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Phase 2a Sheffield Medicine > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Name 4 modifiable risk factors for atherosclerosis?

A
  • Hypertension
  • Diabetes Mellitus → Hyperglycaemia.
  • Smoking
  • Dyslipidaemia (↑LDL, ↓HDL)
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2
Q

Name 4 non-modifiable risk factors for atherosclerosis?

A
  • Age
  • Male
  • Family history
  • African descent
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3
Q

Name some preventative measures for Atherosclerosis?

A
  • Cessation of smoking
  • Blood pressure control - anti-hypertensive
  • Reducing BMI
  • Low-dose aspirin (inhibits aggregation of platelets)
  • Statins (Cholesterol reducing drugs)
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4
Q

Name some complications of atherosclerosis?

A
  • Angina
  • Claudication
  • Clot formation
  • Aneurysm
  • Cholesterol emboli
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5
Q

Describe the pathogenesis of atherosclerosis?

A
  1. Endothelial cell damage.
  2. LDL leak into the intima layer where it is oxidised which causes a pro-inflammatory antigen that induces an immune response.
  3. Macrophages are recruited to the site of damage which digest lipids and become foam cells.
  4. Formation of a fatty streak.
  5. Activated macrophages release cytokines and growth factors.
  6. Smooth muscle proliferation around the lipid core and formation of fibrous cap.
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6
Q

Define stable angina?

A

Angina refers to classic cardiac pain that is felt when there is a reduction in blood supply to the heart.

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7
Q

Name the non-modifiable risk factors for stable angina?

A
  • Increasing age
  • Gender → Male > Female
  • Family History
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8
Q

Name modifiable risk factors for stable angina?

A
  • Hypertension
  • Diabetes
  • Obesity
  • Hypercholesterolaemia
  • Smoking
  • Cocaine use
  • Stress
  • Sedentary lifestyle
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9
Q

What are the primary investigations for stable angina?

A
  • Physical Examination (heart sounds, signs of heart failure, BMI)
  • First line:12-lead ECG (ST segment depression) and CT angiography (gold standard)
  • Second line:functional imaging (stress echo, or cardiac MRI) if CT angiography is non-diagnostic
  • Third line: transcatheter angiography
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10
Q

What are other investigations to consider for stable angina?

A
  • FBC:may reveal anaemia as an underlying cause of angina
  • Ambulatory blood pressure monitoring: if hypertension is suspected in clinic
  • Fasting blood sugar and HbA1c: diabetes is associated with an increased risk of ischaemic heart disease
  • Fasting lipid profile:hyperlipidaemia is associated with an increased risk of ischaemic heart disease
  • Thyroid function tests: check for hypo / hyper thyroid
  • U&Es: prior to ACEi and other meds
  • LFTs: prior to statins
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11
Q

What are the 3 characteristics of stable angina?

A
  • Discomfort to the chest, neck, jaw, shoulders or arms
  • Symptoms brought on by exertion
  • Symptoms relieved within 5 minutes by rest or glyceryl trinitrate (GTN)
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12
Q

What are some complications of stable angina?

A
  • MI:a plaque may continue growing until the coronary artery is completely obstructed
  • Chronic heart failure:theunderlying causes of ischaemic heart disease are also associated with an increased risk of chronic congestive heart failure
  • Stroke:atherosclerosis may also develop within the cerebrovascular system
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13
Q

How would you manage a patient with angina for symptomatic relief?

A
  • GTN spray or tablet: vasodilator
  • If pain persists for 5 minutes after the first dose, then repeat the dose. If after 5 minutes the pain still remains, then an ambulance should be called
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14
Q

Name some anti-anginal medications?

A
  • 1st line: β-blocker OR non-hydropyridine calcium channel blocker
  • 2nd line: dual therapy with dihydropyridine calcium channel blocker AND β-blocker
  • 3rd line: add additional anti-anginal medication e.g.
    • Nitrates
    • Ivabradine
    • Nicorandil
    • Ranolazine
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15
Q

Name 4 management strategies for angina?

A

Symptomatic relief
Anti-anginal medication
Revascularisation options
Prevention

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16
Q

Name two revascularisation options for stable angina?

A
  • Percutaneous coronary intervention (PCI):aballoon is inflated in a stenosed vessel and a stent is placed to ensure the lumen remains open.
  • Coronary artery bypass graft (CABG): involves opening the chest along the sternum (causing a midline sternotomy scar), taking a graft vein from the patient’s leg (usually the great saphenous vein) and sewing it on to the affected coronary artery to bypass the stenosis. Associated with a better overall outcome, however, is associated with greater perioperative risks
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17
Q

What is the main pathological cause of angina and acute coronary syndromes?

A
  • Almost always due to atherosclerosis
  • Atherosclerotic plaque rupture and thrombus formation
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18
Q

What are some non-modifiable risk factors for acute coronary syndromes?

A
  • Age (>65 years of age)
  • Male
  • Family history of premature coronary heart disease
  • Premature menopause
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19
Q

What are some modifiable risk factors for acute coronary syndromes?

A
  • Smoking
  • Diabetes mellitus
  • Hyperlipidaemia
  • Hypertension
  • Obesity
  • Sedentary lifestyle
  • Recreational drug use e.g. cocaine
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20
Q

What are signs of acute coronary syndrome?

A
  • Hypotension or hypertension
  • Reduced 4th heart sound
  • Signs of heart failure: e.g. increased JVP, oedema; red flag symptom
  • Systolic murmur: if mitral regurgitation or a ventricular septal defect develops
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21
Q

What are symptoms of an acute coronary syndrome?

A
  • Chest pain
    • Central, ‘heavy’, crushing pain
    • Radiation to the left arm or neck
    • Symptoms should continue at rest for more than 20 minutes
    • Certain patients e.g. diabetics or elderly, have atypical presentation and may not have chest pain (‘silent MI’)
  • May sometimes feel like indigestion
  • Shortness of breath
  • Sweating and clamminess
  • Nausea and vomiting
  • Palpitations
  • Anxiety: often described as a ‘sense of impending doom’
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22
Q

What are the primary investigations for an acute coronary syndrome?

A
  • ECG:perform within 10 minutes. Aim to perform serial ECGs every 10 minutes to detect dynamic changes.
    • ECG findings
      • Unstable angina: non-specific changes
      • NSTEMI: ST-segment depression; T-wave inversion; pathological Q waves; a normal ECG may be seen
      • STEMI: ST-segment elevation; T-wave inversion; new left-bundle branch block
  • Troponin:for a STEMI and NSTEMI, troponin levels will begin to elevate 4-6 hours after injury and will remain elevated for roughly 10 days. In unstable angina, there isnoelevation in troponin.
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23
Q

What other investigations should you consider for acute coronary syndromes?

A
  • Perform other tests that you would for stable angina e.g.
    • Physical Examination (heart sounds, signs of heart failure, BMI)
    • Lipid profile
    • Thyroid function tests: check for hypo / hyper thyroid
    • HbA1C and fasting glucose: check for diabetes
  • Coronary angiogram:aim to carry out angiography within 90 minutes if required; diagnostic investigation of choice
  • FBC:Hb and haematocrit may reveal a secondary cause in type 2 MI e.g. anaemia
  • U&Es:electrolyte imbalances may predispose the patient to cardiac arrhythmias; also done prior to ACEi and other meds
  • LFTs: done prior to statins
  • Other biomarkers: less commonly used biomarkers of cardiomyocyte injury include creatine kinase-MB (increases at 3-6 hours), andmyoglobin (earliest to rise, usually within 2 hours)
  • CXR:to exclude other potential causes, if needed
  • Echocardiogram after the event to assess the functional damage
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24
Q

What are the immediate management protocols for unstable angina and NSTEMI?

A
  • Oxygen:only if SpO2is <94%, and aim for 94-98%
  • Analgesia:morphine and sublingual glyceryl trinitrate
  • Dual antiplatelets:
    • Aspirin
    • The choice of the second antiplatelet agent depends on if the person is having PCI or not, and will vary based on local guidance:
      • Prasugrel or ticagrelor or clopidogrelif undergoing PCI
      • Ticagrelor or clopidogrelif not undergoing PCI
  • Anticoagulation:
    • Fondaparinux:offer to all patientsunlessundergoing immediate coronary angiography
    • Unfractionated heparin:an alternative to fondaparinux if the patient has renal failure
  • Beta blockers: e.g. atenolol or metoprolol, unless contraindicated
  • Remember ‘MONA’: Morphine,Oxygen,Nitrates,Aspirin
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25
Q

What are the immediate management protocols for a STEMI?

A
  • Oxygen:only if SpO2is <94%, and aim for 94-98%
  • Analgesia:morphine and sublingual glyceryl trinitrate
  • Dual antiplatelets:
    • Aspirin
    • The choice of the second antiplatelet agent depends on if the person is having PCI or not, and will vary based on local guidance:
      • Prasugrel or clopidogrelif undergoing PCI
      • Ticagrelor or clopidogrelif undergoing fibrinolysis
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26
Q

What are some secondary prevention techniques for cardiovascular disease?

A
  • Lifestyle changes: exercise, diet change, smoking cessation, reducing alcohol intake
  • Manage cardiovascular risk factors: lipid, diabetes, hypertension management
  • Antiplatelet therapy:
    • Aspirin 75mg OD continued indefinitely
    • The second antiplatelet depends on the one chosen in the acute setting i.e. prasugrel, ticagrelor, or clopidogrel, and is usually continued for 12 months.
  • Angiotensin-converting enzyme inhibitors(ACEi) andbeta-blocker
  • Statin:usually atorvastatin 80mg
  • Cardiac rehabilitation: must be offered following myocardial infarction
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27
Q

List some early complications of acute coronary syndromes?

A
  • Post-MI pericarditis
  • Cardiac arrest
  • Bradyarrhythmia’s
  • Ventricular septal defect
  • Cardiogenic shock
  • Mitral regurgitation
  • Left ventricular wall rupture
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28
Q

List some late complications of acute coronary syndromes?

A
  • Dressler’s syndrome
  • Heart failure
  • Left ventricular aneurysm
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29
Q

What are the four types of MI?

A
  • Type 1: a classic MI and occurs due to atheromatous plaque rupture
  • Type 2: secondary to ischaemia due to either increased oxygen demand or decreased supply, such as vasospasm, anaemia and sepsis. Management involves treating the underlying cause.
  • Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
  • Type 4: MI associated with PCI / coronary stenting / CABG
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30
Q

What is a GRACE score?

A

The Global Registry of Acute Coronary Events (GRACE) score is recommended by NICE to risk-stratify patients with unstable angina and non-ST elevation myocardial infarction (NSTEMI).

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31
Q

What is Aspirin used for?

A

An antiplatelet: predominantly for COX-1 inhibition and this preventing the synthesis of thromboxane A2

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32
Q

What are clopidogrel, prasurgrel and ticagrelor used for?

A

Antiplatelet therapy: inhibit the binding of adenosine diphosphate to its platelet P2Y12 receptor.

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33
Q

What are Tirofiban, Abciximab and Eptifbatide used for?

A

Antiplatelets: glycoprotein IIb/IIIa receptor antagonists.

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34
Q

What are enoxaparin and fondaparinux used for?

A

Anticoagulants: activate antithrombin III, this causing the inhibition of clotting factor Xa.

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35
Q

What is bivalirudin used for?

A

Anticoagulant: reversible direct thrombin inhibitor.

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36
Q

Define acute decompensated heart failure?

A

Cardiac output is not able to meet metabolic demands.

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37
Q

What are the risk factors of acute decompensated heart failure?

A
  • Increasing age
  • Coronary artery disease
  • Hypertension
  • Valvular disease: commonly senile calcifiction of the aortic valve.
  • Diabetes
  • Atrial fibrillation
  • Renal insufficiency
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38
Q

What are the signs of acute decompensated heart failure?

A
  • Cool peripheries
  • Signs of congestive heart failure:peripheral, pitting oedema and raised JVP
  • Displaced apex beat
  • Hypotension
  • Crackles on auscultation:left-sided failure; usually coarse bi-basal crackles
  • Third heart sound (S3)
  • Stony dull percussion:if an effusion is present
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39
Q

What are the symptoms of acute decompensated heart failure?

