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Phase 1 Exam > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Definition of DVT

A
  • Thrombosis formed within deep vein, usually leg. Can be proximal (involving the knee) or further distal isolated in the calf. It can involve the arms, mesentery and other areas.
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2
Q

Causes of DVT

A
  • Common.
  • Related to the stasis of blood flow and/or the increased coagulability of the blood.
  • Patient’s can have many different risk factors and causes for DVT all contributing.
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3
Q

Risk factors of DVT

A
  • Immobility, pregnancy, recent surgery, long haul flight, malignancy, use of OCP or HRT, smoking, obese, over 40 or PMH.
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4
Q

Pathology of DVT

A
  • Sluggish blood flow through the vein with or without increased coagulability of the blood means that the body overcomes it’s natural anticoagulation activity and leads to thrombus formation. The thrombus continues to grow as it occludes the vein.
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5
Q

DD of DVT

A

Cellulitis, superficial thrombophlebitis

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6
Q

Presentation of DVT

A
  • Unilateral pain, swelling and/or tenderness with or without fever in the limb.
  • Pitting oedema
  • Distension of collateral superficial viens.
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7
Q

Investigations of DVT

A
  • Use of Wells score in patients - 2 or more = referral
  • Serum D dimer
  • Ultrasound D doppler for confirmation.
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8
Q

Management of DVT

A
  • Prevention of PE.
  • LMWH, warfarin, DOAC
  • Compression stockings.
  • Below knee - 6 weeks anti coag, above knee - 3 months anticoag
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9
Q

Complications of DVT

A
  • PE, reoccurence
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10
Q

Prophylaxis of DVT

A
  • LMWH in admitted patients who are bed bound.
  • Post partum patients.
  • Prophylaxis in patients with recurrent VTE events.
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11
Q

Definition of AF

A
  • Common disturbance of heart rhythm, which can be episodic (Paroxysmal).
  • Characterised by rapid irregularly irregular narrow QRS complex tachycardia with an absence of P waves..
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12
Q

Types of AF

A
  • Paroxysmal (Episodic, resolves within 7 days).
  • Persistent (Lasts longer than 7 days)
  • Long standing (Lasts longer than 12 months).
  • Permanent.
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13
Q

Causes of AF

A
  • Congenital heart disease
  • Abnormal heart valves
  • High BP
  • Coronary artery disease
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14
Q

RF of AF

A
  • Age
  • High BP
  • Heart Disease
  • Chronic conditions such as diabetes and thyroid issues.
  • Alcohol user (especially binge drinkers)
  • Family History
  • Obesity
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15
Q

Pathophysiology of AF

A
  • Normal heart: Impulses sent for SAN node across the atria to the AV node causing them to contract, there is a small pause before the signals are sent down the bundle of His into the Purkinje fibres to cause the ventricles to contract.
  • AF heart: The signals in the atria are chaotic causing them to flutter/quiver, this bombards the AV node with multiple signals and causes the ventricles to constrict.
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16
Q

Presentation of AF

A

Heart palpitations, chest pain, fatigue, breathlessness, syncope and lightheadness.

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17
Q

Differentials of AF

A
  • Atrial Flutter (Saw tooth appearance on ECG)
  • Wolff Parkinson’s White Syndrome (Late teens/early 20’s).
  • Atrial Tachycardia (Patient’s present with COPD)
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18
Q

Investigations of AF

A

ECG (Resting/Ambulatory)
Bloods (TFT’s, U&Es and FBC)
CXR

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19
Q

Management of AF

A
  • Urgent admissions or referral if patient is acutely unwell.
  • Assess patients for stroke risk using CHADSVASC2 , if the patient has a score of 2 or more, then consider anti coag.
  • If patient considered for anti coag, weigh up bleeding risk using HAS BLED. Anti coag includes warfarin and DOACs (Rivaoxiban/apixiban).
  • Beta blocker (Bisoprolol) andCCB can be used (Verapmil) for rate limiting to reduce heart rate at rest and exercise.
  • Specialist care includes cardioversion, cardiac ablation and artificial pacemakers.
  • ‘Pill in pocket’ approach for Paroxysmal AF = Beta blocker PRN.
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20
Q

Complications of AF

A
  • Thrombus, stroke, dementia, MI, cardiac arrest.
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21
Q

Definition of Aortic Stenosis

A
  • Represents an obstruction of blood flow through the aortic valve due to a pathological narrowing.
  • Most common valvular disease.
  • Progressive disease that has a long sub clinical period.
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22
Q

Causes of Aortic Stenosis

A
  • 3 main causes: degeneration and calcification of a normal aortic valve (Elderly), calcification of a congenitally bicuspid aortic valve (Middle age) and rheumatic heart disease.
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23
Q

RF of Aortic Stenosis

A

Over 60, RHD, congenital bicuspid valve, radiotherapy, High levels of LDL and CKD.

