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MD3001 > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What 6 questions do you think about from any paper?

A
  1. When and where was it published?
  2. Why was it conducted?
  3. Who conducted the research?
  4. Where was it conducted?
  5. How was it conducted?
  6. What were the results and take home message?
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2
Q

What is the difference between sympathy and empathy?

A

SYMPATHY- quality/state of being affected by the condition of another with a feeling similar. Capacity of entering or sharing the feelings of another.
EMPATHY- the ability to understand and appreciate another person’s feelings, experience etc

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3
Q

What care must a doctor provide according to GMC?

A
  • Must act in accordance with relevant legislation
  • Must not treat patients unfairly
  • Must not deny patients access to appropriate services or care
  • Must not cause patients distress
  • You must not refuse to treat a particular patient because of personal belief
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4
Q

When do the BMA support doctors freedom of choice/ Conscientious Objection (3)?

A
  1. Abortion
  2. Fertility treatment
  3. Withdrawal of life-sustaining treatment
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5
Q

What does the Abortion Act, 1967 say about conscientious objection and abortion?

A

Nothing shall affect any duty to participate in treatment which is necessary to save the life or to prevent grave permanent injury to the physical or mental health of a pregnant woman

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6
Q

How do Human Rights Acts come into play?

A
  • Everyone has the right to freedom of thought, conscience and religion.
  • Freedom to manifest one’s religion or beliefs shall be subject only to such limitations… in the interests of public safety, for the protection of public order, health or morals or protection of right and freedoms of others
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7
Q

How does CO affect medical students?

A
  • You also have the right to hold a conscientious objection to some types of treatment and you should discuss this with your medical school
  • Treating patients fairly and communicating in a polite way, not expressing your personal beliefs
  • Do not discriminate!
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8
Q

What are the 4 arguments against the practice of CO?

A
  1. Inefficiency and inequity
  2. Inconsistency
  3. Commitments of a doctor
  4. Discrimination
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9
Q

What is Pre-load?

A

Determined by venous return and EDV (end diastolic volume)

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10
Q

What is afterload?

A

Force the contracting heart must generate to eject blood from the heart depending on vascular resistance and ventricular wall tension

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11
Q

What is myocardial contractility dependent on (inotropy)?

A

Influenced by Ca2+:

  • L type channels (opening faciliatated by cAMP)
  • Na+/Ca2+ exchange (inhibited indirectly by cardiac glycosides)
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12
Q

What is the difference between systolic and diastolic dysfunction?

A

SYSTOLIC ventricular dysfunction - impaired cardiac contractility, thus a decreased ejection fraction. (less than 40%)
DIASTOLIC ventricular function - normal ejection fraction but impaired diastolic ventricular relaxation and decreased filling, meaning a decrease in stroke volume and cardiac output.

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13
Q

What does systolic dysfunction lead to?

A
  • Contractility problems such as cardiomyopathy and ischaemic heart disease
  • Volume overload
  • Pressure overload such as in valvular stenosis and hypertension.
  • Results in increased EDV (preload), ventricular dilation and increased ventricular wall tension
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14
Q

What causes systolic dysfunction?

A
  • MI and transient myocardial ischaemia
  • Mitral regurgitation
  • Aortic regurgitation
  • Severe hypertension
  • Aortic stenosis
    (all REDUCE ejection fraction)
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15
Q

What causes diastolic dysfunction?

A
  • Left ventricular hypertrophy
  • Myocardial fibrosis
  • Transient myocardial ischaemia
  • Pericardial constriction or tamponade
    (all PRESERVE ejection fraction but DECREASE SV and CO)
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16
Q

What is the effect of right heart failure?

A
  • Congestion of peripheral tissues as increased preload.

- Leads to oedema and ascites, liver congestion and GI tract congestion which may lead to anorexia and GI distress

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17
Q

What is the effect of left heart failure?

A
  • Decreased cardiac output which leads to intolerance of activity and decreased tissue perfusion, leading to cyanosis and hypoxia (deficiency of oxygen reaching tissues)
  • Also get pulmonary congestion, which leads to orthopnea (breathlessness when flat), paroxysmal nocturnal dyspnea and cough with frothy sputum
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18
Q

What are the causes of right heart failure?

A
  • Conditions impeding flow into lungs such as pulmonary hypertension and valve damage/stenosiss
  • Infarction of cardiomyopathy in right ventricle
  • Left ventricular failure
  • Congenital heart defects
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19
Q

What are causes of left heart failure?

