Week 5 Cardiac A

Introduction

• This module introduces the cardiovascular system over two weeks.
• Focuses on acute coronary syndrome, ECG interpretation (sinus rhythm and atrial fibrillation), and chest pain management.
• The cardiovascular system circulates blood, delivering oxygen and nutrients while removing waste.
  • Consists of the heart, blood vessels (arteries, veins, capillaries), and blood.
  • Regulates body temperature, transports hormones, and maintains pH and electrolyte balance.
• Learning Outcomes:
  • Cardiac assessment skills.
  • Understanding cardiovascular disease (CVD) and coronary heart disease (CHD).
  • Knowledge of risk factors like hypertension and dyslipidaemia.
  • Understanding acute coronary syndrome.
  • Identifying sinus rhythm (SR) and atrial fibrillation (AF) on ECG.
  • Safe administration of heart-related medications.

Resources

• Reading Materials:

  • Brown et al., (2023). Lewis's Medical-Surgical Nursing: Assessment and Management of Clinical Problems (6th ed). Elsevier

    • Section 7: Problems of oxygenation: Perfusion
    • Chapter 31: Nursing assessment- Cardiovascular system (pp. 792-818)
    • Chapter 32: Nursing management- Hypertension (pp. 819-840)
    • Chapter 33: Nursing management- Coronary artery disease and acute coronary syndrome (pp. 842-878)

  • Craft, J & Gordon, C. (2023). Understanding pathophysiology (4th ed). Elsevier

    • Chapter 23: Alterations of cardiovascular function across the life span (pp. 612-635)

  • Burchum, J.R., Rosenthal, L.D., (2022) Lehne's Pharmacology for Nursing Care (11th ed). Elsevier

    • Chapter 54: Drugs for Angina Pectoris
    • Chapter 55: Anticoagulant, Antiplatelet, and Thrombolytic Drugs
    • Chapter 56: Management of ST-Elevation Myocardial Infarction

  • Tollefson, J. & Hillman, E. (2025) Clinical Psychomotor Skills (9th ed). Cengage.

    • Chapter 17: Focused cardiovascular health history and physical assessment, p. 90-95
    • Chapter 18: 12-lead electrocardiogram, p. 96-99

Brief Revision of Cardiac Anatomy and Physiology

• Revise cardiac anatomy and physiology.
  • Cardiac structure and function.
  • Cardiac cycle.
  • ECG lead placements.
• Identify the main functions of the cardiovascular system.
• Review the completion of a focused cardiovascular system assessment.
• Video Resources:
  • Cardiac Anatomy and Physiology.
  • Heart Structure and Function.
  • Cardiac Cycle.
  • Pulmonary and Systemic Circulation.
  • Coronary Circulation.
• Reading:
  • Craft, J & Gordon, C. (2023). Understanding pathophysiology (4th ed). Elsevier.
    • Chapter 22: The structure and function of the cardiovascular and lymphatic systems (pp 565-610)

Cardiovascular Assessment

• Revise elements of cardiovascular assessment for Clinical Learning Environment (CLE) application and clinical placements.
• Assessment Skills:
  • Vital for care, prioritization, and identifying deterioration.
• Objective Data:
  • Primary assessment (DRSABCDE).
    • Important for Emergency Department (ED) presentations.
  • Secondary assessment.
    • Focused assessment for ward-based patients.
  • Full set of vital signs.
• Focused Cardiovascular Assessment:
  • Use "Look, Listen, Feel" or "Inspect, Auscultate, Percuss, Palpate" approach.
  • General appearance: Conscious state, posture, skin/nails, speech, affect/mood, eye contact, weight.
  • Blood pressure (BP): Assess both arms, consider orthostatic BP (lying, sitting, standing), review trends.
  • Capillary refill.
  • Pulses: Peripheral and central.
  • Heart sounds: Identify auscultatory areas, S1/S2 sounds, adventitious sounds, extra heart sounds, murmurs.
  • Peripheries: Peripheral oedema, warmth, vascular changes, lower extremity ulcers/wounds, clubbing.
  • Special populations: Paediatrics, pregnant women, older people.
• Subjective Data:
  • Chest Pain.
• Cardiac History:
  • Personal cardiac history: Specific details, management, changes, tests, pending treatment.
  • Family/genetic history: Cardiac issues, stroke, obesity, diabetes mellitus, age of onset.
• Reading:
  • Brown, D. & Edwards, H. (2023). Lewis's Medical-Surgical Nursing (6th edition). Elsevier, p. 792-818.

