ILP 5: Cardiac Conditions Flashcards

Question

What are 4 **managements** for ***hypertension***?

Answer 1

1. Alter modifiable risk factors 2. Dietary = restrict sodium intake, increase potassium (K+) intake 3. Exercise (level I evidence for 40-70% VO2 max) 4. Medications: 1. Diuretics to increase urine output, eg: Frusemide (Lasix) 2. Angiotensin-converting enzyme (ACE) inhibiters, eg: Captopril (Capoten)

Answer 2

Monitor BP - if too high (actual figure depends on patient) then physiotherapy may have to be delayed as activity may further increase BP. Ensure patient is having their regular medications and reassess.

Answer 3

A relative decrease in perfusion to the heart muscle (myocardium), whereby it is not adequate to meet metabolic demands of the myocardium.

Answer 4

Often appears on exertion because the coronary arteries are unable to provide adequate blood to the myocardium to meet the increased metabolic demand

Answer 5

left ventricle

Answer 6

1. higher myocardial oxygen demand 2. larger mass

Answer 7

Caused by atherosclerosis, a chronic and progressive inflammatory disease of the arterial endothelium with formation of ‘plaques’ (intimal thicke ning and accumulation of lipids)

Answer 8

atherosclerosis of the coronary arteries

Answer 9

1. Stable angina 2. Unstable angina pectoris (UAP) 3. Acute myocardial infarction (AMI)

Answer 10

A temporary disturbance in myocardial function, but without myocardial necrosis (so the muscle cells do not die) \*Imagine you take a fish out of water… the fish is struggling, and two things can happen: 1) put the fish back in water, so it survives (this is angina - so if the patient receives medications and the blood supply is restored, the heart muscle survives); 2) leave the fish out of water so it dies (this is then an AMI (‘heart attack’), where the heart muscle dies from lack of oxygen). Signs & Symptoms: 1. Retrosternal pain/discomfort, relieved by rest or nitrates 2. SOBOE 3. reduced exercise capacity. 4. \*Individuals with Diabetes Mellitus may be asymptomatic.

Answer 11

1. Antiplatelet eg: Aspirin (blood thinner) 2. Nitrates eg. Anginine to dilate peripheral blood vessels and coronary arteries. 3. Beta Blockers eg. Propranolol, Atenolol (↓ myocardial contractility, HR, SVR and BP thus ↓ myocardial oxygen demand) 4. Calcium channel blockers eg verapamil, diltiazem (systemic vasodilation, thus ↓ systemic vascular resistance (SVR) ↓ myocardial contractility, ↓ HR).

Answer 12

Angina 1. Stop activity 2. Call other staff - nursing/medical (buzzer) 3. Don’t leave patient 4. Give O2 if required ; nitrate if available (eg. Anginine) 5. Monitor colour, LOC, symptoms 6. Commence CPR if required

Answer 13

Avoid isometric exercises; use a wheelie walker rather than crutches

Answer 14

‘Acute coronary syndrome’ describes the signs and symptoms during unstable angina and/or AMI.

Answer 15

1. Can be life threatening. Thrombus within the artery leads to subtotal or total occlusion meaning the heart muscle is deprived of oxygen. 2. Less predictable than stable angina; can occur anytime even during sleep. 3. Signs & symptoms: Frequent and prolonged episodes of retrosternal pain or discomfort, at rest or with minimal exertion. 4. Immediate hospitalisation as highly likely to progress to AMI.

Answer 16

1. Often referred to as a ‘heart attack’ 2. Occurs when blood flow to part of the heart decreases or stops, causing damage or death to the heart muscle; prolonged myocardial ischaemia (\>20mins) (\*Remember, the fish dies if it stays out of water) 3. Signs & symptoms: Prolonged discomfort/pain in chest, upper extremity, jaw or epigastric with exertion or rest, and/or SOB, diaphoresis, nausea and syncope. 4. Classification of an AMI depends on which vessel is occluded eg. Right coronary artery occlusion means an inferior AMI. 5. Blood test biomarkers and ECG will help determine the type of AMI.

Answer 17

1. ST Elevation Myocardial Infarction (STEMI) 2. Non ST Elevation Myocardial Infarction (NSTEMI)

Answer 18

1. Necrosis through wall of heart 2. ST elevation on ECG - see Figure 4-1 (right), with arrows showing ST elevation (STEMI) 3. Large Troponin rise

Answer 19

Reperfusion ONLY if patient can reach centre within 2 hours If late presenting would receive thrombolysis, see below MONASH = Morphine, Oxygen, Nitrates, Aspirin, Statin, Heparin

Answer 20

1. Sub-endocardial injury 2. Either no ECG change or ST depression 3. Elevated Troponin

Answer 21

Thrombolysis – an intravenous clot dissolving drug, dissolves the blood clot but does not treat the underlying plaque. MONASH

Answer 22

If a patient presents with a history of angina: 1. Perform a thorough patient interview to confirm aggs, signs & symptoms, Mx. 2. Ensure medications are handy when mobilising patient. * IHD = Regular exercise is encouraged (unless patient develops UAP)… * UAP = Exercise is **CONTRAINDICATED.** * AMI = Exercise is **minimised** – avoid increases in HR, BP, CO. Initial management is medically driven: reperfusion of the damaged area of the heart and prevention of cardiac arrest.

