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Cardiovascular Flashcards

1
Q

What are the symptoms of an aortic dissection?

A
  • Chest pain- sudden, tearing, severe, anterior or interscapular
  • Dizziness
  • SOB
  • Sweating
  • Neuro deficit
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2
Q

What are the signs of an aortic dissection?

A

Unequal radial pulses

Tachycardia

Hypo/hypertension

Difference in BP between arms >15mmHg

Aortic regurgitation

Pleural effusion

Neurological deficit if carotid artery dissection

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3
Q

What urgent investigation would you do for a suspected aortic dissection?

A

Urgent CT aorta

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4
Q

What might a CXR show in aortic dissection?

A

Widened mediastinum >8cm (rare)

Irregular aortic knuckle

Small left pleural effusion

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5
Q

What is the acute treatment of aortic dissection?

A

Senior help

If HYPOtensive - oxygen, 2x large bore cannulae, Xmatch, IV opioids

If HYPERtensive - keep systolic BP <100mmHg

BOTH - Surgery (Type A, involving ascending aorta) or conservative management (Type B, involving descending aorta only)

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6
Q

What are the risk factors for an aortic dissection?

A

Smoking, obesity, diabetes, HTN, high cholesterol, family hx, previous IHD

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7
Q

What is the definition of an aneurysm?

A

A permanent and irreversible dilatation of a blood vessel by at least 50% of the normal diameter

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8
Q

What are the 2 types of aortic aneurysm and which is most common?

A

Abdominal and thoracic

Abdominal most common

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9
Q

What is the normal diameter of the abdominal aorta and what diameter would be classed as a AAA?

A

Normal= 2cm

AAA= 3cm +

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10
Q

Where do most AAA’s arise from?

A

Below the level of the renal arteries

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11
Q

What are the symptoms/signs of an unruptured AAA?

A
  • Most are asymptomatic
  • Back/loin/groin pain
  • Pulsatile swelling on examination
  • Distal embolisation- gives features of limb ischaemia but with easily palpable pulses
  • Uterohydronephrosis
  • Severe recent onset lumbar pain may indicate impending rupture!
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12
Q

What is the monitoring requirement for AAAs? At what diameter would surgery be recommended?

A

3-4.4cm annual US

  1. 5-5.4cm 3 monthly US
  2. 5cm or bigger consider surgery
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13
Q

What are the surgical options for AAA repair?

A

Open surgery

Endovascular repair: stent-graft introduced through femoral arteries

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14
Q

What is the NHS screening for AAA and when/to whom is it offered?

A

One US offered to men aged 65- if negative, rules out AAA for life

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15
Q

What are the symptoms of pericarditis?

A

Pleuritic chest pain, worse on lying flat/deep inspiration, better when sat forwards Fever

Recent viral illness

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16
Q

What signs may be found in pericarditis

A

None, or pericardial rub

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17
Q

What would a saddle shaped ST segment on ECG suggest?

A

Pericarditis

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18
Q

What investigations would you do for suspected pericarditis and what would they show?

A

Bedside- temp

Bloods- Raised WCC and CRP, troponin

ECHO- bright pericardium +/- pericardial effusion

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19
Q

What is the management of acute pericarditis?

A

Reassurance

Paracemtaol/NSAIDs

If continues >14d, use colchicine/steroids

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20
Q

What is constrictive pericarditis?

A

Chronic inflammation of the pericardium resulting in a thickened, scarred pericardium which impairs heart function

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21
Q

What are the signs/symptoms of constrictive pericarditis?

A

Similar to R heart failure- SOB, peripheral oedema, raised JVP with Kussmaul’s sign

Pulsatile hepatomegaly (70%)

Pericardial knock

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22
Q

What investigation would distinguish constrictive pericarditis from restrictive cardiomyopathy?

A

ECHO

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23
Q

What is the management of constrictive pericarditis?