A
  • Dyspnoea: due to pulmonary oedema
    • Often a history of orthopnea and paroxysmal nocturnal dyspnoea
  • Fatigue and weakness
  • Cardiogenic wheeze
  • Symptoms of congestive heart failure:swelling of the peripheries and ascites
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40
Q

List some investigations for acute decompensated heart failure?

A
  • FBCs
  • U&Es
  • ABG
  • BNP or NT-proBNP
  • ECG
  • CXR
  • Transthoracic echocardiogram
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41
Q

What are acute management strategies for acute decompensated heart failure?

A
  • Stabilise the patient: administer oxygen to maintain a SpO2≥94%
  • Fluid restriction: fluid intake is usually limited to <1.5L/day
  • IV diuretic: usually a loop diuretic e.g. furosemide to relieve fluid overload
  • Inotropes or vasopressors e.g. dobutamine: only offer to patients with heart failure and cardiogenic shock (i.e. haemodynamically unstable)
  • Non-invasive ventilation (NIV): consider NIV if the patient does not stabilise with initial medical management
    • Continuous positive airway pressure (CPAP)
  • Intubation and ventilation: if CPAP is unsuccessful
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42
Q

What are surgical management options for acute decompensated heart failure?

A
  • If acute heart failure is due to aortic stenosis: offersurgical aortic valve replacement
  • Mechanical assist device:pump that can temporarily help the pumping action of the heart
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43
Q

What are long term management options for acute decompensated heart failure?

A
  • ACE-inhibitor e.g. ramiprilanda cardioselective β-blocker e.g. bisoprolol
    • Improved prognosisby slowing, or even reversing, ventricular remodelling
  • Fluid restriction: fluid intake is usually limited to <1.5L/day
  • Loop diuretic (e.g. furosemide)forsymptomaticrelief of oedema
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44
Q

What are some complications associated with acute decompensated heart failure?

A

Arrhythmias:can both precipitate acute heart failure and occur as a result of it. Atrial fibrillation is one of the most common arrhythmias associated with heart failure.

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45
Q

What are some poor prognostic markers for acute decompensated heart failure?

A
  • Old age
  • Hypotension
  • Male
  • Ischemia
  • Renal dysfunction
  • Previous chronic HF
  • Low respiratory rate (<30)
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46
Q

Define heart failure?

A

Heart cannot supply enough blood to the heart to meet its own demands.

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47
Q

Define systolic heart failure?

A

Heart cannot pump hard enough.
- Ejection fraction of below 40% (50% and below is borderline).
- The stroke volume is decreased.

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48
Q

Define diastolic heart failure?

A

Heart cannot fill enough during diastole.
- Stroke volume is low but the ejection fraction is preserved due to reduced filling (reduced pre-load)

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49
Q

Define biventricular heart failure?

A

Both right sided and left sided heart failure.

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50
Q

Define right-sided heart failure?

A

Usually caused by systolic dysfunction.
- Usually due to damage to the myocardium.
- Cannot contract hard enough.

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51
Q

Name some risk factors for congestive heart failure?

A
  • Ischemia
  • Valvular disease
  • Cardiomyopathy
  • Left sided heart failure → Biventricular
  • Atrial septal defect
  • Ventricular septal defect
  • AF
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52
Q

Name some clinical manifestations for left sided heart failure?

A
  • Increased pressure in the pulmonary artery.
  • Fluid in the interstitial space (congestion)/pulmonary oedema.
  • Dyspnea and Orthopnea as oxygen cannot enter the alveoli as efficiently when there is fluid build up.
  • Crackles - when the patient breathes.
  • S3 heard.
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53
Q

Name some clinical manifestations for right-sided heart failure?

A
  • Jugular venous distention
  • Hepatosplenomegaly (painful)
  • Cirrhosis of the liver (cardiac cirrhosis)
  • Ascites
  • Pitting oedema (legs when standing and sacrum
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54
Q

Name some causes of left-sided systolic heart failure?

A
  • Ischemia
  • Long standing hypertension
  • Dilated cardiomyopathy
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55
Q

Name some causes of left-sided diastolic heart failure?

A
  • Long standing hypertension
  • Aortic stenosis
  • Hypertrophic cardiomyopathy
  • Restrictive cardiomyopathy
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56
Q

Name some causes of right sided heart failure?

A
  • Pulmonary hypertension.
  • Shunt
  • Cor Pulmonale
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57
Q

What investigations would be performed on a patient with congestive heart failure?

A
  • Hemosiderin-Laden macrophages (LSHF)
  • ECG - broad QRS complex (LV hypertrophy)
  • CXR
    • Alveolar oedema
    • Kerley B lines
    • Cardiomegaly
    • Dilated upper lobe vessels
    • Pleural effusion
  • Transthoracic echocardiogram (diagnostic) - LVEF, diastolic function and valvular abnormalities.
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58
Q

What are the management options for congestive heart failure?

A
  • ACEi → dilate blood vessels
  • Diuretics → reduce fluid build up
  • Ventricular assist device (VAD)
  • Heart transplant
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59
Q

What are the severity criteria classifications for congestive heart failure?

A

Class I (mild) - No limitation for physical activity.
Class II (mild) - Slight limitations of physical activity
Class III (moderate) - Marked limitation of physical activity
Class IV (severe) - Cannot carry out physical l activity without discomfort

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60
Q

Define an abdominal aortic aneurysm?

A

An abdominal aortic aneurysm (AAA) describes a dilatation in vessel wall diameter of >50%, which typically means a diameter of >3 cm.

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61
Q

Describe the pathophysiology behind an abdominal aortic aneurysm?

A
  • Degradation of the tunica media and adventitia→ vessel dilatation
    • The most important risk factor for abdominal aortic aneurysms is atherosclerosis.
    • In atherosclerosis, chronic inflammation results in the release of enzymes called matrix metalloproteinases which degrade the extracellular matrix in the tunica media, weakening the aortic wall.
  • An AAA most commonly forms below the level of the renal arteries, known as an infra-renal aneurysm.
    • This is because below this level, the abdominal aorta lacks vasa vasorum (small blood vessels in the adventitial layer that provide nutrients to the aorta). The absence of vasa vasorum in this part of the aorta makes the tunica media particularly susceptible to ischaemia.
    • Thickening of the intima makes it harder for oxygen to diffuse to the tunica media.
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62
Q

What are some risk factors associated with abdominal aortic aneurysms?

A
  • Gender → Male > Female
  • Age → >60 years
  • Atherosclerosis
  • Smoking
  • Hypertension
  • Hyperlipidaemia
  • Diabetes
  • Connective tissue disorders: such as Ehlers Danlos and Marfan syndrome, due to changes in the balance of collagen and elastic fibres
  • Family history
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63
Q

List the signs associated with an AAA?

A
  • Pulsatile abdominal mass
  • Tachycardia and hypotension: red flags signifying ruptured AAA
  • Grey-Turner’s sign: flank bruising secondary to retroperitoneal haemorrhage
  • Cullen’s sign: pre-umbilical bruising
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64
Q

List symptoms associated with an AAA?

A
  • Flank, back or abdominal pain
  • Pulsating abdominal sensation
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65
Q

What primary investigations would take place for a suspected AAA?

A

Abdominal ultrasound.

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66
Q

What other investigations would take place for a suspected AAA?

A
  • FBC
  • U&Es
  • CRP/ESR
  • Group and save and crossmatch
  • CT angiogram
  • MRI
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67
Q

What is the screening programme in England for AAA?

A

The screening programme in England is offered to all males aged 65 and over as a one-off abdominal ultrasound, and further surveillance is organised if the aneurysm exceeds 3 cm.

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68
Q

How would you manage an AAA?

A
  • Surveillance
  • Surgical repair
  • Steroids or immunosuppressants if inflammatory AAA.
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69
Q

Define aortic dissection?

A

Aortic dissection describes the condition when a separation has occurred in aortic wall intima, causing blood flow into a new false channel between the tunica intima and tunica media.

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70
Q

Where would an aortic dissection normally occur?

A

This most commonly occurs around the ascending aorta and aortic arch, but can affect any part of the aorta.

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71
Q

List some risk factors for aortic dissection?

A
  • Hypertension: the most important risk factor
  • Smoking
  • Family history of aortic aneurysm or dissection
  • Coarctation of the aorta: narrowing of vessel
  • Bicuspid aortic valve
  • Connective tissue disorders:Marfan and Ehlers-Danlos syndrome
  • Turner and Noonan syndrome
  • Trauma
  • Pregnancy: increased blood plasma volume
  • Syphilis
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72
Q

What are the signs of an aortic dissection?

A
  • Weak downstream pulses: radio-radial and/or radio-femoral delay
  • A difference in blood pressure between two arms: >10 mmHg
  • Hypertension
  • Tachycardia and hypotension: as condition progresses
  • Diastolic murmur: due to aortic regurgitation
  • Involvement of specific arteries
  • Marfans syndrome signs
  • Ehlers-Danlos syndrome signs
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73
Q

What symptoms are associated with an aortic dissection?

A
  • Sudden onset, severe ‘tearing’ or ‘ripping’ chest pain that may radiate to the back
  • Syncope: red flag symptom
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74
Q

What primary investigations would you carry out for a suspected aortic dissection?

A
  • ECG
  • FBC
  • Group and save and crossmatch
  • Chest X-Ray
  • U&Es
  • Contrast enhanced CT
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75
Q

What other investigations would you carry out for a suspected aortic dissection?

A

Echocardiogram -> transthoracic or transoesophageal should be considered in unstable patients.

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76
Q

What is type A management for a aortic dissection?

A
  • Blood transfusion
  • Beta blockers
  • Urgent surgical repair
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77
Q

What is type B management for aortic dissection?

A
  • Conservative management
  • Beta blockers
  • Thoracic endovascular aortic repair
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78
Q

What complications can arise from an aortic dissection?

A
  • Aortic regurgitation
  • MI
  • Stroke
  • Renal failure
  • Tamponade
  • Haemorrhagic shock
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79
Q

Define hypertension?

A
  • Hypertension refers to a persistent elevation of arterial blood pressure.
  • Hypertension is defined as a blood pressure reading of ≥140/90 mmHg (ambulatory blood pressure monitoring ≥135/85 mmHg) and is categorised into primary or secondary hypertension, depending on whether a cause can be identified.
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80
Q

Define primary hypertension?

A
  • Primary (essential) hypertension: has no known underlying cause and is responsible for 90-95% of cases of hypertension. Some contributing factors include:
    • Genetic susceptibility
    • Excessive sympathetic nervous system activity
    • Abnormalities of Na+/K+ membrane transport
    • High salt intake
    • Abnormalities in renin-angiotensin-aldosterone system
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81
Q

Define secondary hypertension?

A
  • Secondary hypertension indicates a known underlying cause. Examples include (ROPED):
    • R - Renal disease: glomerulonephritis, polycystic kidney disease, renal artery stenosis, chronic kidney disease
    • O - Obesity
    • P - Pregnancy (pre-eclampsia)
    • E - Endocrine disorders: primary hyperaldosteronism, phaeochromocytoma, Cushing’s syndrome, hyperthyroidism, acromegaly
    • D - Drugs:glucocorticoids, ciclosporin, atypical antipsychotics, the combined oral contraceptive pill
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82
Q

Name some non-modifiable risk factors for hypertension?

A
  • Increasing age
  • African heritage
  • Family history
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83
Q

Name some modifiable risk factors for hypertension?

A
  • Obesity
  • Sedentary Lifestyle
  • Alcohol excess
  • Smoking
  • High Sodium intake
  • Stress
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84
Q

Name the 3 stages of hypertension and their readings?

A

Stage 1 - >140/90 clinic reading or >135/85 home reading.
Stage 2 - >160/100 clinic reading or >150/95 home reading.
Stage 3 - >180/120 clinic reading.

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85
Q

What are the signs associated with hypertension?

A
  • Hypertensive retinopathy
  • Visual disturbance
  • Cardiac symptoms e.g. chest pain
  • Oliguria or polyuria
  • Weight loss
  • Sweating
  • Palpitations
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86
Q

What are the symptoms associated with hypertension?

A
  • Asymptomatic: most common presentation
  • Headaches: classically occipital and worse in the morning
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87
Q

What investigations should be done for hypertension?

A

Blood pressure readings.

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88
Q

What other investigations should be done for hypertension?