Answer 23

Patients often rest in bed (RIB) for the first 24 hours following an AMI. Therefore start foot and leg exercises + breathing exercises to prevent pulmonary complications whilst RIB.

Answer 24

Troponin, HR, heart rhythm (telemetry/ECG), BP, SpO2, medication timing.

Answer 25

1. Describes diseases of the myocardium and also associated cardiac disease, including: vascular, valvular, inflammatory and other processes 2. Associated with mechanical and/or electrical dysfunction

Answer 26

1. dilated cardiomyopathies (DCMs) 2. restrictive cardiomyopathies 3. hypertrophic cardiomyopathies 4. arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVC)

Answer 27

1. Characterised by dilatation of the left or both ventricular chambers, impaired contraction and hence systolic dysfunction 2. DCM is commonly idiopathic but may also be related to genetic abnormalities, or occur secondary to cardiac toxins (chemotherapeutic agents), infection (eg. myocarditis) and autoimmune diseases (eg. HIV) 3. May progress to severe heart failure

Answer 28

1. Characterised by an increase in stiffness of the ventricular walls, resulting in impaired ventricular filling (diastolic dysfunction) 2. Commonly caused by abnormal deposition of amyloid proteins in the myocardium causing fibrosis 3. Restrictive cardiomyopathies may be idiopathic, familial in origin, related to ‘storage’ diseases (eg. haemochromatosis) or endomyocardial fibrosis (secondary to radiation therapy) 4. Leads to impaired ventricular fillings and impaired ability to supplement cardiac output

Answer 29

1. Genetic cardiovascular disease characterised by thickening of the left ventricle 2. Can result in impaired transmission of the cardiac impulse with potential for ventricular tachyarrhythmias and sudden cardiac death

Answer 30

1. Predominantly affects the right ventricle 2. Most commonly genetically determined but may also be related to congenital abnormalities and myocarditis 3. Progressive atrophy of the right ventricular myocardium occurs with formation of adipose and fibrous tissue 4. Structural changes interfere with myocardial contractility and normal transmission of the cardiac impulse

Answer 31

1. Varied symptoms primarily relate to the progression of heart failure and/or cardiac arrhythmia 2. Typical symptoms include: dyspnoea, reduced exercise capacity, fatigue, +/-pulmonary oedema and hepatomegaly 3. For HCM and ARVC, typical symptoms are caused by cardiac arrhythmia including: pre-syncope, dizziness and light-headedness

Answer 32

Based on symptoms and exclusion of other structural/functional causes (through detailed patient interview, family history, physical examination and clinical investigation including ECG and echocardiography)

Answer 33

1. Primarily around surveillance, patient education regarding activity (avoiding excessive exertion but maintaining regular exercise) and medical management for arrhythmias 2. Surgery may be indicated for valvular dysfunction

Answer 34

1. Physiotherapists may encounter patients with cardiac myopathy under the following circumstances: (1) those requiring surgery, (2) those hospitalised for management of heart failure and (3) those with undiagnosed cardiomyopathy experiencing ventricular tachyarrythmia and syncope. 2. Physiotherapists should complete careful in-hospital mobilisation and/or respiratory care whilst monitoring signs and symptoms during exertion.

Answer 35

HF results when the cardiac pump is: 1. Unable to maintain adequate output to support the body, and/or 2. Unable to accommodate venous return.

Answer 36

(Left = Lungs develop oedema) * Left-sided heart failure causes blood to back up through the left atrium and into the pulmonary veins. Thus patients commonly present with pulmonary oedema. * Most common causes are coronary artery disease, hypertension, cardiomyopathy and rheumatic heart disease. * When a myocardial infarction occurs (STEMI) an area of the myocardium is damaged and replaced by scar tissue. The scar tissue has reduced elasticity and less contractility than normal. Thus the remaining viable tissue has to work harder. If the damaged area is large, the functioning myocardium cannot compensate for the loss and the ejection fraction is reduced leading to heart failure. * In the case of hypertension, the heart must pump against an increased afterload that may lead to left ventricular hypertrophy. The hypertrophic muscle has reduced contractility and heart failure may result over time.

Answer 37

most common cause Hallmark finding: decreased left ventricular ejection fraction Due to 1. Impaired contractile function (e.g. STEMI) 2. Increased afterload (e.g. hypertension) 3. Cardiomyopathy ie enlargement 4. Mechanical abnormalities (e.g. valve disease)

Answer 38

Normal ejection fraction 1. Impaired ability of ventricles to relax and fill during diastole --\> decreased SV and CO 2. Diagnosis based on presence of pulmonary congestion, pulmonary hypertension, ventricular hypertrophy

Answer 39

(Right = Rest of body develops oedema) High blood pressure within the pulmonary arteries. Diagnosis is made with right heart catheterisation. Pulmonary hypertension can be secondary to any respiratory or cardiac disorder that causes narrowing or increased volume or pressure within the pulmonary circulation. If pulmonary hypertension progresses, hypertrophy of the right ventricle may occur, with eventual cor pulmonale. Acute respiratory infection (eg of COPD) may worsen right heart failure so respiratory treatment is indicated.

