Cardiolovascular Flashcards

(42 cards)

1
Q

Define aortic dissection.

A

Tear in the tunica intima of the aorta

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2
Q

What are the RFs for aortic dissection?

A
  • HTN
  • Smoking
  • Raised cholesterol
  • Pre-existing aortic disease or AV disease
  • FH of aortic disease
  • History of cardiac surgery, cigarette smoking, direct blunt chest trauma
  • IV drug use
  • Marfan’s syndrome. Ehlers-Danlos syndrome and familial thoracic aneurysm type 1 and 2
  • Congenital bicuspid valve
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3
Q

How do we classify aortic dissections?

A

The Stanford Classification in common use classifies the dissections into type A and type B:

  • Type A involves ascending aorta (DeBakey types I and II).
  • Type B does not involve the ascending aorta (DeBakey type III).

The DeBakey Classification classifies the dissections into:

  • Type I: originates in the ascending aorta, then aortic arch, and maybe descending aorta.
  • Type II: ascending aorta only.
  • Type III: descending aorta distal to left subclavian.
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4
Q

How do aortic dissections present? How should we investigate them?

A
  • Classical: tearing chest pain, radiates to the back, >20mmHg difference BP between arms
  • Weak distal pulses
  • Aortic regurgitation
  • Myocardial Ischaemia
  • Neurological complaints (i.e. hemiplegia, frontal headache, neck pain), incl. Horner’s syndrome

Investigations

  • Definitive:
    • Stable (most commonly) → CTA CAP
    • Unstable (cannot be taken to CT) → TOE/TTE
  • Organ hypoperfusion → FTs (liver), U&Es (renal), lactate (GIT)
  • ECG (ischaemia)
  • CXR (widened mediastinum)
  • FBC (haemoglobin)
  • X-match/G&S
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5
Q

How do we manage aortic dissections?

A
  • Type A (ascending) → surgery, IV beta blockade
  • Type B (descending) → bed rest, IV beta blockade

General

  • Intravenous access.
  • Adequate analgesia - eg, morphine.
  • Transfer to an intensive care unit or high dependency unit.
  • Hypertension must be managed aggressively in all cases to reduce further damage. The aim is a systolic pressure of between 100 and 120 mm Hg.
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6
Q

What are the clinical features of aortic stenosis?

A

Features of severe aortic stenosis

  • narrow pulse pressure
  • slow rising pulse
  • delayed ESM
  • soft/absent S2
  • S4
  • thrill
  • duration of murmur
  • left ventricular hypertrophy or failure
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7
Q

What are the causes of aortic stenosis?

A

Causes of aortic stenosis

  • degenerative calcification (most common cause in older patients > 65 years)
  • bicuspid aortic valve (most common cause in younger patients < 65 years)
  • William’s syndrome (supravalvular aortic stenosis)
  • post-rheumatic disease
  • subvalvular: HOCM
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8
Q

How do we investigate aortic stenosis?

A
  • ECG (LVH, arrhythmias)
  • Bloods (FBC, U&E, BNP, lipids, glucose)
  • CXR (calcified valves, LVH, pul. oedema)
  • Echo ± doppler (severity, cause, LV function); severe AS
    • Valve area <1cm2
    • Pressure gradient >40mmHg
    • Jet velocity >4m/s
  • Coronary angiography
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9
Q

How do we manage Aortic stenosis?

A
  • if asymptomatic then observe the patient is a general rule
  • if symptomatic then valve replacement
  • if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery
  • General Management
    • MDT (cardiologist, GP, specialist nurses, cardiothoracic surgeon, dietician, OT/physiotherapist)
    • RF modification (QRISK : statin, anti-platelet; manage HTN, angina, etc.)
    • Regular f/u
  • Valve replacement
    • Surgical AVR - usually for young patients
      • Artificial:
        • Starr-Edwards / ball-in-cage [3 artificial sounds]
          • Quiet click as valve opens
          • Rumbling as ball rolls in the cage
          • Loud thud as valve closes
        • Tilting disc / bileaflet [1 artificial sound]
          • High-pitched click as valve closes
      • Biological:
        • Biological valve [normal heart sounds]
    • Transcatheter AVR (TAVR) is used for patients with a high operative risk
    • Balloon valvuloplasty
      • may be used in children with no aortic valve calcification
      • in adults limited to patients with critical aortic stenosis who are not fit for valve replacement
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10
Q

How does aortic regurgitation present?