A
  • Hypertension
  • Acute MI
  • Aortic or mitral stenosis or regurgitation
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20
Q

What are the compensatory mechanisms for heart failure?

A
  1. Renin-angiotesin-aldosterone
  2. Frank-Starling
  3. Sympathetic nerve activity
  4. Fluid movements
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21
Q

What is the problem with the Frank Starling mechanism?

A
  • Increase in vascular volume leads to increased EDV
  • Increase in muscle stretch and oxygen consumption leads to decline of SV as we go past optimum sarcomere length.
  • Flattened curve in contractility of heart in heart failure, even though EDV increases, CO does not increase comparatively, increase pressure.
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22
Q

What is the problem with sympathetic activity as a compensatory mechanism?

A
  • Leads to tachycardias, decreased perfusion of tissues, cardiac arrythmias and renin release
  • This leads to increased workload on the heart, leading to ischaemia and damage to myocytes.
  • Get desensitisation of beta receptors
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23
Q

What is the problem with renin angiotensin compensatory mechanism?

A
  • Decrease in renal blood flow stimulates release of renin, increasing angiotensin II formation. This is a vasoconstrictor and stimulates aldosterone release
  • Thus there is sodium and water resportion which is increased both by decreased flow rate through kidneys and indirectly via aldosterone
  • Angiotensin II and aldosterone are also involved in inflammatory responses leading to deposition of fibroblasts and collagen in the ventricles, increasing stiffness and decreasing contractility of the heart
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24
Q

What 4 strategies would be used for treatment?

A
  1. Increasing cardiac contractility
  2. Decreasing preload and or after load by relaxing smooth muscle and reducing blood volume
  3. Inhibit the RAAS
  4. Prevent inappropriate increase in heart rate
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25
Q

What is the Definition of Heart Failure?

A
  • Failure of the heart to pump sufficient blood to satisfy metabolic demands
  • Results in under-perfusion which causes fluid retention and increases blood volume
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26
Q

What is Acute Heart Failure?

A

Rapid onset of symptoms, often with definable cause ie. Myocardial infarction

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27
Q

What is Chronic Heart Failure?

A

Slow onset of symptoms, associated with, ischaemic or valvular heart disease

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28
Q

What is Acute-on-Chronic Heart Failure?

A

Chronic failure becomes worsened by an acute event

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29
Q

List Systemic Diseases which have an affect on the CVS?

A
  • Diabetes Mellitus
  • Hypertension
  • Chronic Obstructive Pulmonary Disease
  • Amyloidosis
  • Rheumatoid Arthritis
  • Vasculitides & SLE
  • Thyroid disease
  • Sarcoidosis
  • Nutrition
  • Drugs
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30
Q

What is “forward failure”?

A

Reduced perfusion of tissues, more associated with advanced failure

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31
Q

What is “backwards failure”?

A

Due to increased venous pressures, dominated by fluid retention and tissue congestion

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32
Q

What happens pathologically when there is too much circulating glucose (diabetes mellitus)?

A
  • Non-enzymatic glycation occurs

- Glucose is in excess so sticks to proteins and membranes

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33
Q

Which protein is an ideal marker for blood glucose control in diabetics?

A

Glycated Heamoglobin

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34
Q

What would be classed as a primary cause of hypertension?

A

Cardiovascular disease

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35
Q

How does emphysema cause ischaemic damage to the heart?

A

Vessels within the scar tissue within the lungs are non-functional and present a high resistance for blood to force through, this increases the workloads of the right side of the heart, which causes pulmonary hypertension and right ventricular hypertension- leading to ischaemic damage to the heart muscle

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36
Q

What is amyloid and what does it do?

A
  • Extracellular beta-pleated sheet material

- Deposited on organs, impairing it’s function

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37
Q

What pathologcial condition produces AA and what does this stand for?

A

AA= amyloid associated protein

Chronic inflammation produces excess amyloid associated proteins

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38
Q

What pathological condition produces AL and what does this stand for?

A

AL= amyloid light chains

Myeloma produces excess amyloid light chains (related to immunoglobulin)

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39
Q

What is vaculitis?

A

Damage to blood vessels due to hyper sensitivity

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40
Q

What is type 1 hypersensitivity?

