Cardiology IV

Question 2

Desribe the pathophysiology of AS

Answer 2

A pressure gradient develops across the valve

Initially, this leads to systolic dysfunction, the heart can not pump out a normal proportion of its end-diastolic volume and causes increased resistance to ejection and increases the systolic pressure gradient.

Compensatory mechanisms result in left ventricular (concentric) hypertrophy - hence, a sustained apex.

This then causes diastolic dysfunction by reducing ventricular filling during diastole

This reduces the compliance of the left ventricle and reduces overall myocardial contractility.

This causes left heart failure

ALSO: the back-pressure from the left ventricle also increases pulmonary artery pressure and can lead to pulmonary hypertension. This eventually progresses to right heart failure.

Question 3

Describe the symptoms of AS

Answer 3

Patients with aortic stenosis (AS) may be asymptomatic for a prolonged period of 10-20 years.

• Exertional dysopnea
  Most common complaint
• Exertional angina
  Increased o2 demand due to more LV mass and decreased perfusion pressure gradient due to elevated LV end diastolic pressure
• Exertional syncope or presyncope
  Due to exercise induced vasodilation and inability to increase CO
• Atrial fibrillation
• Epistaxis or bruising

Classical triad of ‘SAD’ is often described.
Syncope; Angina; Dysopnea

Question 4

Describe the signs of AS [4]

Answer 4

Murmur:
* Loud mid-to-late peaking systolic ejection murmur
* Radiates to the carotids and becomes more prominent with sitting forward and in expiration
* Murmur becomes softer the more severe the stenosis
* Murmur radiates to carotids

Sustained apex
Slow rising pulse
Narrow pulse pressure
Soft S2
S4 - caused by the atria contracting against stiff, hypertrophied ventricles.

Question 5

What ECG changes would you expect in AS? [1]

Answer 5

Left ventricular hypertrophy:
- deep S-waves in V1 and V2
- tall R-waves in V5 and V6).

Question 6

How can you tell from a murmur in AS if it is mild-moderate c.f severe murmur? [2]

Answer 6

Early peaking is more consistent with mild or moderate AS and late peaking is consistent with severe AS

Murmur becomes softer the more severe the stenosis

Question 7

When is dobutamine stress echo indicated in AS patients? [1]

By what mmHg does AS gr

Answer 7

Dobutamine stress echocardiogram:
- useful for patients who have low-gradient AS
- patients may be symptomatic but have seemingly low pressures due to a low ejection fraction
- gradient will increase > 40 mmHg after administration of low dose dobutamine

Question 8

Describe the work conducted prior to a surgical aortic valve replacement {SAVR) or transcatheter aortic valve implantation (TAVI) [3]

Answer 8

• Coronary angiogram:
  to ID CAD and concomitant coronary revascularization if possible
• Trans-oesophageal echocardiogram (TOE):
  assess for endocarditis and mitral valve abnormalities as well as monitoring the TAVI procedure
• MSCT:
  assess the anatomy and dimensions of the aortic root, shape of the aortic valve annulus and the number of aortic valve cusps

Question 9

How do you classify AS as being severe? [3]

Answer 9

Severe AS classified as:
- aortic jet velocity ≥4 m/s (direct measurement of the highest antegrade systolic velocity signal across the aortic valve)
- mean trans-valvular pressure gradient ≥ 40 mmHg
- aortic valve area ≤1 cm2.

Question 10

What indicates surgery for AS? [3]

Answer 10

If symptomatic

If asymptomatic but have:
- LVEF < 50%
- Undergoing other cardiac surgery
- low surgical risk factors

Question 11

Which treatment option is used for palliative measures / not suitable for surgery / young children with congenital AS? [1]

Answer 11

Percutaneous balloon valvotomy

Question 12

What is Heyde’ syndrome? [1]

Answer 12

Triad of
- AS
- Recurrent bleeding due to angiodysplasia causing anaemia
- Acquired coagulopathy - VWDS

Question 13

Describe the valve leaflet causes of AR [3]

Answer 13

• rheumatic infection
  Inflammation is a result of molecular mimicry to streptococcal infection: immune system produces antibodies that confuse foreign and self-antigens.
• infective endocarditis
  Infective causes include Strep. viridans, Staph. aureus, Enterococci.
• congenital & degenerative disease
  Congenital (e.g. bicuspid, quadcuspid valve).
  Degenerative (e.g. calcification).

