Week 6 + 7 Flashcards
(129 cards)
1
Q
Atherosclerosis
A
a progressive disease that develops over decades and remains silent for many years and the first manifestation is often myocardial infarction
2
Q
Atherosclerosis major cause
A
of cardiovascular disease (CVD) including coronary heart disease (ischaemic heart disease), stroke, and peripheral vascular disease. It is the ‘hardening of the arteries’ that can occur in any artery in the body.
3
Q
Pathophysiology Atherosclerosis
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The progression of disease develops over many years and is usually advanced by the time symptoms become apparent. Soft deposits of fat and fibrin within the arterial walls harden over time. Inflammation is fundamental in all of the pathophysiological processes of atherosclerosis.
4
Q
Endothelial dysfunction
A
Chronic endothelium damage with associated endothelial dysfunction. This initiates the process of atherosclerosis and can occur from injury caused by hypertension, tobacco use, hyperlipidaemia or diabetes.
5
Q
Fatty Streak formation
A
There is an abnormal accumulation of lipid or fatty substances and fibrous tissues, leading to fatty streak formation.
6
Q
Fibrous Plaque formation
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Collagen covers the fatty streak, resulting in fibrous plaque formation, and the vessel lumen becomes narrowed.
7
Q
Complicated Lesion
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It can be considered as a repetitious inflammatory process that occurs within the endothelium. Ultimately, plaque rupture can occur, leading to thrombus formation and may result in complete blockage. This can cause ischaemia and infarction and lead to irreversible myocardial damage and death.
8
Q
Clinical Manifestations Atherosclerosis
A
There are often no or minor clinical manifestations until the disease has progressed. The signs and symptoms are often due to inadequate perfusion of the tissues due to the narrowing of the vessels that supply them.
Obstruction of the peripheral arteries can lead to significant pain, disability and poor wound healing.
Obstruction of the coronary arteries can cause myocardial ischaemia and present as:
* high blood pressure
* extreme tiredness, shortness of breath on exertion
* loss of appetite, nausea
chest pain and/or discomfort
9
Q
Angina
A
Angina is the manifestation of coronary artery disease that results in the inadequate blood flow to the cardiac muscle (myocardium). Angina can be classified into stable and unstable.
10
Q
Stable Angina
A
Angina pectoris, commonly known as chest pain, stems from an imbalance between myocardial oxygen supply and demand, leading to inadequate blood supply to the heart muscle and myocardial ischaemia. Factors such as physical exertion or emotional stress elevate myocardial oxygen demand, while conditions like atherosclerosis can impede oxygen supply. Even a partial narrowing of the vessel by an atheroma can induce chest pain as myocardial cells receive insufficient oxygen even though there may be some blood supply. Atherosclerosis is the primary cause of inadequate blood flow due to the narrowing of coronary arteries.
10
Q
Chronic Stable Angina
A
Stable angina is a common symptom of coronary artery disease, characterized by transient chest discomfort triggered by exertion or stress. It can indicate narrowing arteries but not permanent damage, increasing the risk of acute cardiac events. Unstable angina can be the first clinical sign.
10
Q
Unstable Angina
A
Unstable angina is chest pain that is new in onset, occurs at rest and/or has a worsening pattern.
Unstable angina is unpredictable and occurs when there is reversible myocardial ischaemia. However it can be a strong indicator of impending myocardial infarction (heart attack). For this reason, it should be considered an emergency because it can signal that the atherosclerotic plaque has ruptured and an infarction may soon follow.
11
Q
Acute Coronary Syndromes
A
ACS encompasses various presentations such as unstable angina and myocardial infarction. Myocardial infarction can be further categorised into non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI).
12
Q
Stable Angina Pathophysiology
A
Angina is a heart condition where coronary arteries are narrowed or blocked due to conditions like atherosclerosis. This causes a thrombus to form, obstructing the coronary artery and reducing blood flow to the myocardium. This reduces oxygen levels, restricts aerobic metabolism, and causes lactic acid buildup, causing pain in the shoulder, neck, lower jaw, and arm. Angina is a primary indicator of reversible myocardial ischaemia, where oxygen supply is diminished due to increased demand or reduced supply. An atheroma can still allow blood flow but may cause chest pain.
13
Q
Unstable Angina Pathophysiology
A
Unstable angina is a condition characterized by plaque erosion, thrombotic vessel occlusion, and vasoconstriction. It progresses when plaque damage exposes underlying tissue, leading to transient episodes of thrombus formation and myocardial necrosis. Endothelial dysfunction, impaired vasodilation, increased vasoconstriction, and platelet aggregation further compromises blood flow.
14
Q
Clinical Manifestations
Stable Angina
A
- Substernal chest pain/discomfort: can be described as stabbing, heaviness, pressure, squeezing, burning and/or fullness (provoked by exertion or emotional stress and relieved by rest and/or nitrates within minutes). This is the typical presentation.
- Pain: can radiate to arms, neck, jaw, shoulder or back
- Nausea
- Shortness of breath (Atypical presentations like shortness of breath and nausea in the absence of chest pain are often found in women, older people, and people with diabetes)
- Epigastric pain - Postmenopausal women may describe epigastric burning which could be angina.
15
Q
Clinical Manifestations
Unstable Angina
A
- Pain - severe chest pain/discomfort (as described above) however not relieved by rest, position change or nitrate administration is the hallmark of a unstable angina and ACS. Pain can originate or radiate down the arms, neck, jaw, shoulder or back
- Nausea and vomiting - these symptoms can result from reflex stimulation of the vomiting centre by the severe pain. They can also result from vasovagal reflexes initiated from the area of the infarcted myocardium
- In response to the release of catecholamines (e.g. adrenaline/noradrenaline) , BP and HR may be elevated initially. Later, the BP may drop because of decreased cardiac output
- Dyspnoea
- Diaphoresis
- Anxiety - chest pain often increases a patient’s worry or concern and this in-turn can exacerbate the symptoms. It is important as nurses we provide calm and offer reassurance
- Fever - temperature may increase within the first 24 hours up to 38°C. The temperature elevation may last for as long as 1 week. This increase in temperature is due to a systemic inflammatory process caused by myocardial cell death
16
Q
What is an ECG?
A
An ECG is a diagnostic tool that visually represents the heart’s electrical conduction, detecting pathological conditions like arrhythmias, acute myocardial infarction, and cardiac ischaemia. It’s crucial for patients with a cardiac history or risk factors, and medical staff should complete it within 10 minutes of chest pain onset or hospital presentation.
17
Q
Components of an ECG
A
P waves: Represent atrial depolarization which is the electrical activity that triggers atrial contraction.
PR interval: measures the time from the beginning of the P wave to the beginning of the QRS complex. It represents the time taken for the electrical impulse to travel from the atria to the ventricles.
QRS complex: Represents ventricular depolarization which indicates the electrical activity that precedes ventricular contraction.
ST segment: This segment reflects the time between ventricular depolarization and repolarization. It is often analysed for signs of myocardial ischaemia or injury.
T waves: Ventricular repolarization, indicating the recovery of the ventricles following contraction.