A

Allergic reaction

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41
Q

If a middle aged, possibly overweight, female patient presents with a cold, what diagnosis should be kept in mind?

A

Hypothyroidism

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42
Q

What is sarcoidosis?

A

Abnormal collections of inflammatory cells that form nodules in multiple organs

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43
Q

What could have happened in a patient with sarcoidosis and arrthymia?

A

Granuloma formed in the conducting tissue

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44
Q

List Drugs that affect CVS?

A
  • Anti-cancer
  • Immunosuppressive
  • Diabetogenic
  • Anti-inflammatory
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45
Q

What are the valve components (4)?

A
  • Valve rings
  • Cusps
  • Chordae tendiniae
  • Papillary muscles (mitral/tricuspid only)
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46
Q

Define stenosis of valve?

A

Narrowing of valve outlet caused by thickening of valve cusps, or increased rigidity/scarring

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47
Q

Define valve incompetence?

A

Insufficency or regurgitation caused by incomplete seal when valves close, allowing blood to flow backwards

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48
Q

What are vegetations?

A
  • Something growing on valve

- Platelets and fibrin accumulations that form hard plaque

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49
Q

What are the three main causes of cardiac valve stenosis and incompetence

A
  1. Congenital heart disease
  2. Cardiomyopathy
  3. Acquired
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50
Q

What types of valve problems would be expected from congenital heart disease?

A

Bicuspid valve incompetence or atresia

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51
Q

What types of problems in valves are found with cardiomyopathy?

A

Incompetence from hypertophic heart, therefore dilated valve ring

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52
Q

What sorts of things can cause acquired valve problems?

A
  • Rhematic fever
  • MI
  • Age related (idiopathic)
  • Endocarditis
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53
Q

What are the risks of aortic stenosis?

A
  • Left ventricular hypertrophy
  • Syncope
  • Sudden cardiac death
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54
Q

What are causes of aortic stenosis?

A
  • Calcification of congenital biscuspid valve
  • Senile calcification degeneration
  • Rheumatic fever
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55
Q

What is rheumatic fever?

A
  • An inflammatory disease that can involve the heart, joints, skin, and brain.
  • Typically develops 2-4 weeks after a throat infection from Streptococcus pyogenes.
  • The heart is involved in about half of cases
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56
Q

What are the consequences of aortic stenosis?

A
  • Increases the work of the heart
  • Ventricular hypertrophy
  • Causes cardiac failure
    (symptoms: dyspnoea, angina, syncope)
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57
Q

What are causes of aortic valve incompetence?

A
  • Marfan’s syndrome
  • Rheumatic fever
  • Infective endocarditis
  • post MI
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58
Q

What are the consequences of aortic valve incompetence?

A
  • Aortic regurgitation
  • Increases volume of blood to be pumped significantly
  • Increases the workload of the heart
  • Causes left ventricular hypertrophy and cardiac failure
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59
Q

What are the causes of mitral valve incompetences?

A

Cusp/chordae- rheumatic disease scarring/contraction, floppy valve & marfans, infective endocarditis (perforation)

Papillary muscles- post MI

Valve ring- age

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60
Q

What is almost always the cause of mitral valve incompetence?

A

Childhood rheumatic fever

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61
Q

What are the risks of Mitral valve incompetence?

A

Pulmonary hypertension, and so right ventricular hypertrophy

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62
Q

What are the 2 main causes of mitral valve stenosis?

A
  • Congenital

- Post rheumatic fever

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63
Q

What is the consequence of mitral valve stenosis?

A
  • Restricts blood flow to left ventricle
  • Atrial fibrillation
  • Back pressure causes pulmonary hypertension and finally right heart failure
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64
Q

Define infective endocarditis?

A
  • Infection of valve with formation of thrombotic vegetations.
  • Virulence of organisms determines damage and severity.
  • Classed as acute and subacute
  • Bacteraemia is common
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65
Q

What is the biggest risk factor for infective endocaridits?

A

Rheumatic fever in childhood

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66
Q

Name the 3 main risk factors for infective endocarditis

A
  1. Valve damage- especially in rheumatic fever
  2. Bacteraemia (dental, catheterisation)
  3. Immunosupression
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67
Q

Describe the principles of diagnosis and treament of infective endocarditis?