Question 14

Describe the aortic root causes of AR

Answer 14

Connective tissue disorders
- Aortic regurgitation may feature in a number of connective tissue disorders. Aortic root diameter should be monitored in these individuals.
- Marfan’s syndrome - caused by a defect in the FBN1 gene.
Ehlers-Danlos syndrome - caused by collagen defects.

Aortitis
- inflammation of the aortic root.
- May be associated with chronic inflammatory conditions such as rheumatoid arthritis (RA) and ankylosing spondylitis (AS).

Aortic dissection
- Aortic regurgitation may complicate in Stanford A dissections, secondary to impaired leaflet coaptation or prolapse. Causes acute disease regurgitation and is a medical emergency.

Question 15

Describe the pathophysiology of acute AR

Answer 15

MEDICAL EMERGENCY:

• Causes an acute rise in left atrial pressure
• Causes pulmonary oedema and cardiogenic shock
• Also get reduced coronary flow - the coronaries fill predominantly during diastole, regurgitant flow at this time reduces filling. Results in angina or in severe cases myocardial ischaemia.

Question 16

Describe the pathophysiology of chronic AR [4]

Answer 16

Regurgitation of blood during diastole causes an increase in the left ventricular end-diastolic volume (essentially the preload).

Leads to systolic and diastolic dysfunction

LV dilatation occurs with eccentric hypertrophy

The dilation allows for an increased stroke volume compensating for regurgitant flow supported by the ventricular hypertrophy

These changes maintain ejection fraction, with a greater preload leading to greater contractility

Question 17

Describe the following signs of AR [5]

de Musset’s
Quincke’s
Traube’s
Duroziez’s
Müllers’

Answer 17

de Musset’s - head nodding with the heart beat.
Quincke’s - pulsation of nail beds.
Traube’s - pistol shot femorals.
Duroziez’s - to and fro murmur heard when stethoscope compresses femoral vessels.
Müllers’ - pulsation of uvula.

Question 18

Describe the managment of acute AR

Answer 18

Acute AR is a surgical emergency: Aortic valve replacement or repair should be performed as soon as possible. It primarily occurs secondary to infective endocarditis or aortic dissection, both of which carry very high morbidity and mortality:

Aortic dissection (Stanford type A):
- management depends on the patients pre-morbid state and severity of presentation. If not already there, patients are transferred to the local on-call dissection centre. Emergency open surgery is typically required, management depends on the exact pattern of findings but may consist of root replacement and valve repair or replacement.

Infective endocarditis:
- management depends upon pattern of valvular involvement (multiple valves may be affected) and complications (e.g. annular/aortic abscess, septic emboli). Coronary angiogram may be performed in selected stable patients prior to operative management. AR is generally an indication for early surgery.

-

Question 19

The normal size of the aortic valve area is more than [] cm2, in mild AS it is more than [] cm2, in moderate AS it is from [] to []cm2, and in severe AS < [] cm2.

Answer 19

The normal size of the aortic valve area is more than 2 cm2, in mild AS it is more than 1.5 cm2, in moderate AS it is from 1.0 to 1.5 cm2, and in severe AS < 1 cm2.