A
  • Fundoscopy: assess for hypertensive retinopathy
  • 12-lead ECG: assess for ischaemic changes and evidence of left ventricular hypertrophy
  • Albumin:creatinine ratio (ACR) and urinalysis: assessing for renal dysfunction, as evidenced by elevated ACR and proteinuria or haematuria on urinalysis
  • Bloods: HbA1c, U&Es, total cholesterol and HDL cholesterol
  • It is also important to formally estimate cardiovascular risk using a tool such as QRisk to discuss prognosis and healthcare options.
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89
Q

What is the diagnosis criteria for hypertension?

A
  • Hypertension is confirmed when the following criteria are met:
  • Clinic blood pressure of 140/90 mmHg or higherand
  • ABPM daytime average or HBPM average of 135/85 mmHg or higher
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90
Q

What is the management for hypertension?

A

A – ACE inhibitor (e.g., ramipril)
B – Beta blocker (e.g., bisoprolol)
C – Calcium channel blocker (e.g., amlodipine)
D – Thiazide-like diuretic (e.g., indapamide)
ARB – Angiotensin II receptor blocker (e.g., candesartan)

Step 1: Aged under 55 or type 2 diabetic of any age or family origin, use A. Aged over 55 or Black African use C.
Step 2: A + C. Alternatively, A + D or C + D.
Step 3: A + C + D
Step 4: A + C + D + fourth agent (see below)

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91
Q

What is the fourth line management for hypertension dependent on?

A

Step 4 depends on the serum potassium level:

Less than or equal to 4.5 mmol/L consider a potassium-sparing diuretic, such as spironolactone
More than 4.5 mmol/L consider an alpha blocker (e.g., doxazosin) or a beta blocker (e.g., atenolol)

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92
Q

What are the treatment targets for above 80yo and below 80yo patients with hypertension?

A
  • <80 years: <140 systolic; <90 diastolic
  • > 80 years: <150 systolic; <90 diastolic
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93
Q

What are the NICE guidelines regarding hypertension monitoring?

A

NICE recommend measuring blood pressure every 5 years to screen for hypertension. It should be measured more often in patients that are on the borderline for diagnosis (140/90) and every year in patients with type 2 diabetes.

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94
Q

What are some complications associated with hypertension?

A
  • Coronary heart disease.
  • Cerebrovascular accident.
  • Congestive heart failure.
  • Chronic kidney disease
  • Hypertensive retinopathy
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95
Q

Define hypotension?

A

While there is not an accepted standard hypotensive value, pressures less than 90/60 are recognized as hypotensive.

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96
Q

What are some signs for hypotension?

A

Commonly asymptomatic.
- Shortness of breath
- Irregular heartbeat
- Fever
- Cough
- Vomiting
- Dysuria
- Fatigue

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97
Q

What are some symptoms for hypotension?

A

Commonly asymptomatic.
- Dizziness
- Syncope
- Chest pain
- Headache
- Stiff neck

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98
Q

Name some investigations for hypotension?

A
  • FBC: with TSH, free T4 and cortisol levels.
  • If patient is in shock then → ECHO immediately with IVC variability test.
  • Pulse pressure variation measurement.
  • CT angiogram to rule out saddle embolus pulmonary embolisms.
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99
Q

What are treatment options for hypotension?

A
  • The treatment of hypotension should focus on reversing the underlying etiology.
  • Fluid resuscitation.
  • Vasopressors may be indicated if the mean arterial pressure is less than 65 mm Hg.
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100
Q

What are some differential diagnosis options for hypotension?

A
  • Benign hypotension
  • Distributive shock
  • Cardiogenic shock
  • Hypovolemic shock
  • Obstructive shock
  • Combined-type hypotensive shock
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101
Q

What are some complications associated with hypotension?

A
  • Sudden cardiac death.
  • Multi-organ failure.
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102
Q

Define venous thromboembolism?

A

DVT of the leg is the development of a blood clot in one of the major deep veins in the leg or thigh, which leads to impaired venous blood flow, usually causing leg swelling and pain.

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103
Q

What are the signs of a VTE?

A
  • Cyanosis
  • Swollen and tended red leg.
  • Cardiac: Increased HR, AF, Increased JVP.
  • Chest: Increased RR, pleural rub, pleural effusion.
  • Pulsus paradoxus.
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104
Q

What are the symptoms of a VTE?

A
  • Leg pain, which may be along the vein.
  • Respiratory: SOB, pleuritic chest pain, haemoptysis, cough.
  • Systemic: dizziness, fever.
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105
Q

What is the DICE mnemonic for risk factors for VTE?

A
  • DVT or PE in past medical history.
  • Immobility
  • Cancer which effects thrombin (prostate and ovarian heavily linked)
  • (O)Estrogen which increases fibrinogen, prothrombin and clotting factor levels.
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106
Q

What is the THROMBOSIS mnemonic for risk factors for VTE?

A
  • T - Trauma or Travel
  • H - Hospitalisation or Hormones
  • R - Relatives (family history)
  • O - Old age
  • M - Malignancy (cancer)
  • B - Long bone fractures
  • O -Obesity or Obstetrics
  • S - Surgery or Smoking
  • I - Immobilisation
  • S - other Sickness (Antiphospholipid syndrome, nephrotic syndrome, paroxysmal nocturnal haemoglobinuria)
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107
Q

How is VTE diagnosed?

A
  • 2-level Wells DVT score or 2-level Wells PE score.
  • Pulmonary embolism rule out criteria (PERC)
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108
Q

What other investigations may be done for VTE?

A
  • CXR → may show wedge shaped infarct, more often used to rule out other conditions.
  • ECG → Sinus tach, RV strain (T inversion in V1-V3), S1Q3T3 (prominent S in lead I, Q wave and inverted T wave in lead III), RBBB, right axis deviation.
  • ABG → Decreased O2, decreased CO2, Increased pH.
  • Unprovoked VTE → consider thrombophilia.
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109
Q

What management strategies would be performed for VTE?

A
  • Anticoagulation to prevent recurrent VTE (Warfarin or LMW Heparin/Fondaparinux)
  • DOACs
  • If O2 <90% then give O2.
  • Aspirin or other anti-platelet drugs.
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110
Q

What are some complications for VTE?

A
  • Recurrent risk of VTE.
  • DVT complications → Cellulitis, Thrombophlebitis, post-thrombotic syndrome.
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111
Q

Define pulmonary embolism?

A

Pulmonary embolism (PE) refers to obstruction of the pulmonary vasculature, secondary to an embolus.

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112
Q

Describe the pathophysiology behind a PE?

A
  • Emboli typically originate in the lower extremities, most commonly secondary to a deep vein thrombosis (DVT) in the calf:
    • Once the clot has formed, the increased pressure in the vein can cause a part of the main clot to break free, becoming a thromboembolism which can travel downstream towards the heart and gets into the right atrium, and then into the right ventricle to get pumped into the lungs where it can get lodged.
  • When a pulmonary embolism happens, a blockage in any of the arteries leads to a decrease in blood flow to lung tissue downstream.
  • If there is no blood flowing past an alveoli, then this means that the alveoli getting ventilated with fresh air but not getting perfused with blood. This is called a ventilation perfusion mismatch or a V/Q mismatch. The body needs oxygenated blood to function and can therefore only tolerate a bit of a V/Q mismatch, before the lungs are no longer able to meet the needs of the body.
  • After some hours, the non-perfused lung no longer produces surfactant resulting in alveolar collapse which in turn exaggerates hypoxaemia.
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113
Q

What are some risk factors for PE?

A
  • Virchow’s triad causing clots:
    • Hypercoagulability
    • Venous Stasis
    • Endothelial cell damage .
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114
Q

What are the signs of PE?

A
  • Hypoxia
    • Cyanosis may be present
  • Deep vein thrombosis: swollen, tender calf
  • Pyrexia may be present
  • Tachypnoea and tachycardia
  • Crackles
  • Hypotension: SBP <90 mmHg suggests a massive PE
  • Elevated JVP: suggests cor pulmonale
  • Right parasternal heave: suggests right ventricular strain
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115
Q

What are the symptoms of PE?

A
  • Pleuritic chest pain
  • Dyspnoea
  • Cough +/- haemoptysis
  • Fever
  • Fatigue
  • Syncope: a red flag symptom
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116
Q

What is the Wells score used for?

A
  • Wells Two-Level score, in conjunction with clinical judgement, is utilised to determine the probability of PE.
    • > 4: high probability of PE
    • ≤ 4: low probability of PE
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117
Q

What primary investigations should be performed for suspected PE?

A
  • CXR - rule out an alternative pathology.
  • ECG (sinus tachy, RBBB, S1Q3T3)
  • CT pulmonary angiogram
  • D-Dimer (fibrin breakdown products)
  • All patients with unprovoked PE should have FBC for suspected cancer.
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118
Q

What other investigations can be performed for suspected PE?

A
  • ABG - quantify the degree of hypoxia.
  • V/Q scan
  • Pulmonary angiography (gold standard, but more invasive and has higher complications)
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119
Q

What are some complications of PE?

A
  • Cor pulmonale
  • Pulmonary infarction
  • Sudden death
  • Respiratory alkalosis
  • Embolic stroke
  • Heparin-associated thrombocytopenia
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120
Q

What are some prevention management options for PE?

A
  • Compression stockings
  • Frequent calf exercises during long periods of sitting still
  • Prophylactic treatment with low molecular weight heparin
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121
Q

What are some supportive management options for PE?

A
  • Admission to hospital
  • Oxygen, as required
  • Analgesia, if required
  • Adequate monitoring for any deterioration
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122
Q

What management can be given for PEs?

A
  • Thrombolysis e.g. alteplase: injecting a fibrinolytic medication that rapidly dissolves clots.
  • Anticoagulation therapy
  • Inferior vena cava filter
  • Surgical embolectomy
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123
Q

Define peripheral vascular disease?

A

Peripheral arterial disease (PAD) is a major circulatory disorder characterised by arterial obstruction, leading to reduced blood supply and ischaemia in the lower limbs.

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124
Q

What are some risk factors for PVD?

A
  • Age → Higher risk when older.
  • Gender → Male > Female
  • Smoking: thesingle greatest risk factorand is thought to confer more than a 4-fold increased risk of PAD
  • Diabetes mellitus
  • Hypercholesterolaemia
  • Hypertension
  • Chronic kidney disease
  • High serum homocysteine
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125
Q

What is the Fontaine classification used for?

A

PVD.
- Stage I - Asymptomatic
- Stage 2 - Intermittent claudication
- Stage 3 - Critical limb ischemia
- Stage 4 - Tissue loss: ulceration or gangrene

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126
Q

Which sites are claudication relate to the site of disease in PVD?

A
  • Common iliac:unilateral buttock
  • Common femoral:unilateral thigh
  • Superficial femoral:unilateral calf
  • Aortoiliac (Leriche syndrome)may cause the triad of:
    • Bilateral buttock and thigh claudication
    • Absent or decreased femoral pulses
    • Erectile dysfunction
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127
Q

What primary investigations should be done for PVD?

A
  • History
  • Ankle-brachial pressure index (ABPI)
  • Duplex ultrasound
  • Assessment of cardiovascular risk factors (ECG, FBC, U&E, random glucose or HbA1c, serum cholesterol, and lipid profiles)
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128
Q

What other investigations should be considered for suspected

A
  • Exercise ABPI: for people in whom the diagnosis is uncertain on the basis of resting ABPI
  • Computed tomography angiography
  • Magnetic resonance angiography
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129
Q

How would you manage intermittent claudication in relation to PVD?

A
  • Exercise
  • Management of cardiovascular risk factors: smoking cessation, HbA1c control, BP control, diet and weight management, lipid modification (statins), antiplatelet agents (e.g. clopidogrel)
  • Surgical intervention
  • Consideration of naftidrofuryl oxalate: vasodilator
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130
Q

List some complications of PVD?

A
  • Critical limb ischaemia and acute limb ischaemia
  • Ulceration and gangrene
  • Infection and poor tissue healing
  • Amputation
  • Multiorgan dysfunction may occur, especially in people with acute limb ischaemia
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131
Q

Define pericarditis and pericardial effusion?

A
  • Pericarditis is inflammation of the pericardium.
  • Pericardial effusion is a condition in which extra fluid collects between the heart and the pericardium.
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132
Q

What are some risk factors for pericarditis and pericardial effusion?