A
  • Initially treat strep. infection
  • Prophylatic antibiotics in at risk patients for invasive procedures (like dental work)
  • Replacement of damaged valves
  • Imaging, blood cultures, clinical signs
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68
Q

What is the most common cause of CVS?

A

Smoking

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69
Q

What does atherosclerotic coronary disease cause?

A
  • Chronic coronary insuficciency (Angina)
  • Unstable coronary disease (MI, sudden ischaemic coronary disease)
  • Heart failure
  • Arrythmia (acute is ischaemic, scar related)
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70
Q

What surface of the heart do the coronary arteries lie on?

A

Epicardial (outer surface of the heart)

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71
Q

What causes resistance in coronary arteries?

A

Presence of atheromas

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72
Q

Where does ischaemia occur first in the heart?

A

Subendocardial region (water shed area) when there is no cell death.

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73
Q

How can the coronary arteries be imaged?

A
  • Coronary Angiography
  • CT
  • MR imaging (more functional but not as much accuracy)
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74
Q

What is the usual pathology of atherosclerotic coronary artery disease?

A
  • Fatty streak (already found in young people)
  • Fibro fatty plaques
  • Plaque disruption
  • Plaque rupture & plaque erosion
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75
Q

What are the risk factors for atherosclerotic coronary arteries?

A 
Age
Hypertension
Hypercholesterolaemia
Smoking
Diabetes 
Obesity
Physical Inactivity
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76
Q

What is the histology of coronary atherosclerosis?

A

Lipid rich core, fibrous cap and a lumen

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77
Q

What is the mechanism of coronary atherosclerosis?

A
  • LDL becomes oxidised and taken up by a macrophage
  • Macrophage responds to it thinking it is a germ, eats it and stores the fat in lysosomes
  • In fibro fatty plaques, cytokines drive macrophage to form the fibrous cap
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78
Q

What is Angina and how does it present?

A
  • It presents as: Gripping central chest pain, radiation to arm and jaw.
  • Clear and precise relationship to exercise.
  • Worse after food and in the cold.
  • No autonomic features and flat of hand to describe pain.
  • The cause is sub endocardial ischaemia.
  • ECG shows depression in the ST segment
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79
Q

What is the mechanism of Angina?

A

Mismatch of blood supply to demand because of epicardial stenosis.
Supply = coronary blood flow
Demand = myocardial oxygen consumption
50% of the lumen diameter reducing usually signifies limitation of maximal flow. Coronary flow reserve must always be able to accomodate myocardia 02 demand. Angina is when it becomes inadequate.

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80
Q

What is Coronary Flow Reserve?

A

Coronary flow reserve (CFR) is the maximum increase in blood flow through the coronary arteries above the normal resting volume

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81
Q

What are two regulatory systems of coronary circulation?

A
  • Autoregulation (myogenic control, where blood flow is kept constant)
  • Metabolic regulation (Blood vessels sense the changes in BP)
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82
Q

How does exercise affect myocardial blood flow?

A

Rise up to 5 fold to accommodate a 20 fold increase in total body 02 consumption

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83
Q

What are the 3 types of resistive compartments in the coronary circulation?

A
  1. Conductive vessels
  2. Prearteriolar vessels
  3. Arteriolar vessels
84
Q

What is adenosine’s function?

A

Metabolic signalling agent in coronary vasodilation

85
Q

What are the determinants of myocardial oxygen consumption?

A 
Variable per unit mass of tissue: 
- Tension development - LV Pressure and LV Volume
- Contractility
- Heart rate
Fixed per unit mass of tissue: 
- Basal activity (10-20%) 
Mass of tissue
86
Q

What is the treatment for angina?

A

Drugs to reduce myocardial oxygen consumption
Percutaneous Coronary Intervention (stents and balloons) and Coronary Artery Bypass Grafting - improve coronary flow reserve

87
Q

What are the types of drugs for angina?

A
  • Beta adrenoreceptor blockers
  • Organic Nitrates (GTN)
  • Calcium channel blocker
  • Potassium Channel activators
88
Q

How do Beta adrenoreceptor blockers work?

A

Reduce heart rate and BP, thus reducing work of heart

89
Q

How do nitrates (GTN) work?

A

Venodilation, thus reduced LV size, reduced wall tension.

Also has small effect on epicardial stenosis dilation (improving supply)

90
Q

How do calcium channel blockers work?

A

Reduce heart rate, small effect on from epicardial dilation (mixed)

91
Q

How do channel inhibitors work?