QT interval: Measures the total time for ventricular depolarization and repolarization, indicating the time for one complete cycle of ventricular electrical activity.
U wave: only seen sometimes, represents late repolarisation of the Purkinje fibres.
18
Q
Sinus Rhythm
A
Sinus rhythm is a cardiac rhythm originating from the sinus node, running through the AV node, bundle of His, bundle branches, and Purkinje fibres, requiring a normal rate of 60-100 beats per minute.
19
Q
Sinus Tachycardia
A
Sinus tachycardia is a rhythm with a rate greater than 100 beats per minute, often associated with physiological or psychological stressors like exercise, fever, pain, hypovolemia, hypoxia, hypoglycaemia, anemia, acute myocardial infarction, heart failure, caffeine, and certain medications.
20
Q
Atrial Fibrillation
A
Atrial fibrillation (AF) is a condition characterized by abnormal electrical pathways in the atria, resulting in irregular ventricular contractions. It can be a clinical manifestation of conditions like myocardial ischaemia, heart failure, electrolyte disturbances, thyroid dysfunction, hypovolaemia, and postoperative complications. AF is often associated with underlying cardiac diseases like coronary artery/heart disease, valvular heart disease, heart failure, cardiomyopathy, hypertension, and pericarditis.
20
Q
Sinus Bradycardia
A
Sinus bradycardia is a rhythm with sino-atrial node origin and conduction pathway, typically less than 60 beats per minute. Symptoms include hypotension, weakness, dizziness, confusion, pale skin, and angina. Common disease states include hypothyroidism, increased pressure, hypoglycaemia, and inferior acute myocardial infarction.
20
Q
Atrial Fibrillation types
A
Occasional (paroxysmal): atrial fibrillation and associated symptoms may come and go, usually lasting for a few minutes to hours. The patient may need treatment.
Persistent: atrial fibrillation lasts longer than a week; can become permanent. Treatment can include cardioversion and/or medications.
Permanent: heart rhythm cannot be restored, and requires medication to minimise the effects and complications.
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Atrial Fibrillation causes
The causes can come from a range of pathophysiological mechanisms:
* Excess catecholamines: adrenaline infusion, stress, thyrotoxicosis
* Increased atrial automaticity: alcohol, caffeine, myocarditis, electrolyte derangement
* Atrial enlargement: pulmonary hypertension, septal defects, valvular disease
* Abnormality of the conducting system: congenital cardiac disease, ischaemic heart disease, hypothermia
The following factors also increase the risk of developing atrial fibrillation:
* Advancing age
* Congenital heart disease
* Heart disease - congenital, valvular, coronary artery disease, structural heart disease, atrial ischaemia, heart failure, hypertension
* Endocrine disorders - diabetes, hyperthyroidism
* Sleep apnoea
* Lifestyle - sedentary, obesity, increased alcohol consumption
* Genetics
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Atrial Fibrillation Pathophysiology
Cardiac remodelling in the atria causes structural and electrical changes, leading to atrial fibrillation (AF). This irregular electrical rhythm creates a "quivering" of the atria, a classic presentation of AF. Multiple re-entry circuits develop, leading to chaotic activity. The SA node becomes the pacemaker, and the AV node is bombarded by rapid atrial impulses, resulting in an irregular response. AF can occur suddenly or persist as a chronic arrhythmia.
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The characteristics of atrial fibrillation on a rhythm strip:
* P wave: not identifiable (notice the squiggly lines before the QRS in the picture below)
* QRS complex: could be normal or wide
* Rate: usually variable with an irregular rhythm (notice the varying gaps between the QRS complexes)
* Mechanical contraction: present
* Pathophysiology: impulse does not originate in the SA but elsewhere in the atria and leads to the atria quivering
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Clinical Manifestations Atrial Fibrillation
* Fatigue, altered conscious state, dizziness, syncope
* Irregular pulse - may be normal or rapid rate
* Palpitations, chest pain
* Hypotension
* Shortness of breath, anxiety
* Diaphoresis, pallor
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Complications Atrial Fibrillation
Adverse effects include the loss of the "atrial kick," decreased diastolic filling time, thrombosis in the atria, potential blood clots, stroke, and heart failure.
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Nursing Assessment Atrial Fibrillation
Focused cardiovascular assessment
This can be performed alongside your primary and secondary assessments, as soon as you have identified this is a required focused assessment.
A non-invasive tell-tale sign of atrial fibrillation that may prompt you to conduct an ECG is an irregular heart rate on palpation of the patient's pulse.
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Nursing Management Atrial Fibrillation
Nursing management of atrial fibrillation (AF) involves controlling symptoms, preventing complications, and improving the patient's quality of life. Strategies include regular assessment, symptom management, education about AF, lifestyle modifications, medication adherence, anticoagulant therapy, risk factor modification, collaboration with healthcare teams, referrals to cardiac rehabilitation programs, and psychosocial support.
28
Medical Investigations Atrial Fibrillation
Further investigations for the diagnosis of and to determine the cause of atrial fibrillation may include:
* Electrocardiogram (ECG)
* Holter monitor
* Echocardiogram
* Blood tests, e.g. thyroid, electrolytes
* Stress test
* Chest X-ray
29
Atrial Fibrillation Medical Management
1. Anti-arrhythmic agents to normalise the heart’s rhythm
2. Beta-blockers, some calcium channel blockers and/or digoxin to slow the heart rate
3. Anticoagulation medications may be prescribed to reduce the risk of stroke
* Electrical cardioversion (synchronised cardioversion) - an electrical shock to attempt to restore the heart's normal electrical rhythm
* Pharmacological cardioversion – Medication to restore the heart’s normal electrical rhythm in a short period of time
* Catheter ablation - a procedure that utilises a catheter to ablate any areas that may be causing the arrhythmia
* Pacemaker - can electrically stimulate the heart to maintain a regular rhythm
* Management of other medical conditions - hypertension, cardiac failure, heart valve disease and diabetes mellitus
* Management of obstructive sleep apnoea
* Referrals to specialised cardiac services
30
Hypertension
Hypertension is a significant risk factor for coronary heart disease, contributing to atherosclerosis, angina, and myocardial infarction. It increases the risk of atherosclerosis, endothelial injury, and myocardial hypertrophy, increasing coronary flow demand. Diagnosis is based on repeated blood pressure measurements, with systolic blood pressure >140mmHg or diastolic pressure 90mmHg or greater.
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Hypertension- Pathophysiology
Hypertension is caused by genetics and environmental factors, triggering neural and hormonal responses. Pathophysiological pathways involve the sympathetic nervous system, renin-angiotensin-aldosterone system, and natriuretic peptides. Inflammatory processes, endothelial dysfunction, and insulin resistance contribute to elevated peripheral resistance and blood volume.