Question 20

What is an austin flint murmur? [1]

Answer 20

Early diastolic murmur heard in AR; the blood flows out of of atrial valve on onto mitral valve; heard on apex beat

Question 21

VSDs are associated with

Aortic regurgitation
Aortic stenosis
Mitral stenosis
Mitral regurgitation

Answer 21

VSDs are associated with

Aortic regurgitation
Aortic stenosis
Mitral stenosis
Mitral regurgitation

Question 22

Why are VSDs associated with aortic regurgitation? [1]

Answer 22

poorly supported right coronary cusp resulting in cusp prolapse

Question 23

Which drug class are CI in AS? [1]
Why? [1]

Answer 23

GTN are CI in AS due to the fact that they are potent vasodilators, meaning that they would reduce BP, and the heart would have to work even harder (and likely cause blood back into the Pulmonary Circulation and Right Ventricle)

Question 24

What are the symptoms of MR? [4]

Answer 24

SOB & dysopnoea (to increase in left atrial pressure)
Fatigue
Signs of RHF (ankle swelling; distended abdomen)
Palpitations due to afib

Question 25

Describe the signs of MR [6]

Answer 25

• Pan systolic, high pitched whistling murmur (due to high velocity of blood flow through the leaky valve)
• Murmur radiates to left axilla
• Soft S1: due to incomplete closure.
• 3rd heart sound may be present due to rapid filling of a dilated ventricle.
• Thrill on palpitation
• Signs of HF
• Signs of pulmonary oedema
• Afib

Question 26

What is a tell tale sign of left atrial enlargement on CXR? [1]

Answer 26

double-density sign, also known as the double right heart border

Normally the left atrium is located posteriorly and only the atrial appendage component is visible. But left atria becomes englarged enlarged, the right aspect may become visible as an extra shadow next to the right atria

Question 27

If the double density sign is present on a CXR, what measurement can be taken to confirm left atrial enlargement? [1]

Answer 27

Olbique left atrial measurement: outer edge of atrium to midpoint of left main bronchus: > 7 cm = LA enlargement

Question 28

Acute MR is characterised by which two features? [2]

Answer 28

Patients with acute MR are normally profoundly unwell. Condition characterised by shock and flash pulmonary oedema

Question 29

Which drug can be used to reduce afterload before acute MR surgery? [3]

Answer 29

• diuretics
• sodium nitroprusside
• positive inotropes: dobutamine
• intra-aortic balloon counterpulsation (helpes the by heart indirectly by decreasing the afterload but increases cardiac output)

Question 30

When is surgery indicated for chronic MR patients?

Answer 30

Chronic MR:

• asymptomatic & LVEF < 60%
  OR
• asymptomatic & LV end systolic diameter >40mm
• All symptomatic if fit for surgery

BMJ BP

Question 31

Describe the symptoms of mitral stenosis [6]

Answer 31

• Mitral stenosis normally presents with exertional dyspnoea. Dysopnea due to left atrial pressure increasing causing pulmonary venous hypertension
• Haemoptysis due to pulmonary pressures and vascular congestion
• Malar flush
• Chest pain
• Atrial fibrillation is caused by the left atrium struggling to push blood through the stenotic valve causing strain, electrical disruption and resulting fibrillation.
• Signs of right ventricular failure - ankle swelling & distended abdomen: due to the development of pulmonary hypertension

Question 32

Describe the signs of mitral stenosis [6]

Answer 32

• Mid-diastolic rumbling murmur: low velocity of blood flow (due to narrow area - rumbles way through). LENGTH OF RUMBLE CORRELATES TO THE INTENSITY
• Loud S1 caused by thick valves closing
• Tapping apex beat that is palpatable (due to loud S1)
• Atrial fibrillation: left atrium can’t push through stenotic valve - disrupts electrical signal
• RFH: Increase in JVP, basal creps, ankle oedema

Question 33

Describe the pathophysiology of mitral stenosis [3]

Answer 33

Mitral stenosis results in raised left atrial pressures and atrial hypertrophy.