A

Features

  • early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre
  • collapsing pulse
  • wide pulse pressure
  • Quincke’s sign (nailbed pulsation)
  • De Musset’s sign (head bobbing)
  • mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
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11
Q

What causes aortic regurgitation?

A
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12
Q

How do we investigate Aortic regurgitation?

A
  • ECG (LVH, LV strain – lateral lead TWI)
  • Bloods (FBC, U&E, NT-proBNP, lipids, glucose, ESR, HLA-B27, ANA)
  • CXR (cardiomegaly, LVH, pul. oedema)
  • Echo ± doppler (severity, cause, LV function); severe AR
    • Jet width (>65% outflow tract)
    • Regurgitant jet volume
    • Premature closing of mitral valve
  • Coronary angiography
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13
Q

How should we manage aortic regurgitation

A
  • medical management of any associated heart failure
  • surgery: aortic valve indications include
    • symptomatic patients with severe AR
    • asymptomatic patients with severe AR who have LV systolic dysfunction
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14
Q

What is mitral stenosis? What are the consequences of it?

A

Mitral stenosis describes the obstruction of blood flow across the mitral valve from the left atrium to the left ventricle.

This leads to increases in pressure within the left atrium, pulmonary vasculature and right side of the heart.

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15
Q

What causes MS?

A

It is said that the causes of mitral stenosis are rheumatic fever, rheumatic fever and rheumatic fever.

Rarer causes that may be seen in the exam include mucopolysaccharidoses, carcinoid and endocardial fibroelastosis

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16
Q

How do patients with MS present?

A

Features

  • dyspnoea
    • ↑ left atrial pressure → pulmonary venous hypertension
  • haemoptysis
    • due to pulmonary pressures and vascular congestion
    • may range from pink frothy sputum to sudden haemorrhage secondary to rupture of thin walled and dilated bronchial veins
  • mid-late diastolic murmur (best heard in expiration)
  • loud S1, opening snap
  • low volume pulse
  • malar flush
  • atrial fibrillation
    • secondary to ↑ left atrial pressure → left atrial enlargement

Features of severe MS

  • length of murmur increases
  • opening snap becomes closer to S2
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17
Q

What are examples of evidence of Pulmonary hypertension?

A
  • Malar flush
  • ­ JVP with large V-waves
  • Right ventricular heave
  • Loud S2 (P2)
18
Q

How do we investigate MS?

A
  • ECG (P-mitrale, AF)
  • Bloods (FBC, U&E, NT-proBNP, lipids, glucose)
  • CXR (LA hypertrophy (splaying of carina), calcified mitral valve, pul. oedema)
  • Echo ± doppler (severity, cusp calcification, LV function, ? TOE); severe MS
    • Valve orifice <1cm2
    • Pressure gradient >10mmHg
    • Pul. artery SBP >50mmHg
  • Coronary angiography
19
Q

How do we manage MS?

A
  • patients with associated atrial fibrillation require anticoagulation
    • currently warfarin is still recommended
  • asymptomatic patients
    • monitored with regular echocardiograms
    • percutaneous/surgical management is generally not recommended
  • symptomatic patients
    • percutaneous mitral balloon valvotomy
    • mitral valve surgery (commissurotomy, or valve replacement)
20
Q
A

This patient has had a sternotomy and a prosthetic mitral valve. There is splaying of the carina with elevation of the left main bronchus, a double right heart border and cardiomegaly. The features are those of left atrial enlargement. Although the entire heart is enlarged, a double contour is seen through the right side of the heart. The more medial line is the enlarged left atrium (white dotted line) and the heart heart border is more lateral (blue dotted line).