A

Treat cause

Anti-inflammatories

Pericardiectomy

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24
Q

What are the causes of cardiac tamponade?

A

Pericarditis, aortic dissection, haemodialysis, warfarin, trans-septal puncture during cardiac catheterisation, post cardiac biopsy

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25
Q

What are the signs of cardiac tamponade?

A

Tachycardia

Hypotension

Pulsus paradoxus

Raised JVP

Kussmaul’s sign

Muffed S1/2

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26
Q

What investigations would you do for cardiac tamponade? What would they show?

A

CXR: large globular heart

ECG: low voltage QRS +/- electrical alternates

ECHO is DIAGNOSTIC: echo-free zone around heart +/- diastolic collapse of right atrium and ventricle

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27
Q

What is the management of cardiac tamponade?

A

Urgent drainage of pericardial effusion

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28
Q

What is cardiac tamponade? What is its pathogenesis?

A

Accumulation of pericardial fluid, resulting in increased intrapericardial pressure causing poor ventricular filling and reduced cardiac output

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29
Q

What are the clinical features of pericardial effusion?

A

SOB

Raised JVP (with prominent x descent)

Bronchial breathing at left base

Signs of cardiac tamponade

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30
Q

What is the management of pericardial effusion?

A

Treat cause

Pericardiocentesis (diagnostic/therapeutic)

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31
Q

What would CXR, ECG and ECHO show in pericardial effusion?

A

CXR: enlarged globular heart

ECG: low voltage QRS and electrical alternans

ECHO: echo-free zone around heart

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32
Q

What is the target BP for those without diabetes age >80 and <80?

A

<80 = <140/90

>80 = <150/90

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33
Q

What rise in creatinine/decrease in eGFR is acceptable when on an ACEi?

A

eGFR decrease up to 25%

or

Creatinine rise up to 30%

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34
Q

What 4 things could cause hypertension with low potassium?

A

Conn’s

Cushing’s

Renal artery stenosis

Liddle’s

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35
Q

What is the first line treatment for HTN in a diabetic?

A

ACEi

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36
Q

What is the treatment for resistant hypertension if further diuretics are not tolerated, contraindicated or ineffective?

A

Consider alpha blocker or beta blocker

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37
Q

What should an adult <80yrs with stage 1 HTN, no end organ damage and a QRisk >10% but <20% be treated with?

A

Lifestyle advice PLUS a statin

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38
Q

Antihypertensive drug treatment should be offered to those <80yrs with stage 1 HTN if they have 1 or more of???

A

Target organ damage

Established CV disease

Renal disease

Diabetes

10yr CV risk >20%

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39
Q

If HTN is uncontrolled on ACEi, Ca channel blocker and thiazide diuretic what is the next step?

A

If K+ <4.5 = spiro

If K+ >4.5 = increase dose of thiazide

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40
Q

What are the sx/signs of idiopathic intracranial HTN?

A

Headache

Blurred vision

Papilloedema

Enlarged blind spot

+/- 6th nerve palsy

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41
Q

What are the risk factors for idiopathic intracranial HTN?

A

Obesity

Female

Pregnant

Drugs: COCP, steroid, vit A, lithium, tetracycline

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42
Q

What is the management of idiopathic intracranial HTN?

A

Weight loss

Diuretics e.g. acetazolamide

Topiramate

Repeated LPs

Surgery

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43
Q

What is aleading cause of sudden cardiac death in young athletes?

A

Hypertrophic obstructive cardiomyopathy

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44
Q

What would an ECHO show in hypertrophic obstrcutive cardiomyopathy?

A

Mitral regurg

Systolic anterior motion of anterior mitral valve

Asymmetric septal hypertrophy

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45
Q

What is the inheritance of HOCM?

A

Autosomal dominant

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46
Q

What are the causes of dilated cardiomyopathy?

A

Alcohol

Coxsackie B virus

Doxorubicin

Wet beriberi

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47
Q

What are the causes of restrictive cardiomyopathy?