Cardiovascular Disease (CVD)

• Cardiovascular disease (CVD) is an umbrella term for diseases of the heart and blood vessels.
  • Includes stroke (covered in semester 2), coronary artery disease, and acute coronary syndrome.
• Impact:
  • Significant health problem: 1 in 6 Australians have CVD (over 4.5 million people, approx. 18%).
  • Mortality: CVD accounts for 1 in 4 deaths (24%), about 118 people per day or 1 person every 12 minutes.
  • Higher incidence in lower socioeconomic groups, Aboriginal and Torres Strait Islander people, and rural/remote areas.
  • Financial cost: Approximately 5 billion annually on public hospital services for CVD treatment (11% of total hospital expenditure).

Coronary Heart Disease (CHD)

• Overview:
  • Coronary heart disease (CHD) is a subcategory of CVD, affecting the heart's structure and function.
    • Primarily involves coronary arteries via atherosclerosis.
  • Also known as coronary artery disease (CAD) or ischaemic heart disease (IHD); terms are generally interchangeable.
  • CHD results from atherosclerosis, with associated risk factors.
• Risk Factors:
  • Conditions increasing CVD/CAD risk.
  • Divided into modifiable and non-modifiable factors.
  • Other conditions increasing risk:
    • Diabetes mellitus (Type I, Type II, gestational).
    • Fasting BGL >6.4mmol/L.
    • Kidney function issues (microalbumin +/- urine protein, eGFR <45mL/min/1.73m^2).
    • Familial hypercholesterolaemia.
    • Homocysteine levels.
    • Evidence of AF.

Atherosclerosis

• Atherosclerosis is the primary cause of CHD, potentially leading to acute coronary syndrome.
• Arteriosclerosis vs. Atherosclerosis:
  • Atherosclerosis is a form of arteriosclerosis.
  • Arteriosclerosis is a general term for thickening and stiffening of arterial walls.
    • Includes non-atheromatous arteriosclerosis, Monkeberg's arteriosclerosis, hyaline arteriolosclerosis, hyperplastic arteriolosclerosis, and atherosclerosis.
  • Atherosclerosis involves soft deposits of intra-arterial fat and fibrin that harden over time.
• Arterial Wall Layers:
  • Tunica Intima.
  • Tunica Media.
  • Tunica Adventitia.
• Pathophysiology:
  • Develops over decades, beginning with fatty streaks progressing to plaque.
  • Can lead to artery blockage, causing acute coronary syndrome (ACS).
  • Narrowing of coronary arteries by 50% or more can impair myocardial oxygen delivery and cellular metabolism.

Hypertension

• Hypertension (HT) is a prevalent cardiovascular condition.
  • Approximately 3.7 million Australians over 25 (30% of adults) have HT or are medicated for it.
  • Major modifiable risk factor for CHD; contributes to atherosclerosis, angina, and myocardial infarction progression.
• Impact:
  • High morbidity, mortality, and economic burden.
  • Increases atherosclerosis risk by two to three-fold.
  • Contributes to endothelial injury and myocardial hypertrophy, increasing myocardial oxygen demand.
• Pathophysiology:
  • Blood pressure (BP) is the pressure exerted by blood in intravascular space.
  • Control occurs via systemic and peripheral vascular systems, regulated by baroreceptors.
  • HT results from changes in factors affecting peripheral vascular resistance or cardiac output.
  • Diagnosis is based on repeated BP measurements >140mmHg (systolic) and/or >90mmHg (diastolic).
  • Multifaceted combination of genetic and environmental influences triggers neural and hormonal responses.
  • Pathways involve activation of sympathetic nervous system, renin-angiotensin-aldosterone system, and natriuretic peptides.
  • Inflammatory processes, endothelial dysfunction, and insulin resistance elevate peripheral vascular resistance and blood volume; impede sodium excretion.
• Clinical Manifestations:
  • Elevated BP.
  • Effects distributed throughout the body; implicated in several conditions.
  • Many people asymptomatic or have mild symptoms; organ damage can occur before symptoms are evident.
• Complications:
  • Dizziness, fatigue.
  • Palpitations and dyspnoea.
  • Retinal changes, papilloedema.
  • Coronary heart disease/angina/ACS.
  • Left ventricular hypertrophy (LVH).
  • Chronic renal impairment.
  • Stroke, TIAs.

