Cardiovascular

Question 1

What is chronic congestive heart failure?

Answer 1

Heart failure = heart is unable to generate a cardiac output sufficient to meet the demands of the body (without increasing diastolic pressure)

• It can result from any cardiac disease that affects ventricular systolic or diastolic function or both.
• ‘congestive heart failure’ (CHF) = patients with breathlessness and abnormal sodium and water retention –>oedema.

Heart failure comprises a wide range of clinical scenarios, from patients with normal left ventricular ejection fraction (LVEF) >50% to those with reduced myocardial contractility (LVEF <40%).

Based on LVEF, heart failure is defined as follows:

1. Heart failure with reduced ejection fraction (HFrEF): symptoms and signs with LVEF <40%.
2. Heart failure with mid-range ejection fraction (HFmrEF): symptoms and signs with LVEF 40% - 49%.
3. Heart failure with preserved ejection fraction (HFpEF): e.g. Diastolic failure can be this as the ejection fraction is proportional to the reduced ventricle size to try and compensate via preload- its still pathological though even if EF is >50%

Then with both 2. & 3:

• elevated natriuretic peptides
  
  • [BNP] >35 nanograms/L
  • N-terminal pro-brain natriuretic peptide [NT-pro-BNP] >125 nanograms/L
• and at least one additional criterion:
  
  • (a) relevant structural heart disease (e.g., left ventricular hypertrophy [LVH] or left atrial enlargement),
  • (b) diastolic dysfunction.

NB: acute heart failure means new onset acute or decompensation of CHF –> characterised by pulmonary and/or peripharal oedema with.out signs of hypoperfusion in peripheries. In CHF there is venous congestion but arterial pressure is well maintained until very late.

Question 2

What are the causes of chronic congestive heart failure?

Answer 2

It can result from any cardiac disease that affects ventricular systolic or diastolic function or both. TF there are numerous and varied causes of heart failure.

Some of these conditions tend to increase metabolic demand, which may not be matched by a sufficient increase in cardiac output by the failing heart.

Common causes of chronic heart failure include:

• Coronary artery disease
• Hypertension
  
  • Maybe the first clin manifest: Uncontrolled hypertension dc systolic function by ic the afterload against which the failing ventricle must pump blood.
• Valvular disease
  
  • treatment: valvuloplasty or valve replacement for valvular heart disease
• Myocarditis.

Other causes include:

• Infiltrative diseases: amyloidosis, haemochromatosis, sarcoid
• Congenital heart diseases
  
  • Familial cardiomyopathy
• Pericardial disease
• Toxin-induced: heroin, alcohol, cocaine, amfetamines, lead, arsenic, cobalt, phosphorus
• Infection: bacterial, fungal, viral (HIV), Borrelia burgdorferi (Lyme disease), parasite (e.g., Trypanosoma cruzi[Chagas disease], importnant in central and south america)
• Endocrine disorders: diabetes mellitus, thyroid disease, hypoparathyroidism with hypocalcaemia, phaeochromocytoma, acromegaly, growth hormone deficiency
• Systemic collagen vascular diseases: lupus, rheumatoid arthritis, systemic sclerosis, polyarteritis nodosa, hypersensitivity vasculitis, Takayasu syndrome, polymyositis, reactive arthritis
• Chemotherapy-induced: for example, adriamycin, trastuzumab
• Nutritional deficiencies: thiamine, protein, selenium, L-carnitine
• Pregnancy: peripartum cardiomyopathy (high outpu cardiac failure)
• Tachycardia-induced cardiomyopathy.
  
  • Tachyarrhythmias also decrease the diastolic ventricular filling time and increase myocardial oxygen demand.
  • Give standard treatment and adjunctive rate control therapy

Many of these causes may be completely reversible given appropriate and timely treatment/intervention. (e.g., revascularisation for stunned or hibernating myocardium; peripartum, HTN, valves and tachycardia induced).

Other causes, such as scarred myocardium or dilated cardiomyopathy, are currently considered irreversible.

Question 3

What is the pathophysiology of heart failure?

Answer 3

Heart failure: initial myocardial insult –> over-expression of multiple peptides with different ST and LT CVS effects. In the acute phase, neurohormonal activation seems to be beneficial in terms of maintaining adequate CO and peripheral perfusion.