A

Amyloidosis

Post-radiotherapy

Loeffler’s endocarditis

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48
Q

What is the name for stress-induced cardiomyopathy?

A

Takotsubo

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49
Q

What is the management of Takosubto cardiomyopathy?

A

Supportive

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50
Q

What do new widening QRS complexes and an RSR pattern in v1 suggest?

A

RBBB

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51
Q

What would widened QRS complexes and a notched morphology of the QRS complexes in the lateral leads suggest?

A

LBBB

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52
Q

What are the risk factors for mitral regurg?

A

Female

Low BMI

Prior MI/mitral stenosis/valv prolapse

Collagen disorders e.g. Marfans, Ehlers-Danlos

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53
Q

What wpuld a pan-systolic blowing murmur heard best at the apex, radiating to the axilla suggest?

A

Mitral regurgitation

54
Q

Secondary causes of HTN

A
  • Renal disease
  • Primary hyperaldosteronism
  • Phaeochromocytoma
  • Cushing’s
  • Acromegaly
  • Hyper/hypothyroidism
  • Alcohol
  • Connective tissue disorders
  • OSA
  • Coarctation of aorta
  • Renal artery stenosis
55
Q

Annual review for HTN

A
  • Check blood pressure
  • Check renal function by measuring creatinine, electrolytes and EGFR
  • Dip urine to check for proteinuria
  • Q risk
56
Q

What is accelerated hypertension?

A

Blood pressure >180/110 mmHg with signs of papilloedema and/or retinal haemorrhage

57
Q

Complications of hypertension

A
  • Heart Failure
  • Coronary artery disease
  • Stroke
  • Chronic kidney disease
  • Peripheral arterial disease
  • Vascular dementia
58
Q

Symptoms of postural hypotension

A

Dizziness

Lightheaded

Blurred vision

Weakness

Fatigue

Nausea

Palpitations

Headache

Less common; syncope, dyspnoea, chest pain, neck/shoulder pain

59
Q

Positive tilt table test

A

Systolic BP falls below 20mmHg and diastolic BP below 10mmHg of baseline

60
Q

What is the tilt table test for orthostatic hypotension

A

Tilt testing to an angle between 60 and 80° for three minutes

61
Q

First line drug for orthostatic hypotension

A

Fludrocortisone

62
Q

Symptoms of hypotensive shock

A
  • Feeling cold, unwell, anxious, faint, short of breath
  • Fainting
  • Patient may look pale and sweaty
  • Tachypnoea
  • Tachycardia
  • Fall in blood pressure
  • Late features include confusion, coma
63
Q

Causes of hypovolaemic shock

A
  • Loss of blood
  • Trauma
  • Burns
  • Severe loss of water and salt from heat, poor intake, diarrhoea and vomiting, inappropriate diuresis
64
Q

Investigations for hypovolaemic shock

A

Bedside – monitor urine output with catheter, may need CVP monitoring

Bloods – Hb, U&Es, LFTs, group and save, crossmatch, coagulation screen, blood gas

Imaging- ultrasound vena cava to distinguish hypovolaemic vs cardiogenic shock

65
Q

Stages of loss of blood volume

A

Class 1: 10-15% blood loss; physiological compensation

Class 2: 15-30% blood loss; postural hypotension, generalised vasoconstriction, reduction in UO to 20 to 30ml/hour

Class 3: 30-40% blood loss; hypotension, tachycardia, tachypnoea, UO under 20ml/hour, patient confused

Class 4: 40% blood loss; marked hypotension, tachycardia and tachypnoea, no UO, patient comatose

66
Q

Management of hypovolaemic shock

A

Oxygen

Venous access

Crystalloid e.g. Hartmann’s, normal saline (or blood if haemorrhage)