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24
Q

Types of Aortic Stenosis

A

Supravalvular, subvalvular and valvular

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25
Q

Pathophysiology of Aortic Stenosis

A
  • Increase pressure gradient between LV and AA due to increased afterload in the LV. Initially LV compensates through LV hypertrophy but eventually this becomes unsustainable due increased myocardium oxygen demand and therefore myocardium ischaemia.
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26
Q

Presentation of Aortic Stenosis

A
  • Presentation once patients are moderate disease.
  • 3 main symptoms include exertion syncope, angina and dyspnoea.
  • Signs - carotid pulse = slow rising, apex beat = thrusting, harsh systolic ejection murmur heard at the right sternal angle and into the neck.
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27
Q

Investigations of Aortic Stenosis

A
  • CXR = Normal heart size, potential prominence of the AA and possible valve calcification.
  • ECG = LV Hypertrophy and strain = severe.
    = Echo = Diagnostic - looks at valve size, gradient, flow, LV dilation and hypertrophy.
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28
Q

Differentials of Aortic Stenosis

A
  • Aortic sclerosis, IHD and hypertrophic cardiomyopathy.
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29
Q

Management of Aortic Stenosis

A
  • IE prophylaxis and attentive dental care.
  • Valve replacement - open or transcatheter.
  • Potential balloon valvotomy in children and teens.
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30
Q

Complications of Aortic Stenosis

A
  • IE, infection, thrombus, stroke and cardiac arrest.
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31
Q

Definition of Mitral Stenosis

A
  • Obstruction between LA to LV that leads to inadequate filling of the LV due to pathological narrowing.
  • Usually symptoms after the valve is less than 2cm2. Normal size = 4 - 6cm.
  • Decease in prevalence and incidence.
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32
Q

Causes of Mitral Stenosis

A

Previous Rheumatic Heart Disease

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33
Q

Risk Factors of Mitral Stenosis

A

Female, infections of strepotoccoccal, SLE, amyloidosis, certain medications.

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34
Q

Pathophysiology of Mitral Stenosis

A
  • Increased size of valve leaflets means obstruction between LA and LV. Leads to increased pressure in LA, ultimately cause LA hypertrophy, leading to pulmonary hypertension and eventually right sided heart failure.
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35
Q

Presentation of Mitral Stenosis

A
  • Initial signs are externtional dyspnoea that becomes progressively worse, patients may have cough or haempotysis, it is a disease of plateauing phases.
  • Signs include mitral facietis (flushed colour on tops of cheeks), tapping apex beat, low pulse volume and loud S1 sounds.
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36
Q

Investigations of Mitral Stenosis

A
  • CXR (Left atrial hypertrophy/ pulmonary hypertension).
  • ECG (AF or in normal sinus rhyhtm potential bifid P waves).
  • Echo = diagnostic - assess severity and valve area.
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37
Q

Differentials of Mitral Stenosis

A

Left atrium tumour

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38
Q

Management of Mitral Stenosis

A
  • If patient has mild then no mechanical interventions, just symptomatic control using beta blockers/digixoin, anti coag and diuretics.
  • Valve replacement ultimately required - offered to all patients with HF at class 3 or more or those particularly symptomatic.
  • Balloon valvectomy can be used to relieve symptoms.
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39
Q

Complications of Mitral Stenosis

A
  • AF, stroke, bleeding for warfarin, IE.
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40
Q

Definition of Mitral Regurgitation

A
  • Backflow of blood between LV and LA.

- 80% of people have mild MR.

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41
Q

Aetiology of Mitral Regurgitation

A
  • Mitral valve prolapse.