Sustained neurohormonal activation, however, eventually results in:

1. increased wall stress,
2. dilation, and
3. ventricular remodelling,

–> These contribute to disease progression in the failing myocardium, eventually –> further neurohormonal activation.

Left ventricular remodelling is the process by which mechanical, neurohormonal, and possibly genetic factors alter ventricular size, shape, and function. Remodelling occurs in several clinical conditions, including:

• myocardial infarction,
• cardiomyopathy,
• hypertension, and
• valvular heart disease

The signs of remodelling:

• hypertrophy,
• loss of myocytes (dilation of ventricles)
• increased interstitial fibrosis (scarring)
• From remodelling –> Mitral regurgitation
  
  • as the left ventricle dilates and the heart assumes a more globular shape,
  • Mitral regurgitation results in an increasing volume overload on the overburdened left ventricle (as it comes back into the ventricle, it doesnt leave,) that further contributes to remodelling and progression of disease and symptoms.

Question 4

What are the signs and symptoms of congestive heart failure?

Answer 4

The incidence and prevalence of heart failure increases with increasing ag Male sex (esp. >80 y/o) has also been linked to a higher risk of developing heart failure & Excess body weight is an established risk factor.

A number of precipitating factors leading to impaired cardiac function & potentially acute heart failure episode - want to detect and treat these: e.g. salt intake, lack of adherence to medication and diet, MI, PE, uncontrolled hypertension, cardiac arrhythmias, infection, hypothyroidism, hyperthyroidism, renal dysfunction, and alcohol and drug abuse.

The complexity and variety of potential causative factors means that a multitude of patient historical factors may be relevant.

Hx: of hypertension; diabetes mellitus; dyslipidaemia; tobacco use; coronary, valvular, or peripheral vascular disease; rheumatic fever; heart murmur or congenital heart disease; personal or family history of myopathy; mediastinal irradiation; and sleep-disturbed breathing should be enquired about.

The DH should record the past or current use of illicit drugs; alcohol; ephedra; or antineoplastic agents such as anthracyclines, trastuzumab, or high-dose cyclophosphamide, because heart failure may occur years after exposure to doxorubicin or cyclophosphamide.

The history and physical evaluation should include specific consideration of non-cardiac diseases such as collagen vascular disease, bacterial or parasitic infection, obesity, thyroid excess or deficiency, amyloidosis, and phaeochromocytoma.

FH: for pre-disposition to atherosclerotic disease but also to identify relatives with cardiomyopathy, sudden unexplained death, conduction system disease, and skeletal myopathies.

• Dyspnoea on exertion or at rest is the most common symptom of left-sided heart failure.
• Increasing failure = patient may develop leg oedema and abdominal distension due to ascites.

General examination:

• tachycardia and cyanosis.

A focused CVS examination:

• elevated jugular venous pressure
• ankle oedema
• displaced apex beat (–>cardiomegaly).

Auscultation:

• pulmonary rales/crepitation,
• S3 gallop - a large amount of blood striking a very compliant ventricle through the mitral valve (on diastole, just after s2)

Particular attention should be paid to factors like

1. pallor (which may reflect anaemia),
2. irregularly irregular pulse (reflecting atrial fibrillation),
3. systolic murmur of aortic stenosis and
4. mid diastolic murmur of mitral stenosis, or
5. overt signs of thyrotoxicosis (hand tremor, muscle weakness, lid lag etc)
6. In dialysis patients, a large atrioventricular fistula may occasionally be the precipitating factor.

dyspnoea

The most common symptom of left-sided heart failure. May occur with exertion or in more severe cases, at rest (NYHA IV).

This is considered a minor criterion for the diagnosis of heart failure (Framingham criteria) along with:

• tachycardia (heart rate >120 beats per minute)
  
  • This may be the result of frequent ectopic supraventricular or ventricular beats or may reflect paroxysms of atrial flutter/fibrillation; permanent atrial fibrillation may or may not cause palpitations
• hepatomegaly
  
  • may cause abdominal discomfort/distension and nausea.
• ankle oedema
• night cough
• signs of pleural effusion

Or the major Framingham criterion for the diagnosis of heart failure:

• neck vein distension
• S3 gallop
• cardiomegaly
  
  • Left ventricular dilation or hypertrophy are common findings.
• hepatojugular reflux
  