A
  • Gender → Male > Female
  • 20-50 years of age
  • Previous MI
  • Viral or bacterial infection
  • Systemic autoimmune disorders
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133
Q

What are some signs for pericarditis and pericardial effusion?

A
  • Pericardial rub
    • Heard at the left sternal edge as the patient leans forward
    • Extra heart sound of a to-and-fro character
    • High-pitched or squeaky
  • Diminished heart sounds: if there is large effusion
  • Tachycardia
  • Tachypnoea
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134
Q

What is the difference between acute pericarditis and chronic pericarditis?

A

Acute pericarditis generally lasts just a few weeks, whereas chronic pericarditis lasts longer, usually more than 6 months.

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135
Q

What are some symptoms associated with pericarditis and pericardial effusion?

A
  • Chest pain
    • Sudden onset, sharp, central and pleuritic
    • Relief upon sitting up or leaning forward
    • Exacerbated by lying flat
    • May last from hours to days
  • Fever and myalgia
  • Shortness of breath
  • Hiccups: if phrenic involvement
  • Low BP and light headedness: if effusion is large
  • Peripheral oedema: suggests right-sided heart failure secondary to constrictive pericarditis
  • Prodromal viral illness: e.g. upper respiratory tract infection
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136
Q

What primary investigations should be done for pericarditis and pericardial effusion?

A
  • ECG:
    • Pericarditis: widespread saddle-shaped ST-elevation (highly sensitive) and PR depression (highly specific) followed by T-wave flattening and eventual T-wave inversion.
    • Pericardial effusions: low QRS complex voltage or electrical alternans (QRS complexes have different heights)
  • Chest X-ray: may demonstrate an associated pericardial effusion showing “water-bottle heart”as there is pooling of fluid at the bottom of the heart
  • Transthoracic echocardiogram: pericardial effusion shows a ‘dancing’ heart as it moves around in the fluid
  • ESR and CRP:elevated secondary to inflammation
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137
Q

What other investigations can be done for pericarditis and pericardial effusion?

A
  • Troponin:elevated in 35-50% of patients
  • Urea:elevated levels indicate a uraemic cause
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138
Q

What management strategies should be considered for acute idiopathic or viral pericarditis?

A
  • 1st line: NSAIDs and colchicine are often both used together
  • 2nd line: NSAIDs, colchicine and low-dose prednisolone
139
Q

What management strategies should be considered for bacterial pericarditis?

A

IV antibiotics and pericardiocentesis (removal of fluid) with washout, culture and sensitivities

140
Q

What management strategies should be considered for refractory pericarditis?

A

Pericardectomy may be considered for refractory cases of pericarditis unresponsive to medical therapy

141
Q

What complications are associated with pericarditis and pericardial effusion?

A
  • Myocarditis
  • Constrictive pericarditis
142
Q

What are some causes of pericarditis and pericardial effusion?

A
  • Idiopathic
  • Viral
  • Bacterial
  • Dressler syndrome
  • Uraemia secondary to kidney disease
  • Systemic autoimmune disorders
  • Connective tissue disorders
  • Hypothyroidism
  • Trauma
  • Malignancy
  • Certain medications such as penicillin or anticonvulsants
143
Q

What 6 viruses are most associated with pericarditis and pericardial effusion?

A
  • Coxsackievirus
  • Mumps
  • Epstein-Barr virus (EBV)
  • Cytomegalovirus (CMV)
  • Varicella-Zoster virus (VZV)
  • HIV
144
Q

What bacteria is most associated with pericarditis and pericardial effusion?

A
  • Tuberculosis
145
Q

What are some clinical manifestations of constrictive pericarditis?

A
  • Kussmaul’s sign: rise in jugular venous pressure and increased neck vein distension during inspiration
  • Pulsus paradoxus
  • Diffuse heart sounds
  • Right heart failure signs
  • Ascites
  • Oedema
  • Atrial dilatation
146
Q

What are the primary investigations for constrictive pericarditis?

A
  • CXR: small heart with/without pericardial calcification
  • ECG: low voltage QRS
  • ECHO: thickened calcified pericardium restricting the heart’s movement; small ventricular cavities
147
Q

What management strategy should be considered for constrictive pericarditis?

A
  • May require complete resection of the pericardium; pericardiectomy
148
Q

What complications are associated with constrictive pericarditis?

A
  • Congestive heart failure.
149
Q

Define cardiac tamponde?

A
  • Cardiac tamponade describes a reduction in cardiac output due to a raised intrapericardial pressure secondary to a pericardial effusion.
150
Q

What are some causes of cardiac tamponade?

A
  • Idiopathic
  • Viral
  • Bacterial
  • Dressler syndrome
  • Uraemia secondary to kidney disease
  • Systemic autoimmune disorders
  • Hypothyroidism
  • Trauma
  • Malignancy
  • Aortic dissection
  • Rheumatological
151
Q

What are the signs of cardiac tamponade?

A
  • Beck’s triad
    • Hypotension
    • Kussmaul’s sign
    • Muffled heart sounds
  • Tachycardia
  • Cool peripheries
  • Pulsus paradoxus
  • Prolonged capillary refill time
152
Q

What are the symptoms of cardiac tamponde?

A
  • Dyspnoea
  • Coughing
  • Chest discomfort
  • Lightheadedness: if large effusion
  • Peripheral oedema: heart failure
  • Confusion: decreased CNS perfusion
153
Q

What are the primary investigations for cardiac tamponade?

A
  • ECG:tachycardia, low QRS complex voltage andelectrical alternans (QRS complex varies in amplitude as the heart moves in the fluid)
  • Bloods (inflammatory markers and troponin)
  • Imaging (ECHO, chest X-ray)
154
Q

What other investigations can be done for a cardiac tampondade?

A

Pericardial fluid analysis - obtained through a pericardiocentesis.

155
Q

What management should be done for pericardial effusion with no sign of tamponade?

A
  • Conservative management:repeat echocardiograms and monitor blood pressure
  • NSAIDsorcolchicineif the underlying cause is suspected pericarditis
  • Pericardiocentesis:may be required for larger effusions
156
Q

What management should be done for pericardial effusion evidence of tamponade?

A
  • Urgent pericardiocentesis:a needle is inserted between the xiphisternum and left costal margin and directed towards the left shoulder. This can be done under ultrasound guidance. Pericardial fluid can be aspirated to relieve intrapericardial pressure
  • Urgent surgicaldrainage is usually indicated in cases related to neoplasia, a purulent effusion, or hemopericardium (e.g. trauma)
157
Q

What are some complications of cardiac tamponade?

A
  • Cardiac arrest
  • Constrictive pericarditis
158
Q

Define bradycardia?

A

Bradycardia is defined as a heart rate below 50 beats per minute, which can either be physiological or due to sinus node or atrioventricular (AV) node conduction dysfunction.

159
Q

Define first-degree AV block?

A

First-degree AV block: occurs where there is delayed atrioventricular conduction through the AV node but every atrial impulse leads to a ventricular contraction.

160
Q

Define second degree Mobitz type I AV block?

A

Atrial inputs becomes gradually weaker until it does not pass through the AV node. After failing to stimulate a ventricular contraction the atrial impulse returns to being strong.

161
Q

Define second degree Mobitz type II AV block?

A

Usually due to disease of the His-Purkinje system which causes intermitted failure or interruption of AV conduction. This results in missing QRS complexes. There is usually a set ratio of P waves to QRS complexes.

162
Q

Define third-degree AB block?

A

Complete heart block. This is no observable relationship between P waves and QRS complexes.

163
Q

What are some risk factors for heart block?

A
  • Increasing age.
  • Hypothyroidism
  • Electrolyte imbalances
  • Recent MI
  • Hypothermia
  • Drugs
  • Drugs: e.g. beta-blockers, non-dihydropyridine calcium channel blockers, digoxin, adenosine and amiodarone
164
Q

What are some signs for heart block?

A

Cushings triad
- Bradycardia
- Hypertension
- Irregular respirations (apnoea)
- JVP

165
Q

What are some symptoms of heart block?

A
  • Dizziness
  • Fatigue
  • Shortness of breath
  • Syncope
166
Q

What are the primary investigations for heart block?

A
  • First-degree AV block: PR interval >0.2s
  • Mobitz type I / Wenckebach: increasing PR interval culminating in a dropped QRS complex. The PR interval resets and the cycle repeats.
  • Mobitz type II: the PR interval remains constant, but with intermittent dropped QRS complexes (2:1, 3:1, etc).
  • Third-degree AV block: P wave and QRS complex are completely dissociated
167
Q

What other investigations can be done for suspected heart block?

A
  • TFTs
  • U&Es
  • Serum digoxin
  • Holter monitoring
  • Tilt-table test
  • ECHO
168
Q

What is the management for a stable patient with heart block?

A

If stable - observe.

169
Q

What is the management for a patient who is unstable due to heart block?

A
  • First line: atropine500mcg IV
  • If no improvement:
    • Atropine500mcg IV repeated
    • Otherinotropes(such as noradrenalin)
    • Transcutaneous cardiac pacing(using a defibrillator)
170
Q

What is the management for a patient who is at high risk of asystole due to heart block?

A
  • Temporary transvenous cardiac pacing
  • Permanent implantable pacemakerwhen available
171
Q

What are some complications of heart block?

A
  • Syncope
  • Arrhythmias:some patients may go on to develop asystole, ventricular tachycardia or ventricular fibrillation
  • Congestive heart failure: due to poor cardiac output
172
Q

What is the definition of infective endocarditis?

A
  • Infective endocarditis (IE) is an infection of the endocardium (including the valvular structures, the chordae tendineae, sites of septal defects etc).
  • Endocarditis typically affects valves - native valves or prosthetic valves.
173
Q

What common bacteria cause infective endocarditis?

A
  • Staphylococcus aureus
  • Staphylococcus epidermidis
  • Streptococcus bovis
  • Viridans streptococci
  • Streptococcus mitis and sanguinis
174
Q

What are some risk factors of infective endocarditis?

A
  • Male gender:men are 2.5 times more prone to endocarditis than women
  • Previous infective endocarditis
  • Prosthetic heart valves or implantable cardiac device
  • Congenital heart disease especially affecting the valves
  • Rheumatic heart disease causing damage to the valves
  • Poor dental hygiene/ dental treatment: a way of microbes entering
  • Intravenous drug use (IVDU) typically affects tricuspid valve
  • Intravenous catheter
  • Immunosuppression
175
Q

What are some signs of infective endocarditis?

A
  • Heart murmur: due to turbulent blood flow
  • Splinter haemorrhages: red-plum lines under the nails due to microemboli deposition
  • Janeway lesions: painless plaques on palms and soles due to septic microemboli deposition
  • Osler’s nodes: painful nodules on fingers or toes due to immune complex deposition
  • Roth’s spots: white centred retinal haemorrhages due to immune complex deposition
  • Signs of glomerulonephritis: due to immune complex deposition in kidneys
  • Mild splenomegaly
176
Q

What are some symptoms of infective endocarditis?

A
  • Fever or chills
  • Headache
  • Shortness of breath
  • Night sweats, malaise, fatigue, weight loss
  • Joint pain: may be due to septic emboli
177
Q

What are the primary investigations of infective endocarditis?

A
  • inflammatory markers (WCC, Neutrophilia)
  • CRP/ESR
  • 3 x blood cultures 1 hour apart
  • ECHO - confirms diagnosis (transthoracic is first line, transoesophageal if clinical suspicion remains)
  • Chest X-ray
  • 12-lead ECG
  • Urinalysis
178
Q

What is the modified duke criteria used for?

A

The Modified Duke Criteria requires 2 major criteria, or 1 major and 3 minor criteria, or 5 minor criteria for a diagnosis of infective endocarditis.

179
Q

What is the 1st line management for infective endocarditis?

A

IV antibiotics:generally for 4-6 weeks. Patients usually require a central line or peripherally inserted central catheter (PICC)

180
Q

What is the 2nd line management for infective endocarditis?

A
  • Surgery:aim to remove infected tissue and repair or replace affected valves
    • Indicationsinclude: decompensated heart failure, resistance to antibiotic therapy, severe sepsis, perivalvular abscess, intracardiac fistulae, prosthetic valve endocarditis
181
Q

What are some complications associated with infective endocarditis?

