Cardiology - Part 3

Notes

Overview

Heart failure is a clinical syndrome that results from an inability of the heart to maintain adequate cardiac output.

Heart failure (HF) is a clinical syndrome with multiple aetiologies. It is commonly secondary to ischaemic heart disease or hypertensive heart disease. The condition is characterised by progressive shortness of breath, fatigue and fluid overload. Unfortunately, HF is a progressive disorder associated with high morbidity and mortality. Prognosis is generally poor; approximately 50% die within five years.

There are many different ways to classify heart failure that reflect the complexity of the condition:

  • Acute versus chronic: rate of development of heart failure.
  • Right-sided versus left-sided: predominant ventricle affected. Congestive heart failure refers to biventricular failure.
  • Systolic (HFrEF) versus diastolic (HFpEF): impaired ventricular ejection in systole (systolic). Impaired ventricular filling in diastole (diastolic)
  • High output versus low output: low output - low cardiac output and high systemic vascular resistance. High output - high cardiac output and reduced systemic vascular resistance

In these notes, we review the important concepts of heart failure. For more detailed information, check out our notes on Heart failure.

Aetiology

The aetiology of heart failure is complex.

We can broadly divide the causes of heart failure based on the site of pathology within the heart. The most common cause of heart failure is coronary artery disease.

1. Vascular

These are the most common causes of heart failure.

  • Ischaemic heart disease
  • Hypertension

2. Muscular

  • Cardiomyopathy (e.g. hypertrophic, restrictive, dilated)
  • Congenital heart disease

3. Valvular

Valvular disease may lead to either acute or chronic heart failure.

  • Stenotic valves
  • Regurgitant valves

4. Electrical

Arrhythmias (abnormalities of normal conduction) may cause acute heart failure through decompensation.

5. High-output

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. Causes include:

  • Anaemia
  • Septicaemia
  • Thyrotoxicosis
  • Liver failure

Pathophysiology

Mean arterial pressure is dependent on cardiac output and systemic vascular resistance.

To understand the mechanisms leading to heart failure, we need to understand what is governing our blood pressure.

Mean arterial pressure

Mean arterial pressure (MAP) is the average arterial pressure throughout one cardiac cycle. It can be calculated as follows:


MAP = diastolic blood pressure + 1/3rd of the pulse pressure

Pulse pressure is the difference between the systolic and diastolic blood pressure.


MAP is dependent on the cardiac output and systemic vascular resistance

  • Cardiac output: amount of blood pumped out the heart each minute. Measured in litres per minute (L/min).
  • Systemic vascular resistance: resistance to blood flow offered by all of the systemic vasculature, excluding the pulmonary vasculature.

Cardiac output is determined by heart rate x stroke volume:

  • Heart rate: number of times the heart beats each minute.
  • Stroke volume: amount of blood pumped by the left ventricle with each contraction.

Systemic vascular resistance is determined by factors that alter vessel size:

  • Vasodilatation: reduced vascular resistance
  • Vasoconstriction: increased vascular resistance

MAP

Stroke volume

Stroke volume is the amount of blood pumped out of the left ventricle in one contraction. It can be calculated as the end-diastolic volume (i.e. amount of blood left in the ventricle at the end of diastole) minus the end-systolic volume (i.e. amount of blood left in the ventricle at the end of systole).

Several factors can influence the stroke volume and thus the cardiac output.

  • Preload: stretching of cardiomyocytes at the end of diastole.
  • Afterload: pressure or load against which the ventricles must contract.
  • Contractility (Inotropy): refers to myocardial contractility (i.e. the force of muscular contractions)

Preload in influenced by venous return and filling time

  • Venous return: increased venous return increases the preload and thus stretch on the cardiomyocytes
  • Filling time: a longer filling time in diastole increases the preload

Afterload is influenced by vascular resistance and valvular disease

  • Vascular resistance: vasoconstriction increases the pressure the heart has the pump against decreasing stroke volume
  • Valvular disease: a stenotic valve increases the pressure the heart has to pump against decreasing stroke volume

Contractility is influenced by myocardial strength and the autonomic nervous system

  • Muscular function: increased muscular bulk (e.g. hypertrophy) is a physiological and pathological response to increase stroke volume
  • Autonomic nervous system: innervation from the parasympathetic and sympathetic nervous systems alter the strength of contraction

Stroke volume

Frank-Starling Law

The Frank-Starling law describes the relationship between ventricular stretch and contractility, which is at the core of heart failure.