IV analgesia if pain

Surgery if bleeding

67
Q

Complications of hypovolaemic shock

A

AKI

Gut ischaemia

Hypoxia

Metabolic acidosis

Cardiac arrhythmias/arrest

Haemoconcentration- smudging and venous sinus thrombosis

68
Q

Virchow’s triad of risk factors for thrombophlebitis

A

Damage to vessel wall (due to infection, inflammation or trauma)

Stasis of blood flow

Hypercoagulability of blood

69
Q

Risk factors for thrombophlebitis

A
  • Obesity
  • Thrombophilia
  • Smoking
  • Oral contraceptives
  • Pregnancy
  • IVDU
  • IV infusion
70
Q

Signs of thrombophlebitis

A

Painful, hard lump, often with surrounding erythema

71
Q

Management of superficial phlebitis

A

Topical anti-inflammatory

Resolves spontaneously in 10-14 days

72
Q

Mitral stenosis murmur

A

Mid diastolic murmur heard best with patient leaning to left side

73
Q

Causes of mitral stenosis

A

Rheumatic fever

Degenerative calcification

Congenital

SLE

RA

Carcinoid

Infective endocarditis

Amyloid deposition

74
Q

Signs associated with mitral stenosis

A

Malar flush

Raised JVP

Laterally displaced apex beat

RV heave

Loud SI with opening snap in early diastole

A mid-late diastolic murmur, heard best with patient in left lateral position, with the bell of the stethoscope

AF

Signs of RV failure including hepatomegaly, ascites and peripheral oedema

75
Q

What does this ECG show?

A

LBBB

76
Q

ECG features in RBBB

A

QRS duration >120ms

An “M-shaped” QRS complex in V1 (rSR pattern)

Wide, slurred S wave in lateral leads (aVL, V5-6)

77
Q

ECG features in LBBB

A

QRS duration >120ms

Broad R wave in I, aVL and V6

Lack of septal Q waves in I and V6

78
Q

Causes of RBBB

A

Normal variant- more common with increasing age

RVH

Cor pulmonale

PE

MI

Atrial septal defect

Cardiomyopathy

Myocarditis

79
Q

Causes of LBBB

A

Acute anterior MI

Coronary artery disease

LVH

Heart failure

Idiopathic

Hyperkalaemia

Digoxin toxicity

80
Q

ECG findings in atrial flutter

A
  • ‘sawtooth’ appearance
  • as the underlying atrial rate is often around 300/min the ventricular or heart rate is dependent on the degree of AV block. For example if there is 2:1 block the ventricular rate will be 150/min
  • flutter waves may be visible following carotid sinus massage or adenosine
81
Q

Clinical features of complete heart block

A
  • syncope
  • heart failure
  • regular bradycardia (30-50 bpm)
  • wide pulse pressure
  • JVP: cannon waves in neck
  • variable intensity of S1
82
Q

Describe atrial flutter and its pathophysiology

A

Due to re-entry circuit in the atrium

Atria contract at 300-400bpm

Refractory period of AV node means not every P is conducted

The result is that there are several P waves and then a QRS which is conducted regularly e.g. 3 P waves then a QRS complex is 3:1

83
Q

Describe the ECG features of atrial fibrillation and its pathophysiology

A

Supraventricular tachycardia

Indiscernable P waves

Irregularly irregular pulse

Narrow irregular QRS complex

Due to uncoordinated atrial activation resulting in an irregular ventricular response

84
Q

Management of atrial fibrillation

A

1st line treatment is rate-control with beta blocker or rate-limiting calcium channel blocker

Assess stroke risk with CHA2DS2VASc score

If 2 or more (F) or 1 ore more (M) need anticoagulation

Assess risk of major bleed using HAS-BLED tool

Anticoagulants: apixaban, dabigatran, rivaroxaban, Vit K antagonist (e.g. warfarin)

85
Q

Risks associated with AF and atrial flutter

A

Ineffective contraction of atria results in stasis of blood and promotes clot formation, increasing the risk of stroke and other thromboembolic complications