This predisposes to atrial fibrillation

Elevated left atrial pressure also causes pulmonary venous hypertension and subsequent pulmonary arterial hypertension resulting in right ventricular hypertrophy and dilation, ultimately progressing to right-sided heart failure

Question 34

What signs would indicate that MS has become more severe? [2]

Answer 34

length of murmur increases
opening snap becomes closer to S2

Question 35

Which form of ECHO is best for investigating mitral valve? [1]

Answer 35

transthoracic echocardiography

Question 36

Mitral valve prolapse is associated with with

Early diastolic murmur, high pitched and blowing
Holosystolic murmur, harsh in character
Continous machinery murmur
Ejection systolic murmur
Mid-late diastolic murmur, rumbling
Late systolic murmur

Answer 36

Mitral valve prolapse is associated with with

Late systolic murmur

Question 37

coarctation of aorta is associated with

Early diastolic murmur, high pitched and blowing
Holosystolic murmur, harsh in character
Continous machinery murmur
Ejection systolic murmur
Mid-late diastolic murmur, rumbling
Late systolic murmur

Answer 37

coarctation of aorta is associated with

Late systolic murmur

Question 38

patent ductus arteriosus is associated with

Early diastolic murmur, high pitched and blowing
Holosystolic murmur, harsh in character
Continous machinery murmur
Ejection systolic murmur
Mid-late diastolic murmur, rumbling
Late systolic murmur

Answer 38

Continous machinery murmur

Question 39

According to NICE guidelines, what is the recommended threshold for the mitral valve area below which intervention is considered in patients with mitral stenosis?
A) 2.0 cm²
B) 1.5 cm²
C) 1.0 cm²
D) 0.5 cm²

Answer 39

According to NICE guidelines, what is the recommended threshold for the mitral valve area below which intervention is considered in patients with mitral stenosis?
A) 2.0 cm²
B) 1.5 cm²
C) 1.0 cm²
D) 0.5 cm²

Question 40

Which pharmacological intervention is recommended by NICE guidelines for managing symptoms in patients with mitral stenosis?
A) Beta-blockers
B) ACE Inhibitors
C) Calcium Channel Blockers
D) Diuretics

Answer 40

Which pharmacological intervention is recommended by NICE guidelines for managing symptoms in patients with mitral stenosis?
A) Beta-blockers
B) ACE Inhibitors
C) Calcium Channel Blockers
D) Diuretics

Question 41

According to NICE guidelines, what is the recommended anticoagulation therapy for patients with mitral stenosis and atrial fibrillation?
A) Aspirin
B) Warfarin
C) Clopidogrel
D) Heparin

Answer 41

According to NICE guidelines, what is the recommended anticoagulation therapy for patients with mitral stenosis and atrial fibrillation?
A) Aspirin
B) Warfarin
C) Clopidogrel
D) Heparin

Question 42

What is de-novo acute heart failure caused by? [4]

Describe pathophysiology of de-novo acute heart failure [3]

Answer 42

De-novo acute HF: caused by and increased cardiac filling pressures and myocardial dysfunction usually as a result of ischaemia.

This causes reduced cardiac output & therefore hypoperfusion.

This, in turn can cause pulmonary oedema.

Caused by:
* Ischaemia
* Viral myopathy
* Toxins
* Valve dysfunction

Question 43

Decompensated heart failure accounts for most cases of AHF.

What are the most common precipitating causes of acute AHF? [4]

Answer 43

• Acute coronary syndrome
• Hypertensive crisis: e.g. bilateral renal artery stenosis
• Acute arrhythmia
• Valvular disease

There is generally a history of pre-existing cardiomyopathy. It usually presents with signs of fluid congestion, weight gain, orthopnoea and breathlessness.

CHAMP

Acute coronary syndrome (ACS)
Hypertensive crisis
Arrhythmias, e.g. atrial fibrillation, ventricular tachycardia, bradyarrhythmia
Mechanical problems, e.g. myocardial rupture as a complication of ACS, valve dysfunction
Pulmonary embolism

Question 44

Explain how the heart tries to compensate for a failing heart [4]

Answer 44

Increasing preload (increasing venous pressures):
* Increases end-diastolic volume (EDV) compensating for the reduced ejection fraction, thus maintaining cardiac output.
* In severe disease, large increases result in pulmonary oedema, ascites and peripheral oedema.