Dyslipidaemia

• Lipids (cholesterol) are essential for cell membrane function; triglycerides are a major energy source.
• Dyslipidaemia Definition:
  • Imbalance of lipids (cholesterol, LDLs, triglycerides, HDLs).
• Pathophysiology:
  • Elevated levels can make artery walls 'sticky,' damaging the endothelial wall, leading to atherosclerosis.
• Detection:
  • Often asymptomatic; regular check-ups and blood tests required for at-risk patients.

Nursing Assessment and Management

• Covers nursing assessment and management for atherosclerosis, hypertension, and coronary heart disease.
  • Also relates to angina and heart failure.
• Key Concepts Summary for CVD-Focused Assessment:
  • Subjective Data:
    • Important health information.
      • History of present illness: Current symptoms.
      • Past health history: Chest pain, shortness of breath, palpitations, dizziness, syncope, fatigue, substance use, anaemia, rheumatic fever, congenital heart disease, known duration/workup of high BP, cardiovascular/renal/thyroid disease, diabetes, obesity, dyslipidaemia, thrombophlebitis, intermittent claudication, varicosities, oedema, menopause/hormone replacement status.
      • Medications: Prescription, OTC, illicit, herbal; previous antihypertensive therapy.
      • Surgeries/Treatments: Specific treatments, past surgeries/hospital admissions for cardiovascular issues.
  • Objective Data:
    • Physical examination.
      • Vital signs:
        • BP (bilateral measurements, orthostatic readings).
      • Inspection:
        • Thorax and bony structures.
        • Skin: Colour, oedema, clubbing, varicosities, lesions/ulcers.
        • Large veins in neck.
      • Palpation:
        • Upper/lower extremities: Temperature, moisture, pulses, oedema.
        • Pulse strength and rhythm.
        • Capillary refill.
        • Central pulses.
      • Auscultation:
        • Major arteries.
        • Heart sounds.
  • Functional Health Patterns:
    • Health perception-health management: Risk factors, family history, substance use, allergies.
    • Nutritional-metabolic: Salt/fat intake, food habits, weight changes.
    • Elimination: Nocturia, incontinence, constipation, medication use.
    • Activity-exercise: Fatigue, dyspnoea, palpitations, exertional chest pain, claudication, cramps, exercise patterns.
    • Sleep-rest: Paroxysmal nocturnal dyspnoea, pillow use, sleep apnoea.
    • Cognitive-perceptual: Dizziness, blurred vision, paraesthesia.
    • Sexual-reproductive: Erectile dysfunction, decreased libido.
    • Coping-stress tolerance: Stressful life events.
    • Self-perception: Quality of life impacted by CVD.
    • Role-relationship: Age, gender, socioeconomic status, roles, employment, living environment, satisfaction with life roles.
  • Focused Cardiovascular Assessment Findings:
    • Cardiovascular:
      • SBP consistently >140mmHg, DBP >90 mmHg, orthostatic changes in BP/pulse, bilateral BP differences, abnormal heart sounds, displaced apical pulse, diminished/absent peripheral pulses, bruits, peripheral oedema, strict fluid balance/restriction, ECG changes.
    • Neurological: Mental status changes, anxiety, restlessness.
    • Gastrointestinal: Obesity, high waist-hip ratio, nausea/vomiting, weight changes, constipation.
    • Renal: Poor urine output, increased urea/creatinine.
    • MSK/Integ: Low muscle tone, arterial/venous ulcers, pressure sores, pigmented skin, cool peripheries.
  • Possible Diagnostic Findings:
    • Abnormal serum electrolytes, increased urea/creatinine/glucose/cholesterol/triglyceride levels, proteinuria, microalbuminuria, haematuria, ischaemic heart disease/LVH on echocardiogram, arteriovenous nicking, retinal haemorrhages, papillo-oedema.
• Nursing Management:
  • Combination of lifestyle modification, medication management, and regular assessment.
  • Education:
    • Educate about CVD, risk factors, lifestyle modifications and medication adherence to improve outcomes.
    • Provide practical recommendations for modifiable risk factors (obesity, dyslipidaemia).
  • Medication Management:
    • Educate and check understanding of medications, including dosage, indications, timing, and side effects.
    • Encourage reporting of side effects to specialist/GP.
    • Pharmacist involvement: Hospital pharmacist education, then local pharmacist for ongoing questions.
    • Address barriers to medication management (access/cost).
  • Collaboration and Referrals:
    • Refer to cardiac rehabilitation to reduce readmission and improve outcomes.
    • Collaborate with specialists, GPs, pharmacists, and allied health.
  • Patient Advocacy:
    • Ensure understanding of healthcare journey; assist navigation from acute hospital to discharge with resources/services.
  • Risk Factor Reduction:
    • Maintain healthy weight, healthy diet (reduce salt), avoid tobacco/alcohol, increase exercise, manage psychosocial risk factors.
  • Adapted from Lewis's Medical-Surgical Nursing (6th ed.), Table 33.3:
    • Hypertension: Monitor home BP, attend check-ups, take medications, reduce salt, stop tobacco, control weight, move/walk daily.
    • Elevated serum lipids: Reduce total/animal fat, take medications, adjust intake for ideal weight, engage in daily physical activity, increase complex carbs/fibre/vegetable proteins.
    • Tobacco use: Quit program, change routines, substitute activities, ask for support, avoid exposure.
    • Physical activity: 30 minutes moderate activity daily (5/7 days).
    • Psychological state: Increase awareness of harmful behaviours, alter stress patterns, set realistic goals, reassess priorities, manage stress, seek help, plan rest/sleep.
    • Obesity: Change eating patterns, reduce energy intake (BMI 18.5-24.9 kg/m2), increase activity, avoid fad diets/heavy meals, consider smaller more frequent meals.
    • Diabetes: Follow diet, control weight, take medications, monitor blood glucose.
    • Complementary therapies: Breathing exercise, meditation/mindfulness, tai chi, yoga, hypnosis, biofeedback, acupuncture, supplements (fish oils after consultation).
• Impact of High Dietary Salt Intake
• Cardiac Rehabilitation:
  • Important interprofessional program for those recovering from acute MI, heart failure, or requiring surgery/medical treatment for CHD.
  • Improves quality of life and reduces risk of another cardiac event.
  • Includes physical activity, healthy living education, medication adherence, and stress relief counselling.