A
  • Regurgitation
  • Congestive HF
  • Septic embolisation
  • Valvular rupture
  • Aortic rot abscess
182
Q

Define rheumatic fever?

A

Acute rheumatic fever is an autoimmune condition triggered by group A β-haemolytic Streptococcus pyogenes infection (rheumatic fever usually follows strep throat)

183
Q

What are some risk factors of rheumatic fever?

A
  • Childhood and adolescence: peak age 5-17 years old
  • Developing world: rheumatic fever is considered a disease of poverty, with lower rates in the developed world due to improvements in antibiotic use and hygiene
  • Malnutrition
  • Overcrowding
  • Family history of rheumatic fever
  • HLA class II
184
Q

What are some signs of rheumatic fever?

A
  • Heart murmur (mitral stenosis and aortic regurgitation)
  • Tachycardia or bradycardia
  • Pericardial rub on auscultation
  • Palpitations
  • Tender joints: usually not swollen
  • Erythema marginatum
  • Subcutaneous nodules
  • Pan-carditis
185
Q

What are some symptoms of rheumatic fever?

A
  • Recent sore throat or scarlet fever (occurs 2-4 weeksbeforechest pain)
  • Chest pain: pleuritic
  • Shortness of breath
  • Fever and rigors
  • Non-pruritic rash
  • Joint pain: oligo- or poly-arthritis
    • Severe pain
    • Often involves the lower limbs
    • Migratory
  • Sydenham’s chorea
186
Q

What investigations should be done for suspected rheumatic fever?

A
  • Throat swab
  • Anti-streptococcal antibodies (ASO) titres
  • Chest X-ray: cardiomegaly and/or evidence of congestive heart failure may be seen
  • Echocardiogram: may demonstrate mitral and aortic valvular pathology, as well as the presence of pericarditis or a pericardial effusion
  • Blood cultures: if the patient is pyrexial
  • Raised WCC
  • Raised ESR and CRP
187
Q

What is the Jones criteria used for?

A

Jones Criteria is used to diagnose rheumatic fever and is dependent on evidence of recent streptococcal infection in addition to 2 major criteria, or 1 major and 2 minor criteria:
- Major criteria:
- J – Joint arthritis
- O – Organ inflammation, such as carditis
- N – Nodules
- E – Erythema marginatum rash
- S – Sydenham chorea
- Minor criteria
- Fever
- ECG Changes (prolonged PR interval) without carditis
- Arthralgia without arthritis
- Raised inflammatory markers (CRP and ESR)

188
Q

What is the initial management for rheumatic fever?

A
  • Conservative: bed rest, analgesia, immobilise joints in severe arthritis
  • Antibiotic therapy:benzylpenicillin IV STAT, followed by oral phenoxymethylpenicillin for 10 days
  • Aspirin and steroids: used to treat carditis
  • Haloperidol or diazepam:if severe Sydenham’s chorea is present
189
Q

What prophylaxis is advised for rheumatic fever?

A
  • All patients should be put on long-term, regular antibioticsto lower chance of developing chronic rheumatic heart disease
  • Antibiotics: IM benzylpenicillin. The duration will vary depending on patient factors (e.g. could be for 10 years or life-long)
190
Q

What are some complications of rheumatic fever?

A
  • Rheumatic heart disease:occurs in 30-50% of patients, most commonly affecting the mitral valve, followed by the aortic valve.
  • Heart failure: may occur in chronic or recurrent cases
  • Infective endocarditis: previous rheumatic heart disease increases the risk of infective endocarditis
  • Atrial fibrillation
191
Q

What is the definition for aortic stenosis?

A
  • Aortic stenosis (AS) represents obstruction of blood flow across the aortic valve due to pathological narrowing.
  • It can be supra-valvular (e.g. fibrous ridge above valve), sub-valvular (e.g. fibrous ridge is below valve) or valvular.
192
Q

Describe the normal physiology of the aortic valve?

A

The aortic valve is normally made up of three leaflets: the left, the right, and the posterior leaflet. It opens during systole to allow blood to be ejected to the body. During diastole, it closes to allow the heart to fill with blood and get ready for another systole.

193
Q

Name some causes of aortic stenosis?

A
  • Mechanical stress over time.
  • Bicuspid valve.
  • Other congenital variations of the valve.
  • Chronic rheumatic fever.
194
Q

Describe the pathology behind aortic stenosis?

A
  • Aortic stenosis refers to when the aortic valve doesn’t fully open, making it harder for blood to be pumped out. Usually, the aortic valve opens to about 3-4 cm^2, but with stenosis it can become less than 1 cm^2.
  • The valve doesn’t open as easily but as the left ventricle contracts, it creates a high pressure that eventually pushes on the valve until it finally snaps open, causing a characteristic “ejection click.”
  • As the blood has to flow through a narrow opening, there’s turbulence which creates a murmur - initially gets louder as more blood flows past the opening, and then becomes quieter as the amount of blood flowing subsides (crescendo-decrescendo murmur).
  • As the left ventricle has to generate higher pressures, it undergoes concentric hypertrophy. Despite this, enough blood may still not leave the heart. This leads to symptoms of heart failure which will vary depending on which organ is affected e.g. brain = syncope
195
Q

Name some risk factors for aortic stenosis?

A
  • Hypercholesterolaemia
  • Hypertension
  • Smoking
  • Diabetes
  • Rheumatic heart disease
  • Bicuspid aortic valve
196
Q

What are some signs of aortic stenosis?

A

Mild aortic stenosis can be completely asymptomatic, discovered as an incidental murmur during routine examination.
- Ejection systolic murmur
- Ejection click
- Soft / ascent S2
- Fourth heart sound (s4)
- Palpable thrill during systole
- Pulsus tarsus
- Left ventricular hypertrophy on imaging

197
Q

What are some symptoms of aortic stenosis?

A

Mild aortic stenosis can be completely asymptomatic, discovered as an incidental murmur during routine examination.
- Fatigue
- Shortness of breath
- Angina
- Dizziness
- Fainting
- Epistaxis and bruising
Symptoms may be worse on exertion.

198
Q

What primary investigations should be carried out for aortic stenosis?

A
  • ECHO (gold standard) - left ventricular size and valve area
199
Q

Define aortic regurgitation?

A

Aortic regurgitation (AR) is the diastolic leakage of blood from the aorta into the left ventricle.

200
Q

Describe the pathophysiology behind aortic regurgitation?

A
  • Patients with aortic regurgitation will have an early decrescendo diastolic murmur, caused by the blood flowing back through the valve.
  • As blood leaks back from the aorta into the left ventricle, the left ventricular blood volume increases, which increases the stroke volume. More blood pumped out of the heart per squeeze requires more pressure, so systolic blood pressure increases. During diastole, though, there’s less blood volume in the aorta so diastolic blood pressure decreases. A high systolic pressure and low diastolic pressure is known as hyperdynamic circulation.
  • Patients with a hyperdynamic circulation have bounding pulses, or water-hammer pulses, as the blood slams against the walls of the arteries with each heartbeat.
  • Over time, the increase in blood volume in the left ventricle causes it to undergo eccentric ventricular hypertrophy.
  • Aortic regurgitation can be acute or chronic. Chronically, there can be compensation (LV hypertrophy). However, acutely valvular incompetence develops and blood starts to back up in the atria → pulmonary system etc
201
Q

Name 3 cause of aortic regurgitation?

A
  • Aortic root dilation: most are idiopathic but can also be caused by aortic dissection, aneurysms, syphilis, connective tissue disorders and aortitis.
  • Valvular damage e.g. due to infective endocarditis or rheumatic fever: chronic inflammation leads to fibrosis, but instead of fusing the valve leaflets together, it makes it so that they don’t form a strong seal, and instead let blood leak through.
  • Congenital causes: e.g. bicuspid or quadcuspid valve
202
Q

Name some risk factors of aortic regurgitation?

A
  • Infective endocarditis
  • Rheumatic fever
  • Congential abnormalities e.g. bicuspid valve
  • Connective tissue disorders
  • Aortic dissection
  • Aortic aneurysms
  • Gender → Male > Female
203
Q

Name some signs of aortic regurgitation?

A
  • Early decrescendo murmur: due to blood flowing back into LV
  • Soft S1 and S2
  • Apex beat is displaced laterally
  • Wide pulse pressure: due to high systolic pressure and low diastolic pressure
  • Bounding pulses/ water-hammer pulse
  • de Musset’s: head bobbing with each beat due to severe bounding pulses
  • Quincke’s sign: pulsation of capillary beds in fingernails due to bounding pulses
  • Traube’s: pistol shot femoral pulses
  • Duroziez’s: to and fro murmur heard when stethoscope compresses femoral vessels.
  • Müller’s: pulsation of uvula.
  • Raised JVP: if acute regurgitation as blood backs up
  • LV hypertrophy seen on imaging
204
Q

Name some symptoms of aortic regurgitation?

A
  • Dyspnoea
  • Chest pain
  • Palpitations
  • Syncope
    In chronic regurgitation, patients remain asymptomatic for a long time.
205
Q

What is the primary investigations of aortic regurgitation?

A

ECHO: gold standard investigation; allows visualisation of the origin of regurgitant jet and its width, detection of aortic valve pathology and compensatory changes e.g. LV hypertrophy and function

206
Q

List some other investigations for suspected aortic regurgitation?

A
  • BP
  • ECG: left ventricular hypertrophy (deep S-waves in V1 and V2, tall R-waves in V5 and V6) in chronic AR
  • CXR: may show a dilated ascending aorta; may show cardiomegaly if chronic AR
  • MRI: can be used to show regurgitant fraction
  • CT: can show aortic dilation and maximum diameter; LV hypertrophy
  • Angiography: can be done prior to surgery to look for concomitant coronary artery disease
207
Q

How would you monitor someone with aoritc regurgitation?

A

Serial echocardiograms to monitor progression.

208
Q

What is the management for someone with aortic regurgitation?

A
  • Vasodilators e.g. ACE-inhibitors (ramipril) will improve stroke volume and reduce regurgitation (only if patient is symptomatic or has hypertension)
  • Root replacement, if needed
  • Replacement of the valve: can be mechanical or bioprosthetic
  • Infective endocarditis prophylaxis no longer recommended
209
Q

Define mitral stenosis?

A

Mitral stenosis is a narrowing of the mitral valve orifice, making it difficult for blood to flow from the left atria to the left ventricle.

210
Q

Describe the normal physiology of the mitral valve?

A
  • The mitral valve has two leaflets: the anterior leaflet and the posterior leaflet. Together, they separate the left atrium from the left ventricle. During systole the valve closes, which means blood is ejected out of the aortic valve and into circulation. During diastole, the mitral valve opens and lets blood fill into the ventricle.
  • It is supported by the chordae tendineae and papillary muscles.
211
Q

Describe the pathology behind mitral stenosis?

A
  • As the volume of blood in the left atrium increases it causes higher pressures in the left atrium. Higher pressures flowing through the fibrotic valve make a “snap” sound when the valve opens, which is followed by a diastolic rumble as the blood is forced through the smaller opening.
  • A constant elevation in both blood volume and pressure in the left atrium causes it to dilate, and can allow blood to back up into the pulmonary circulation (pulmonary congestion and pulmonary oedema). This can ultimately result in pulmonary hypertension and right sided heart failure.
  • As the left atrium dilates, the muscle walls stretch and the pacemaker cells become more irritable, increasing the risk of atrial fibrillation.
  • The dilated atria may also press on nearby structures, causing certain symptoms.
212
Q

What are some causes of mitral stenosis?

A
  • Rheumatic fever.
  • Congenital MS
  • Mitral annular calcification
  • Radiation associated MS
  • Carcinoid associated valve disease
  • Fabry’s disease
213
Q

What are some signs of mitral stenosis?

A
  • Loud S1 snap
  • Atrial fibrillation
  • Mitral facies (malar flush)
  • Signs of RSHF
  • Signs of pulmonary hypertension
  • Mid-diastolic murmur
    • the more severe the stenosis the longer the diastolic murmur and the closer the opening snap is to S2
214
Q

What are some symptoms of mitral stenosis?

A
  • Dyspnoea
  • Fatigue
  • Haemoptysis
  • Angina
  • Dysphagia
  • Ortner syndrome
    Usually there are no symptoms until the valve orifice is moderately stenosed i.e. area is less than 2cm^2
215
Q

What are the primary investigations for mitral stenosis?