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Hypertension- Clinical Manifestations
The clinical manifestation of hypertension is an elevated blood pressure. In addition to this, the effects of hypertension are distributed throughout the body and are implicated in several conditions. However many people can live with hypertension for years without symptoms (asymptomatic), or with mild symptoms they may not seek medical attention for. This means that organ disease and damage can occur long before symptoms are evident
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Hypertension- Complications
* Coronary artery disease (can cause an AMI (heart attack))
* Left ventricular hypertrophy (from sustained high BP increasing the cardiac workload; a cause of heart failure, covered in later chapters)
* Heart failure
* Cerebrovascular disease (can cause a stroke, aneurysm, dementia)
* Peripheral vascular disease
* Nephrosclerosis (kidney damage, renal impairment or failure)
* Retinal damage
34
Beta blockers
HPT, angina, chronic heart failure with reduced ejection fraction, tachyarrhythmias, MI, migraine prevention (not bisoprolol)
Block mainly beta1 receptors in the heart - ↓HR, ↓force of contraction and rate of impulse conduction through the AV node - ↓CO and myocardial oxygen demand
C - shock, bradyarrhythmias, poorly controlled asthma
P - hyperthyroidism, phaeochromocytoma, history of anaphylactic reactions, PAD, patients with diabetes
Bradycardia, hypotension, orthostatic hypotension, precipitation of heart failure
Note patient's vital signs prior to administration; particularly bradycardia or hypotension.
Monitor closely patients with congestive heart failure. Advise not to stop medication abruptly as this may lead to angina pectoris, acute myocardial infarction or cardiac arrhythmias
Educate patient about reduced exercise induced tachycardia (HR won’t increase with exercise)
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*Non-selective Beta blockers
HPT, angina, tachyarrhythmias, MI, prevention of migraine
Non-selectively block beta receptors in heart, peripheral vessels, bronchi, pancreas, uterus, kidney, brain and liver
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*Non-selective Beta and Alpha blockers
HPT, chronic heart failure with reduced ejection fraction.
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Angiotensin-converting enzyme (ACE) inhibitors
HPT, heart failure, diabetic nephropathy, MI
Prevents the conversion of angiotensin I to angiotensin II by inhibiting the action of angiotensin conversion enzyme in the lungs. This reduces vasoconstriction, sodium retention and aldosterone release
P - Caution with initiation of treatment when patient on a diuretic; caution in patients with PVD and renal failure; check with anaesthetist pre-operatively. Potentially need to withhold due to excessive hypotension.
C - avoid when patient on other drugs that ^potassium; avoid in pregnancy and caution in breastfeeding.
Common: Hypotension, headache, dizziness, cough, hyperkalaemia, fatigue, nausea, renal impairment.
Rare: Angioedema, rash, diarrhoea, ^hepatic aminotransferases and bilirubin.
Monitor BP and K+, educate patient about dry cough, hypotension, side effects, and avoid potassium supplements. Inform GP if severe, warn about standing up, dizziness, and driving restrictions. Avoid NSAIDs and ACEi interactions.
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Angiotensin II receptor antagonists (ARBs)
Competitively block binding of angiotensin II to type 1 angiotensin (AT1) receptors. Reduce vasoconstriction, sodium reabsorption and aldosterone release.
P - Use cautiously in patients who have had angioedema post ACEis. Ensure adequate fluid volume and sodium levels. Avoid additional potassium.
Use cautiously in elderly, seek advice pre surgery.
Avoid in pregnancy and with breast feeding.
Common - dizziness, headache, hyperkalaemia
Infrequent - first-dose hypotension, rash, diarrhoea, dyspepsia, muscle cramp, yalgia, back pain
Rare - vogue, psoriasis, hypersensitivity reactions, abnormal liver function
Monitor blood pressure, educate patient on fluid maintenance, adverse effects, and medication commencement. Inform GP if diarrhoea occurs, avoid potassium replacements, and minimize NSAID use.
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Calcium channel blockers
Calcium blockers reduce coronary vascular resistance and oxygen requirements, affecting cardiac and arteriolar smooth muscle.
P- Avoid with myasthenia-like neuromuscular disease, heart failure, and aortic stenosis. Seek advice for pregnancy and breastfeeding.
C - cardiogenic shock
Common side effects include nausea, headache, flushing, dizziness, hypotension, and peripheral oedema.
Patient should be informed about the gradual reduction of hypotension, dizziness, and headache, avoid grapefruit juice due to potential toxicity, and be advised to abruptly discontinue therapy.
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DIURETIC THERAPY
Hypertension medications, such as hydrochlorothiazide, are used alone or in combination with diuretics to reduce fluid volume, lower blood pressure, and aid cardiac failure patients by reducing blood pressure.
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Thiazide diuretics
HPT, Cardiac failure
This medication inhibits sodium and chloride reabsorption in the proximal segment of the distal convoluted tubule, causing K+ excretion.
P- It is contraindicated for those with gout, diabetes, heart failure, or elderly individuals due to electrolyte imbalances.
C - anuria, hepatic coma
Common side effects include dizziness, weakness, muscle cramps, and hypotension. Infrequent side effects include rash, hyperglycemia, dyslipidemia, impotence, renal impairment. Rare side effects paraesthesia, cholestatic jaundice, cholecystitis, pancreatitis.
Dosing timing, dizziness risk, and monitoring BP and electrolytes are crucial.
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Coronary Heart Disease
Coronary heart disease (CHD) is a progressive condition affecting the heart's structure and function, primarily affecting coronary arteries. It is characterized by plaque buildup, causing reduced blood flow, leading to ischaemia or infarction. Risk factors include atherosclerosis and hypertension.
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Dyslipidaemia
Abnormal blood lipoprotein concentrations, including lipids, phospholipids, cholesterol, and triglycerides, are significant indicators of coronary risk. High LDL levels, primarily cholesterol and protein, contribute to endothelial injury and inflammation, while low HDL levels reverse cholesterol transport, aid in endothelial repair, and reduce thrombosis.
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Hypertension risk factors
is responsible for a 2-3 times increase risk of atherosclerosis contributes to endothelial injury and lead to myocardial hypertrophy, increasing myocardial demand for coronary blood
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Cigarette smoking
* both direct and passive spoking increase the risk of coronary heart disease
* nicotine stimulates the release of catecholamines increasing blood pressure, cardiac workload and oxygen demand.
* associated with an increase in LDL and a decrease in HDL and damages the endothelial lining, blood vessel inflammation and thrombosis
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Diabetes and insulin resistance
* increases cardiovascular risk by endothelial damage, thickening of the vessel wall, increased inflammation, increased thrombosis and decreased production of endothelial-derived vasodilators
* associated with dyslipidaemia
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Obesity and sedentary lifestyle
* abdominal obesity has the strongest link with increased coronary heart disease risk
* exercise improves cardioprotective mechanisms - increased nitric oxide generation, decreased cytokine production and increased antioxidant defences
* Metabolic syndrome - is a combination of central (abdominal) obesity, abnormal glucose tolerance or impaired glucose tolerance, raised triglycerides, decreased HDL and elevated blood pressure
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Nursing Management coronary Heart Disease
- Education
- Medication management
- Collaboration and Referral
- Patient advocacy
- Risk factor reduction
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HMG-CoA reductase inhibitors
This medication inhibits HMG-CoA reductase, increasing hepatic cholesterol uptake and reducing total cholesterol, LDL, and triglyceride concentrations.
p- It's not recommended for patients with infection, trauma, or metabolic disorders, as it increases risk of myopathy and renal failure.