Acute Coronary Syndrome (ACS)

• ACS is the umbrella term for conditions related to atherosclerosis buildup in coronary arteries, leading to ischaemia or infarction.
• Three categories:
  • Unstable angina (UA):
    • New onset or worsening chest pain with minimal exertion.
    • Unpredictable; considered an emergency.
    • May or may not have ECG changes, but no cardiac biomarkers.
    • Warning sign for NSTEMI or STEMI.
  • Non-ST elevation infarction (NSTEMI):
    • Prolonged ischaemia leading to myocardial cellular death.
    • No ST elevation on ECG, but detectable cardiac biomarkers.
  • ST elevation myocardial infarction (STEMI):
    • ST segment elevation on ECG; life-threatening emergency.
    • Considerable delay or lack of treatment results in increased morbidity/mortality.
• Clinical manifestations of myocardial ischaemia/infarction:
  • Possible ACS pain locations.
  • Other symptoms: Nausea/vomiting, dyspnea, fatigue, diaphoresis, syncope.
• Diagnosis of ACS:
  • ECG
  • Cardiac biomarkers
  • Coronary angiogram
  • Other tests: exercise stress test, echocardiogram.
• ACS management is guided by the Acute coronary syndrome guidelines (2016).
  • 2.3 Initial Clinical Management, p. 905-907
  • 6 Discharge Management and Secondary Prevention, p. 933-936