- Rheumatic heart disease

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42
Q

Risk Factors of Mitral Regurgitation

A
  • IE, history of cardiac trauma, MI, IHD, congenital heart disease, ventricular systolic dysfunction, hypertrophic cardiomyopathy.
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43
Q

Pathophysiology of Mitral Regurgitation

A
  • Circulatory changes depend on speed of onset and severity.
  • Overtime increase LA pressure compensated for by increased LA hypertrophy.
  • Leads to pulmonary hypertension and right sided heart failure then CHF.
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44
Q

Presentation of Mitral Regurgitation

A
  • Acute presentation as pulmonary oedema.
  • Chronic presentation as progressive extertional dyspnoea, fatigue and lethargy.
  • Eventually symptoms of right sided heart failure and CHF.
  • Signs and symptoms include apex beat displaced, soft heart sounds and 3rd heart beat.
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45
Q

Investigations of Mitral Regurgitation

A
  • CXR, ECG, Echo and doppler/colour flow doppler to assess severity.
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46
Q

Differentials of Mitral Regurgitation

A
  • ACS, Mitral stenosis, atrial stenosis.
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47
Q

Management of Mitral Regurgitation

A
  • Mild = no interventions, symptomatic treatment and re echo every 1 to 5 years.
  • More severe symptoms include valve replacement.
  • IE prophylaxis.
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48
Q

Complications of Mitral Regurgitation

A
  • AF, pulmonary hypertension, recurrent regurgitation, prosthetic stenosis.
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49
Q

Definition of Atrial Regurgitation

A
  • Leaking of blood into the LV during diastole due to ineffective coapulation of the aortic cusp.
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50
Q

Causes of Atrial Regurgitation

A
  • Infective endocarditis or rheumatic fever complicating an already damaged valve.
  • Occurs in patients in their 40’s or 50’s.
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51
Q

Risk Factors of Atrial Regurgitation

A
  • Bicuspid aortic valve, rheumatic fever, IE, Marfan’s syndrome, systemic hypertension and older age.
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52
Q

Pathophysiology of Atrial Regurgitation

A
  • Increased pressure in the LV, ultimately leeds to LV hypertrophy and then LV dilatation.
  • Increased stroke volume leads to increased pulse.
  • Eventually leading to LV HF and ultimately CHF.
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53
Q

Presentation of Atrial Regurgitation

A
  • Asymptomatic for a long period of time.
  • Dyspnoea, orthnopea and fatigue.
  • Signs = collapsing pulse, displaced thrusting apex beat, and diastolic blowing murmur heard at the left sternal border.
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54
Q

Investigations of Atrial Regurgitation

A
  • CXR = Enlarged heart size.
  • ECG = LVH
  • Echo with doppler = Severity and blood flow.
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55
Q

Differentials of Atrial Regurgitation

A
  • Mitral regurgitation, mitral stenosis, atrial stenosis, pulmonary regurgitation.
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56
Q

Management of Atrial Regurgitation

A
  • Mild symptoms treated with medication such as vasodilators, ACE inhibitors (Ramipril), diuretics (Fursoemide) etc.
  • Valve replacement = patients with less than 50% EF or symptomatic when at rest.
  • Consider IE prophylaxis.
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57
Q

Complications of Atrial Regurgitation

A
  • IE, op mortality, arrhythmias, CHF, MI, sudden death.
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58
Q

Definition of Pulmonary Insufficiency

A
  • Back flow of blood from the pulmonary arteries into the right ventricle.
  • Rare and often symptomatic.
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59
Q

Causes of Pulmonary Insufficiency

A
  • Congenital (Congenital heart defects)

- Acquired (Trauma, syphillis, left sided heart conditions, rheumatic heart disease)

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60
Q

Risk Factors of Pulmonary Insufficiency

A
  • Left sided HF, rheumatic heart disease, RA, IE, permanent pacemaker.
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61
Q

Pathophysiology of Pulmonary Insufficiency

A
  • Increased fluid build up in the RV, increase pressure causing RV dilatation leading to RV hypertrophy, eventually causing heart failure.
  • Decrease stroke volume leading to decreased pulse.
  • Leads to symptoms such as peripheral oedema, dyspnoea and fatigue.
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62
Q

Presentation of Pulmonary Insufficiency

A
  • Dyspnoea, fatigue or palpitations.

- Some murmurs may be able to be heard and also differences in the internal jugular pulse.

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63
Q

Investigations of Pulmonary Insufficiency

A
  • CXR - Cardiomegaly/RVH
  • Transthoracic echo
  • ECG - AF/Previous MI
64
Q

Management of Pulmonary Insufficiency

A
  • Symptomatic treatment/ treatment of cause.

- Valve replacement.