Essentially stretching of cardiac muscle (within physiological limits) will increase the force of contraction.

Discovered in the mid-19th century by Otto Frank and Ernest Starling. The ability of the heart to respond to increased venous return by increasing the stroke volume is essential to normal cardiac function. Failure to do so would result in input-output mismatch and pooling of blood in either the systemic or pulmonary circulation.

Frank-Starling Curve

In a normal heart, increased venous pressure leads to increased venous return and raised end diastolic volume (EDV). This increased EDV means an increase in the preload, as there is increased stretch on the cardiomyocytes. This increased stretching - an increase in the length of the sarcomere - leads to a more forceful contraction. In turn, this increase in contractility leads to an increase in the stroke volume.

Frank-starling curve

Interestingly, the heart does not sit on a single curve, rather it is affected by afterload and the inotropic state.

  • Reduced afterload and increased inotropy - move the curve up and to the left (green)
  • Increased afterload and decreased inotropy - move the curve down and to the right (red).

In effect, venous return governs where on the curve the heart sits while the pre-existing afterload and inotropic environment control which curve it sits on.

The failing heart

The relationship between stretch and contractility has a physiological limit to how much it can compensate for an incresase in preload. In a heart that is failing, continued increaases in preload actually leads to a depressed contractility and subsequent fall in stroke volume.

Frank-Starling

The fall in stroke volume leads to a fall in cardiac output. This leads to a reduction in mean arterial pressure. As a consequence, the heart has several physiological mechanisms to prevent a sustained fall in mean arterial pressure. This includes increasing vasoconstriction through the sympathetic nervous system and renin-angiotenin system (RAS). The RAS system has the added benefit of increasing sodium reabsoprtion in the kidney nephrons that helps to retain water and thus leads to an increase in preload. However, as we have seen a failing heart is already beyond its physiological limit and the increases in preload now place strain on the failing heart leading to worsening function. We can see how in a failing heart, all of these normal physiological adaptations to maintain cardiac function and mean arterial pressure become progressively ineffecive.

Cardiac strain

Clinical features

Heart failure typically manifests with dyspnoea and fatigue (which may limit exercise tolerance) and signs associated with fluid retention.

Symptoms

  • Shortness of breath (SOB)
  • Wheeze
  • Fatigue
  • Weight loss
  • Paroxysmal nocturnal dyspnoea
  • Orthopnoea
  • Ankle swelling

Signs

  • Raised JVP
  • Displaced apex
  • Crackles
  • Ankle swelling
  • Heart sounds S3/S4
  • Pulsus alternans
  • Hepatomegaly
  • Ascites

Clinical features heart failure

Diagnosis

NICE recommends echocardiography and specialist assessment in patients with suspected heart failure based on BNP.

In patients with suspected heart failure, the first step is taking a detailed history and performing a clinical examination. The next step is measuring a BNP, which is used to risk stratify patients and determine the urgency of referral.

BNP

B-type natriuretic peptide (BNP) is a protein released by cardiomyocytes in response to excessive stretching. It is used to assess the likelihood of heart failure. Conditions other than heart failure which may raise BNP levels include diabetes, sepsis, old age, hypoxaemia (PE and COPD), kidney disease, and liver cirrhosis. It has an excellent negative predictive value. This means a negative test should warrant investigation into others causes.

The BNP, along with a detailed history, examination and other relevant investigations, may be used to decide who to refer for further assessment:

Heart failure diagnosis

Investigations

A variety of investigations should be used to investigate for the possible cause of heart failure and any suspected complications.

Investigations are discussed in detail in our notes on Heart failure.