86
Q

Acute and long term management of atrial flutter

A

Acute:

Rate control with beta blocker or Ca channel blocker

DC cardioversion for immediate restoration of sinus rhythm- if patient is hypotensive, or 1:1 AV conduction

Elective restoration of sinus rhythm: antiarrythmic drug, DC cardioversion or rapoid atrial pacing

Long term:

Anticoagulation to prevent clots

Catheter ablation usually curative

87
Q

Pathophysiology of ectopic beats (ventricular ectopics/premature beats)

A
  • Ectopic firing of a focus within the ventricles bypasses the His-Purkinje system and depolarises the ventricles directly.
  • This disrupts the normal sequence of cardiac activation, leading to asynchronous activation of the two ventricles.
  • The consequent interventricular conduction delay produces QRS complexes with prolonged duration and abnormal morphology.
88
Q

ECG features of premature ventricular ectopics

A
  • Broad QRS complex (≥ 120 ms) with abnormal morphology.
  • Premature — i.e. occurs earlier than would be expected for the next sinus impulse.
  • Discordant ST segment and T wave changes.
  • Usually followed by a full compensatory pause.
  • Retrograde capture of the atria may or may not occur.
89
Q

What is cardiogenic shock?

A

Occurs when there is failure of the pump action of the heart, resulting in a decrease in cardiac output causing reduced end-organ perfusion. This leads to acute hypoperfusion and hypoxia of the tissues and organs, despite the presence of an adequate intravascular volume.

Defined as:

  • Sustained hypotension (systolic blood pressure (BP) <90 mm Hg for more than 30 minutes)
  • Tissue hypoperfusion (cold peripheries, or oliguria <30 ml/hour, or both)

(Despite adequate LV filling pressure)

90
Q

Most common cause of cardiogenic shock

A

MI

91
Q

Symptoms of varicose veins

A

aching legs

discomfort or itching over the veins

swollen feet and ankles

92
Q

Management of varicose veins

A

Weight loss, light activity

93
Q

Most common cause of infective endocarditis

A

Staph aureus

94
Q

Valves most commonly affected by infective endocarditis

A

Mitral

Aortic

Mitral + aortic

Tricuspid

Pulmonary (rare)

95
Q

Signs and symptoms of infective endocarditis

A

Signs:

  • Heart murmur (may be new)
  • Splinter haemorrhages
  • Osler’s nodes (small tender red-purple nodules on terminal phalanges)
  • Janeway’s lesions (irregular painless erythematous macules on thenar and hypothenar eminence)
  • Roth’s spots (retinal haemorrhages with pale centres)
  • Cerebrovascular accident
  • Arthritis
  • Splenomegaly (long standing disease)
  • Meningism

Symptoms:

  • Infection e.g. fatigue, fever, flu-like symptoms, pain, anorexia, weight loss
  • May present as an acute rapidly progressive infection
96
Q

Risk factors for infective endocarditis

A

Valvular heart disease

Valve replacement

Structural congenital heart disease

Previous infective endocarditis

Hypertrophic cardiomyopathy

Drug abuse

Invasive vascular procedures

97
Q

Investigations for endocarditis

A

Bloods- CRP, FBC

Blood cultures

CXR

ECG

ECHO (TTE is initial investigation of choice)

98
Q

Diagnostic criteria for infective endocarditis

A

2 major or 1 major + 3 minor or 5 minor criteria

Major criteria:

  • Positive blood cultures
  • Evidence of endocardial involvement (e.g. positive ECHO)

Minor criteria:

  • Predisposition: predisposing heart condition or intravenous drug use.
  • Fever: temperature >38°C.
  • Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhages and Janeway’s lesions.
  • Immunological phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots and rheumatoid factor.
  • Microbiological phenomena: positive blood culture but does not meet a major criterion as noted above or serological evidence of active infection with organism consistent with IE.
  • PCR: broad-range PCR of 16S (polymerase chain reaction using broad-range primers targeting the bacterial DNA that codes for the 16S ribosomal subunit).
  • Echocardiographic findings consistent with IE but do not meet a major criterion as noted above.
99
Q