65
Q

Complications of Pulmonary Insufficiency

A
  • AF, MI, AV block and liver disease.
66
Q

Definition of Tricuspid Insufficiency

A
  • Back flow of blood between the right ventricle and the right atrium.
67
Q

Causes of Tricuspid Insufficiency

A
  • Congenital

- Acquired (Trauma, RA, rheumatoid heart disease)

68
Q

Risk Factors of Tricuspid Insufficiency

A
  • Left sided HF, RA, Rheumatic heart disease, Marfan’s
69
Q

Pathophysiology of Tricuspid Insufficiency

A
  • Decrease in cardiac output caused by increase in RA pressure, leading RA dilatation and RA hypertrophy.
70
Q

Presentation of Tricuspid Insufficiency

A
  • Fatigue, extertional intoleralbitly, dyspnoea and palpitations
71
Q

Investigations of Tricuspid Insufficiency

A
  • Transoesophageal/ transthoracic echo
  • CXR - Cardiomegaly/Heart Failure
  • ECG - AF/Previous MI
  • Bloods - Renal/liver complications and abnormalities
72
Q

Management of Tricuspid Insufficiency

A
  • Treat symptoms, symptoms of HF.
  • Treat cause.
  • Valve replacement.
73
Q

Complications of Tricuspid Insufficiency

A
  • AV block, MI, AF and liver problems.
74
Q

Differences in Signs/Symptoms of Mitral Stenosis and Aortic Stenosis.

A
  • Mitral Stenosis = extertional dyspnoea, cough + haemoptysis, AF. Signs include flushed pink cheeks, apex beat tapping, low rising pulse and loud S1 sound.
  • Aortic Stenosis = Angina, exertional fatigue and dyspnoea. Signs include apex beat is thrusting, carotid pulse is slow rising and systolic murmur on the right sternal border.
75
Q

Differences in Signs/Symptoms of Mitral Regurgitation and Aortic Regurgitation.

A
  • Mitral regurgitation = Extertional dyspnoea, fatigue and lethargy. Signs include apex beat is displaced, heart sounds soft and 3rd heart sound.
  • Aortic Regurgitation = Asymptomatic then dyspnoea, orthopnoea and fatigue. Signs include apex beat is displaced and thrusting, collapsing pulse and diastolic murmur on left sternal border.
76
Q

Hypertrophic Cardiomyopathy

A
  • LV outflow portion obstruction due to asymmetric septal hypertrophy.
  • Uncommon
  • Genetic
  • Asymptomatic until predominant involvement with septum.
  • Presents with breathlessness, fatigue, palpitations, angina or sudden death.
  • Investigations = ECG (Showing LVH - Progressive T wave inversion and deep Q waves in the inferior and lateral leads).
  • Management = Symptoms (BB/CCB), Arrythmias (Amdidrone), Anti coag and potential implantation of defib device.
77
Q

Idiopathic Dilated Cardiomyopathy

A
  • Uncommon
  • Genetic, X linked
  • Increased in mass due to dilatation but thinning of cardiac chambers.
  • Presentation with breathlessness, palpitations, pulmonary oedema and fatigue.
  • Investigations include bloods (Low sodium), CXR (Cardiomegaly) and ECG (Tachycardia).
  • Management include bed rest, meds and transplantation.
78
Q

Arrhythmaogenic RV cardiomyopathy

A
  • Caused by mutations that lead to detachment and apoptosis of the myocytes under mechanical strain, leading to replacement with fat and scarring.
79
Q

Restrictive Cardiomyopathy

A
  • Idiopathic causes.
  • Presents with oedema and ascites.
  • Investigations include MRI, Echo and Cardiac catheterisation.
  • Treat the cause.
80
Q

Definition of Stable Angina

A
  • Recurrent persistent episodes of chest pain, caused by myocardial ischaemia.
  • Caused by exercise, relieved by rest, good prognosis.
  • More prevalent in men, and very common.
81
Q

Aetiology of Stable Angina

A
  • Coronary artery atherosclerosis.

- Hypertension/aortic stenosis

82
Q

Risk Factors of Stable Angina

A
  • Non modifiable: Age, gender, family history, PMH.

- Modifiable: Smoking, hypertension, diabetes, hypercholesterolemia, hyperlipidemia, stress, sedentary lifestyle.