Angina

• Angina is a manifestation of CHD resulting in inadequate blood flow to the myocardium; classified as stable or unstable.
• Pathophysiology:
  • Coronary arteries narrowed or blocked by conditions like atherosclerosis.
  • Prevents vessel expansion during heightened myocardial demand.
  • Plaque disruption leads to thrombus formation, reducing blood flow.
  • Lactic acid buildup irritates myocardial nerve fibres, causing referred pain.
  • Increased vasoconstriction further reduces blood flow.
  • Angina indicates reversible myocardial ischaemia, triggered by increased oxygen need or diminished supply.
  • Impact to the supply of oxygen with ischaemia occurring typically happens when an artery is obstructed by 70-75% or more.
• Stable Angina:
  • Chest pain stems from imbalance between myocardial oxygen supply and demand due to artery narrowing.
  • Chronic Stable Angina:
    • Predictable transient chest discomfort precipitated by exertion/stress relieved by rest/GTN within minutes.
    • Pain indicates artery narrowing; permanent damage does not occur.
    • Episodes indicate increased risk of cardiac event.
• Unstable Angina:
  • New onset chest pain, occurs at rest, and/or has a worsening pattern. Impending acute myocardial infarction.
  • Small fissuring/erosion of plaque triggers thrombotic vessel occlusion; endothelial dysfunction.
  • Thrombus partially occludes vessel for up to 10-20 minutes with return of perfusion occurring before significant myocardial necrosis occurs.

Chest Pain Assessment and Management

• Comprehensive and accurate assessment of chest pain is required to determine whether the chest pain is the results of stable or unstable angina, acute coronary syndrome (including myocardial infarction) or an alternative diagnosis.
• Important factors for nurses:
  • PQRST chest pain assessment.
  • ECG - and medical review
  • Patient and/or family history
  • Medications
  • Allergies
  • Cardiovascular risk factors
  • Vital signs
  • In some settings - IV access and pathology taken
• PQRST Assessment of Chest Pain:
  • P - Precipitating factors: What events or activities precipitated the pain (e.g. argument, exercise, resting)?
  • Q - Quality of pain: What does the pain feel like (e.g. pressure, dull, aching, tight, squeezing, heaviness)?
  • R - Region/Radiation of pain: Where is the pain located? Does the pain radiate to other areas (e.g. back, neck, arms, jaw, shoulder, elbow)?
  • S - Severity of pain: On a scale of 0–10 with 0 indicating no pain and 10 being the most severe pain you could imagine, what number would you give the pain?
  • T - Timing: When did the pain begin? Has the pain changed since this time, what relieved it? Have you had pain like this before?
  • BUT always suspect the chest pain is caused by the heart until proven otherwise, because "time is muscle" (ie the longer the artery if the patient is having a heart attack (AMI) is blocked, the more muscle is damaged or dies)

Electrocardiogram (ECG)

• The electrical conduction system of the heart coordinates contraction of the heart.
• Definition:
  • ECG is a visual representation of the electrical conduction system of the heart.
  • Allows for detection of abnormalities in depolarisation and repolarisation of atrial and ventricular activity.
  • Electrical conduction begins with sinus node firing.
    • Impulse travels through internodal branches and Bachmann's branch to the AV node.
    • Brief pause for atrial contraction.
    • AV node transmits impulse down the bundle of His to the left and right bundle branches and to the Purkinje fibres.
    • Causes ventricular contraction.
  • Another way to record the electrical activity of the patient's heart is continuous cardiac monitoring.
• If patient complains of 'chest pain', 'chest discomfort' or other symptoms suspected of being related to the patient's heart, you MUST do a 12-lead ECG immediately and get this ECG reviewed by a doctor preferrablely within 10 minutes of symptoms commencing.

Sinus Rhythm (SR)

• Sinus rhythm is the most common rhythm seen in health hearts. The sinoatrial (SA) node generates the impulse which is conducted throughout the heart via the normal conduction pathway.