A

Selective heart rate reduction by inhibiting channels in SA node - IVABRIDINE

92
Q

What is clinical presentation of an MI?

A
  • Chest pain, classicaly severe, crushing, radiating to jaw and arm.
  • Associated autonomic symptoms such as nausea, sweating, terror.
  • Breathlessness.
  • Some people, generally male, are not able to feel cardiac pain.
93
Q

What are the causes for an MI?

A 
Plaque rupture - 70-75%
Plaque erosion - 25-30% 
Coronary embolism
Coronary artery spasm and drug
Coronary anomaly 
Spontaneous coronary dissection
94
Q

What is the pathology of an MI?

A
  • Occlusive thrombus forming on an atherosclerotic plaque.
  • Two mechanisms: platelet aggregation / coagulation.
  • Unstable plaques
95
Q

What are events modifying presentation of an MI?

A 
Time of day (more common in early hours of the morning) 
Inflammatory activity
Infection
Elevation of BP
Catacholamines
96
Q

How are MIs classified?

A
  • Site of infarction: full thickness, transmural or sub endocardial
  • By ECG: ST elevation STEMI or Non-ST elevation non-STEMI
97
Q

What are the 3 tests done to diagnose an MI?

A
  1. A clinical history
  2. ECG defining STEMI or NSTEMI
  3. Blood tests to look for raised Troponin T or I, creatine kinase
98
Q

How is STEMI managed?

A

Antiplatelet agents: Aspirin and clopidrogel
Immediate revascularisation: Primary PCI (percutaneous coronary intervention) or thrombolysis (not in the UK anymore)
Adjunctive Therapy or STEMI: after the above, use beta blockers, statin drugs (reduce cholesterol) and ACE inhibitors (inhibit dilation of left ventricle)

99
Q

What are the complications of a STEMI?

A

Immediate: ventricular arrythmia and death. Acute left heart failure
Early: myocardial rupture, mitral valve insufficiency, ventricular septal defect, mural thrombus and embolisation
Late: LV dilation and heart failure, arrythmia, recurrent MI

100
Q

What are the features of NSTEMI?

A

Getting more frequent - STEMI less common
More common in elderly and implies sub-endocardial ischaemia.
Caused by : threatened STEMI, small branch occlusion, occlusion of well collaterised vessel, or lateral STEMI in territory not well seen by an ECG.

101
Q

How is NSTEMI treated?

A

Antiplatelet therapy (aspirin and clopidrogel)
Anti-ischaemics (beta blockers and nitrates)
Statins
ACE inhibitors
Coronary angiography and revascularisation : early if symptoms continue, early if troponin raised, risk score (eg GRACE)

102
Q

What is the accepted scale for ECGs?

A

1cm=1mv, 25mm (5 big boxes)=1 sec

103
Q

How much time does one small box represent on an ECG?

A

0.04s

104
Q

How much time does one big box represent on an ECG?

A

0.2s

105
Q

How do you calculate heart rate from an ECG

A

Count big boxes between R-R peaks, divide 300 by this

106
Q

In which leads should the P waves be upright/positive?

A

II, III and aVF

107
Q

What is the normal size range for P wave amplitude?

A

<0.25mv

108
Q

What is the normal time range for the QRS complex?

A

under 120ms (0.12s)

109
Q

How do you assess if there is regular sinus rhythm?

A

Mark the position of 3 regular R waves on piece of paper, slide this mark forward and check intervals are equal

110
Q

What is the appearance of an ECG in atrial fibrillation?

A

No discernible P waves (lots of small seperate ones)and irregular QRS complexes

111
Q

What is the appearence of atrial flutter on an ECG?

A

Sawtooth appearance, frequent regular atrial depolarisation P waves, several between regular QRS complexes

112
Q

What is the appearence of an ECG in Junctional (nodal) tachycardia?

A

Normal QRS complexes very frequently, without P waves

113
Q

What is the appearence of an ECG in ventricular tachycardia?

A

Frequent, broad QRS complexes, T waves are difficult to identify

114
Q

In what situations may the P wave be absent?

A
  1. Atrial fibrillation

2. Nodal/junctional rhythm

115
Q

What would a bifid P wave indicate?

A

Left atrial hypertrophy (P-mitrale)

116
Q

What would a peaked P wave indicate?