83
Q

Pathophysiology of Stable Angina

A
  • Oxygen demand outweighs supply.
  • Stenosis of coronary artery means that blood is obstructed when oxygen demand increases during exercise.
  • Circumference less than 75%
84
Q

Investigations of Stable Angina

A
  • Resting ECG: ST depression, T wave flattening or inversion.
  • Cardioangiography can be used to identify a blockage if diagnosis is uncertain.
85
Q

Differential Diagnosis of Stable Angina

A
  • Aortic dissection, PE, Pneumothorax and pericarditis.
86
Q

Management of Stable Angina

A
  • Prevention of attacks and also other cardiovascular events including MI/Stroke.
  • GTN (If patient feels pain –> rest, use spray/tablets, wait 5 mins, if still in pain use medication again, wait 5 mins, if still in pain dial 999).
  • BB/CCB or long acting nitrates.
  • 2nd prevention = anti platelet (Aspirin 75mg) or if patient is already taking Clopidogrel then continue.
  • Surgical procedure - PCI/ CABG.
87
Q

Complications of Stable Angina

A
  • Stroke, MI, CHF and depression.
88
Q

What is included in the term acute coronary syndrome?

A
  • NSTEMI, STEMI and Unstable angina.
89
Q

Management of Acute Coronary Syndrome

A
  • If STEMI urgent revascularisation = PCI/CABG (Using internal mammary artery in the chest, saphenous vein in the leg or the radial artery in the arm).
  • If NSTEMI - serial troponin bloods to distinguish between MI and Unstable Angina.
  • MONA (Morphine, oxygen (sats > 94%) , nitrates (GTN ) and Antithrombin (300mg aspirin)).
  • Modify risk factors = smoking cessation, treat diabetes, cardiac rehab, mental health and diet.
  • Cardio protective meds = Antiplatelet (Aspirin/clopidegrol), anti coag, BB (Gradual increase), ACE/ARB, statin (Atorvastatin 80mg) and echo for LV assessment.
  • General advice (no driving for 1 week post revasc, no driving for 4 weeks if no revasc).
90
Q

Definition of NSTEMI

A
  • Partial thickness necrosis of the myocardium.

- Common

91
Q

Aetiology and Risk Factors for Acute Coronary Syndrome

A
  • Coronary artery atherosclerosis
  • Modifiable risk factors: hypertension, diabetes, smoking, hyperlipidaemia, hypercholeseteromia, sedentary lifestyle, obesity, stress, type A personality and cocaine use.
  • Non modifiable risk factors: Age, family history, personal past medical history and gender.
92
Q

Pathophysiology of NSTEMI

A
  • Cracking or fissuring of an atherosclerotic plaque causing the accumulation of platelets leading to thrombus forming.
  • The thrombus partial occludes the artery causing a restriction in the blood flow to the heart leading to myocardial necrosis.
93
Q

Presentation of NSTEMI

A
  • Central crushing chest pain for more than 20 mins.
  • Associated with palpitations, syncope, feeling faint, dyspnoea and nausea.
  • Silent MI - no chest pain but syncope, nausea and epigastric pain possible.
94
Q

Investigations of NSTEMI

A
  • ECG - Ischaemia but not ST elevation. ST segment may be depressed with inverted T waves.
  • Troponin - Increased (15 - 40).
95
Q

Differentials of ACS

A
  • Stable angina, pericarditis, PE, pneumothorax, aortic dissection.
96
Q

Complications of NSTEMI

A
  • Future ACS events or LV heart failure.
97
Q

Definition of STEMI

A
  • Full thickness necrosis of the myocardium.

- Common but declining.

98
Q

Pathophysiology of STEMI

A
  • Unstable plaque ruptures causing the aggregation of platelets leading to thrombus.
  • Thrombus completely occludes the artery and leads to full necrosis of the tissue preventing flow of blood into the muscle.
99
Q

Investigations of STEMI

A
  • ECG = ST elevation or new onset LBBB. Also showing T wave inversion and pathological Q waves in the hours and days post MI.
  • Troponin = Levels more than 100.
100
Q

Complications of STEMI

A
  • Immediate risk = cardiac arrest, sudden cardiac failure or arrhythmias.
  • Future risk for ventricular arrhythmias or LVHF.
101
Q

Definition of Unstable Angina

A
  • Acute severe myocardial ischaemia as opposed to myocardial necrosis.
  • Increase in frequency/severity, and onset during minimal exertion/ at rest leads to increase risk of MI.
  • Common
102
Q

Pathophysiology of Unstable Angina

A
  • Erosion of atherosclerotic plaque leads to build of platelets over time creating a thrombus.
  • The thrombus begins to occlude the vein reducing blood flow, but does this when oxygen demand is not more than available as well.
  • Potential for embolus to occur, temporarily blocking blood flow.
103
Q

Investigations of Unstable Angina

A
  • ECG = Ischaemia but not ST elevation.