Basic tests

  • ECG
  • Blood tests
  • Chest radiograph
  • ECHO

Chest radiograph

Heart failure causes pulmonary oedema/congestion that may be seen on x-ray.

Classic x-ray findings in heart failure can be remembered using ‘ABCDE’:

  • Alveolar oedema: white opacities that typically extend from the hilum in a 'batwing' pattern
  • Kerley B lines: thin white lines in the lung periphery that represent thickened interlobular septa
  • Cardiomegaly: Cardiothoracic ratio > 50% on PA film
  • Upper lobe Diversion: prominence of the upper pulmonary veins
  • Pleural Effusions: blunting of the costophrenic angles

Pulmonary oedema

Heart failure on CXR demonstrating cardiomegaly, upper lobe diversion and Kerley-B lines

Image courtesy of Dr Roberto Schubert and Radiopaedia


Alveolar oedema

Heart failure on CXR demonstrating alveolar oedema

Image courtesy of Dr Frank Gaillard via Wikimedia Commons

Echocardiography

A transthoracic echocardiography (TTE) is the main investigation for the confirmation of heart failure. It should be completed in patients with an elevated BNP. A TTE may still be warranted, regardless of BNP, if clinical examination reveals a murmur or the ECG is abnormal.

The main determinant of an TTE is to look at the ejection fraction of the heart. This helps to differentiate suspected heart failure into three groups:

  • Heart failure with reduced ejection fraction (HFrEF): LVEF <40%
  • Heart failure with minimally reduced ejection fraction (HFmrEF): LVEF 40-49%
  • Heart failure with preserved ejection fraction (HFpEF): LVEF ≥50%

NOTE: additional echo criteria are used to help diagnose HFpEF or 'diastolic heart failure'. These are broadly based on ventricular thickness, chamber size and other features.

Management

Management follows NICE guidance and is based upon the type of heart failure.

Here, we summarise the key treatments for the management of heart failure. For a more detailed discussion see our additional notes on Heart failure.

Heart failure reduced ejection fraction

Conservative measures

  • Manage co-morbidities (e.g. hypertension, diabetes mellitus)
  • Address lifestyle factors (e.g. obesity, smoking)
  • Patient education
  • Vaccinations (influenza, pneumococcal)

First-line (prognostic) treatments

  • Beta-blockers (e.g. beta-blockers)
  • Angiotension-converting enzyme inhibitors (e.g. ramipril)

Next-line (prognostic) treatments

  • Mineralcorticoid-receptor antagonists (e.g. spironolactone)

Ad-hoc (non-prognostic) treatments

  • Diuretics (e.g. furosemide)

Second-line interventions

  • Medical: Ivabradine, Sacubitril/valsartan, Hydralazine in combination with nitrate, Digoxin
  • Interventional: Implantable devices, revascularisation, transplant

Heart failure preserved ejection fraction

Conservative measures

  • Manage co-morbidities (e.g. hypertension, diabetes mellitus)
  • Address lifestyle factors (e.g. obesity, smoking)
  • Patient education
  • Vaccinations (influenza, pneumococcal)

Medical therapies

There is no clear evidence of benefit for using many of the medications that are given in heart failure with reduced ejection fraction.

Some medications can be trailed that may reduce admissions such as mineralcorticoid receptor antagonists. However, the mainstay of treatment is the use of diuretics such as furosemide to manage fluid overload and addressing the underlying cause (e.g. blood pressure control in hypertension).

Acute heart failure

Acute heart failue may represent a sudden acute insult in a previously well individual such as secondary to a myocardial infarction, acute valvular abnormality or arrhythmia. Alternatively, patients with pre-existing heart failure may develop an 'acute decompensation' due to a concurrent illness or ongoing precipitating factor. Patients with acute heart failure can be extremely sick and may need intensive care support.

The principal management of acute heart failure is 'offloading' that refers to removing fluid from the body with the use of diuretics (e.g. furosemide).

Other options depend on the severity and mechanism of heart failure and can include:

  • Intravenous nitrate infusion
  • Continuous positive airway pressure (CPAP)
  • Inotropes
  • Invasive ventilation

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