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PHTY3250 > ILP 5: Cardiac Conditions > Flashcards

ILP 5: Cardiac Conditions Flashcards

1
Q

Left side of the heart receives blood from the______ (_____)

A

Lungs (oxygenated)

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2
Q

Right side of the heart receives blood from the______ (_____)

A

Rest (of the body) (deoxygenated)

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3
Q

Arteries pump blood _____ (Towards/Away) from the heart to the body (veins return blood to the heart)

A

Away

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4
Q

What prevents blood mixing between the right and left sides of the heart?

A

Interatrial septum & interventricular septum

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5
Q

Which has the thickest wall – the atria (left or right) or ventricles (left or right) – and why?

A

The left ventricle has the thickest wall as it needs to pump blood around the body [remember, the Left receives oxygenated blood from the Lungs and pumps this around the body, whereas the Right ventricle only needs to pump deoxygenated blood from the Rest of the body to the lungs]. The atria only need to squeeze blood into the adjoining ventricle (much closer, so the atria are smaller and thinner walled).

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6
Q

What is the role of the pericardial fluid? What happens when there is an increase in pericardial fluid? What is this condition?

A

The pericardial fluid lubricates and creates a frictionless environment for the heart. An increase in pericardial fluid will compress the heart and impair its ability to pump. This is termed cardiac tamponade.

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7
Q

How many cusps does the right atrioventricular valve have? And the left?

A

RIght = tRIcuspid valve (3) ; Left = bicuspid valve (2) (also termed ‘mitral’).

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8
Q

Are the coronary arteries superficial or deep? What is the implication of this for surgery?

A

Superficial. This means they are relatively easily located for coronary artery bypass graft (CABG) surgery.

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9
Q

What is systole? And diastole?

A

Heart contracts ; heart relaxes.

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10
Q

Heart Sounds

How many heart sounds are there? What are they termed?

A

Two heart sounds = ‘lub, dup’

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11
Q

Electrical Conductivity of the Heart

Where is the first electrical stimulus generated?

A

Sinoatrial (SA) node in the right atrium

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12
Q

Electrical Conductivity of the Heart

Where is the next impulse? How does this then travel to the ventricles?

A

Atrioventricular (AV) node –> AV Bundle of His & Purkinje fibres to the ventricles.

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13
Q

What does ECG (Electrocardiogram) look like?

A
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14
Q

What are 4 ECG physiotherapy considerations?

A
  1. Be able to identify a normal and abnormal rhythm and know what arrhythmias means.
  2. If patient is on ECG monitoring, ensure that all leads are on firmly and that you can identify a good rhythm trace prior to treatment.
  3. When repositioning the patient you may have to recheck the trace.
  4. Percussion & vibration may interfere with the trace.
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15
Q

Autonomic Regulation of Heart Rate

An increase in sympathetic nervous system (SNS) will have what result on the heart? What hormones stimulate this action?

A

↑SNS activation –> ↑HR. This is caused by release of catecholamines, adrenalin and noradrenalin.

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16
Q

Blood Pressure & Total Peripheral Resistance

What three mechanisms affect blood pressure (BP)?

A
  1. HR (beats per minute)
  2. Stroke volume (SV) (volume of blood ejected from a ventricle per contraction)
  3. Total peripheral resistance (TPR) (friction encountered by blood as it passes through a peripheral artery)
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17
Q

Blood Pressure & Total Peripheral Resistance

What is CO? How is it calculated?

A

Cardiac Output = SV x HR (the amount of blood ejected from a ventricle per minute)

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18
Q

Stroke Volume

What three methods can increase stroke volume (SV)?

A
  1. Increased venous return (Frank Starling’s law)
  2. Reduced after-load
  3. Increased contractility of the ventricle (inotropy)
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19
Q

Renal System & Auto Regulation of Blood Pressure

What organ has an important role in regulating blood pressure by secreting the hormone renin?

A

Kidneys

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20
Q

Renal System & Auto Regulation of Blood Pressure

Along with the kidneys, what other factors influence TPR?

A
  1. Temperature (cold  vasoconstriction)
  2. Chemicals
    1. nicotine –> vasoconstriction –> ↑BP
    2. alcohol –> vasodilation –> ↓BP
  3. Diet (salt, saturated fat, cholesterol –> narrowed vessels –> ↑BP)
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21
Q

Renal System & Auto Regulation of Blood Pressure

If blood volume is low, which hormone is released from the pituitary gland? What does this hormone do?