- Troponin levels = Normal

104
Q

Presentation of STEMI

A
  • Central crushing chest pain lasting more than 20 minutes.
  • Silent MI seen in diabetics and the elderly.
  • ‘I feel like I’m going to die
105
Q

Presentation of Unstable Angina

A
  • Sudden central crushing chest pain.

- Not resolved by rest or medication.

106
Q

Definition of Hypertension

A
  • Persistently elevated BP where the treatment benefit is clear cut.
  • Anyone over BP of more than 160/100 are treated.
  • It is very common, there is a geographical/racial differences and more common in the western world.
107
Q

Aetiology of Hypertension

A
  • 95% of causes is unknown.

- 5% - CKD, OCP, endocrine disease.

108
Q

Risk Factors of Hypertension

A
  • Obesity, central obesity, lack of exercise, increased alcohol, diabetes, black ancesteory, over 60’s.
109
Q

Pathophysiology of Hypertension

A
  • Highly complex with lots of multiple factors.
  • Promotes atherosclerosis.
  • Increased LV function –> LVH and LVD = LVHF.
110
Q

Presentation of Hypertension

A
  • Asymptomatic, picked up on routine BP.

- Some patients get headaches/visual disturbances.

111
Q

Diagnosis of Hypertension

A
  • Increase of 2mmHg in systolic pressure leads to 7% increase IHD and 10% stroke.
  • Normal BP –> 120/80 - 90/60.
  • Stage 1 –> > 140/90 or average > 135/85
  • Stage 2 –> >160/100 or average > 150/95
  • Severe –> More than or equal 180 systolic OR More than or equal 110 diastolic.
112
Q

Differentials of Hypertension

A
  • Drug induced, CKD
113
Q

Management of Hypertension

A
  • Lifestyle medications.
  • Statin –> Patients over 40 with CVD complications and patients with 10y CVD risk of more than 20%.
  • Stage 1 –> Over 80 OR one or more of: CVD, diabetes, target organ damage, CKD or 10y risk 20%.
  • Stage 2 –> Treat all patients.
  • Less than 55 —> ACE/ARB then add CCB then add diuretic then refer.
  • More than 55 or afro/carribean –> CCB then add ACE/ARB then diuretic then refer.
114
Q

Definition of Infective Endocarditis

A
  • Infection of the endocardium or the vasculature of the endothelium of the heart.
  • Used to be a disease of the young with rheumatic heart disease but now affects older patients, IVDU, younger patients with congenital heart disease and anyone with a replacement valve.
115
Q

Aetiology of Infective Endocarditis

A
  • Acute = staph aureus, step pneumoniae.

- Sub acute = strep viridians, enterococci.

116
Q

Pathophysiology of Infective Endocarditis

A
  • Staph aureus - through IV drugs or vessel lines.
  • Strep viridians - through oropharynx due to dental care and toothbrushing.
  • Enterococci - Through instruments in the bladder/bowel.
  • Platelets/fibrin/organism = vegetatations.
117
Q

Presentation of Infective Endocarditis

A
  • Systemic presentation but depends on organism and position in heart.
  • Heart murmurs possible.
118
Q

Investigations of Infective Endocarditis

A
  • Blood culture - 3 samples over 24 hrs in 6 bottles pre antibiotics.
  • Transoesophageal/transthoracic echo to look for vegetations.
119
Q

Differentials of Infective Endocarditis

A

Rheumatic heart disease.

120
Q

Diagnosis of Infective Endocarditis

A
  • Dukes classification:

- 2 Major OR 1 Major + 3 Minor OR 5 minor

121
Q

Management of Infective Endocarditis

A
  • Antibiotics (2w IV then 2 - 4w oral) - give all IV benzopenniciln and gentamicin initially.
  • Surgical replacement of valve.
122
Q

Definition of Pericarditis

A
  • Inflammation of the pericardium with or without effusion.
123
Q

Aetiology of Pericarditis

A
  • Infection - viral (EBV) , bacterial (pneumonia) or fungal.