A
  • ECG - atrial fibrillation; p-mitrale signifying enlarged atria; right axis deviation and tall R-waves in V1 if right ventricular hypertrophy
  • CXR: left atrial enlargement - double right heart border, splayed trachea, prominent atrial appendage; pulmonary oedema and congestion; calcified mitral valve
  • Transthoracic ECHO (gold standard) - both the valve area and trans-mitral gradient can be assessed
216
Q

Name some other investigations to consider for mitral stenosis?

A
  • Transoesophageal ECHO: performed to look for left atrial thrombosis either after an embolic episode (e.g. stroke) or prior to percutaneous mitral commissurotomy.
  • Stress testing e.g. exercise stress echo or dobutamine stress test.
217
Q

What is the management for a patient with mitral stenosis?

A
  • Beta-blockers e.g. atenolol and digoxin: control heart rate and prolong diastole for improved diastolic filling
  • Valve repair or surgical replacement of the valve. Options include:
    • Percutaneous mitral commissurotomy (PMC): balloon enters via right femoral vein. Balloon is inflated to alleviate the stenosis.
    • Open surgery
  • Diuretics: for fluid overload
  • Anticoagulation/ Vitamin K antagonist: due to risk of thrombus formation
218
Q

Name some causes of mitral regurgitation?

A
  • Mitral valve prolapse
  • Damage to the papillary muscles post MI
  • Dilated and hypertrophic cardiomyopathy
  • LSHF
  • Infective endocarditis
  • Medications - ergotamine, bromocriptine, pergolide
219
Q

Describe the pathology behind mitral regurgitation?

A

Mitral regurgitation refers to when the mitral valve doesn’t completely shut allowing blood to leak back into the left atria from the left ventricle.

220
Q

List some risk factors of mitral regurgitation?

A
  • Associated with females
  • Advanced age
  • Connective tissue disease e.g. Marfans syndrome or Ehlers-Danlos syndrome
  • Prior MI
  • Infective endocarditis
  • Rheumatic fever
  • Cardiomyopathies
  • Certain medications e.g. ergotamine, bromocriptine, pergolide
221
Q

Name some signs of mitral regurgitation?

A
  • Mid-systolic click
  • Pan-systolic murmur
  • Soft S1
  • Additional S3 sound
  • Apex beta displaced laterally
  • Systolic thrill
  • Tachycardia
  • Signs of HF
222
Q

What effect does squatting have on the signs of mitral regurgitation?

A
  • When squatting down, the click comes later and the murmur is shorter
    • Squatting increases venous return, which fills the left ventricle with slightly more blood and the left ventricle gets larger. Therefore, the larger leaflets have more space, and as the ventricle contracts it takes just a little longer for the leaflet to get forced into the atrium.
223
Q

What effect does standing or doing the valsalva maneuver have on the signs of mitral regurgitation?

A
  • When standing or doing a valsalva maneuver, the click comes sooner and the murmur lasts longer
    • Standing reduces venous return so there’s a little less blood in the ventricle and so less room for the valve leaflets. This results in the leaflets being forced out earlier during contraction.
224
Q

What are the symptoms of mitral regurgitation?

A
  • Dyspnoea and orthopnoea: due to pulmonary hypertension
  • Fatigue and malaise: due to reduced cardiac output
  • Palpitations: due to initial compensation and increased stroke volume
  • Peripheral oedema: if right sided heart failure
225
Q

What are the primary investigations of mitral regurgitation?

A
  • ECHO - confirmation of an incompetent valve, assessment of the severity and identification the underlying cause.
  • CXR: left sided enlargement; pulmonary oedema in acute MR
  • ECG: may reflect recent MI; p-mitrale suggestive of left atrial enlargement; may be AF; signs of LV hypertrophy
226
Q

What other investigations should be considered for mitral regurgitation?

A
  • Exercise testing
  • Cardiac MRI
  • Cardiac catheterisation: used for evaluation of the coronary vessels prior to valvular surgery. Right sided catheterisation can be used to confirm pulmonary hypertension.
227
Q

What is the management for mitral regurgitation?

A
  • Vasodilators e.g. ACE-inhibitors (Ramipril or hydralazine)
  • Diuretics e.g. furosemide or spiranolactone: for fluid overload
  • Beta blockers e.g. atenolol/ calcium channel blockers/ digoxin: for heart rate control
  • Cardiac resynchronisation therapy (CRT) used when appropriate
  • Anticoagulation in atrial fibrillation and flutter: to prevent thrombus formation
  • Valve repair or surgical replacement of the valve.
  • Other surgical measures include: ventricular assist devices, cardiac restraint devices and heart transplantation.
228
Q

How should a patient with mitral regurgitation be monitored?

A
  • Serial echocardiography:
    • Mild: 2-3 years
    • Moderate: 1-2 years
    • Severe: 6-12 months
229
Q

What complications are associated with mitral regurgitation?

A
  • Left sided heart failure
  • Pulmonary congestion, hypertension and right sided heart failure: in acute MR
  • Cardiogenic shock: as cardiac output isn’t maintained
  • Atrial fibrillation: due to enlarged atria
  • Thrombus formation: due to atrial fibrillation
230
Q

Define hypertrophic cardiomyopathy?

A

Hypertrophic cardiomyopathy (HCM) is a genetic disorder characterised by left ventricular hypertrophy (LVH).

231
Q

What is the cause of hypertrophic cardiomyopathy?

A
  • Autosomal dominant trait: genetic missense mutation in one of the genes that encode proteins in the sarcomere of heart muscle.
    • Beta-myosin heavy chain mutation is the most common, but it could also be mutations in the myosin binding protein C and Troponin T.
    • 50% of mutations are sporadic
232
Q

Name some risk factors of hypertrophic cardiomyopathy?

A
  • Family history
  • Friedreich’s Ataxia(autosomal recessive neurodegenerative disease): patients with Friedreich’s ataxia often develop hypertrophic cardiomyopathy
233
Q

What are some signs of hypertrophic cardiomyopathy?

A
  • Ejection systolic murmur:crescendo-decrescendo character due to blood flowing through the obstructed left ventricular outflow tract.
  • Bifid pulse:two pulses due to mitral valve moving towards outflow tract mid-systole and causing further obstruction
  • S4 sound:due to atria contracting and pushing blood into a non-compliant ventricular wall during diastole.
  • Systolic thrillmay be felt
  • Arrhythmias
  • Hypertrophy seen on imaging
234
Q

Describe how a murmur caused by hypertrophic cardiomyopathy can change depending on whether someone is standing or squatting?

A
  • When squatting vascular resistance increases, which makes it harder to eject blood out and increases afterload. This means that the ventricle has more blood stretching it out, so it becomes less obstructed, and the murmur becomes less intense.
  • When standing or doing a valsalva maneuver, venous return decreases. This decreases preload so less blood is stretching out the ventricle before ejection. The obstruction gets larger and the murmur’s intensity increases.
235
Q

What are some symptoms of hypertrophoic cardiomyopathy?

A
  • Dyspnoea
  • Palpitations
  • Chest pain
  • Dizziness
  • Syncope
  • Sudden death,may be first manifestation
236
Q

What are the primary investigations for hypertrophic cardiomyopathy?

A
  • ECG:shows signs of left ventricular hypertrophy with progressive T wave inversion and deep Q waves; may also be AF, WPW syndrome, ventricular ectopics, VT
  • Echocardiogram:shows ventricular hypertrophy and a small left ventricular cavity; mid-systolic closure of aortic valve; anterior movement of mitral valve mid-systole
237
Q

Name some other investigations to consider to suspected cardiomyopathy?

A
  • MRI
  • Exercise test
  • Genetic analysiscan confirm diagnosis since most cases are autosomal dominant and familial
238
Q

What is the management strategy for hypertrophic cardiomyopathy?

A
  • Beta blockers or calcium channel blockers:control heart rate.
    • Digoxin is contraindicated because it tends to increase force of contraction, which can increase the obstruction.
  • Anti-arrhythmic medicatione.g. amiodarone
  • Consider defibrillatorif at high risk of arrhythmias
  • Anticoagulation:if AF is present as there is higher risk of thrombus formation
  • Septal myectomy:surgery to remove part of septum causing obstruction
239
Q

What are some complications of hypertrophic cardiomyopathy?

A
  • Left ventricular outflow obstruction
  • Heart failure
  • Arrhythmias:as there is disarray of cardiac myocytes as well as due to the heart becoming ischaemic
  • Sudden death:due to fast arrhythmias
240
Q

Define dilated cardiomyopathy?

A

Dilated cardiomyopathy refers to when all 4 chambers of the heart dilate (but don’t get thicker).

241
Q

What are some causes of dilated cardiomyopathy?

A
  • Most often idiopathic
  • Autosomal dominant- familial
  • Certain genetic conditionse.g. Duchenne Muscular Dystrophy and haemochromatosis
  • Infectione.g. coxsackievirus B or Chagas disease, a protozoal infection
  • Alcohol abuse:alcohol and its metabolites have a direct toxic effect on the myocardium
  • Chemotherapy drugse.g. doxorubicin and daunorubicin
  • Drugse.g. cocaine
  • Thyroid disorder
  • Wet beriberi:Vitamin B1 deficiency
  • Peripartum cardiomyopathy:dilated cardiomyopathy can develop in the third trimester of pregnancy or in the weeks following delivery. About half of patients recover following pregnancy.
242
Q

What are some risk factors of dilated cardiomyopathy?

A
  • Family history
  • Certain conditionse.g. haemochromatosis
  • Alcohol abuse
  • Drug abuse
  • Chemotherapy
  • Certain infections
  • Thyroid disorders
  • Increased BP
243
Q

What are the signs of dilated cardiomyopathy?

A
  • Larger heart seen on imaging
  • Systolic murmur:due to regurgitation
  • S3 gallop:due to blood rushing hitting the dilated ventricular wall during diastole
  • Increased pulse
  • Decreased BP
  • Displaced and diffuse apex
  • Arrhythmias
  • Signs of heart failuree.g. pulmonary oedema, increased JVP
244
Q

What are the symptoms of dilated cardiomyopathy?

A
  • Fatigue
  • Dyspnoea
245
Q

What investigations should be done for dilated cardiomyopathy?

A
  • Bloods:BNP elevated; low Na+ implies poor prognosis
  • CXR:cardiac enlargement; pulmonary oedema
  • ECG:tachycardia, non-specific T wave changes and poor R-wave progression; may be AF or VT
  • ECHO:shows dilated heart and low ejection fraction
246
Q

What is the management for dilated cardiomyopathy?

A
  • Bed rest
  • Diuretics:to deal with oedema
  • Beta blockers:to control heart rate
  • ACE inhibitors:dilate vessels to improve blood flow
  • Anticoagulation:due to increased risk of thrombus
  • Biventricular pacing
  • ICD
  • Left ventricular assist device (LVAD):mechanical pump that assists the heart in distributing blood
  • Heart transplant, in extreme cases
247
Q

What are some complications of dilated cardiomyopathy?

A
  • Heart failure
  • Mitral and tricuspid valve regurgitation
  • Arrhythmias
  • Risk of thromboembolism
  • Sudden death
248
Q

Define restrictive cardiomyopathy?

A

Restrictive cardiomyopathy describes when the heart muscle becomes stiffer and less compliant.

249
Q

List some of the causes of restrictive cardiomyopathy?

A
  • Idiopathic
  • Amyloidosis
  • Sarcoidosis
  • Endocardial fibroelastosis
  • Loffler syndrome
  • Haemochromatosis
  • Scleroderma
  • Radiation
250
Q

What are the signs of restrictive cardiomyopathy?

A
  • 3rd and 4th heart sounds
  • Signs of heart failure
    • Increased JVP
    • Elevation of venous pressure with inspiration
    • Oedema
    • Hepatomegaly
251
Q

What are the symptoms of restrictive cardiomyopathy?

A
  • Dyspnoea
  • Fatigue
  • Embolic symptoms
252
Q

What are the investigations for restrictive cardiomyopathy?

A
  • ECG:low amplitude QRS
  • ECHO
  • CXR
  • MRI
  • Cardiac catheterisation helps diagnosis
    The others are all abnormal but not specific enough to be diagnostic
253
Q

What is the management for suspected restrictive cardiomyopathy?