A

Right atrial hypertrophy (P-pulmonale)

117
Q

What is the normal time range for the PR interval?

A

120-200ms

118
Q

Where is the P-R interval measured from?

A

Beginning of P to beginning of Q (if Q absent, beginning of R)

119
Q

What does a prolonged PR interval imply?

A

Delayed AV conduction

120
Q

Where is the QRS interval measured from?

A

Beginning of Q to the end of S wave

121
Q

What are the normal Q wave dimensions?

A

Less than 40ms (0.04s), and less then 2mm in depth

122
Q

What does a QRS complex duration longer than 120ms indicate?

A

Ventricular conduction defects, e.g. bundle branch block (left and right)

123
Q

What does a low voltage QRS complex indicate?

A

Hypothryoidism, COAD, myocarditis, pericarditis and pericardial effusion

124
Q

What is the nomal voltage range for a QRS complex?

A

> 5mv

125
Q

What QRS sign indicates left ventricular hypertrophy?

A

R wave in v5 greater than 25mm in length
OR
Sum of S wave in v1 and R in V5/v6 is greater than 35mm in length

126
Q

What QRS sign is indicitive of right ventricular hypertrophy?

A
  • Dominant R wave in V1
  • T wave inversion in V1-V3/4
  • Deep S wave in V6
127
Q

What defines a ‘significant Q wave’?

A

Greater than 40ms, deeper than 2mm.

128
Q

In what situations would a significant Q wave usually be present?

A

Couple of days/hours after MI,

If in lead III consider pulmonary embolism

129
Q

How is the QT interval measured?

A

Start of QRS to end of T wave (varies with rate)

130
Q

How is the corrected QTc interval obtained?

A

QTc= QT/√RR

131
Q

What is the normal range for QTc?

A

0.38-0.42s

132
Q

What could a prolonged QT be a sign of?

A
  • Acute myocardial ischaemia
  • Myocarditis
  • Bradycardia
  • Head injury
  • Hypothermia
  • U&E imbalance (low K+, low Ca++, low Mg++)
  • Congenital
  • Drugs
133
Q

Where is the ST segment measured from?

A

End of ventricular depolarisation to start of ventricular repolarisation

134
Q

What is the definition of elevated ST segment in limb and chest leads?

A

Limb: >1mm in two adjascent limb leads
chest: >2mm in two adjascent chest leads

135
Q

What does ST depression indicate?

A

Ischaemia

136
Q

In which leads is the T wave usually inverted?

A

VR and V1 (also V2 in young people)

137
Q

In which leads is it abnormal to have an inverted T wave? What is this indicative of?

A

I, II and V4-V6 (ischaemia/ infarction)

138
Q

What is the effect of digoxin overdose on T wave?/ ST segment?

A

T wave inversion & ST segment sloping depression

139
Q

What is the degree range of the normal axis of the heart?

A

-30 to +90

140
Q

What is the degree range for left axis devation?

A

-30 to -90

141
Q

In which leads would there be negative QRS deflections in left axis deviation?

A

II, III

142
Q

What is left axis devation indicative of?

A

LV hypertrophy/ MI

143
Q

What is right axis deviation indicative of?

A

RV hypertrophy/ PE/ MI

144
Q

What degree range is it for right axis deviation?

A

+90 to +180

145
Q

In which lead would there be a negative QRS in right axis deviation?

A

Lead I

146
Q

What are the 3 stages of ECG change in a myocardial infarction?

A

T wave peaking followed by T wave inversion,
ST segment elevation,
Appearence of new Q waves

147
Q

In anterior infarct, change in ECG can occur in leads?

A

V1 to V6

148
Q

In lateral infarction, change in ECG can occur in leads?

A

I, V5 and V6

149
Q

In inferior infarction, a change in ECG can occur in leads?

A

II, III, and aVF

150
Q

In a posterior infarction reciprocal changes (ST depression, tall R wave) occur in lead?

A

V1

151
Q

In anterior infarction, Q waves are visible in?

A

Leads V2-V4

152
Q

In anterior infarction, Inverted T waves are visible in leads?

A

V4-V6

153
Q

In atereolateral infarction, Q waves are in leads?

A

I, II, aVL and v3-v5

154
Q

In an atereolateral infarction, raised ST segments are visible in leads?

A

V2-V6

155
Q

In inferior infarction, Q waves are seen in leads?