21
Q

What is Mitral regurgitation?

A

Also known as mitral insufficiency, mitral regurgitation (MR) occurs when blood leaks back through the mitral valve on systole

22
Q

How does MR present and progress?

A

MR is common in otherwise healthy patients to a trivial degree and does not need treatment.

As the degree of regurgitation becomes more severe, the body’s oxygen demands may exceed what the heart can supply and as a result, the myocardium can thicken over time. While this may be benign initially, patients may find themselves increasingly fatigued as a thicker myometrium becomes less efficient, and eventually go into irreversible heart failure.

Symptoms

  • Most patients with MR are asymptomatic, and patients suffering from mild to moderate MR may stay largely asymptomatic indefinitely. Symptoms tend to be due to failure of the left ventricle, arrhythmias or pulmonary hypertension. This may present as fatigue, shortness of breath and oedema.

Signs

  • The murmur heard on auscultation of the chest is typically a pansystolic murmur described as “blowing”. It is heard best at the apex and radiating into the axilla. S1 may be quiet as a result of incomplete closure of the valve. Severe MR may cause a widely split S2
23
Q

What are the RFs for MR?

A
  • Female sex
  • Lower body mass
  • Age
  • Renal dysfunction
  • Prior myocardial infarction
  • Prior mitral stenosis or valve prolapse
  • Collagen disorders e.g. Marfan’s Syndrome and Ehlers-Danlos syndrome
24
Q

What are the causes of MR?