Increasing heart rate (a sinus tachycardia)

Activation of the renin-angiotensin-aldosterone system (RAAS)
* due to renal hypoperfusion from the reduced cardiac output.
* contributes to increased venous pressures through vasoconstriction and there is retention of water and sodium that contributes to oedema.

Sympathetic nervous system activation
* via baroreceptors; increasing myocardial contractility and heart rate

Question 45

What are the five overarching causes of chronic heart failure? [5]

State common causes for each [+]

Answer 45

Vascular
* Ischaemic heart disease
* Hypertension

Muscular
* Dilated cardiomyopathy (30%)
* Hypertrophic cardiomyopathy
* Congenital heart disease

Valvular
* Commonly aortic stenosis

Arrhythmias
* commonly atrial fibrillation

High-output failures
* Anaemia
* Septicaemia
* Thyrotoxicosis
* Liver failure

High output failures:
- Typically heart failure is caused by a reduced cardiac output. In some cases, however, the cardiac output may be raised but the systemic vascular resistance very low

Question 46

Describe the signs of HF [+]

Answer 46

• Tachycardia (raised heart rate)
• Tachypnoea (raised respiratory rate)
• Hypertension
• Murmurs on auscultation indicating valvular heart disease
• Peripheral oedema of the ankles, legs and sacrum
• Raised JVP
• Displaced apex
• Heart sounds S3/S4
• Pulsus alternans
• Hepatomegaly
• Ascites

Question 47

Describe why right sided heart failure may occur [4]

Answer 47

Right-sided heart failure commonly occurs as a result of advanced left-sided failure.

Primary right-sided heart failure is uncommon and broadly related to three categories:
* Pulmonary hypertension
* Pulmonary/Tricuspid valve disease
* Pericardial disease

Also:
* Pneumonia
* Pulmonary embolism (PE)
* Mechanical ventilation
* Acute respiratory distress syndrome (ARDS)

Pulmonary hypertension may occur secondary to left-sided heart disease, primary pulmonary hypertension or significant pulmonary disease (e.g. COPD).

Question 48

Describe what is meant by Paroxysmal Nocturnal Dyspnoea (PND) [2]

Explain why this occurs [3]

Answer 48

Experience that patients have of suddenly waking at night with a severe attack of shortness of breath, cough and wheeze.

They may describe having to sit on the side of the bed or walk around the room, gasping for breath

Pathophysiology:
- Fluid settles across a large surface area of the lungs as they lie flat to sleep, causing breathlessness. As they stand up, the fluid sinks to the lung bases, and the upper lung areas function more effectively
AND
- respiratory centre in the brain becomes less responsive. the respiratory rate and effort do not increase in response to reduced oxygen saturation like they would when awake.
AND
- there is less adrenalin circulating during sleep. Less adrenalin means the myocardium is more relaxed, reducing cardiac output.

Question 49

A [] is the main investigation for the confirmation of heart failure.

Answer 49

A transthoracic echocardiography (TTE) is the main investigation for the confirmation of heart failure.

Question 50

What are you looking for to that might indicate HF in an ECHO [3] or CXR [5]

Answer 50

Echocardiogram:
* Evidence of previous MI
* Left ventricular strain / hypertrophy
* Conduction abnormalities / AF

CXR:
* Cardiomegaly (Cardiothoracic ratio > 50% on PA film)
* Alveolar shadowing oedema
* Kerley B lines (fluid in septae of secondary lobules)
* Pleural effusion
* Upper lobe diversion

Question 51

What are normal, raised and high levels of BNP and NTproBNP? [9]

Answer 51

Question 52

Name some causes apart from HF that raise BNP [5]

Answer 52

diabetes, sepsis, old age, hypoxaemia (PE and COPD), kidney disease, and liver cirrhosis