A

Antidiuretic Hormone (ADH). This causes the renal system to increase the reabsorption of water (ie, less urine is produced) to increase blood volume, VR and pre-load.

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22
Q

What are the 6 Cardiac conditions & implications for physiotherapy?

A
  1. Hypertension
  2. Ischaemic heart disease (IHD)
  3. Cardiomyopathy
  4. Heart Failure
  5. Peripheral artery disease (PAD)
  6. Venous thrombombolism (VTE)
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23
Q

What are 5 characteristics of hypertension? What is primary and secondary hypertension?

A
  1. A consistent elevation of blood pressure
  2. Systolic >140mmHg; Diastolic >90mmHg
  3. ~30% of population have hypertension
  4. Primary (idiopathic): accounts for >90% of cases
  5. Secondary: renal disease, adrenal tumour, recreational drugs, medications
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24
Q

What are 8 risk factors for hypertension?

A
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25
Q

What are 4 managements for hypertension?

A
  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)
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26
Q

What are the physiotherapy implications for hypertension?

A

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.

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27
Q

What is Ischaemic Heart Disease (IHD)?

A

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

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28
Q

When does Ischaemic Heart Disease (IHD) appear?

A

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

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29
Q

The _______ is most susceptible to ischaemia and injury due to its higher myocardial oxygen demand and larger mass

A

left ventricle

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30
Q

Why is the left ventricle the most susceptible to ischaemia and injury?

A
  1. higher myocardial oxygen demand
  2. larger mass
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31
Q

What is ischaemia heart disease (IHD) caused by?

A

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

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32
Q

As IHD is caused by __________ , the term IHD is often used interchangeably with ‘coronary artery disease’ (CAD) or ‘coronary heart disease’ (CHD).

A

atherosclerosis of the coronary arteries

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33
Q

What are the risk factors of IHD?

A
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34
Q

What are 3 primary clinical manifestations of IHD?

A
  1. Stable angina
  2. Unstable angina pectoris (UAP)
  3. Acute myocardial infarction (AMI)
35
Q

What is stable angina for IHD? What are the 4 signs & symptoms?

A

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.
36
Q

What are 4 medications for IHD?

A
  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).
37
Q

Mr A, 48yo male, d2 post TKR; PMHx = hypertension. You are exercising him when he complains of chest tightness and tingling in his fingers.

What could this be? Describe your actions.

A

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
38
Q

Mr A, 48yo male, d2 post TKR; PMHx = hypertension. You are exercising him when he complains of chest tightness and tingling in his fingers.

If investigations are clear, what precautions could you take?

A

Avoid isometric exercises; use a wheelie walker rather than crutches

39
Q

What is Unstable Angina Pectoris (UAP) & Acute Myocardial Infarction (AMI) ?

A

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

40
Q

What are 4 characteristics of UAP in IHD?

A
  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.
41
Q

What are 5 characteristics of AMI in IHD?

A
  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.
42
Q

What are blood tests for biomarkers of myocardial necrosis?

A
43
Q

What are 2 ECG for types of AMI for IHD?

A
  1. ST Elevation Myocardial Infarction (STEMI)
  2. Non ST Elevation Myocardial Infarction (NSTEMI)
44
Q

What are 3 characteristics of ST Elevation Myocardial Infarction (STEMI) as a type of AMI for IHD?

A
  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
45
Q

What is the management of ST Elevation Myocardial Infarction (STEMI) as a type of AMI for IHD?

A

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

46
Q

What are the 3 characteristics of Non ST Elevation Myocardial Infarction (NSTEMI) as a type of AMI for IHD?

A
  1. Sub-endocardial injury
  2. Either no ECG change or ST depression
  3. Elevated Troponin
47
Q

What is the management of Non ST Elevation Myocardial Infarction (NSTEMI) as a type of AMI for IHD?

A

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

MONASH

48
Q

What are the physiotherapy considerations for IHD?

A

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.
49
Q

Mrs B, 52yo female admitted to Coronary Care Unit (CCU) via ambulance with chest pain >20minutes. ECG shows ST elevation. Troponin I results = 1.0ng/L. Diagnosis is confirmed as ST elevated myocardial infarction (STEMI).

You are asked to see Mrs B Day 1 - what will your management be?