C- Caution for patients with Myasthenia Gravis, renal and hepatic impairment, and advanced elderly over 80.
Monitor for myalgia, headache, sleep disturbances, dizziness, and myopathy, taking medication simultaneously.
Advise patient to take medication simultaneously, especially in the evening, for better effectiveness. Inform them about side effects and monitor for dark urine, muscle pain, tenderness, or weakness.
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Bile acid sequestrants: Cholestyramine, Colestipol
This medication inhibits bile acid reabsorption in the intestinal lumen, increasing bile acid excretion in feces and causing increased hepatic LDL uptake and removal from plasma.
P - avoid when triglyceride level >3mmol/L
C- It should be avoided in patients with high triglyceride levels, constipation, diverticular disease, severe haemorrhoids, and in children, pregnancy, and breastfeeding.
Dosage-related side effects include constipation, abdominal pain, dyspepsia, nausea, vomiting, diarrhea, anorexia, and increased triglycerides.
Mix with water, juice, or fluids for compliance. Take 1 hour before or 4-6 hours after other medications.
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Cardiac Rehabilitation
Cardiac rehabilitation is a crucial interprofessional program for recovering from heart failure, acute myocardial infarction, or coronary heart disease. It involves physical activity, education on healthy living, and counseling to improve quality of life and reduce the risk of future cardiac events.
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Cholesterol absorption inhibitor
Reduces absorption of dietary and biliary cholesterol by inhibiting its transport across the intestine wall. Demand for cholesterol is increased with an increase in LDL uptake and its removal from the plasma.
P - avoid combining with fenofibrate - ^risk of gall bladder disease;
C - moderate to severe hepatic failure, pregnancy and breastfeeding.
Common - headache, diarrhoea
Infrequent - myalgia, raised ALT/AST (liver enzymes)
Rare - allergic reactions, pancreatitis, cholelithiasis, myopathy, raised creatinine.
Ensure patients are advised about side effects and the importance of reporting any unexplained myalgia or malaise to the GP.
Absorption of medication is not affected by food.
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Fibrates and Vitamin B
Modulate lipoprotein synthesis and catabolism. Reduce plasma triglyceride, moderately increase HDL with a varying effect on LDL concentrations.
Third line choice for treatment of dyslipidaemia.
C - pancreatitis, renal failure with creatinine clearance <30ml/min; hepatic impairment including biliary cirrhosis, gallstones and gall bladder disease.
P - reduce dose in renal failure with creatinine clearance 30-60ml/min.
Seek specialist advise for use in pregnancy and breast feeding
Common - increased aminotransferase concentrations
Infrequent- Venous thromboembolism, urticaria, rash
Rare - cholestatic jaundice, anaemia, leucopenia, myopathy, rhabdomyolysis.
Advise patients about adverse effects, seek medical advice if urine turns brown, wear protective clothing, use sunscreen, and monitor liver enzymes for signs of rhabdomyolysis.
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Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors
Inhibit PCSK9 activity, increasing LDL clearance from the blood
Seek specialist advice regarding pregnancy and breast feeding
Common - injection site reactions, rash, nasopharyngitis, infections
Rare - Hypersensitivity reactions
Educate patient to have medication at room temperature for at least 30-40 minutes prior to administration and to rotate injections between upper arm, thigh or abdomen.
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Complications of Unstable Angina
* Electrical dysfunction causing arrhythmia
* Mechanical dysfunction (heart failure, cardiogenic shock)
* Thrombotic complications (recurrent coronary ischaemia)
* Inflammatory complications (pericarditis)
* Death
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PQRST Assessment of Angina
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?
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Management of Stable Angina
Patients with stable angina are not always admitted to the hospital but should be started on treatment while awaiting investigations (usually non-invasive testing) to confirm the diagnosis of CHD.
The goals of treatment of stable angina are to:
1. reduce symptoms and improve quality of life
2. improve survival by preventing myocardial infarction and death
3. slow disease progression
4. identify and treat aggravating factors that can worsen angina
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Management of Unstable Angina
1 Immediate management
Acute chest pain or symptoms of acute coronary syndrome are treated using a documented chest pain assessment pathway.
2 Early assessment
A 12-lead ECG is performed on a patient with acute chest pain or coronary syndrome symptoms, with results analyzed by a trained clinician within 10 minutes of emergency contact.
3 Timely reperfusion
A patient with an acute ST-segment-elevation myocardial infarction (STEMI) who requires emergency reperfusion is recommended to undergo percutaneous coronary intervention (PCI) or fibrinolysis.
4 Risk stratification
A patient with a non-ST-segment-elevation acute coronary syndrome (NSTEACS) is managed based on a documented, evidence-based assessment of their risk of an adverse event.
5 Coronary angiography
The discussion discusses the importance of coronary angiography in diagnosing and revascularizing patients with non-ST-segment-elevation acute coronary syndrome (NSTEACS) at intermediate or high risk of adverse cardiac events.
6 Individualised care plan
Acute coronary syndrome patients receive an individualized care plan, including lifestyle modifications, medications, psychosocial needs, and referrals to cardiac rehabilitation or secondary prevention programs, provided within 48 hours of discharge.
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Medical Management of Unstable Angina
* Medications for pain (e.g. glyceryl trinitrate, fentanyl, morphine)
* Baseline blood/pathology (e.g. cardiac markers (troponin & CK), electrolytes)
* ECG and consider continuous telemetry/ECG monitoring
* Portable chest X-ray
* Aspirin for cardiac-related chest pain
* Antiarrhythmic medications if needed
* Plan for other medications
* Other interventions either thrombolytic therapy or PCI as appropriate
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Percutaneous Coronary Interventions (PCI)
* a catheter is inserted into the blocked or narrowed part of the coronary artery
* a wire with a deflated balloon is passed through the catheter to the narrowed area
* the balloon is then inflated, opening the artery by compressing the plaque deposits against the artery walls
* a stent is inserted to help keep the artery open
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Coronary Artery Bypass Graft Surgery (CABG)
* redirects blood flow around a section of a blocked or partially blocked coronary artery
* a healthy blood vessel may be taken such as the internal thoracic artery, saphenous vein or radial artery and used to connect above and below the blocked artery/arteries in your heart
* it doesn't cure atherosclerosis or coronary artery disease. It can reduce symptoms, improve blood flow, oxygenation and function of the heart and reduce the risk of dying of heart disease
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Fibrinolysis: tissue plasminogen activator (tPA)
* administered to dissolve blood clots that may cause serious complications promptly
* used to maximise tissue reperfusions by restoration of coronary blood flow
* can improve early and long-term survival
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Nitrates
Exogenous source of nitric oxide - vasodilation. Mostly venous dilation reducing venous return, preload and hence myocardial oxygen requirement.
C - hypotension, hypovolaemia, raised intracranial pressure hypertrophic obstructive cardiomyopathy, cardiac tamponade, aortic or mitral stenosis or cor pulmonale.
P - seek specialist guidance for use in pregnancy and breastfeeding.
Common - headache, flushing, palpitations, orthostatic hypotension, fainting, peripheral oedema.