Atrial Fibrillation (AF)

• Overview:
  • Atrial fibrillation (AF) is the most common arrhythmia in Australia and New Zealand, with prevalence increasing with age.
  • Types:
    • Occasional (paroxysmal) AF: atrial fibrillation and associated symptoms may come and go, usually lasting for a few minutes to a hours. The patient may or may not require treatment.
    • Persistent AF: atrial fibrillation lasts longer than a week and can become permanent. Treatment can include cardioversion, however, as the duration is generally unknown, medications would be the first treatment option.
    • Permanent AF: the rhythm has become a permanent condition for the patient, and the normal heart rate cannot be restored with interventions. At this stage, the patient will require specific medications to prevent the assocaiated complications of AF (such as thrombus formation).
  • Causes: The cuase can come from a range of pathophysiological mechanisms:
    • Excess catecholamines such as adrenaline infusion, stree, thyrotoxicosis
    • Incerased atrial automaticity caused by alcholol, caffeine, myocarditis, electrolyte imbalances
    • Atrial enlargement caused by pulmonary hypertension, septal defects, heart failure or valvular disease
    • Abnormality fo the conductin system as a result of congenital cardiac disease, ischaemic heart disease or hypothermia.
  • The following factors can also increase the risk of developing AF:
    • Advanced age Congentail heart disease Other heart disease: valvular, CHD, structural heart disease, atrial ischaemia, heart failure, hypertension Endocrine disorders: diabetes, hyperthroidism Sleep apnoea Lifestyle: sedentary, obesity, increased alcohol consumption Genetics
  • Pathophysiology: Cardiac remodelling, such as atrial enlargement, can lead to structural and electrical changes that cause AF.
    • The enlargement of the atrium results in stetching of the myocytes, extracellular matrix and fibrous tissue depostis. This then leads to abnormal sites firing off in the atrium. Some of these abnormal firing sites electrical stimuluses make it through to the ventricles resulting in an irregular rhythm.
  • Clinical Manifestations
    • Fatigue, altered conscious state, dizziness, syncope Irregular pulse - may be controlled or uncontrolled Palpitations, chest pain Hypotension Shortness of breath, anxiety Diaphoresis, pallor
  • Nursing Assessment and Management:
    • Nursing Assessment: For patients with CVD, a primary, secondary assessment and vital signs can be completed as part of an admission, start of shift and/ or clincially indicated. It is a good idea to adopt the 'head-to-toe' approach as discussed in Module 1: Acute Clincial Concepts. But in this situation (as with any system related condition) a focused cardiovascular assessment should be also completed.
    • Nursing Management: Nursing management of AF involves controlling symptoms, preventing complications and improving patient’s quality of life.
    • If you notice a new irregular pulse when assessing heart rhythm, please escalate this immediately to the nurse-in-charge and/or the medical team.
    • Regular assessment of vital signs; cardiac rhythm and/ or cardiac monitoring/ telemtry ( which is continuous ECG monitoring) may be indicated; symptoms identification, management and control; cardiovascular system assessment at least once per shift Assessing and management of associated complications.
    • Medication management: Administer medications as prescribed and indicated, including rate or rhythm control agents, anticoagulants, and antiarrhythmics. This needs special consideration when patients are unwell. Always check with medical staff before withholding rate and rhythm control medication.
    • Anticoagulant therapy: Ensure patients understand the importance of anticoagulation therapy in reducing the risk of thromboembolic events (for example stroke).Monitor international normalised ratio (INR) levels for patients on warfarin and ensure that the dose is adjust as necessary by the medical team.
    • Risk factor modification and lifestyle management: Discuss with patients the modifiable risk factors such as hypertension, diabetes, obesity, sleep apnoea and reducing stimulants such as caffeine and nicotine.
    • Medical Management: Electrocardiogram (ECG) Holter monitor Echocardiogram Blood test (such as thyroid function and electrolytes) Stress test Chest x-ray

Cardiovascular Pharmacology

• Pharmacology related to the cardiovascular system has many different treatments that are generally related to slowing the disease process.