- Post MI

124
Q

Pathophysiology of Pericarditis

A
  • Anything that injures the pericardium leading to an inflammatory response.
125
Q

Presentation of Pericarditis

A
  • Pleuritic sharp sudden chest pain that is worse with inspiration and when lying down and is relieved by leaning forward.
  • Sudden left anterior chest and epigastric pain.
  • Pericardial rub heard, which sounds like crunching snow which is pathonemonic.
126
Q

Investigations of Pericarditis

A
  • ECG = diagnostic = saddle shaped ST elevation in all leads.
127
Q

Differentials of Pericarditis

A
  • PE, pleurisy, pneumothorax
128
Q

Management of Pericarditis

A
  • Treat cause.
  • Prescribe NSAIDs with gastro protection (1 to 2 wks).
  • Use of Colchicine 500mg OD/BD in order to reduce risk of reoccurance for 3 months if tolerated (Side effects include nausea and diarrhoea)
  • Rest until healed - 3m for athletes
129
Q

Complications of Pericarditis

A
  • Cardiac tamponande
130
Q

Definition of an aneurysm

A
  • A permanent localised dilation of an artery.

- The dilation has to more than 50%.

131
Q

Abdominal Aortic Aneurysm

A
  • After T12.
  • Ruptured or unruptured.
  • Presents due to degeneration, usually in elderly men - screening programme for over 65’s.
  • Asymptomatic / or presents with epigastric/back pain when pressing on other structures.
  • Ruptured AAA = Medical emergency - patient presents with severe epigastric pain radiating into the back in a hypovalemic state. Needs immediate emergency surgery to graft the artery back together.
  • Management of unruptured includes mointoring and also potential grafting/stenting.
132
Q

Thoracic Aortic Aneurysm

A
  • Asymptomatic or if pressing on other structures can cause symptoms such as back pain, dysphagia or cough.
  • Usually caused by atherosclerosis.
133
Q

Definition of Pericardial Effusion

A
  • Accumulation of fluid within the pericardial sac.
134
Q

Aetiology of Pericardial Effusion

A
  • Infection, post MI, hypothyroidism.
135
Q

Presentation of Pericardial Effusion

A
  • Obstructed apex beat and soft heart sounds.
136
Q

Investigations of Pericardial Effusion

A
  • CXR = Globular heart.
  • ECG = Low voltage complexes and possible tachycardia.
  • Echo = Diagnostic = fluid round the heart.
  • Pericardialcentesis + biopsy = aetiology
137
Q

Management of Pericardial Effusion

A
  • Most spontaneously resolve themselves.

- Pericardial segment can be removed if need be to allow fluid to drain into the lymphatics.

138
Q

Cardiac Tamponade

A
  • Medical emergency.
  • Large amounts of fluid in the pericardial sac restricting diastolic ventricular filling and causing a marked reduction in cardiac output.
  • Emergency pericardiocentesis required.
139
Q

Definition of Heart Failure

A
  • A progressive complex condition where the heart muscle can’t adequately function enough to meet the demand of the rest of the body.
  • Poor outcome, around 50% of patients die within 5 years.
140
Q

Aetiology of Heart Failure

A
  • Most common causes include IHD, hypertension and cardiomyopathies.
  • Anything that increases the work of the myocardium to extent where it loses the ability to function.
141
Q

Pathophysiology of Heart Failure

A
  • When the heart begins to fail, the heart has mechanisms that compensate for this in order to maintain cardiac output and peripheral perfusion for as long as possible. When these begin to become overwhelmed this is when symptoms start to occur and pathology occurs in the body.
    1. Activation of the sympathetic nervous system.
    2. Renin angio tension system.
    3. Natriuretic Peptides - BNP released from the ventricles, good measure of severity of heart failure.
    4. Ventricular dilation
    5. Ventricular structural changes
142
Q

Presentation of Heart Failure

A
  • Gradual, subtle onset of symptoms.
  • Depending on the type of heart failure.
  • Extertional dyspnoea, orthnopnoea, paroxysmal nocturnal dyspnoea and fatigue.
  • Ankle oedema, increased internal jugular pulse, 3rd and 4th heart sounds and cardiomegaly with displaced apex beat.
143
Q

Types of Heart Failure

A
  • Left ventricular systolic dysfunction (reduced ejection fraction) - commonly caused by IHD.
  • Right ventricular systolic dysfunction (Most commonly secondary to LVSD).
  • Diastolic heart failure (Normal ejection fraction) - usually seen in hypertensive elderly patients.
144
Q

Investigations of Heart Failure

A
  • ECG - LVH and arrhythmias.
  • CXR - Enlarged heart.
  • Echo = Diagnostic = looks at ventricular diastolic/systolic function and also ejection fraction.
  • pro BNP levels in the blood ( More than 100).
145
Q