Infrequent - contact dermatitis, rebound angina
Treatment of angina
Educate patient regarding need to be sitting or lying down prior to taking nitrates medication as it may cause dizziness.
Depending on form of nitrate used, ensure priming of nozzle for sprays, s/l tablets to be placed under tongue, not to be swallowed.
Medication to be kept in a glass bottle away from direct light. Date opened to be placed on bottle as effectiveness of medication decreases once exposed to air.
Prevention
Transdermal patches - ensure nitrate free period to prevent tolerance to medication. Applied to coincide with most frequent episodes of angina.
Educate re need to rotate transdermal patches and apply to clean, dry skin on upper arm or chest.
Oral isosorbide mononitrate tablets to be swallowed whole. Educate re need to stand up slowly as risk of dizziness from medication.
Other
For any interventional procedures requiring diathermy, ensure patient informs staff about any transdermal patches to have them removed and skin wiped.
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Other antianginal
Venous and arterial dilation due to its nitrate moiety and its effect on potassium channels in vascular smooth muscle; improves myocardial oxygen balance and decreases angina.
C - hypotension, cardiogenic shock or acute MI with acute left ventricular failure and low filling pressures is present.
P - seek specialist guidance in patients with diverticular disease. Adjust dose for those with liver impairment.
Avoid in pregnancy and breastfeeding.
Common - headache (especially when starting), dizziness, lethargy, nausea, palpitations, flushing, myalgia
Infrequent - hypotension, ulceration and fistula formation especially genital and GIT
Rare - conjunctivitis
Warn patient that they may feel dizzy and to avoid driving or operating machinery. Educate patient about risks of ulcers, wounds or skin problems and to seek medical advice if slow to heal.
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Anti-platelet medication
ACS
Symptomatic atherosclerosis
Inhibits platelet aggregation by irreversibly inhibiting cyclo-oxygenase.
C - allergy to aspirin/NSAIDs, some asthma, severe bleeding or disease states with ^risk of severe bleeding. Avoid use in pregnancy
P - People >75 have an increased risk of major bleeding (especially GI); seek guidance with surgery as some minor procedures safe to remain on aspirin whilst others require stopping up to 7 days.
Common - GI irritation, asymptomatic blood loss, increased bleeding time
Infrequent - Stevens-Johnson syndrome, iron deficiency anaemia, GI haemorrhage
Rare - Intracranial haemorrhage, GI ulcer
Allergy - watch for bronchospasm, angioedema, urticaria and rhinitis.
Educate patient to take medication with food, only remove medication from packaging immediately prior to taking it (aspirin can break down rapidly outside of packaging), and to swallow enteric coated and slow release medication whole.
Advise patient to seek medical advice when undertaking any interventional procedure.
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P2Y12 antagonist
ACS in combination with aspirin
Symptomatic atherosclerosis
Irreversibly binds to the platelet P2Y12 receptor and inhibits platelet aggregation.
C - hypersensitivity to clopidogrel and other P2Y12; severe active bleeding or disease states with an increased risk of severe bleeding.
P - seek advice regarding stopping with surgery as some minor procedures safe to remain on medication whilst others require stopping. Seek guidance regarding use in pregnancy and breastfeeding
Common - bleeding, skin reactions
Rare - angioedema, thrombotic thrombocytopenic purpura.
Educate patient to avoid grapefruit juice and that any bleeding may take longer to stop than normal.
Advise patient to avoid over-the-counter NSAIDs (^risk of bleeding) and to report any unusual or prolonged bleeding or bruising.
Educate patient to inform dentist and doctors about medication prior to any procedures.
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Heparins
Prevention of VTE and other thrombosis in surgical and high risk medical patients
Treatment of:
- VTE
- ACS
Inactivation of clotting factors IIa (thrombin) and Xa by binding to antithrombin III
C - severe thrombocytopenia, active bleeding, severe hepatic impairment
P - consider dose reduction with renal impairment and older peoples
Safe for use in pregnancy and breast feeding
Common - bleeding, bruising and pain at injection site, hyperkalaemia, mild, reversible thrombocytopenia
Infrequent - transient elevation of liver aminotransferases, severe thrombocytopenia
Rare - skin necrosis (at injection site), osteoporosis and alopecia with long-term use, allergic reactions
Educate patient about risks of bleeding, monitoring for bleeding (nosebleeds, black or tarry bowel motions, unexplained bruising) and protective measures - use of electric over safety razor for shaving, soft toothbrushes, caution with sharp edges around the home.
If self administering, educate re correct injection technique to avoid IM and haematoma
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Direct thrombin inhibitors
Prevention of VTE
Non-valvular AF
Reversibly inhibit both free and fibrin-bound thrombin preventing conversion of fibrinogen to fibrin thus preventing thrombus formation.
C - GI haemorrhage within 12 months, prosthetic heart valve, significant renal and liver impairment. Do not use if patient on verapamil or some antifungal medications.
P - reduce dose in elderly and patients with reduced renal function.
Avoid use in pregnancy and breastfeeding.
Common - gastritis, dyspepsia, GI bleeding
Infrequent - oesophageal ulcers, increased liver enzymes and bilirubin
Rare - anticoagulant-related nephropathy
Patients should avoid chewing, crushing, or opening capsules to reduce bleeding risk. Take medication with food and water daily, inform doctors and pharmacists before stopping or starting other medications, and be alert for bruising, bleeding, and feces.
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Factor Xa inhibitors
Non-valvular AF, VTE prevention and treatment
Selectively inhibit factor Xa, blocking thrombin production, conversion of fibrinogen to fibrin and thus thrombus development.
C - Hepatic impairment
P - Adjust dose with renal impairment
Avoid use in pregnancy and breastfeeding.
Common - nausea
Infrequent- thrombocytopenia, abnormal liver function tests
Rare - allergic reactions, anticoagulant-related nephropathy
Inform patient that tablets may be crushed and mixed with water, apple juice or apple sauce but should be taken at the same time every day. See above information regarding bruising and bleeding and informing medical professionals.
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Warfarin
VTE prevention and treatment.
Prevention of stroke with previous AMI and increased embolic risk.
Valvular AF
Inhibits synthesis of vitamin K-dependent clotting factors (II, VII, IX, X) and the antithrombotic factors protein C and protein S.
C - Alcoholism due to poor compliance, severe active bleeding or disease states with increased risk of severe bleeding (e.g. severe hepatic disease).
P - use cautiously in those with increased risk of falls and renal impairment. Consider dose adjustment in the elderly.
Seek specialist advice in pregnancy but safe to use if breastfeeding.
Common - bleeding
Rare - skin necrosis, calciphylaxis, purple discolouration of toes, alopecia, fever, rash, nausea, vomiting, diarrhoea, hepatic dysfunction, allergic reactions.
Patients should be educated on the importance of taking the same brand of warfarin, taking medication at the same time daily, recording doses and INR, maintaining stable vitamin K intake, avoiding excessive alcohol and cranberry juice, and note other anti-coagulants.
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Magnesium Sulfate
Arrhythmias associated with hypokalaemia
Increases serum magnesium and associated serum potassium, stabilising the myocardial cell membrane
C - heart block, hypermagnesaemia,
P - use cautiously in patients with myasthenia gravis, renal impairment and obstetric patients on nifedipine.