Answer 40

1. Respiratory management as indicated (eg, if underlying infection, exacerbation). However, ACTs are NOT indicated for pulmonary oedema if there is no evidence of retained secretions. 2. Management of SOB, recovery positions, purse-lipped breathing, NIV, exercise prescription, falls prevention, formal cardiac rehabilitation. 3. Avoid HDT, bilateral above shoulder arm exercises, flat supine. 4. For peripheral oedema, do NOT use compression therapy (eg TEDs) as this will increase the pre-load which will further stress the already compromised heart.

Answer 41

Right heart failure, secondary to acute exacerbation of COPD

Answer 42

Treat the acute infective exacerbation of COPD using ACTs such as ACBT, P&V; manage SOB with BC, recovery positions. Addressing airway clearance will improve PaO2, decrease vasoconstriction of pulmonary vessels, decrease the load on the right heart so it can pump more effectively and reduce backflow to the brain, liver and extremities.

Answer 43

1. Describes obstructive disorders of blood supply to the lower and upper limbs 2. Highly associated with coronary atherosclerosis and IHD, thereby increasing the risk of major cardiovascular events 3. Primary causes are atherosclerosis and thromboembolism leading to vessel stenosis (narrowing) and/or occlusion 4. Impaired perfusion to distal tissues may cause temporary (exercise-induced) ischaemia and/or prolonged ischaemia and necrosis 5. Also terms ‘peripheral vascular disease’ (PVD)

Answer 44

1. Can be asymptomatic but typically presents as intermittent claudication ie. exertional discomfort, pain and/or fatigue localised to the muscle supplied by the affected vessels, during walking 2. May cause alterations to skin colour, temperature and integrity (delayed wound healing) 3. Can result in critical limb ischaemia and impending limb loss

Answer 45

1. Known risk factors – atherosclerotic coronary, carotid or renal artery disease 2. Vascular symptoms – claudication 3. Vascular assessments – auscultation of femoral arteries, peripheral pulse palpation and skin inspection 4. Non-invasive vascular laboratory tests

Answer 46

1. Initial management includes reducing risk factors – smoking cessation, treatment of hypertension, dyslipidaemia, diabetes mellitus, antiplatelet therapy 2. Angioplasty with or without stenting is indicated for patients with lifestyle-limiting symptoms or whose symptoms are unresponsive to exercise and pharmacology interventions

Answer 47

1. Physiotherapists will supervise patients during intermittent walking-based programs often undertaken in a cardiac rehabilitation setting. These programs have been shown to substantially improve average maximal walking distance. 2. Monitor symptoms and objective measures (HR, BP, RPE) during exertion. 3. Be aware of claudication distance; this will impact tolerance and inform exercise approach.

Answer 48

Venous thromboembolism (VTE) refers to the disease process whereby thrombi (blood clots) form within the venous circulation.

Answer 49

1. **Deep vein thrombosis (DVT):** occurs more commonly in the lower limbs however may occur in the upper limbs. The primary concern of DVT is embolization such as a PE (next). 2. **Pulmonary embolism (PE):** occurs when a thrombus detaches from the site of formation and lodges in the pulmonary arterial circulation.

Answer 50

1. Often asymptomatic 2. Local pain, tenderness, redness, swelling of affected limb

Answer 51

1. May also be asymptomatic 2. Acute onset SOB, tachypnoea, chest pain, haemoptysis/cough, tachycardia, syncope 3. Approximately 10% of patients with symptomatic PE will die within 1h of symptom onset.

Answer 52

1. Ultrasound 2. Blood test for fibrin D-dimer 3. P/E tests for colour, temperature, pain, Homan’s sign (but these have limited specificity and sensitivity)

Answer 53

1. Computed tomographic pulmonary angiogram (CTPA) 2. Blood test for fibrin D-dimer

Answer 54

1. Prophylaxis/prevention++ 2. Blood thinners eg. heparin 1. Compression stockings (TEDs) 2. Sequential compression devices (SCDs, “scuds”) 3. Anticoagulation therapy 3. +/- catheter or surgical thrombolysis/embolectomy

Answer 55

1. Physiotherapists play an integral role in preventing VTE in hospitalised patients 2. Perform routine assessment (DVT, circulation) of those at risk 3. Bed exercises as indicated for patients on bed rest 4. For patients with a confirmed DVT or PE, early mobility is indicated only when a patient has reached therapeutic levels of anticoagulation (INR 2.0-3.0), the patient is haemodynamically stable and medical clearance has been approved.

ILP 5: Cardiac Conditions Flashcards

(84 cards)