Management of Heart Failure

A
  • All about reducing symptoms, improving quality of life and prolonging life.
  • Pharm treatments: ACE inhbitiors/ARBS, diuretics , Betablockers, digoxin in patients with AF and inotropic agents if required.
  • Non pharm treatments: revascularisation, cardiac resync, implant defib device, cardiac transplant.
146
Q

Definition of Congenital Heart Disease

A
  • Severity can vary.
  • Prognosis used to be poor, but now with increased use of surgery and cardiology interventions mean that many patients survive for longer than 18 yrs.
147
Q

General Investigations of Congenital Heart Disease

A
  • Echo with/without bubble contrast.
  • Cardiac MRI/CT
  • Cardiac cathertirsation to assess pressures and oxygen sats.
  • Exercise testing to assess capacity and capability.
148
Q

What is tetralogy of fallot?

A
  • Most common cyanotic congenital heart disease.
  • Features include VSD, pulmonary stenosis, right ventricular hypertrophy and the aorta overcomes the VSD and accepts blood from the right side of the heart.
  • Babies can be born acyanotic but then become blue has the blood moves through circulation.
  • Older patients presents with extertional dyspnoea, palpitations etc.
  • Investigations include ECG = RVH and CXR = Boot shaped heart.
  • Management = Surgical
  • Prognosis = 85% of patients survive over the age of 35 with surgery but 85% death if no surgery before the age of 20.
149
Q

What is ventral septal defect?

A
  • The most common type of congenital heart disease.
  • A hole between the two ventricles.
  • Leads to increase in blood flow from the left ventricle into the right ventricle due to higher pressure, this means that there is increased flow of blood into the lungs. It means that the patient is not cyanotic.
  • Depends on the size of the hole as to the range of symptoms.
  • Large hole leads to large increased in pulmonary blood flow leading to breathlessness. Babies would have poor feeding as well as tachycardia, a large heart on CXR, murmurs and increased resps.
  • Small hole would only see a small increase in blood flow leading to systolic murmur, thrill but normal HR and heart size on CXR.
  • It could be congenital or acquired (Post MI).
  • Management would be medical at first due to possibility of spontaneous closure and then surgical repair if required.
  • Complications include Eisenmenger’s Syndrome.
150
Q

What is atrial septal defect?

A
  • A hole between the two atrium.
  • It leads to blood flow from the slightly high pressure LA into the RA, increasing right heart circulation and blood flow to the lungs.
  • Leads to symptoms such as chest pain, dyspnoea and palpitations - severity depends on the size of the hole.
  • Investigations would include CXR showing a small aortic knuckle.
  • Management would be medication initially due to spontaneous closure and then surgical if required.
151
Q

What is atrioventricular septal defect?

A
  • A hole basically in the centre of the heart, taking over the ventricle septum, atrial septum, tricuspid valve and mitral valve.
  • Complete defect = breathlessness, poor weight + feeding, torrential pulmonary blood flow.
  • Partial defect = Can present in late adulthood.
152
Q

What is Patent Ductus Arteriosus?

A
  • Persistent opening between the pulmonary arteries and the ascending aorta.
  • Presents with a continuous machinery murmur.
  • Management with surgical procedures.
153
Q

What is coarctation of the aorta?

A
  • Congenital narrowing of the descending aorta.
  • More common in boys.
  • Presents with hypertension and murmurs.
  • Surgical intervention required.
154
Q

What physical exam findings would you see with infective endocarditis?

A
  • Splinter haemorrhages - fine, thread-like, blood clots appearing vertically in the bed of the fingernail
  • Osler’s nodes - small, tender, purple subcutaneous lesions on the pulp of the finger tips
  • Janeway lesions - erythematous, macular, nontender lesions on the fingers, palms and/or soles of the feet
  • Roth spots - retinal haemorrhages wit white or pale centers seen on fundoscopy
  • New heart murmur
  • Petechiae
155
Q

What are the two most common causes of pericarditis?

A
  • Viral infection and autoimmune disease
156
Q

What are the diagnostic criteria for acute pericarditis?

A

Diagnosis is based on two of the following:

  • chest pain (sharp and pleuritic
  • relieved with sitting forward and worse with lying down)
  • ECG changes (diffuse ST elevation)
  • friction rub on examination (pathppneumonic - “crunching snow”)
  • pericardial effusion
157
Q

Other than CAD what other conditions does atherosclerosis predispose patients to?

A
  • Ischaemic stroke or cerebrovascular accident (CVA)
  • critical limb ischaemia
  • Sudden cardiovascular death

Phase 1 Exam (25 decks)

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