  • e.g. on firm pressure over the liver.
• rales

May see: orthopnoea and paroxysmal nocturnal dyspnoea

• Orthopnoea worsens immediately after lying down, because of a sudden increase in venous return (i.e., pre-load).
• Paroxysmal nocturnal dyspnoea occurs several hours after the patient lies down to sleep; it results from the central re-distribution of extravascular fluid that progressively increases the venous return.
• Nocturia:
  
  • Increased frequency of uresis occurs several hours after the patient lies down to sleep; it also results from the central re-distribution of extravascular fluid that augments the amount of circulating blood cleared from the kidneys.
• chest discomfort
  
  • A symptom of poor coronary perfusion.
• fatigue, muscle weakness, or tiredness
  
  • Symptom of poor tissue (muscle) perfusion.
• lethargy/confusion
  
  • Symptom of poor tissue (brain) perfusion.

Question 5

What investigations should be done for heart failure?

Answer 5

FOR ALL PTS, initial investigations should include:

• ECG,
  
  • QRS duration above 120 ms should always raise the question of ventricular dyssynchrony.
  • evidence of underlying coronary artery disease, left ventricular hypertrophy, or atrial enlargement; may be conduction abnormalities and abnormal QRS duration
• chest x-ray,
  
  • May reveal pulmonary vascular congestion (vascular redistribution, Kerley B lines), cardiomegaly (increased cardiothoracic ratio), or pleural effusion (usually right-sided but often bilateral).
• Transthoracic Echocardiogram,
  
  • Should be performed in every patient presenting with heart failure symptoms.
    • determies the systolic and diastolic function of both ventricles.
  • With systolic heart failure, echo usually demonstrates a dilated left and/or right ventricle with low ejection fraction.
  • With pure diastolic heart failure left ventricular ejection fraction (LVEF) is normal but there is evidence of left ventricular hypertrophy (LVH) and of abnormal diastolic filling patterns (on Doppler evaluation.)
  • Echo can also identify valvular or pericardial disease or may reveal evidence of underlying coronary artery disease (regional wall motion/thickness abnormalities).
• baseline haematology and blood chemistry, including:
  
  • full blood count,
    
    • Anaemia and high lymphocyte percentage are strong risk factors and prognostic markers of poor survival.
  • serum electrolytes (including calcium and magnesium),
    
    • Baseline electrolytes should be obtained in all patients.
    • May see: decreased sodium (usually <135 millimols/L), altered potassium
  • serum urea and creatinine,
    
    • Reflects tissue perfusion, fluid status, rules out renal disease. (normal to elevated)
  • liver function tests,
    
    • Reflects abdominal congestion -> normal to elevated
  • B-type natriuretic peptide/N-terminal pro-brain natriuretic peptide levels.
    
    • In patients presenting with dyspnoea, measurement of natriuretic peptide biomarkers is useful to support a diagnosis or exclude heart failure.
    • Elevated plasma BNP levels have been associated with reduced left ventricular ejection fraction, left ventricular hypertrophy, elevated left ventricular filling pressures, and acute myocardial infarction and ischaemia,
    • BUT they can occur in other settings, such as pulmonary embolism and chronic obstructive pulmonary disease. & BNP They are sensitive to other biological factors, such as age, sex, weight, and renal function. So clinical judgement is neccessary
    • A low plasma BNP level e.g.<100 nanograms/L can rapidly rule out decompensated heart failure and point to a pulmonary cause.
    • A high plasma BNP level (>400 nanograms/L = supports the diagnosis of abnormal ventricular function (i.e., heart failure).
    • Intermediate values (100 to 400 nanograms/L = ‘grey zone’ -> search for a potential non-cardiac cause of dyspnoea: for example, COPD.
    • BNP levels tend to be less elevated in heart failure with preserved ejection fraction than with low ejection fraction and are lower in obese patients.
    • Levels of BNP may be elevated meaningfully in women and in people over 60 years of age who do not have heart failure, and thus BNP levels should be interpreted cautiously in such individuals.