Management of infective endocarditis

A

Empirical antibiotics whilst awaiting cultures:

native valve, indolent presentation- amoxicillin

native valve and sepsis- vancomycin AND gentamicin

prosthetic valve- vancomycin + gentamicin + rifampicin

Staphylococcal endocarditis- flucloxacillin IV 4 weeks

Streptococcal- benzylpenicillin or ceftriaxone

Surgery if heart failure or inadequate response to antibiotic treatment

100
Q

Management of MI (long-term)

A

Lifestyle advice:

  • Stop smoking
  • Cardioprotective diet (salt <6g/d, minimise refined sugars, wholegrain, 4-5 30g portions nuts/seeds per week, fish 2x per week, 5 a day, olive oil, reduce fat and sat fat)
  • Regular exercise- ideally 150mins per week of moderate intensity aerobic activity and muscle strength on 2 or more days per week
  • Weight loss if overweight
  • <14 units alcohol per week
  • Cardiac rehabilitation programme
  • Annual influenza vaccine

Medication:

  • ACEi
  • Dual antiplatelet therapy (aspirin + clopidogrel or ticagrelor)
  • Beta-blocker
  • Statin

Source: https://cks.nice.org.uk/mi-secondary-prevention#!scenario

101
Q

Management of acute myocardial infarction

A

Morphine 10mg IV (+metoclopramide IV)

Oxygen (to keep O2 sats >94%)

Nitrates

  • sublingual GTN (2 sprays) if not hypertensive, then prn
  • IV GTN/IV isosorbide dinitrate

Aspirin 300mg loading then 75mg OD lifelong

Clopidogrel 300mg loading then 75mg for 12 months OD/Ticagrelor/Prasugrel*

+ LMWH or fondaparinux

+ beta blockers (if no contra-indications)

+ statin

If STEMI- refer for PCI or thrombolysis (if PCI not possible within 90mins, give thrombolysis plus LMWH/fondaparinux)

102
Q

Investigations for ACS

A
  • 12 lead ECG (then continuous cardiac monitoring)
  • Bloods: usual bloods (FBC, U&Es, LFTs, CRP, glucose) plus cardiac enzymes (STAT and again at 10-12 hours post- pain onset), magnesium, phosphate, lipid profile
  • Chest X-ray (LVF signs?)
103
Q

Symptoms suggestive of ACS

A

Pain in chest (or arms/back/jaw) lasting >15mins

Associated with nausea & vomiting, sweating, or breathlessness

Associated with haemodynamic instability

Pain is new-onset, or an abrupt deterioration of stable angina

104
Q

ECG features indicative of ischaemia/previous MI

A

Pathological Q waves

LBBB

ST-segment and T-wave abnormalities

*a normal ECG does not confirm or exclude a diagnosis of ACS*

105
Q

When is serum troponin normally detectable after a myocardial infarction?

A

Within 3-6 hours

106
Q

What is the definition of angina?

A

Chest pain (or constricting discomfort) caused by an insufficienct blood supply to the heart muscle

107
Q

The 3 types of angina and their definitions

A

Stable- occurs with exertion or stress, relieved within minutes of rest or with GTN spray.

Unstable- new onset angina, or abrupt deterioration in stable angina, often occuring at rest. Requires immediate admission.

Prinzmetal’s variant (aka coronary artery vasospasm)- rare angina due to narrowing/occlusion of proximal coronary arteries due to spasm. Occurs at rest, not during exercise. Tends to occur at the same time each day, most often during the night and early morning.