Safe to use in pregnancy and breastfeeding.
These relate to hypermagnesaemia
Common - flushing, nausea, vomiting
Infrequent - headache, dizziness
In these situations, the medication is normally given IV and should be diluted according to the manufacturer and hospital guidelines prior to administration.
Monitor for adverse effects.
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Digoxin
AF and atrial flutter
Heart failure
Slows heart rate and reduces AV nodal conduction. Increases force of myocardial contraction by increasing release and availability of stored calcium.
C - second and third degree heart block, SVT with secondary pathway, VT, VF, cor pulmonale
P - adjust dose in elderly and those with renal impairment. Caution in patients with severe aortic stenosis and some other arrhythmias.
Narrow therapeutic range and may potentiate arrhythmias if serum levels are over this range.
Common - anorexia, nausea, vomiting, diarrhoea, visual disturbances, drowsiness, dizziness, headache, rash, bradycardia, arrhythmia
Infrequent - depression, shortened QRS complex, atrial or ventricular extrasystoles, VT or VF, heart block
Rare - thrombocytopenia, seizures, confusion, psychosis, gynaecomastia
On commencement, and in elderly, serum concentration should be monitored.
Educate patient regarding side effects and that the medication will control the rate but not stop AF.
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Amiodarone
Oral tablets
IV solution
Treatment and prophylaxis of serious tachyarrhythmias including AF, VT and SVT.
Decreases SA node and junctional automaticity, slowing AV conduction and prolonging refractory period of myocardial tissues.
C - allergy, 2nd and 3rd degree AV block, symptomatic bradycardia.
Do not use in pregnancy or breastfeeding
P - Use cautiously in elderly and with hepatic impairment
Common - nausea and vomiting, constipation, anorexia, taste disturbance, transient elevation of hepatic aminotransferases, thyroid dysfunction, fever, photosensitivity, skin pigmentation (blue-grey), corneal microdeposits, headache, dizziness, fatigue, neurotoxicity and more.
Infrequent - AV block, arrhythmias, phlebitis, epididymitis
Rare - hepatotoxicity, optic neuropathy, bronchospasm.
For noting - rapid IV administration may result in severe hypotension and circulatory collapse.
For full information see AMH
IV administration - diluted into 5% glucose as incompatible with normal saline and administered slowly - according to manufacturer and hospital guidelines.
Educate patients about importance of avoiding sun exposure - to wear protective clothing and use of sunscreen when outdoors; avoiding grapefruit as it interacts with amiodarone.
Inform patient that they will need regular blood tests, ECGs and chest x-rays whilst on amiodarone. Educate regarding side-effects and when to inform Dr.
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Flecainide
Oral tablets
IV solution
Paroxysmal AF, maintenance of sinus rhythm post cardioversion, SVT
Slows cardiac conduction and increases refractory period in all myocardial tissues.
C - heart block, cardiogenic shock or history of AMI.
P - Use with caution in ventricular rhythms and heart failure, and with other antiarrhythmics. Dose adjustment may be required for patients with renal and hepatic impairment.
Seek specialist advice for use in pregnancy and breastfeeding.
Common - nausea, vomiting, diarrhoea, constipation, headache, dizziness, tinnitus, visual disturbances, fatigue, tremor, nervousness, paraesthesia, ataxia, numerous effects on the heart, dyspnoea, flushing, increased sweating, rash.
Infrequent - bradyarrhythmias, heart block, hallucinations, amnesia, confusion
Rare - cardiac arrest, sudden death, myalgia, arthralgia, fever, plus more
For further information see AMH
Educate patient about potential dizziness and altered vision and the importance of not driving if impacted. Also to immediately report any chest pain, rapid or irregular heart beat or difficulty breathing.
Prior to commencing, serum electrolyte imbalances must be corrected. As with amiodarone, IV flecainide should only be diluted in 5% glucose.
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Heart Failure
Heart failure is a condition characterized by abnormal ventricular function, resulting in inefficient myocardial performance and compromised metabolic demands. It affects 1-2% of people in Australia but has a high hospitalization rate and 5-year mortality rate. Various underlying cardiovascular conditions weaken the heart muscle, making it difficult to fill.
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Cardiac Function
Understanding key physiological concepts related to cardiac function is crucial for understanding heart failure mechanisms, clinical manifestations, treatment strategies, and medication rationale. Cardiac output, measured by heart rate and stroke volume, measures the volume of blood pumped out of the heart each minute.
Cardiac Output [CO] = Heart Rate [HR] x Stroke Volume [SV]
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Stroke volume is influenced by 3 key aspects:
Preload:The end-diastolic volume, which represents the volume of blood in the ventricles and associated pressure, is determined by venous return and ventricular compliance.
Afterload: Hypertension increases heart workload due to increased resistance in ventricles to eject blood into arteries, requiring greater force of contraction to overcome high arterial pressures.
Contractility: Myocardial contraction is influenced by changes in ventricular myocardium stretching, sympathetic activation of ventricles, and myocardial oxygen supply.
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Ejection Fraction
Ejection fraction (EF) is used to measure how effectively the heart is pumping. This is an important aspect to understand when discussing heart failure as you will see that the type of heart failure is often determined on the ejection fraction of the left ventricle.
Ejection Fraction (%) = [Stroke Volume / End Diastolic Ventricular Volume] x 100
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Classification and staging of Heart Failure- A
At risk for heart failure
People who are at risk for heart failure but do not yet have symptoms or structural or functional heart disease
Risk factors for people in this stage include hypertension, coronary vascular disease, diabetes, obesity, exposure to cardiotoxic agents, genetic variants for cardiomyopathy and family history of cardiomyopathy
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Classification and staging of Heart Failure- B
Pre-heart failure
People without current or previous symptoms of heart failure but with either structural heart disease, increased filling pressures in the heart or other risk factors
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Classification and staging of Heart Failure- C
Symptomatic heart failure
People with current or previous symptoms of heart failure
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Classification and staging of Heart Failure- D
Advanced heart failure
People with heart failure symptoms that interfere with daily life functions or lead to repeated hospitalizations
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Chronic Heart Failure
* Fatigue: one of the earliest symptoms that begins to limit the person's activities. It is caused by reduced cardiac output, impaired perfusion, anaemia and a decrease in oxygenation.
* Dyspnoea: caused by an increase in pulmonary pressures and oedema. Patients can also present with a dry, non-productive cough that isn't alleviated with position change or over the counter cough medication. These symptoms can be worse at night.
* Tachycardia: the body compensates for a failing ventricle and reduced cardiac output by increasing the heart rate.
* Oedema: this can occur peripherally, liver (hepatomegaly), abdomen and lungs. A sudden weight gain of 1.5kg in 2 days can be caused by deteriorating heart failure.
* Nocturia: with a decreased cardiac output a patient will have impaired renal perfusion, decreased urine output particularly during the day. At night when a patient lies down and rests, renal perfusion improves and causes the patient to need to void frequently.
* Skin changes: skin can appear dusky, shiny and/or swollen with diminished or absent hair growth due to poor oxygenation.