Question 53

Describe the treatment algorithm for HF

Answer 53

First-line treatment:
- for all patients is both an ACE-inhibitor and a beta-blocker
- Generally, one drug should be started at a time

Second-line treatment:
- aldosterone antagonist, angiotensin II receptor blocker or a hydralazine in combination with a nitrate

Continued symptoms:
- cardiac resynchronisation therapy
- digoxin
- ivabradine
- SGLT2 inhibitors
- Sacubitril with valsartan (brand name Entresto)

ABAL: ACEin; Beta Blocker; Aldosterone antagonist; Loop diuertic

Question 54

Avoid [] in patients with valvular heart disease until initiated by a specialist.

ACE inhibitor
Beta blocker
Aldosterone antagonist
Loop diuretic

Answer 54

Avoid [] in patients with valvular heart disease until initiated by a specialist.

ACE inhibitor
Beta blocker
Aldosterone antagonist
Loop diuretic

Question 55

Cardiac resynchronisation therapy (CRT) may be used in severe heart failure, with an ejection fraction of less than []%.

What NYHA classification do they need to meet? [2]

Answer 55

Cardiac resynchronisation therapy (CRT) may be used in severe heart failure, with an ejection fraction of less than 35%.

NYHA III or IV

Question 56

What is the difference between Low and High Output Failure?

Answer 56

low output failure:
- Traditional concept of heart failure where the heart cannot maintain an adequate cardiac output to meet the demands of the body.
- results in increased systemic vascular resistance in an attempt to maintain mean arterial pressure

High output failure:
- high cardiac output (i.e. > 8L/min)
- heart is unable to meet the increased demand for perfusion despite normal cardiac function.
- The problem is with reduced systemic vascular resistance, often due to diffuse arteriole vasodilatation or shunting
- It is generally due to states of increased metabolic demand (e.g. hyperthyroidism), reduced vascular resistance (e.g. thiamine deficiency, sepsis) or significant shunting (e.g. large arteriovenosu fistula).

Question 57

If a patient remains symptomatic despite optimal treatment what interventions using a device can be used in selected patients? [4]

Answer 57

Implantable cardiac defibrillator (ICD):
* important for primary and secondary prevention of sudden cardiac death (specific indications)
.
Cardiac resynchronisation therapy (CRT):
* biventricular pacing, which is indicated in certain patients with HFrEF (i.e. ≤ 35%) & prolonged QRS (i.e. ≥ 130 ms). Usually receive combined device with defibrillator.

Percutaneous coronary intervention (PCI):
* patients with ischaemic heart disease may be offered revascularisation therapy if indicated.|

Cardiac transplant:
* highly specialised procedure for certain patient groups with heart failure.

Question 58

Describe how you manage an acute heart failure patient [+]

Answer 58

Oxygen
- Patients often require 15L/minute with a reservoir mask.
- reassess and down-titrate oxygen to avoid hyper-oxygenation which is associated with worsening myocardial ischaemia and other pathology.

Loop diuretics:
- All ‘WET’ patients will require diuretics as the cornerstone of their management.
- 40 milligrams furosemide intravenously initially to improve symptoms of congestion fluid overload.

Nitrates:
- sublingual glyceryl trinitrate or intravenous nitrates
- Do not use nitrates in those with SBP < 90mmHg or aortic stenosis, who rely on sufficient preload to overcome their pressure gradient.

NIV:
- for those with cardiogenic pulmonary oedema or dyspnoea
- improves ventilation to reduce respiratory distress and drives fluid out of alveoli

Question 59

Describe the pathophysiology of acute onset HF [2]

Answer 59

AHF involves the acute failure of the heart to pump blood to meet the body’s demand.

As a result, two courses of pathology develop:

Congestion in the pulmonary or systemic circulation.
* Pulmonary oedema develops when the left ventricle is unable to empty, which increases the hydrostatic pressure in pulmonary vasculature leading to pulmonary oedema and hypoxia.
These patients are ‘WET’.