Comorbid disease:

• Blood glucose,
  
  • Elevated in diabetes. Diabetes mellitus has been associated with a 3- to 5-fold increase in the risk of developing heart failure.
• thyroid function tests
  
  • Both hypo- or hyperthyroidismcan be a primary or contributory cause of heart failure.
    • primary hypothyroidism: elevated TSH, decreased free thyroxine (FT4);
    • hyperthyroidism: decreased TSH, elevated free triiodothyronine, elevated FT4
• blood lipids
  
  • Screening for dyslipoproteinaemias/metabolic syndrome (assoc. w/CVS and T2DM).
  • Elevated in dyslipidaemia,
  • decreased in end-stage heart failure, especially in the presence of cardiac cachexia (heart failure –> loss of body muscle, fat and bone)

Subsequent investigations for assessing severity of heart failure and functional status:

• standard exercise stress testing (bicycle or treadmill),
• cardiopulmonary exercise testing with VO₂ max,
• 6-minute walking test exercise,
• right heart catheterisation,
• endomyocardial biopsy.

if indicated in clinical history:

• HIV screening
  
  • HIV increases risk of heart disease
• Haemochromatosis screen (hereditary iron overload)
  
  • measurement of iron levels & ferratin
  • and fasting transferrin saturation
    
    • [primary iron overload myopathy!]
    • A cardiac MRI scan is particularly useful in the investigation of infiltrative cardiomyopathy e.g. haemochromatosis, amyloidosis, sarcoidosis. Also for myocarditis.

Question 6

What is the management of chronic congestive heart failure?

Answer 6

Acute congestive heart failure:

Patient has tolerance to ACEi:

1. ACE inhibitor OR sacubitril/valsartan
   
   • captopril, enalapril, fosinopril, lisinopril, perindopril, quinapril, ramipril, trandolapril:
   • sacubitril (antihypertensive)/valsartan (ang2 receptor antagonist)
2. LIFESTYLE CHANGES
   
   • sodium restriction
   • fluid restriction (in severe hyponatraemia)
   • weight monitoring (also for daily water intake/output measurement]
   • continuous health screening
   • exercise training
3. Beta-Blocker
   
   • 2º = metoprolol, bisoprolol,nebivolol:
   • 1º =carvedilol
   • Contra indications: bradycardia, reactive airway disease, and unstable or low-output heart failure.

Adjuncts:

Diuretic

• furosemide:bumetanide:torasemide
• chlorothiazide: hydrochlorothiazide:indapamide:metolazone
  
  • All patients with symptoms and signs of congestion should receive the min dose diuretics, to relieve congestion/symptoms and dry weight, irrespective of the left ventricular ejection fraction (LVEF).
    
    • diuretics are not able to maintain HF clinical stability for long periods of time. Combined with ACEi and B-blocker decreases clinical decompensation risk.
  • In loop diuretic resistant paitents; or pts with HTN and only mild fluid retention = use both diuretics or just thiazide respecitvely. Check electrolytes.
  • Few patients with heart failure and fluid retention can maintain sodium balance without the use of diuretic drugs.
• Aldosterone antagonist
• spironolactone; eplerenone
  
  • also called mineralocorticoid receptors
    
    • Amiloride and triamterene (potassium-sparing diuretics) should be used with caution with aldosterone antagonists, because of the increased risk of developing hyperkalaemia. Close monitoring of serum potassium levels (and renal function) is suggested in this situation.
• Hydralazine + isosorbide dinitrate
  
  • Good for black patients
  • And for pts who cant have ACE inhibitor or angiotensin-II receptor antagonist because of drug intolerance, hypotension, or renal insufficiency, unless contraindicated
• Digoxin
• • For pts w/reduced left ventricular ejection fraction (LVEF), especially those with atrial fibrillation.
    
    • Effective with: ACE inhibitors, beta-blockers, and diuretics,
    • Digoxin reduces the composite end point of mortality or hospitalisations, but does not reduce all-cause mortality.
    • toxicity is with levels >2.6 nanomols/L =toxicity. and may occur at lower levels w/hypokalaemia, hypomagnesaemia, or hypothyroidism co-exists
    • Use Low doses if the patient is over 70 years old, has impaired renal function, or has a low lean body mass.
• Ivabradine
  
  • SPECIALIST ONLY & ONLY after 4W of standard therapy
    
    • Inhibits pacemaker currents = cardiotionic e.g. strengthens heart/increases CO
    • sinus rate >75 beats per minute and an ejection fraction <35%, and who remain symptomatic despite optimal therapy. It can also be used in patients who are unable to take beta-blockers.
• Vasopressin antagonist
  