A
  • Following coronary artery disease or post-MI: if the papillary muscles or chordae tendinae are affected by a cardiac insult, mitral valve disease may ensue as a result of damage to its supporting structures.
  • Mitral valve prolapse: Occurs when the leaflets of the mitral valve is deformed so the valve does not close properly and allows for backflow. Most patients with this have a trivial degree of mitral regurgitation.
  • Infective endocarditis: When vegetations from the organisms colonising the heart grow on the mitral valve, it is prevented from closing properly. Patients with abnormal valves are more likely to develop endocarditis as opposed to their peers.
  • Rheumatic fever: While this is uncommon in developed countries, rheumatic fever can cause inflammation of the valves and therefore result in mitral regurgitation.
  • Congenital
25
What are the investigations of MR?
* ECG (P-mitrale, AF, LVH) * Bloods (FBC, U&E, NT-proBNP, lipids, glucose) * CXR (LA/LV hypertrophy, calcified mitral valve, pul. oedema) * Echo ± doppler (severity, cusp calcification, LV function); **severe MR**… * Jet width \>0.6cm * Systolic pul. flow reversal * Regurgitant volume \>60mL * Coronary angiography
26
What is the initial management of patients with ACS?
Initial drug therapy * aspirin 300mg * oxygen should only be given if the patient has oxygen saturations \< 94% in keeping with British Thoracic Society oxygen therapy guidelines * morphine should only be given for patients with severe pain * previously IV morphine was given routinely * evidence, however, suggests that this may be associated with adverse outcomes * nitrates * can be given either sublingually or intravenously * useful if the patient has ongoing chest pain or hypertension * should be used in caution if patient hypotensive
27
Describe the STEMI criteria.
* clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (\> 20 minutes) ECG features in ≥ 2 contiguous leads of: * 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years * 1.5 mm ST elevation in V2-3 in women * 1 mm ST elevation in other leads * new LBBB (LBBB should be considered new unless there is evidence otherwise)
28
What is the immediate management for a STEMI?
There are two types of coronary reperfusion therapy: * percutaneous coronary intervention * should be offered if the presentation is within 12 hours of the onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI) * if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered * drug-eluting stents are now used. Previously 'bare-metal' stents were sometimes used but have higher rates of restenosis * radial access is preferred to femoral access * fibrinolysis e.g. altepase * should be offered within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given * a practical example may be a patient who presents with a STEMI to a small district general hospital (DGH) that does not have facilities for PCI. If they cannot be transferred to a larger hospital for PCI within 120 minutes then fibrinolysis should be given. If the patient's ECG taken 90 minutes after fibrinolysis failed to show resolution of the ST elevation then they would then require transfer for PCI
29
What drug therapy is given before and during the PCI?
Further antiplatelet prior to PCI * this is termed 'dual antiplatelet therapy', i.e. aspirin + another drug * if the patient is not taking an oral anticoagulant: prasugrel * if taking an oral anticoagulant: clopidogrel Drug therapy during PCI * patients undergoing PCI with radial access: * unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus * patients undergoing PCI with femoral access: * bivalirudin with bailout GPI
30
What other procedure can be done during PCI?
Other procedures during PCI * thrombus aspiration, but not mechanical thrombus extraction, should be considered * complete revascularisation should be considered for patients with multivessel coronary artery disease without cardiogenic shock
31
If giving fibrinolysis what should be done?
Patients undergoing fibrinolysis should also be given an antithrombin drug. An ECG should be repeated after 60-90 minutes to see if the ECG changes have resolved. If patients have persistent myocardial ischaemia following fibrinolysis then PCI should be considered
32
What is the management on an NSTEMI?
Further drug therapy * antithrombin treatment * fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography immediately * if immediate angiography is planned or a patients creatinine is \> 265 µmol/L then unfractionated heparin should be given
33
How do we risk assess (6-month mortality) in an NSTEMI?
GRACE Score The Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment. It can be calculated using online tools and takes into account the following factors: * age * heart rate, blood pressure * cardiac (Killip class) and renal function (serum creatinine) * cardiac arrest on presentation * ECG findings * troponin levels
34
How do we use the GRACE score?
Based on this risk assessment key decisions are made regarding whether a patient has coronary angiography (with follow-on PCI if necessary) or has conservative management. * immediate: patient who are clinically unstable (e.g. hypotensive) * within 72 hours: patients with a GRACE score \> 3% i.e. those at intermediate, high or highest risk * coronary angiography should also be considered for patients if ischaemia is subsequently experienced after admission
35
What further drug therapy is needed after a PCI for an NSTEMI/unstable angina?
Further drug therapy * unfractionated heparin should be given regardless of whether the patient has had fondaparinux or not * further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug) prior to PCI * if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor * if taking an oral anticoagulant: clopidogrel
36
What is the immediate management for a STEMI?
There are two types of coronary reperfusion therapy: * percutaneous coronary intervention * should be offered if the presentation is within 12 hours of the onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI) * if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered * drug-eluting stents are now used. Previously 'bare-metal' stents were sometimes used but have higher rates of restenosis * radial access is preferred to femoral access * fibrinolysis e.g. altepase * should be offered within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given * a practical example may be a patient who presents with a STEMI to a small district general hospital (DGH) that does not have facilities for PCI. If they cannot be transferred to a larger hospital for PCI within 120 minutes then fibrinolysis should be given. If the patient's ECG taken 90 minutes after fibrinolysis failed to show resolution of the ST elevation then they would then require transfer for PCI
37
What does cardiac rehabilitation and secondary prevention of an MI involve?
38
What are the stages of hypertension?
39
How should BP be measured? How should stages be decided? Who should be managed?
* *Consider antihypertensive drug treatment in addition to lifestyle advice for adults aged under 60 with stage 1 hypertension and an estimated 10-year risk below 10%.* * For patients \< 40 years consider specialist referral to exclude secondary causes.
40
What are the lifestyle interventions for HTN?
* a low salt diet is recommended, aiming for less than 6g/day, ideally 3g/day. * caffeine intake should be reduced * the other general bits of advice remain: stop smoking, drink less alcohol, eat a balanced diet rich in fruit and vegetables, exercise more, lose weight
41
What are the treatment options for HTN?
* angiotensin receptor blockers should be used where ACE inhibitors are not tolerated (e.g. due to a cough) * for patients of black African or African–Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an angiotensin receptor blocker in preference to an ACE inhibitor *
42
What are the BP Targets?