* Behavioural changes: cerebral circulation can be reduced with a reduced cardiac output. Patients can become restless, confused, and/or have decreased cognitive functioning.
* Chest pain: due to decreased coronary artery perfusion a patient may experience angina
Weight changes: weight gain can be caused by fluid retention. Weight loss can be caused by cardiac cachexia with muscle wasting and fat loss.
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Complications from Heart Failure
* Pleural effusion: fluid accumulates in the pleural space due to increasing pressure in the capillaries (see Respiratory chapters)
* Arrhythmias: enlargement of the chambers of the heart leads to stretching of the cardiac walls and causes changes in the electrical pathways. Atrial fibrillation is a common arrhythmia for patients with heart failure.
* Left ventricular thrombus: increase chance of a thrombus formation due to a decrease in ventricular contractility.
* Hepatomegaly: often caused by right sided heart failure as the liver becomes congested.
* Renal failure: a decreased cardiac output leads to decreased renal perfusion
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There are physiological differences between the left and right ventricle:
* The right ventricle has a greater sensitivity to afterload (which increases workload on the heart) changes and leads to dilatation to preserve stroke volume
* Pressure in the pulmonary circulation is significantly lower than the systemic circulation, therefore the right ventricular myocardium requires less muscle power than the left ventricular myocardium
*The right ventricle is more compliant to accommodate larger variations in venous return without altering end-diastolic pressure
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Heart Failure with REDUCED Ejection Fraction (HFrEF)
Systolic heart failure occurs when left ventricular function decreases, leading to poor contraction and left ventricle emptying, resulting in fluid buildup, causing oedema, orthopnoea, and shortness of breath.
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Heart Failure with PRESERVED Ejection Fraction
This was formally referred to as diastolic heart failure. It is characterised by heart failure symptoms however with a preserved ejection fraction of 50% or higher. There is decreased compliance of the left ventricle and this results in poor filling.
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Right Heart Failure
Right-sided heart failure (RHF) occurs from impaired contractility of the right ventricle (RV) caused by increased pressure, volume overload, intrinsic myocardial contractile dysfunction and/or cardiac rhythm.
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Right Heart Failure- Pathophysiology
Heart failure is a complex cardiac dysfunction causing inadequate oxygen and nutrient perfusion of tissues. Common causes include coronary heart disease, acute myocardial infarction, and hypertension. The pathophysiology of heart failure is complex and influenced by various factors.
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Left Heart Failure
Patients with HPrEF often present with signs of pulmonary oedema (pulmonary vascular congestion) and inadequate perfusion of the systemic circulation. This includes fatigue, dyspnoea, orthopnoea, cough (with frothy sputum), decreased urine output and oedema.
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Right-sided Heart Failure signs
* Murmurs
* Jugular vein distention
* Oedema (peripheral, scrotum, sacrum)
* Weight gain
* Increased heart rate
* Ascites
* Hepatosplenomegaly (enlarged liver and spleen)
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Right-sided Heart Failure Symptoms
* Fatigue
* Anxiety, depression
* Dependent, bilateral oedema
* Right upper quadrant pain
* Anorexia and gastrointestinal bloating
* Nausea
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Compensatory Mechanisms
* sympathetic nervous system
* neurohormonal responses
* ventricular dilation
* ventricular hypertrophy
* ventricular remodelling
* beneficial counter-regulatory mechanisms
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Left-sided Heart Failure Signs
* Increased heart rate
* Crackles (resp auscultation)
* Pleural effusion
* Poor gas exchange (low O2)
* Extra heart sounds
* Changes in mental status
* Restlessness, confusion
* Alternating pulses (strong to weak)
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Left-sided Heart Failure Symptoms
* Weakness, fatigue
* Anxiety, depression
* Shallow respirations
* Orthopnoea
* Dry hacking cough
* Nocturia
* Frothy, pink-tinged sputum
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Heart Failure PREVENTION
Regardless of the type of heart failure, prevention centres around the management of blood pressure and serum cholesterol levels.
Medications used to control BP and for patients with left ventricular (LV) systolic dysfunction to prevent heart failure include:
* ACE inhibitors
* Beta blockers
* Sodium-glucose cotransporter 2 (SGLT2) inhibitors for patients with T2 diabetes.
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Sodium-glucose cotransporter 2 (SGLT2) inhibitors
Type 2 diabetes
Symptomatic heart failure
Chronic kidney disease
Inhibit SGLT2, reducing glucose reabsorption in kidney. How they work in heart failure is not understood but appears to be independent from glucose lowering affect.
C - severe hepatic failure
P - use with caution with impaired renal function and the elderly.
Avoid use in pregnancy and breast feeding.
Common - genital infections, polyuria, dysuria, UTI, dyslipidaemia, hypoglycaemia, ^haematocrit, constipation, nausea, thirst, renal impairment.
Infrequent - volume depletion
Rare- perineal necrotising fasciitis.
Ensure education regarding effect of medication on urine output and encourage discussion regarding thirst and management of this to avoid worsening heart failure.
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Loop Diuretics
Oedema associated with heart failure, hepatic cirrhosis, renal impairment and nephrotic syndrome
Inhibits reabsorption of sodium and chloride in ascending limb of loop of Henle. Increases water excretion.
P - use with NSAIDs may reduce diuresis - dose adjustment required.
-Monitor BP carefully when used with an ACE inhibitor.
C - Anuria, severe sodium and fluid depletion, pregnancy
Common - electrolyte disturbances (⇩sodium, potassium, magnesium, chloride, calcium), dehydration, metabolic alkalosis, ^creatinine, gout, dizziness, hypotension, fainting.
Infrequent- dyslipidaemia, rash
Rare- tinnitus, vertigo, deafness.
If taking more than once a day, educate patient to take second dose at lunch time.
Warn patient regarding side effects of medication including dizziness, and need to monitor electrolytes and weight.
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Potassium Sparing Diuretics
Cardiac failure with reduced ejection fraction
Primary hyperaldosteronism
Cirrhosis of liver
Resistant HPT
Inhibits sodium absorption in distal tubule increasing sodium and water excretion but reducing potassium excretion. Weak diuretics.
P - use with caution in patients with uncontrolled diabetes, severe cardiopulmonary disease and prostate cancer.
C - renal failure, pregnancy
Common - hyperkalaemia, hyponatraemia, hypochloraemia, weakness, headache, nausea, vomiting
Infrequent- GI cramps, diarrhoea, ataxia, drowsiness, confusion, impotence, menstrual irregularities
Rare - agranulocytosis, hepatotoxicity, rash
Educate patients to avoid potassium replacements and minimise potassium rich foods (bananas)..
Ensure patient knows about need to have ongoing monitoring of renal function including monitoring of vital signs, fluid balance and urine output.
Encourage to take medication early in the day (avoid after 4pm)
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Nursing Management
The main goals in the treatment of chronic heart failure are to treat the underlying cause and contributing factors;
* to maximise cardiac output
* reduce symptoms
* improve ventricular function
* improve quality of life
* preserve target organ function
* improve mortality and morbidity risks.