A
  • Treat underlying causee.g. removing excess iron in case of haemochromatosis
  • Heart transplant
254
Q

What is the complication of restrictive cardiomyopathy?

A

Heart failure.

255
Q

What is the definition of atrial flutter?

A

Atrial flutter is usually an organised atrial rhythm with an atrial rate typically between 250-350bpm

256
Q

Describe the differences between type 1 and type 2 atrial flutter?

A

Type 1 (typical)
- Single reentrant circuit, from the right atrium.
- Cavotricuspid isthmus dependent
- Circulates tricuspid annulus usually counterclockwise (from below)

Type 2 (atypical)
- Less common
- Right or left atrium (exact location is less defined.
- Isthmus independent.
- Associated with underlying diseases e.g. ischemia.

257
Q

What are some causes of atrial flutter?

A
  • Idiopathic (30%)
  • Coronary heart disease
  • Obesity
  • Hypertension
  • Cardiomyopathy
  • Heart failure
  • Thyrotoxicosis
  • COPD
  • Pericarditis
  • Acute excess alcohol intoxication
258
Q

What are some risk factors of atrial flitter?

A
  • Previous MI
  • Heart Failure
  • Hypertension
  • Diabetes
  • Valvular Heart Disease
  • Obstructive Sleep Apnoea
259
Q

What are some risk factors of atrial flitter?

A
  • Previous MI
  • Heart Failure
  • Hypertension
  • Diabetes
  • Valvular Heart Disease
  • Obstructive Sleep Apnoea
260
Q

What are the clinical manifestations of atrial flutter?

A
  • Palpitations
  • Tachycardia
  • Breathlessness
  • Chest pain
  • Dizziness
  • Syncope
  • Fatigue
261
Q

What are the primary investigations for suspected atrial flutter?

A
  • ECG: regular sawtooth-like atrial flutter waves (F waves) with P-wave after P-wave (diagnostic)
  • FBC - in all patients
  • Serum electrolytes
  • Renal function test
  • TSH → To exclude thyroid problems
  • Transthoracic ECHO: Evaluate the size of the left and right ventricles, heart disease and assess the ejection fraction.
  • CXR
262
Q

What is the management for atrial flutter?

A
  • Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis)
  • Radiofrequency ablationof the re-entrant rhythm
  • Anticoagulationbased on CHA2DS2VASc score
  • IV Amiodarone to restore sinus rhythm
  • Beta blocker e.g. Bisoprolol to suppress further arrhythmias
  • Electrical cardioversion with anticoagulant (LMW-heparin) such as Enoxaparin
    • Dalteparin if acute (in last 48 hours)
263
Q

What are some complications of atrial flutter?

A
  • Heart Failure
  • Thromboembolic events
  • Atrial Fibrillation
264
Q

Define atrial fibrillation?

A

Atrial fibrillation (AF) is a chaotic irregular atrial arrhythmia and is considered a type of supraventricular tachycardia (SVT).

265
Q

What are some risk factors of atrial fibrillation?

A
  • Increasing age: AF affects approximately 5% of patients aged 70-75 years, and 10% of patients aged 80-85 years
  • Diabetes mellitus
  • Hyperthyroidism
  • Hypertension
  • Congestive heart failure
  • Valvular heart disease
  • Coronary artery disease
  • Dietary and lifestyle factors: excessive caffeine intake, alcohol abuse, obesity, smoking, medication use (e.g. thyroxine or beta-agonists)
266
Q

What are some signs of atrial fibrillation?

A
  • Irregular irregular pulse
  • Hypotension:red flag; suggest haemodynamic instability
  • Evidence of heart failure:red flag; such as pulmonary oedema
267
Q

What are some symptoms of atrial fibrillation?

A
  • Palpitations
  • Dyspnoea
  • Chest pain: red flag
  • Syncope: red flag
268
Q

What does the presence of adverse features indicate in the decision of management for atrial flutter? and what are they?

A

The presence of adverse features guides the decision to undergo DC cardioversion.

  • Shock: hypotension (systolic blood pressure <90 mm Hg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
  • Syncope: transient loss of consciousness
  • Myocardial ischaemia: typical ischaemic chest pain and/or evidence of myocardial ischaemia on 12-lead ECG
  • Heart failure: pulmonary oedema and/or raised jugular venous pressure
269
Q

What are the primary investigations for atrial fibrillation?

A
  • ECG:irregularly irregular QRS complexes with absent P waves and chaotic baseline (gold standard)
    • 24-hour ambulatory ECG monitoring is recommended for those with paroxysmal AF in the community
  • Serum electrolytes, urea and creatinine:in addition to standard electrolytes, magnesium, calcium and phosphate should also be assessed
  • TFTs: hyperthyroidism is a secondary cause of AF
  • FBC in all patients
270
Q

What other investigations should be considered for suspected atrial fibrillation?

A
  • Cardiac biomarkers:request troponin if chest pain is present as this may reflect an MI
  • Chest x-ray:if there is suspicion of heart failureto assess for pulmonary oedema
  • Transthoracic ECHO:consider if there is a suspicion of underlying structural or functional heart disease; usually performed prior to cardioversion in chronic cases
271
Q

What is the management for a patient with atrial fibrillation who is haemodynamically stable vs unstable?

A

Unstable - Emergency electrical synchronised DC cardioversion

Stable - Onset of AF < 48 hours: 1) rate control or 2) rhythm-control
- Onset of AF > 48 hours / unknown onset: offer rate-control and anticoagulation for at least 3 weeks, then offer rhythm control if appropriate e.g. if rate control is unsuccessful or the patient remains symptomatic

272
Q

What should be given for rate control in atrial fibrillation?

A
  • First line: beta-blocker(e.g. bisoprolol) or arate-limiting calcium-channel blocker (e.g. verapamil)
    • Digoxin: may be considered first-line in patients with AF and heart failure
  • Second line: if refractory then consider combination therapy
273
Q

What should be given for rhythm control in atrial fibrillation?

A
  • Pharmacological:
    • Flecainide or amiodarone: if no evidence of structural/ischaemic heart disease
    • Amiodarone: if structural/ischaemic heart disease is present
  • Electrical cardioversion:rapidly shock the heart back into sinus rhythm
274
Q

What are some complications of atrial fibrillation?

A
  • Stroke
  • Myocardial infarction
  • HF
  • Reduced quality of life
275
Q

What is the CHA2DS2-VASc score used for?

A

Used to calculate stroke risk when considering anticoagulation

276
Q

What is the HAS-BLED score used for?

A

Estimates the risk of major bleeding for patients on anticoagulation to assess risk-benefit in AF care

277
Q

Name the components of the CHA2DS2-VASc scoring system?

A
  • Congestive heart failure (1)
  • Hypertension (1)
  • Age (1 - 65-74, 2 - >75)
  • Diabetes (1)
  • Stroke (2)
  • Vascular disease (1)
  • Sex (1 - Female)
278
Q

Name the components of the HAS-BLED scoring system?

A
  • Hypertension (1 - uncontrolled)
  • Abnormal renal/liver function (1 each)
  • Stroke history (1)
  • Bleeding history (1)
  • Liable to INR (1)
  • Elderly (>65 = 1)
  • Drugs (1)
279
Q

Define 1st degree heart block?

A
  • Delayed AV conduction through AV node
  • Every atrial impulse still leads to one ventricular contraction.
  • Prolonged PR interval seen on ECG (>200ms)
  • No treatment required
280
Q

Define 2nd degree heart block - Type 1?

A
  • Some impulses do not make it through the AV node.
  • Some P waves do not lead to QRS complexes.
  • Atrial impulse become gradually weaker until they do not pass through the AV node and repeats.
  • ECG → Longer PR (>200ms) until no QRS and then repeats.
  • No treatment required.
281
Q

Define 3nd degree heart block - type 2?

A
  • Some impulses do not make it through the AV node.
  • Some P waves do not lead to QRS complexes.
  • Intermittent conduction of P waves to QRS complex.
  • Conduction ratio of 2:1 is untypable as cannot tell if there is progressive PR prolongation.
  • High grade 2nd degree heart block is when two successive P wave fail to conduct to the ventricles.
  • P waves are regular.
  • High risk of progression to 3rd degree so pacemaker required.
282
Q

Define 3rd degree heart block?

A
  • Complete heart block.
  • No transmission of P waves into ventricles.
  • QRS usually wide, occasionally the bundle of His takes over and can become narrow.
  • Requires pacemaker.
283
Q

What are the investigations for bundle branch block?

A

ECG - QRS complex becomes wider. >120ms.
- LBBB - W shape seen in V1 and notched M in V6
- RBBB - Terminal R wave (M) in V1 and W shaped in V6

284
Q

What is the management for bundle branch block?

A
  • If acquired through heart disease then a cardiac resynchronisation pacemaker can be inserted.
  • This paces the chambers at the same time and improves cardiac function.
285
Q

Define tetralogy of Fallot?

A

Tetralogy of Fallot (TOF) is a congenital cardiac malformation. It is the most common form of congenital cyanotic heart disease.

286
Q

What is the PROVe mnemonic for tetralogy of Fallot?

A
  • Pulmonary infundibular stenosis
  • Right ventricle hypertrophy
  • Overriding Aorta
  • Ventricular Septal Defect
287
Q

What are the risk factors of tetralogy of Fallot?

A
  • Neonates and babies: typically manifests at around 1-2 months of life
  • Family history of congenital heart disease
  • Rubellainfection
  • Increased age of the mother (over 40 years)
  • Alcohol consumption in pregnancy
  • Diabetic mother
  • Down syndrome: trisomy 21
  • DiGeorge syndrome: chromosome 22q11 deletion
  • Edwards’ syndrome: trisomy 18
  • Patau syndrome: trisomy 13
288
Q

What are some signs of tetralogy of fallot?

A
  • Ejection systolic murmur: due to pulmonary stenosis
  • Reduced SpO2, particularly when distressed
  • Respiratory distress
  • Cyanosis
  • Clubbing
289
Q

What are the symptoms of tetralogy of Fallot?

A
  • Poor weight gain or ‘failure to thrive’
  • Difficulty feeding
  • Hyper-cyanotic or ‘Tet’ spells: cyanosis, breathlessness and syncope, particularly when crying or feeding
  • Squatting posture
290
Q

What are the primary investigations for tetralogy of Fallot?

A
  • ECG:evidence of right ventricular hypertrophy, such as right axis deviation
  • Echocardiogram + doppler flow studies:definitiveinvestigation and will reveal right ventricular outflow obstruction, right ventricular hypertrophy, a ventricular septal defect and an overriding aorta
  • Chest X-ray:demonstrates a characteristic ‘boot-shaped’ heart due to RV hypertrophy, right-sided aortic arch is seen in 25% of patients
291
Q

What are some other investigations to consider for tetralogy of Fallot?

A
  • FBC: secondary polycythaemia may be seen (raised Hb and haematocrit) due to hypoxia-driven erythropoietin release from the kidney
  • Hyperoxia test:the infant is given high flow oxygen and an ABG is performed to measure pO2. In cyanotic heart disease, the pO2 willfail to risesignificantly due to deoxygenated blood being shunted away from the lungs.
292
Q

What is the management for a patient during a ‘tet’ spell?

A
  • Conservative:ensure the infant is kept calm and their knees are placed to their chest to reduce the right to left shunt
  • Supplementary oxygenis essential in hypoxic children as hypoxia can be fatal
  • Beta blockerscan relax the right ventricle and improve flow to the pulmonary vessels
  • IV fluidscan increase pre-load, increasing the volume of blood flowing to the pulmonary vessels
  • Morphinecan decrease respiratory drive, resulting in more effective breathing
  • Sodium bicarbonatecan buffer any metabolic acidosis that occurs
  • Phenylephrine infusioncan increase systemic vascular resistance
293
Q

What is the management for a patient with tetralogy of Fallot?

A

Prostaglandin e.g. alprostadil: used in symptomatic babies at birth to maintain a ductus arteriosus, thus allowing shunting of deoxygenated blood into the pulmonary circulation
- - Blalock-Taussig (BT) shunt: atemporarypalliative measure performed for patients that remain persistently cyanotic whilst awaiting definitive surgery. It increases pulmonary arterial blood flow.
- Definitive surgery: all patients eventually need surgical correction of the abnormality, which involves closure of the VSD with a patch and reconstruction of the right ventricular outflow tract.