Pharmacology of Hypertension

• The pharmacological treatment of HT takes on many different forms and is patient specific, depending on the type and severity of the HT
• The common types of drugs used to treat HT, generally fall into the following class:
  • Diuretics Beta-Adrenergic Blockers Renin-Angiotensin-aldosterone inhibitors (i.e ACE inhibitors) Calcium Channel Blockers
• The following is a list of drugs commonly used to treat HT (click on the drug to review the page in the AMH book)
  • Beta-Blocker: Commonly referred to as the "olols" Beta-blockers work by competitively blocking the beta receptors in the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver. Beta-blockers are used to reduce HR, BP and cardiac contractility which in tern reduce myocardial oxygen demand.
    • The following is a list of Beta-Blockers currently available for use in Australia: Atenolol Bisoprolol Carvedilol Labetalol Metoprolol (probably the most commonly used Beta-Blocker) Nebivolol Propranolol Sotalol
  • Angiotensin- Converting Enzyme (ACE) Inhibitors: Commonly referred to as the 'prils' The primary this family of drugs is to block the conversion of angiotensin I to angiotensin II of the renin-angiotensin-aldosterone system (RAAS).
    • The following is a list of ACE Inhibitors currently available for use in Australia: Captopril Enalapril Enalaprils with hydrochlorothiazide Fosinopril Lisinopril Perindopril Perindopril with amlodipine Prindopril with indapamide Quinapril
  • Angiotensin II Receptor Blockers (ARBs): Commonly referred to as the 'Sartans' This family of drugs work by competitively blocking the ability of angiotensin II binding to type 1 angiotensin receptors
    • The following is a list of ARBs currently available for use in Australia: Candesartan Candesartan with hydrochlorothiazide Irbesartan Irbesartan with hydrochlorothiazide Losartan Olmesartan
  • Calcium Channel Blockers (CCBs): most ending in 'dipine', but don't be fooled there are other CCBs This family of drugs work by blocking the inward current of calcium into the cells of the vascular smooth muscles, myocardium and the cardiac conduction system. Intracellular calcium regulate the contractile force in the myocardium and vascular smooth muscle cells. CCBs decrease the amount of calcium available to the contractile proteins within the cell thereby reducing the contraction force of the myocardium and relaxation of the vascular smooth muscles resulting in vasodilation.
    • The following is a list of CCBs currently available for use in Australia: Dihydropyridines Amlodipine Amlodipine with atorvastatin Amlodipine with valsartan
    • Diuretics: the ones that make you wee Diuretics are mostly used for heart failure (to be discussed in Cardiac B) and HT. The use of diuretics for the control of BP is centred around reducing intravascular volume.

Pharmacology for Dyslipidaemia

• This specific group of drugs play an important role in slowing the progression of the development of atherosclerosis, improve cardiac outcomes and reduce mortality rate.
• Within this group there are a number of different ways in which the drugs work. Some work in the liver by inhibiting cholesterol production (statins), some work by inhibiting cholesterol uptake at the epithelial cell with in the small intestines, while others work directly on the LDL receptor sites themselves and bind to these preventing this site from being available thereby preventing the LDL from entering the cell.
• The main drugs to focus on in this group are the:
  • Statins: the most commonly used Fibrates (not commonly used in Australia, but if you would like more information please see the link below to the AMH). Cholesterol absorption inhibitors: when statins are contraindicated or can't be tolerated
    • Statins: the most commonly used This family of drugs work directly in the liver by competitively inhibiting HMG-CoA reductase which increases hepatic cholesterol uptake from the blood thereby reducing the concentrations of LDL and triglyceride and have a small increase in HDL concentrations.
  • Cholesterol Absorption Inhibitors: Currently there is only one drug available in this family, Ezetimibe. This drug works by inhibiting the absorption of cholesterol in the small intestines, essentially leaving with the lower gastrointestinal tract to be excreted through faeces.

Pharmacology for ACS, Angina & AF

• The primary goal of the medications for ACS and angina are centred around 'dissolving' or slowing the development of clots (thrombus) and controlling chest pain symptoms.
  • Anti-anginal Medications (Acute Ischaemic Therapies): The most common medication used in this family of drugs is the organic nitrates, one of the oldest treatments for angina. The main physiological action of these medications is vasodilation.
    • Anti-platelet and Anti-thrombotic Medications: To understand this family of medication, you will need to have an understanding of the clotting cascade, you may wish to review this.
      • Each of these medications act at different parts of the clotting cascade to slow 'clot formation', but generally don't completely stop it (apart from the antithrombotics).