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Angiotensin receptor neprilysin inhibitor (ARNI)
Heart failure with reduced ejection fraction (HFrEF)
Combination of medication produces vasodilation, increases glomerular filtration rate, reduces sympathetic tone and aldosterone release and increases bradykinin levels.
C - history of angioedema, severe hepatic impairment, pregnancy and breastfeeding.
P - Ensure blood volume, sodium and potassium levels are corrected prior to commencing therapy; adjust dose in those with moderate hepatic impairment and the elderly.
Common- hyperkalaemia, ^serum creatinine, renal impairment, hypotension, dizziness, fainting, headache, cough, anaemia, diarrhoea, back pain
Infrequent - angioedema, rash
Educate patient about side effects and to get up gradually from sitting or lying to avoid dizziness. Also to inform GP if ongoing and to avoid driving.
Ensure patient avoids potassium replacement during therapy with ARNI.
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Self Management
Educating patients and their carers about self-management of heart failure is recommended to decrease hospitalisation and mortality.
The Heart Foundation has created a document intended to guide patients on the important aspects of managing their own condition
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Dietary Therapy
* A diet plan with a list of permitted and restricted foods
* Examine labels (food and OTC medications) for sodium content.
* Avoid the use of salt when cooking
* Daily weigh (at the same time each day, preferably in the morning)
* Eat smaller, more frequent meals
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Activity Program/exercise
* Increase walking and other activities
* Consider a cardiac rehabilitation program
* Avoid extreme cold and hot
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Health promotion
* Annual flu vaccine
* Pneumococcal vaccine
* Develop plan to reduce risk factors
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Ongoing monitoring
* Know the signs and symptoms of worsening heart failure
* Recall symptoms experienced
* Report to the healthcare team any of the following: weight gain of 1.5kg in 2 days, or 2.3kg in 1 week, difficulty breathing, waking up breathless at night, frequent dry cough, swelling of ankles, feet or abdomen, nausea with swelling, pain or tenderness, dizziness or fainting
* Attend regular check-ups with healthcare team
* Consider joining a support group
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Rest
* Plan a regular daily rest and activity program
* After exertion, (exercise and ADL's) plan a rest period. (This is an important aspect of planning your nursing care for patients experiencing exacerbations of heart failure). This should also include avoiding exertion around meal times. Blood is diverted to the GIT post meals so it is wise to avoid exertional activities immediately after meals.
* Avoid emotional upsets, verbalise concerns, fear and feelings of depression to the health care team.
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Medication therapy
* Take medication as prescribed
* Develop a system to ensure medications are taken
* Take pulse rate each day and know the parameters that your healthcare provider wants for your heartrate
* Take BP at determined intervals and know BP limits
* Know signs and symptoms of orthostatic hypotension and how to prevent them
* Know signs and symptoms of internal bleeding and what to do about it if taking anticoagulants. Know INR levels if taking warfarin
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Acute intervention
* Patients with heart failure may experience periods of worsening and acute exacerbations. This requires stabilisation and specialised monitoring and care.
* Support systems need to be in place upon discharge
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Health promotion
* Communication and jointed decision making with the patients and/or carers
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Ambulatory and home care
* Often led and monitored by heart failure specialty nurses and/or nurse practitioners
* Focus on slowing the progression of the disease
* Focus on managing patients out of hospital
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Palliative and end-of-life care
* Refer patients with advanced heart failure to palliative care
* Goals of providing comfort and relieving symptoms remain priorities in the care of patients
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Diagnostic studies
Blood studies
* Cardiac markers (troponin and creatinine kinase [CK]),
* electrolytes (sodium, potassium, calcium, magnesium),
* renal function (estimated glomerular filtration rate [eGFR], urea and creatinine),
* blood glucose,
* C-reactive protein (CRP), homocysteine,
* full blood count, white cell count, haemoglobin,
* activated partial thromboplastin time (aPTT), international normalised ration (INR), natriuretic peptides (B-type, N-terminal pro-brain [BNP and ANP markers]),
* liver function tests,
* serum lipids (cholesterol, triglycerides, lipoproteins [HDL, LDL]), ABG.
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Radiology
Chest x-ray, echocardiogram (ECHO) shows the heart movement, and blood flow and can assess the ejection fraction, transoesophageal echocardiogram, nuclear imaging, 12-lead ECG, Holter monitoring, telemetry, exercise (stress) testing.
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Computerised Tomography and Magnetic resonance imaging
Cardiovascular MRI, magnetic resonance angiography, cardiac CT, coronary CT angiography.
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Pharmacists heart failure
Pharmacists play a crucial role in the interprofessional team, verifying patients' medications, educating them on new ones, and providing information on prescription and over-the-counter medications, interactions, and compliance with medication regimes. They also assist patients with blister packs.
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Dieticians heart failure
* A referral to the dietician can be a handy way for the patient to discuss any necessary changes to their diet, especially when they may have a new diagnosis or an acute exacerbation of their cardiac disease.
* Dietitians share heart-healthy eating guidelines and help develop meal plans. It is crucial in recovery and ongoing nutritional support for patients.
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Physiotherapists heart failure
* Muscle weakness and general fatigue can heavily impact the patients, so physiotherapists can assist in their recovery and strengthen their muscles during their inpatient stay.
* Physiotherapists assist with cardiac rehabilitation and help develop an appropriate plan for regular physical activity.
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Occupational Therapists heart failure
Occupational therapists collaborate with physiotherapists to prepare home equipment for post-discharge community residents, including assist devices and steps. They play a crucial role in multidisciplinary heart failure disease management programs.
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Social Workers heart failure
Social workers play a crucial role in patients dealing with new diagnoses, providing support and community services beyond inpatient stays. They also assist with complex financial, legal, and legal issues, and are essential for the whole family, ensuring the best care possible for the patient.
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General Practitioners heart failure
A primary care doctor, typically a family physician, provides routine preventive health care, manages treatment, and develops care plans for rehabilitation. They monitor cardiac function and pathology, provide education, and refer patients to Allied Health Professionals as needed, ensuring overall care and support.
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Cardiologist heart failure
Whilst much of the management of risk factors for a patient with cardiac disease can be coordinated by a GP, if there are difficulties around diagnosis, progression of the condition or complex management requirements, other heart specialists including cardiologist, cardiac surgeons and/or cardiac electrophysiologists may need to be involved.
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Clinical Nurse Specialists/Nurse Practitioners heart failure
Clinical nurse specialists and nurse practitioners can help treat heart problems, might perform tests and provide care, education and counselling. Note that in the community setting nurses often lead the management strategies.
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Palliative care consultant/team heart failure
For many people with cardiovascular disease, there is a limit to how much treatment will be effective, especially those with chronic heart failure. Optimisation of symptoms is a complex process and often requires input from specialists that work with these on a daily basis. These may include a palliative care consultant and/or a palliative care nurse practitioner. These professionals support both the patient and the family during the end-stages of the disease and this can occur either within the in-hospital environment or in the home.
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Mental Health Professionals heart failure
Being diagnosed with a cardiovascular condition that limits your lifestyle can have impacts on an individual's mental health including anxiety, stress and even depression. Inclusion of a psychologist or counsellor can help the patient and family work through these issues.