Hypoperfusion
* of vital organs as the cardiac output is reduced.
* These patients are ‘COLD’.

Question 60

Explan your answer [1]

Answer 60

Left ventricular aneurysm

The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.

Question 61

Name the four causes of diastolic HF [4]

Answer 61

• cardiac tamponade
• hypertrophic obstructive cardiomyopathy
• constrictive pericarditis
• restrictive cardiomyopathy

Question 62

Name the four causes of systolic HF [4]

Answer 62

• ischaemic heart disease
• arrhythmias
• myocarditis
• dilated cardiomyopathy

Question 63

When considering third line therapy for chronic heart failure, which drugs can be considered?[5]

Answer 63

Ivabradine

sacubitril-valsartan

digoxin

hydralazine in combination with nitrate

cardiac resynchronisation therapy

Question 64

A patient has chronic heart failure. You trial and ACEI but the patient is intolerant.

You then trial an ARB, but the patient is still intolerant.

What treatment should you consider nexr? [1]

Answer 64

Hydralazine and nitrate

Question 65

Describe how you were determine if you give each of the following for third line chronic HF tx?

Ivabradine

sacubitril-valsartan

hydralazine in combination with nitrate

cardiac resynchronisation therapy

Answer 65

Ivabradine
- sinus rhythm > 75/min and a left ventricular fraction < 35%

sacubitril-valsartan:
- criteria: left ventricular fraction < 35%
- is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs

digoxin

hydralazine in combination with nitrate
- this may be particularly indicated in Afro-Caribbean patients

cardiac resynchronisation therapy
- indications include a widened QRS (e.g. left bundle branch block) complex on ECG

Question 66

A patient has chronic heart failure.

You iniate an ACEin and a BB as first line treatment. This does not resolve their EF.

You next trial and aldosterone antagonist. This does also not help.

They are Afro-Carribean.

What is the appropriate third line treatment?

• Ivabradine
• sacubitril-valsartan
• digoxin
• hydralazine in combination with nitrate
• cardiac resynchronisation therapy

Answer 66

• hydralazine in combination with nitrate

Question 67

A patient has chronic heart failure.

You iniate an ACEin and a BB as first line treatment. This does not resolve their EF.

You next trial and aldosterone antagonist. This does also not help.

They have a widened QRS on their ECG.

What is the appropriate third line treatment?

• Ivabradine
• sacubitril-valsartan
• digoxin
• hydralazine in combination with nitrate
• cardiac resynchronisation therapy

Answer 67

A patient has chronic heart failure.

You iniate an ACEin and a BB as first line treatment. This does not resolve their EF.

You next trial and aldosterone antagonist. This does also not help.

They have a widened QRS on their ECG.

What is the appropriate third line treatment?

• Ivabradine
• sacubitril-valsartan
• digoxin
• hydralazine in combination with nitrate
• cardiac resynchronisation therapy

Question 68

When are nitrates considered in the treatment of acute heart failure patients? [3]

Answer 68

Acute HF +
- concomitant myocardial ischaemia
- severe hypertension
- regurgitant aortic or mitral valve disease

Question 69

A patient presents with acute heart failure.

Under what conditions would you consider prescribing intropric agents to them? [1]

Answer 69

Acute HF +
- patients with severe left ventricular dysfunction who have potentially reversible cardiogenic shock

Question 70

A patient presents with acute heart failure. You suspect that they have severe left ventricular dysfunction, with a potentially reversible cardiogenic shock.

What is your next stage in management [1]

Answer 70

Add an inotropic agent (such as dobutamine)

Question 71

When do you discontinue beta-blockers for patients with acute HF? [1]

Answer 71

heart rate less than 50 beats per minute, second or third degree atrioventricular block, or shock

Question 72

A patient has acute HF.

Under what circumstances would you prescribe norepinephrine? [1]

Answer 72

If hypotensive / in cardiogenic shock and have an insufficient response to inotropes and there is evidence of end-organ hypoperfusion