108
Q

Management of stable angina

A

Lifestyle advice:

  • Stop smoking
  • Weight loss
  • Exercise
  • Limit alcohol

Medication:

  • Sublingual GTN
  • Beta-blocker or calcium-channel blocker 1st line
  • 2nd line= isosorbide mononitrate, nicorandil, ivabradine or ranolazine
  • Secondary prevention of CV events:
    • Consider antiplatelet therapy (aspirin 75mg OD)
    • Statin
    • ACEi if co-existing HTN, heart failure, CKD or previous MI. Consider ACEi if diabetic
    • Anti-hypertensive treatment if required as per NICE guidelines
109
Q

In which type of angina are beta blockers contra-indicated? What is the alternative?

A

Prinzmetal’s angina

use rate-limiting calcium-channel blocker e.g. verapamil or diltiazem

110
Q

Causes of cardiac failure

A

Myocardial disease e.g. CAD, HTN, cardiomyopathies

Valvular heart disease e.g. aortic stenosis

Pericarditis/pericardial effusion

Congenital heart disease

Arrythmias e.g. AF/other tachyarrythmias

High output states e.g. anaemia, thyrotoxicosis, phaeochromocytoma, sepsis, liver failure, AV shunts, Paget’s disease, thiamine deficiency

Volume overload

Obesity

Drugs incl. alcohol, cocaine, NSAIDs, beta blockers, calcium channel blockers

111
Q

New York Heart Association classification of heart failure

(4 classes)

A

Class I- no limitation of physical activity

Class II- Slight limitation (ordinary activity results in breathlessness/fatigue/palpitations)

Class III- Marked limitation (less than ordinary physical activity results in breathlessness/fatigue/palpitations)

Class IV- unable to carry out any activity without discomfort. Symptoms at rest may be present.

112
Q

Complications of chronic heart failure

A

Arrythmias (AF most common)

Depression

Cachexia

CKD

Sexual dysfunction

Sudden cardiac death

113
Q

Typical symptoms of heart failure

A
  • Breathlessness — on exertion, at rest, on lying flat (orthopnoea), nocturnal cough, or waking from sleep (paroxysmal nocturnal dyspnoea).
  • Fluid retention (ankle swelling, bloated feeling, abdominal swelling, or weight gain).
  • Fatigue, decreased exercise tolerance, or increased recovery time after exercise.
  • Light headedness or history of syncope.
114
Q

Clinical features of chronic heart failure

A

Tachycardia, abnormal rhythm

Laterally displaced apex beat, murmur, and 3rd/4th HS (gallop rhythym)

HTN

Raised JVP

Enlarged liver (due to engorgement)

Dependent oedema/ascites

115
Q

Management of confirmed heart failure with reduced ejection fraction

A

Stop drugs which may cause/worsen heart failure

Loop diuretic e.g. bumetanide, furosemide, torasemide (to relieve sx of fluid overload)

Prescribe an ACEi and beta-blocker e.g. bisoprolol, carvedilol, nebivolol (but start one at a time)

  • Consider antiplatelet if artherosclerotic disease*
  • Consider statin if indicated*

Manage causes/comorbidites/precipating factors

Annual inflenza vaccine and once-only pneumococcal vaccines

Screen for depression and anxiety

Supervised exercise-based group rehab programme

116
Q

Management of heart failure with preserved ejection fraction

A

Stop drugs which may cause/worsen heart failure

Loop diuretic- up to 80mg furosemide or equivalent (to relieve sx of fluid overload)

Consider antiplatelet if artherosclerotic disease

Consider statin if indicated

Manage causes/comorbidites/precipating factors

Annual influenza vaccine and once-only pneumococcal vaccine

Screen for depression and anxiety

Supervised exercise-based group rehab programme

117
Q

Investigations for suspected chronic heart failure

A

Admit if severe symptoms/pregnant

If previous MI, refer urgently (seen within 2wks)

If has not had previous MI, measure BNP or NT-pro-BNP:

BNP >400pg/mL refer for ECHO + specialist assessment within 2 weeks
BNP 100-400 refer within 6 weeks
BNP <100

12-lead ECG

Consider tests for other conditions/aggravating factorse e.g. CXR, bloods (U&Es, eGFR, FBC, TFTs, LFTs, HbA1c, fasting lipids), urine dip (blood and protein), lung function tests

118
Q

Investigations for new suspected acute heart failure

A

BNP

If BNP raised, do TTE

119
Q

Treatment of acute heart failure

A

Initial treatment:
Pharmacological:

  • IV diuretics (if already on diuretic then increase dose)

​Non-pharmacological:

  • Consider NIV if cardiogenic pulmonary oedema and severe dyspnoea and acidaemia
  • Consider invasive ventilation if heart failure is (despite treatment) leading to respiratory failure, decreased consciousness or physical exhaustion

After stabilisation:

  • Beta blocker if acute heart failure due to left ventricular systolic dysfunction, once IV diuretics are no longer needed
  • ACEi and an aldosterone antagonist if acute heart failure and reduced ejection fraction

Long-term management:

  • As per chronic heart failure
  • Surgical aortic valve replacement if heart failure due to severe aortic stenosis (or transcatheter aortic valve implantation if unfit for surgery)
120
Q

Causes of acute heart failure/decompensation of chronic heart failure

A
  • Further/worsening ischaemia
  • Myocardial infarction
  • Additional valvular or diastolic dysfunction
  • Infections
  • Arrhythmias - commonly atrial fibrillation (AF).
  • Electrolyte imbalance
  • Worsening comorbidities - eg, anaemia, thyroid dysfunction, pulmonary disease, renal dysfunction, diabetes
  • New medications
121
Q

Ejection systolic murmur

Crescendo-decrescendo

Commonly heard in 2nd right intercostal space

A

Aortic stenosis

122
Q

Slow rising pulse is associated with which murmur?

A

Aortic stenosis

123
Q

Symptoms of aortic stenosis

A

May be asymptomatic

SOBOE

Dizziness

Chest pain/angina

Syncope

Swollen ankles

124
Q

Diagnostic investigation for aortic stenosis

A

ECHO

125
Q

Managament of aortic stenosis

A

Avoid heavy exertion

Modify atherosclerotic risk factors

Treat HTN

Maintain sinus rhythm

Surgery or transcatheter aortic valve implantation if symptomatic

126
Q

Early diastolic murmur

Best heard in aortic area with patient sat forward in expiration

Soft S1

Collapsing pulse/wide pulse pressure

A

Aortic regurgitation

127
Q

Causes of aortic regurgitation

A

Most common cause worldwide- rheumatic heart disease

Commonest cause in developed countries- congenital and degenerative valve abnormalities e.g. bicuspid aortic valve, endocarditis, collagen vascular diseases

Transcatheter aortic valve replacement

128
Q

Management of aortic regurgitation

A

Surgery if symptomatic or asymptomatic with deteriorating left ventricular function (valve replacement or repair)

129
Q

Pansystolic murmur

Heard loudest over tricuspid region

Loudest during inspiration

Large v waves in JVP

Hepatic pulsations

Signs of right sided heart failure

A

Tricuspid regurgitation

130
Q

Ejection systolic murmur

Loudest over pulmonary area in inspiration

Radiates to left shoulder

“a waves” in JVP

Widely split S2

A

Pulmonary stenosis

131
Q

Early decrescendo murmur

Loudest over left sternal edge during inspiration

Usually due to pulmonary hypertension

A

Pulmonary regurgitation

132
Q

Mid-diastolic murmur (rarely audible)

Loudest at 3rd/4th intercostal space, left sternal edge, during inspiration

Signs of right atrial enlargment (raised JVP with giant a waves, peripheral oedema, ascites)

A

Tricuspid stenosis

PA (12 decks)

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