstable patients during procedure (a rapid pulse is a normal finding)

Access Route

Cardiac catheterisation is done through the femoral or radial artery. The radial artery is quicker and safer (due to the palmar arch) than the femoral artery since it is wider, making it easier to advance wire through it. It also allows the patient to sit up right after the procedure, whereas in femoral access the patient has to stay on bed rest with the femoral area frequently monitored. However, the femoral artery is still preferred by many operators.

Femoral Arterial Sheats Removal Nurse Responsibilities

Ensure that the patient has been prescribed analgesia prior to sheath removal.

In hypertensive patients, prolonged manual pressure should be applied before sheath removal.

If a haematoma is present, blood flow to the lower limb could be compromised. Thus, the nurse should access the pedal pulse to confirm if blood flow is being impeded. Comparing both limbs and asking the patient to move toes may also help. Manual pressure or through a mechanical device should be used in the case of a haematoma.

Gelafundin, which is a sterile powder indicated in surgical procedures to obtain haemostasis, can be helpful when dealing with a haematoma, however it has an effect on blood pressure. The systolic pressure needs to be less than 90 to use Gelafundin.

Record length and width of haematoma by marking the edges so you can compare later on to confirm whether it is spreading or reducing.

Bleeding

In the case of bleeding from the angio site, occlude femoral artery with manual pressure and assess whether bleeding stops. If it doesn’t stop it means that the bleeding is superficial. In this case apply manual pressure. For mild bleeding apply pressure for 10-20 minutes either using manual pressure or FemoStop, which is a compression device. In the case of major bleeding, a drop in haemoglobin may be noted. This may require blood transfusion. For this reason, the patient should be cross-matched prior to the procedure.

Pseudoaneurysm happens when blood flowing through the tunica media is captured behind the tunica advanticia, which can lead to a rupture due to its weakness. Pseudoaneurysm can cause nerve compression leading to neuralgia.

In retroperitoneal bleeding, which is the result of a ruptured pseudoaneurysm, the patient deteriorates in a very short time, especially since this cavity is very big and can accumulate a large amount of blood which leads to cardiogenic shock. Symptoms of retroperitoneal bleeding include hypotension and severe back pain. It should be reported immediately.

Patient Education

apply pressure to femoral site when coughing or sneezing, or if warmth or wetness is felt
after femoral sheath removal, patient should stay on bed rest for 4 hours
unless contraindicated, fluid intake should be encouraged to promote contrast medium excretion
patient should report any bleeding or pain at the angio site immediately

Below you can find a collection of videos that can help provide a more visual approach to cardiac catheterisation.

Cardiac Catheterisation Procedure

Angioplasty Procedure

Cardiac Catheterisation Sheath Removal

FemStop Femoral Artery Compression Device

TR-Band Radial Compression Device

Special thanks to the creators of the featured videos on this post, specifically Youtube Channels Beaumont Health, Fortis Healthcare, Houston Methodist DeBakey CV Education, Nicole McMullen and Radcliffe Group.

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Smoking Cessation Nicotine Replacement Therapy, ENDDs & Medication

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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.

Maltese Health Promotion Leaflet Download

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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Cardiovascular Health Nutrition – CVD Non Pharmacological Intervention

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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.

cardiovascular health nutrition — Accessed from https://www.pinterest.com/pin/314618723944586389/ on 30th January 2021

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.

ABCDE of primary prevention CVD — Accessed from https://kahn642.medium.com/understanding-the-new-2019-acc-aha-guideline-on-the-prevention-of-cardiovascular-disease-in-under-f7f862980ebb on 30th January 2021

clinical signs and symptoms of nutritional deficiencies — Accessed from https://www.slideshare.net/ahmedabudeif/nutritional-assessment-71093757 on 31th January 2021

ABCD Systematic Approach Assessment

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.

metabolic syndrome CVD — Accessed from https://slideplayer.com/slide/1507908/ on 30th January 2021

Below you can find a collection of videos that can help provide a more visual approach to cardiovascular health nutrition.

Cardiovascular Disease Primary Prevention

Cardiovascular Disease Secondary Prevention

Cardiovascular Health Nutrition: The Dash Diet

Cardiovascular Health Nutrition: the Mediterranean diet

Special thanks to the creators of the featured videos on this post, specifically Youtube Channels Johns Hopkins Medicine, World Heart Federation, Well+Good and LLUHealth.

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Acute Coronary Syndrome – STEMI, NSTEMI, Necrosis and Angina

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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.

acute coronary syndrome diagnosis — Assessed from https://en.wikipedia.org/wiki/Acute_coronary_syndrome on 28th January 2021

Plaque Rupture Triggers

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 serum cardiac biomarkers: necrosis causes sarcolema disruption, releasing macro-molecules in circulation
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
Anti-Ischaemic Therapy: Beta-Blockers, Nitrates and Calcium Channel Blockers (CCB are not to be administered in case of heart block or heart failure)
Anti-Thrombotics – Aspirin (300gm) & Clopidogrel (300-600mg loading dose, then 75mg): balance platelet aggregation
Anti-Coagulants – Enoxaparin OR IV Heparin OR Fondaparinux OR Bivalirudin (the latter only for patients undergoing Percutaneous Coronary Intervention)
Statin: anti-cholesterol drug that reduces infarction and mortality
ACEi: helps control blood pressure – excellent drug for patients with low ejection fraction

Percutaneous Coronary Intervention VS Thrombolytics

PCI vs Thrombolytics — Accessed from https://www.researchgate.net/figure/Advantages-and-disadvantages-of-thrombolysis-vs-PPCI_tbl1_230724181 on 29th January 2021

Myocardial Infarction Complications

Cardiogenic Shock

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.

Acute Coronary Syndrome Detailed Overview

Special thanks to the creator of the featured videos on this post, specifically Youtube Channel Armando Hasudungan and Thrombosis Adviser.

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Cardiac Pacing – Saving Endangered Lives With A Cardiac Pacemaker

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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.

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

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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)

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

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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)
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

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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.

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

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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

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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