294
Q

What are some complications of tetralogy of Fallot?

A
  • Cardiovascular:
    • Hyper-cyanotic (‘Tet’) spells - severe spells can lead to reduced consciousness, seizures and potentially death
    • Congestive cardiac failure
    • Paradoxical emboli
  • Post-surgical:
    • Atrial and ventricular arrhythmias: increased long-term risk
    • Pulmonary regurgitation
295
Q

Define transposition of the great arteries?

A

Transposition of the great arteries refers to the switching of places of the pulmonary artery and the aorta.

296
Q

What are some risk factors for transposition of the great arteries?

A

Cause is idiopathic but risk factors include the expecting mother having:
- Diabetes
- Rubella
- Poor nutrition
- Alcohol consumption
- Being over 40 years old

297
Q

What are some signs of transposition of the great arteries?

A
  • Cyanosis
  • Tachycardia
298
Q

What are some symptoms of transposition of the great arteries?

A
  • Respiratory distress
  • Poor feeding
  • Poor weight gain
  • Sweating
299
Q

What are the investigations for transposition of the great arteries?

A
  • The defect is often diagnosed during pregnancy with antenatal ultrasound scans.
  • ECHO
300
Q

What is the management strategy for a patient with transposition of the great arteries?

A
  • Close monitoring during the pregnancy and arrangements should be made so that the woman gives birth in a hospital capable of managing the condition after birth.
  • Babies are given prostaglandin E to keep ductus arteriosus open (short term solution)
  • Balloon septostomy:insert a catheter into theforamen ovalevia the umbilicus, and inflating a balloon to create a largeatrial septal defect.
  • Open heart surgery: definitive management. Acardiopulmonary bypassmachine is used to perform an “arterial switch” procedure within a few days of birth. If present, a VSD or ASD can be corrected at the same time.
301
Q

What are some potential complications of transposition of the great arteries?

A

Congestive heart failure.
The right ventricle pumps out to the higher-pressure systemic circuit, even though it’s built for low-pressure systems, and the left ventricle pumps out to the lower pressure pulmonary circuit, even though it’s built for high pressure systems. So, in response, the right ventricle can hypertrophy and the left ventricle might atrophy. This can lead to heart failure.

302
Q

Define coarctation of the aorta?

A

Coarctation of the aorta is defined as a narrowing in the aorta. There is an infant (70%) and an adult form (30%).

303
Q

What are the risk factors of coarctation of the aorta?

A
  • Turner syndrome.
304
Q

What are some signs of coarctation of the aorta?

A
  • Weak femoral pulses
    • Tachypnoea
  • Left ventricular heavedue to left ventricular hypertrophy
  • Cyanosis of lower extremities: seen in infantile coarctation
  • Bruits over the scapulae and back from collateral vessels
  • May be a systolic murmur heard below the left clavicle and below the left scapula
  • Hypertension: as reduced kidney perfusion activated RAAS
  • Underdeveloped left arm where there is reduced flow to the left subclavian artery: in infantile form
  • Underdevelopment of the legs: in infantile form
  • Signs of aneurysm and dissection in adult form
  • Rib notching seen on CXR
305
Q

What symptoms are associated with coarctation of the aorta?

A
  • Poor feeding
  • Grey and floppy baby
  • Claudication in lower extremities
  • Headaches and nose bleeds: due to hypertension
306
Q

What are the investigations for coarctation of the aorta?

A
  • CXR: dilated aorta indented at the site of the coarctation
  • ECG: left ventricular hypertrophy
  • CT: accurately demonstrates the coarctation and quantify flow
307
Q

What are the management strategies for coarctation of the aorta?

A

Management depends on severity

  • Infantile coarctation: prostaglandin E is used keep the ductus arteriosus open while waiting for surgery

Surgical options:

  • Balloon dilation: used to widen the aorta
  • Surgical removal of the narrowed area of the aorta
  • Infantile coarctation: surgical ligation of ductus arteriosus
308
Q

Define ventricular septal defect?

A
  • Ventricular septal defect refers to when the ventricular septum has a gap in it.
  • This can vary in size from tiny to the entire septum, forming one large ventricle.
309
Q

What are some risk factors for ventricular septal defect?

A
  • Foetal alcohol syndrome
  • Turner syndrome
  • Down syndrome
  • Other cardiac deformities
310
Q

What are the signs of a ventricular septal defect?

A
  • Pansystolic murmurat the lower left sternal border
  • May be asystolic thrill on palpation
  • Cyanosis:due to deoxygenated blood in systemic circulation
  • Tachypnoea
311
Q

What are the symptoms of a ventricular septal defect?

A

Small VSDs may be asymptomatic while large VSDs may present early.
- Dyspnoea
- Poor feeding
- Failure to thrive

312
Q

What are the investigations for ventricular septal defect?

A
  • May be picked up onantenatal scans or when a murmur is heard during the newborn baby check.
  • CXR:may show large heart or normal heart depending on size of VSD
  • ECHO
313
Q

What is the management for ventricular septal defect?

A
  • Watch and wait:for small VSD as they can close spontaneously
  • Surgical closure of VSD
    • Trans-catheter closure
    • Open heart surgery
  • Antibiotic prophylaxis:should be considered due to increased risk of infective endocarditis
314
Q

What are some complications of ventricular septal defect?

A
  • Right sided heart failure:due to left to right shunt and right sided overload
  • Pulmonary hypertension:as blood is shunted from left to right
315
Q

Define atrial septal defect?

A

An atrial septal defect describes when there’s an opening in the heart between the right and left atria.

316
Q

What are some risk factors for atrial septal defect?

A
  • Down syndrome:associated with ostium primum defects
  • Foetal alcohol syndrome
  • Affects Females > Males
317
Q

What are the signs for atrial septal defect?

A
  • Mid-systolic, crescendo-decrescendo murmurloudest at the upper left sternal border
  • Splitting S2 sound:due to pulmonary valve closing after the aortic valve
  • Cyanosis:if reversal of shunt
318
Q

What are the symptoms of an atrial septal defect?

A

Can often be asymptomatic in childhood, and first presentation in adulthood can sometimes be stroke or heart failure.
- Dyspnoea
- Difficulty feeding
- Poor weight gain
- Lower respiratory tract infections

319
Q

What investigations should be considered for atrial septal defect?

A
  • Atrial septal defects are often picked up throughantenatal scans or newborn examinations.
  • CXR:large pulmonary arteries; may show large heart
  • ECG:may show right bundle branch block due to right ventricle dilatation
  • ECHO:hypertrophy and dilation of right side of heart and pulmonary arteries
320
Q

What is the management for atrial septal defect?

A
  • Watch and wait:for small ASD as it may spontaneously resolve
  • Surgical closure of ASD
    • Trans-catheter closure
    • Open heart surgery
  • Anticoagulants:used to reduce the risk of clots and stroke in adults
321
Q

What are some complications of atrial septal defect?

A
  • Stroke
  • Pulmonary hypertension
  • Atrial fibrillation
  • Eisenmenger syndrome
322
Q

What is Eisenmenger’s syndrome?

A

As right sided pressure increases and blood is shunted from right to left = deoxygenated blood in the systemic circulation

323
Q

Define patent ductus arteriosus?

A

Patent ductus arteriosus (PDA) describes the persistent opening of a foetal structure, known as the ductus arteriosus, after birth.

324
Q

What are some risk factors for patent ductus arteriosus?

A
  • Maternal infectionse.g. rubella
  • Prematurity
325
Q

What are some signs of patent ductus arteriosus?

A
  • Continuous crescendo-decrescendo “machinery” murmur:due to blood moving from the aorta to the pulmonary artery
  • Bounding pulse
  • Cyanosis of lower extremities:initially acyanotic but progresses into being cyanotic as shunt reverses
  • Tachycardia
326
Q

What are some symptoms of patent ductus arteriosus?

A

A small PDA can be asymptomatic, cause no functional problems and close spontaneously.
- Shortness of breath
- Difficulty feeding
- Poor weight gain
- Lower respiratory tract infections

327
Q

What investigations should be used for patent ductus arteriosus?

A

ECHO + doppler flow studies: can confirm diagnosis. Can assess the size and characteristics of the left to right shunt. May also show right ventricular hypertrophy.

328
Q

What is the management for patent ductus arteriosus?

A
  • Monitor with ECHO until 1 years of age:may close spontaneously
  • Indomethacin:NSAID that inhibits prostaglandin E2 so PDA can close
  • Trans-catheter closure of PDA
  • Surgical ligation of PDA
329
Q

What are some complications of patent ductus arteriosus?

A
  • Chronic heart failure
  • Eisenmengers syndrome
330
Q

What are some general clinical manifestations of shock?

A
  • Tachycardia
  • Tachypnoea
  • Pulse pressure is reduced → MAP may be maintained until a very large volume of blood is lost.
  • Skin is flushed → Warm shock
  • Skin is cold → Cold shock
  • Reduced urine output
  • Confusion
  • Collapse
  • Coma
  • Weakness
331
Q

What are the clinical manifestations for hypovolemic shock?

A
  • Cold and clammy skin
  • Confusion and drowsiness
  • Increased sympathetic tone
  • Tachycardia or bradycardia → depending on the stage.
  • Initially weak pulse pressure until compensation → weak pulse when compensation fails.
332
Q

What are the clinical manifestations for cardiogenic shock?

A

Signs of heart failure. Raised JVP, Pulmonary oedema.

333
Q

What are the clinical manifestations for septal shock?

A
  • Warm and flushed skin
  • Pyrexia and rigors
  • Nausea and vomiting
  • Bounding pulse
334
Q

What are the clinical manifestations for anaphylactic shock?

A
  • Warm and flushed skin
  • Itching
  • Sweating
  • May be breathlessness and wheeze
  • Hypotensive
  • Tachycardia
  • Pulmonary oedema
335
Q

What are the investigations for shock?

A
  • Assess using ABCDE.
  • Capillary refill time: takes more than 3 seconds to turn pink after 5 seconds of compression → easliest and most accurate sign of shock.
  • Investigate suspected underlying cause → CXR, Troponin, ECG.
336
Q

What is the management for shock?

A
  • Treatment depends on the cause.
  • ABC
    • Airway → Intubation of necessary.
    • Breathing → give O2.
    • Circulation → Establish IV access, raise legs if hypovolaemic, fluid resuscitation and blood transfusion if necessary, ensure haemostasis.
  • Medications that increase heart contractility, cause vasocontriction, and retail fluid.
  • Manage underlying causes:
    • Septic → Antibiotics
    • Anaphylactic chock → remove causative agent, give adrenaline, chlorphenamine and hydrocortisone.
    • Cardiogenic chock → Revascularisation
337
Q

What are some complications of shock?

A
  • Organ failure due to prolonger hypotension:
    • Kidney - Acute tubular necrosis.
    • Lungs - ARD’s.
    • Heart - Ischemia and MI.
    • Brain - Confusion, Irritability, Coma.
338
Q

Define Kawasaki disease?

A

Acute, febrile, self-limiting, systemic vasculitis of unknown origin. Mainly affects coronary arteries.

339
Q

What is the cause of Kawasaki disease?

A

There is no clear cause. May be related to infection, autoimmune reactions and genetics

340
Q

What are the clinical manifestations of Kawasaki disease?

A
  • Mnemonic - CRASH
    • C - Conjunctivitis
    • R - Rash - erythema and desquamation (skin peeling)
    • A - Adenopathy - enlarged lymph nodes
    • S - “Strawberry tongue”(red tongue with prominent papillae)
    • H - Hand and feet issues - swelling and rash
  • Other:
    • Persistent high fever > 5 days
341
Q

What are the investigations for Kawasaki disease?

A
  • Bloods
    • Anaemia
    • Increased WCC
    • Increased CRP
    • Increased ESR
    • Increased liver enzyme
    • Increased platelets
  • Urinalysis
    • Mononuclear white blood cells in urine without bacteria
  • Echocardiogram
    • Check for complications
  • Diagnostic Criteria
    • Patient’s must meet 4/5 of the CRASH signs
342
Q

What is the management for Kawasaki disease?

A

Aspirin and IV immunoglobulins
- Monitor due to aspirin administration in children

343
Q

What are some complications of Kawasaki disease?

A

Coronary artery aneurysms - leading to MI and ischaemia

Phase 2a Sheffield Medicine (10 decks)

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