A

III and aVF

156
Q

In inferior infarction, Depressed ST segments seen in leads?

A

aVl and V6

157
Q

In PE, There is a large S wave seen in lead?

A

I

158
Q

In PE there is a deep Q wave visible in lead?

A

III

159
Q

In PE, inverted T wave in lead?

A

III

160
Q

What are the ECG abnormalities seen in hyperkalaemia ?

A

Tall, tented T wave, widened QRS

161
Q

What ECG abnormalities are seen in Hypokalaemia?

A

Small T waves, prominent U waves

162
Q

What ECG abnormaities are seen in hypercalcaemia?

A

Short QT interval

163
Q

What ECG abnormalities are seen in Hypocalcaemia?

A

Long QT interval, small T waves

164
Q

What are the strategies of treatment for treating heart failure?

A
  • Increase cardiac contractility
  • Decrease preload and/or afterload to decrease cardiac work demand
  • Inhibiting RAAS
  • Preventing inappropriate increase in heart rate
165
Q

How would you decrease preload and after load?

A

Relax vascular smooth muscle (vasodilation) and decrease blood volume

166
Q

What is the acronym for drugs used in heart failure?

A

DAB (diuretic, ace inhibitor, beta blocker)

167
Q

What are the signs and symptoms of heart failure?

A
  • Shortness of breath
  • Swelling of feet and legs
  • Chronic lack of energy
  • Difficulty sleeping due to breathing problems
  • Swollen or tender abdomen with loss of apetite
  • Cough with frothy sputum
  • Increased urination at night
  • Confusion and/or imparied memory
168
Q

What is class 1 New York Heart Association Classification of Heart Failure (NYHA)?

A

No limitation of physical activity

169
Q

What is class 2 New York Heart Association Classification of Heart Failure (NYHA)?

A

Slight limitation of physical activity, comfortable at rest

170
Q

What is class 3 New York Heart Association Classification of Heart Failure (NYHA)?

A

Marked limitation of physical activity

171
Q

What is class 4 New York Heart Association Classification of Heart Failure (NYHA)?

A

Unable to carry out physical activity without discomfort, pain even during rest.

172
Q

Conditions that increase the chances of developing heart failure?

A
  • Hypertension
  • Coronary heart disease
  • Cardiomyopathy (genetic, alcohol misuse, infections, medications)
  • Atrial fibrillation
  • Anaemia
  • Overactive thyroid gland
173
Q

What does the body mistake heart failure for which leads it to make the condition worse?

A

Haemorrhage

174
Q

What does the body release appropriately in haemmorhage that makes the heart failure worse?

A

Angiotensin II and ADH

175
Q

Why are diuretics used in heart failure?

A

To move/excrete odematous fluid

176
Q

What does heart failure treatments do/dont do?

A

DOES- Treats symptoms, Prolongs life

DOESN’T- Treat cause

177
Q

What are the main drugs used in heart failure?

A
  • Loop diuretic
  • ACE inhibitor
  • ARB
  • Beta blockers
  • Aldosterone receptor antagonists
178
Q

What is the loop diuretic drug?

A

Furosemide

179
Q

What are the ACE inhibitors?

A

Ramipril

Lisonopril

180
Q

What are the ARBs?

A

Candesartan

181
Q

What are the beta blockers used?

A

Bisoprolol

Carvedilol

182
Q

Aldosterone receptor antagonists?

A

Spironalactone

183
Q

What are the benefits of using beta blockers?

A
  • Slow heart rate which could decrease cardiac output
  • Allows ventricles to fill more completely suring diastole
  • May cause vasodilation and decrease afterload
184
Q

What are common side effects of ACE inhibitors?

A

Persistant dry cough, dizziness, tiredness, headache

185
Q

What are common ARB side effects?

A

Dizziness, headaches, back/leg pain

186
Q

Aldosterone receptor antagonists side effects?

A

Hyperkalaemia, hyponataemia, nausea, hypertension

187
Q

What are the loop diuretic side effects?

A

Acute gout is common in higher doses

188
Q

What are the aims fo treating ACUTE heart failure?

A

Normalise ventricular filling pressures and restore adequate tissue perfusion

189
Q

What are the treatments of acute heart failure initally?

A

IV loop diuretics- venodilation and diuresis
IV opiates- reduce anxiety and therefore preload
IV, buccal or sublingual nitrates- reduce preload and afterload

190
Q

What are the second line drug treatments for ACUTE heart failure?