A

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.

50
Q

Mrs B, 52yo female admitted to Coronary Care Unit (CCU) via ambulance with chest pain >20minutes. ECG shows ST elevation. Troponin I results = 1.0ng/L. Diagnosis is confirmed as ST elevated myocardial infarction (STEMI).

You are now seeing the patient Day 2 - what indicators/objective measures would you use to determine if the patient is safe to start gentle mobility?

A

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

51
Q

What are 2 characteristics of cardiomyopathy?

A
  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
52
Q

What are the 4 main categories of cardiomyopathies?

A
  1. dilated cardiomyopathies (DCMs)
  2. restrictive cardiomyopathies
  3. hypertrophic cardiomyopathies
  4. arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVC)
53
Q

What are 3 characteristics of Dilated Cardiomyopathy (DCM)?

A
  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
54
Q

What are 4 characteristics of Restrictive Cardiomyopathy?

A
  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
55
Q

What are 2 characteristics of Hypertrophic Cardiomyopathy (HCM)?

A
  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
56
Q

What are 4 characteristics of Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy (ARVC)?

A
  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
57
Q

What are 3 signs and symptoms for cardiomyopathy?

A
  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
58
Q

What is the diagnosis of cardiomyopathy?

A

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)

59
Q

What are 2 managements of cardiomyopathy?

A
  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
60
Q

What are 2 physiotherapy considerations of cardiomyopathy?

A
  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.
61
Q

What are 2 situations of the cardiac pump where HF (heart failure) is the result?

A

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.
62
Q

What is Left Heart Failure?

A

(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.
63
Q

What is the hallmark of systolic failure? What are 4 causes?

A

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)
64
Q

What are 2 characteristics of diastolic failure?

A

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
65
Q

What are signs and symptoms of left and right heart failure?

A
66
Q

What is Right Heart Failure (Pulmonary Hypertension)?

A

(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.

67
Q

What are 4 physiotherapy considerations of heart failure?

A
  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.
68
Q

Mr C, 52yo male

PMHx = COPD, heavy smoker, supplemental oxygen

FEV1/FVC = 40% of predicted

SpO2 (usual) = 88-92% on 2L via np ; SpO2 (current) = 85% on 2L via np

P/E: Increased SOB, cough, sputum has changed colour (green)

JVP = raised (+5cm)

Swelling of ankles (SOA); swollen abdomen, tender liver

What condition does Mr B have?

A

Right heart failure, secondary to acute exacerbation of COPD

69
Q

Mr C, 52yo male

PMHx = COPD, heavy smoker, supplemental oxygen

FEV1/FVC = 40% of predicted

SpO2 (usual) = 88-92% on 2L via np ; SpO2 (current) = 85% on 2L via np

P/E: Increased SOB, cough, sputum has changed colour (green)

JVP = raised (+5cm)

Swelling of ankles (SOA); swollen abdomen, tender liver

What physiotherapy management can you provide?

A

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.

70
Q

What are 5 characteristics of peripheral artery disease (PAD)?

A
  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)
71
Q

What are 3 signs and symptoms of peripheral artery disease (PAD)?

A
  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
72
Q

What are 4 diagnosis of peripheral artery disease (PAD)?

A
  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
73
Q

What are 2 managements of peripheral artery disease (PAD)?

A
  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
74
Q

What are 3 physiotherapy considerations of PAD?

A
  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.
75
Q

What is the venous thromboembolism (VTE)?

A

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

76
Q

What are 2 most common clinical manifestations of VTE?

A
  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.
77
Q

What are 2 signs and symptoms of DVT of VTE?

A
  1. Often asymptomatic
  2. Local pain, tenderness, redness, swelling of affected limb
78
Q

What are 3 signs and symptoms of PE of VTE?

A
  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.
79
Q

What are risk factors of VTE?

A
80
Q

What are 3 diagnosis of DVT for VTE?

A
  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)
81
Q

What are 2 diagnosis of PE for VTE?

A
  1. Computed tomographic pulmonary angiogram (CTPA)
  2. Blood test for fibrin D-dimer
82
Q

What are 3 managements of VTE?

A
  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
83
Q

What are 4 physiotherapy considerations of VTE?

A
  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.
84
Q

What are common medications in the cardiac and cardiovascular fields?

NOT EXAM QUESTION

A

PHTY3250 (20 decks)

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