  • Tolvaptan
  • Considered for patients with symptomatic or severe hyponatraemia (<130 mmol/L)
  • AND persistent congestion despite attempts to correct sodium levels

If intolerant to ACEi

• eX: patients in cardiogenic shock, low renal output, hyperkalaemia or angio-oedemia

then 1^st line e.g. 1) = beta blocker + angiotensin 2 receptor antagonist (2. lifestyle changes) then 3) = diuretic

If unresponsive

And LVEF <35%: no left bundle branch block

1. Implantable cardiac defibrillator
   
   • Works as 1º prevention against sudden cardiac death for pts with HF
   • Works as 2º to prolong HF, low LVEF, VF & Tachycardic pts
   • 3º for LVEF <30

If LVEF <30%: left bundle-branch block

1. Cardiac re-synchronisation therapy (CRT) with biventricular pacemaker

• Gives simultaneous electrical activation of both R & L ventricles with a biventricular pacemaker to enhance the contraction and reduce mitral regurgitation.
• Can be Combined with an implantable defibrillator

For both <30% or <35% the next line is then:

1. Cardiac transplant
   
   • Refractory end stage disease – all treatments for all/any possible contributing conditions tried.

Question 7

What is the management of Atrial fibrillation?

Answer 7

Management of new-onset atrial fibrillation

Rate control with beta blockers:

• Esmolol, metoprolol, propranolol, atenolol, nadolol
  
  • Beta blockers preferred when new-onset AF assoc. with acute MI or when new onset AF is precipitated after exercise.

Rate control with calcium channel blockers:

• Diltiazem, verapamil
  
  • CCBs preferred in pts with chronic lung disease – where BBlockers may cause bronchospasm

Anticoagulation

• heparin (or enoxaparin) AND warfarin

For pharma cardioversion

• amiodarone or ibutilide

Haemodynamically stable + NO left atrial thrombus: asymptomatic

CHA2DS2-Vasc score 0-1

1. Observation
   
   • rate control and cardioversion only if needed

CHA2DS2-VASc score 2+

1. Anticoagulation
2. Observation
3. ADJUNCT: Rate control with beta-blockers and/or CCBs
   
   • Electrical or pharmacological cardioconversion

If haemodynamically unstable, initial:

1. Direct current cardioversion

If haemodynamically stable with left atrial thrombus & no heart failure:

• NB: If there is a thrombus always do cardioversion after 3-4 weeks of anticoag.

1. Rate control with beta-blockers and/or calcium-channel blockers (CCBs)
2. Anticoagulation
3. Electrical or pharmacological cardioversion following 3-4 weeks of anticoagulation

If haemodynamically stable without left atrial thrombus: symptoms onset <48 hours

W/O heart failure: CHA2DS2-VASc score 0-1 – always (1) rate control and (2) cardioversion but anticoag is not necessary with low score and under 48hrs & no thrombus.

But if over 48hrs & low score then:

1. Rate control with beta blockers and/or CCBs
2. Heparin
3. Electrical or pharmacological cardioversion – ONCE heparin anticoag established
   
   • Provided the transoesophageal echo is negative (e.g. no thromboembolism risk)
4. ADJUNCT: consideration of long-term aspirin post cardioversion

(W/O heart failure) if score is 2+ even if under 48hrs treat with anticoag:

1. Rate control with beta blockers and/or CCBs
2. Electrical or pharmacological conversion + heparin
3. Anticoagulation

If over 48hrs! anticoag then cardiovert following 3-4 weeks of anticoagulation

If patient is in any type of AF WITH heart failure [because of risk of thromboembolism]

ALWAYS:

1. Rate control with digoxin or amidarone (if digoxin is contraindicated)[e.g. not beta blockers or CCBs]
2. Electrical or pharmacological cardioversion + heparin
3. Anticoagulation

May need Electrical or pharmacological cardioversion following 3-4 weeks of anticoagulation if symptoms onset is over 48hrs OR there is arterial thrombus – also wait 3-4 weeks

• Target INR: 2-3 for 3-4 weeks following repeat transoesophageal echocardio to confirm left atrial thrombus