A

Inotropes and beta agonists e.g. DOBUTAMINE (increases myocardial contractility)

DOPAMINE- increases renal perfusion and increases BP

INOTROPES, ADRENALINE- increase myocardial contractility

191
Q

What is Cardiac Rehab?

A

Process in which pts with cardiac disease, in partnership with a multidisciplinary team of health professionals, are encouraged and supported to achieve and maintain optimal physical and psychological health

192
Q

Why is cardiac rehab important?

A
  • Secondary prevention
  • Evidence gives 20-25% reduction in mortality.
  • Exercise-based CR is effective in reducing cardiac deaths, reducing cardiac risk factors and in enhancing psychosocial factors.
193
Q

What Patient Groups can use Cardiac Rehabilitation?

A
  • MI
  • Angioplasty (and stent)
  • CABG
  • Stable/unstable angina
  • Valve repair
  • Congenital repairs
  • Transplant
  • Heart Failure
  • Arrythmias
194
Q

Physiological Benefits of cardiac rehab?

A
  • Improvement in functional capacity
  • Improved cardiovascular efficiency
  • Reduction in atherogenic and thrombotic risk factors
  • Improvement in coronary blood flow, reduced myocardial ischaemia, and severity of atherosclerosis
  • Reduction in risk of cardiovascular disease mortality
  • Pt feels fitter, more exercise with less increase in HR and breathlessness.
  • Most pts have co-morbidities so exercise can help treat these too.
195
Q

Psychological benefits of cardiac rehab?

A
  • Reduced anxiety and depression
  • Enhanced mood
  • Enhanced self-efficacy
  • Restoration of self-confidence
  • Decreased illness behaviour
  • Increased social interaction
  • Resumption of chores/hobbies
  • Resumption of sexual activity
  • Return to work/vocation
196
Q

What is the Initial Assessment of cardiac rehab?

A
  • Individual Assessment with the cardiac rehab physio.
  • Soon as 2 weeks after MI.
  • Setting goals for increasing and maintaining activity in CR is important to help individuals stay motivated
  • Risk Assessment using the AACVPR guidelines
  • Angioplasty, ECG, shuttle/walk walking programme
  • Risk Stratification
  • Majority are post MI
  • Adapt exercise programme to pt level, geared to individual.
  • Pulse ranges for exercise regime
  • Put in classes with those at similar level.
197
Q

6 Cycle of Change in cardiac rehabilitation patients?

A
  1. Not interested
  2. Precontemplation
  3. Contemplation
  4. Doing it
  5. Had enough
  6. Give up or start again
198
Q

What are the Barriers to Exercise?

A 
Bad weather
Too tired
Not in the mood
Dont know how to
Cant afford it
Fear 
Dont have time
199
Q

What does “SMART” stand for?

A 
Specific
Measurable
Achievable
Realistic
Time based
200
Q

Activity/exercise

A
  • Activity is sporadic in nature and inconsistent in intensity eg climbing stairs
  • Exercise is purposeful and sustained eg going for a walk
  • Adults should do 150mins of mod exercise per week.
  • Live active lifestyle, regular exercise sessions.
201
Q

What is the “Warm Up” in cardiac rehab?

A
  • 15 mins
  • Prepare the muscles, nerves, cardiac, respiratory and vascular systems for main work out.
  • Stretches are still included - keep joints supple and lengthens muscles
  • If start/stop suddenly can cause angina/dizziness
202
Q

What is the “Conditioning Phase” in cardiac rehab?

A
  • 20 mins
  • Should be designed to produce a training effect
  • Circuit based exercise - designed to allow different levels of intensity
  • BORG 13-14
  • Comfortably short of breath “TALK”
203
Q

What does “FITT” Stand for?

A

Frequency
Intensity
Time
Type

204
Q

What is the “Cool Down” in cardiac rehab?

A
  • 10 mins
  • Pulse lowering exercises, which aim to reduce the heart rate and BP gradually
  • If have strengthening or lying down exercises do after the cool down to prevent pt getting up and down more than necessary, as if have low BP is very risky
205
Q

What does “STG” stand for in cardiac rehab?

A

Sing - good level to start off with for warm up

Talk - slightly short of breath but able to chat is a good level for moderate exercise

Gasp - If you cannot talk fluently, you are working too hard

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