Caring for patient in acute heart failure

Heart failure it the term used to describe state where the heart fails to maintain an adequate circulation for the needs of the body despite
an adequate venous return. Acute heart failure occurs as a result of a sudden decrease in ventricular function and may be associated with
an acute event such as a viral illness, valvular dysfunction or an acute myocardial infarction. Chronic heart failure develops over time and
is often the result of inability of auto regulatory mechanisms to compensate for decreased ventricular function. Acute heart failure
frequently occurs in patients with chronic, long standing impairment of ventricular function.
Learning Outcomes
Upon successful completion of this section, you should be able to:
describe the pathophysiology and classifications of heart failure
identify the risk factors and conditions that contribute towards heart failure
identify the neuro-hormonal compensatory mechanisms which occur in heart failure
relate the clinical manifestations of heart failure to the relevant pathophysiological processes
identify rationales for the investigations that aid in the diagnosis of heart failure
describe how the pathophysiology of heart failure impacts upon patient care, particularly in relation to pharmacological regimes
discuss the nursing care required for a patient in acute pulmonary oedema
discuss the psychosocial issues surrounding the patient with heart failure.
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Heart failure is associated with a failure of the normal body mechanisms which regulate blood flow. It is important
that you understand the role of the following compensatory mechanisms in the pathophysiology of heart failure.
You may need to consult a pathophysiology text to review the following.
Note the definitions of stroke volume, preload, afterload and contractility.
Describe the Frank Starling mechanism and its effect on cardiac output.
Describe the role of the following compensatory mechanisms for decreased cardiac output.
Include both the short and long term effects of stimulation of these systems
the sympathetic and parasympathetic nervous systems
the rennin angiotensin system
myocardial hypertrophy or remodeling
the naturetic peptides.
Define the following terms:
positive and negative inotropes
positive and negative chronotropes
adrenergic receptor.
Lecture Notes – Click Here
Acute Heart Failure physiology and CP…
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Core text reading
Core text reading
Aitken, A, Marshall, A, & Chaboyer, W., 2015, ACCCN’s critical care nursing, 3nd edn, Elsevier, Australia, Chapter 10, pp 285-304.
Optional Reading
Laurent, D 2010, chapter 24 ‘Heart failure and cardiogenic shock’, in Wood, S, Froelicher, M & Motzer, S (eds),
Bridges cardiac nursing, 6th edn, Lippincott,Williams and Wilkins, Philadelphia, pp. 555-578. (Also available on
Journals at Ovid (Books) database.)
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Heart and lung interaction
Understanding the interaction between the heart and lung in spontaneous breathing is important for understanding some of the clinical
signs and symptoms related to heart failure.
Blood flows through the right side of the heart to the lungs, and then back to the left side of the heart through the aortic valve and root to
the systemic circulation. This flow is mainly dependent on differences in pressure between circulation compartments with blood flowing
from high pressure to low pressure. These pressures are affected by gravity and movement of the chest wall for breathing and the
contraction of the heart muscle. The compartments are the venous bed (mainly the abdominal and splanchnic circulation) the right atrium,
the right ventricle, the pulmonary circulation, the left atrium, the left ventricle, the aortic root and the arterial bed. The pressures are higher
in the thicker walled elastic arterial and left ventricle compartments than the thin walled, easily collapsible venous compartments.
Blood returns to the heart during inspiration when the pleural pressure becomes more negative from chest wall moving out causing the
right atrium to dilate—lowering its pressure hence the gradient between the venous bed (in the abdomen and muscle) is increased to a
point that blood flows from a higher to a lower pressure into the right atrium. The right ventricle dilates to receive the incoming blood as
does the pulmonary bed from the release of atrial naturetic peptide that the dilating right atrium releases. The larger the breath volumes
during inspiration the greater the diaphragm and intercostals movement and hence the lower the pleural pressures. The pulmonary bed
dilates and constricts in response to the lung volumes and compliance and oxygen concentration which is varied throughout the lung. This
pulmonary blood once oxygenated flows into the left atrium and left ventricle during diastole from a high to a low pressure with some
assistance from gravity.
The term transmural pressure (PTM) or the difference in pressure across the walls of each of the compartments or vessel or organ
(Transmural pressure = internal surface pressure—external surface pressure) is referred to in literature you will read. There is a transmural
pressure of the heart, the aortic root and the lung—but the lung is explained in terms of transpulmonary pressure (pressure difference
between blood vessels and alveolar) and intrathoracic pressure as the large vessels in the thoracic as well as the pleural space have a
larger impact on pressure than just the lung and lung tissue.
As ventricular afterload is defined as the force opposing ejection, ventricular afterload is represented by the level of transmural pressure,
in the course of systole, within either the aortic root (LV afterload) or the pulmonary artery trunk (RV afterload). In terms of the LV; at the
onset of spontaneous inspiration, the intraluminal pressure in the aortic root decreases less than does intrathoracic pressure, due to the
connection of this vessel with extrathoracic arteries. As a result, aortic transmural pressure increases.
Spontaneous deep breathing places the acute failing heart under stress as it increases preload and afterload
With spontaneous breathing therefore, LV afterload is greater in inspiration than in expiration. Respiration has a profound effect on LV
afterload in pathologic conditions, such as when negative intrathoracic pressures (from large spontaneous breaths and increased work of
breathing) are exaggerated (e.g. in sleep apnoea, acute pulmonary oedema or respiratory failure) or when LV systolic function is impaired.
This concept is exampled in sleep apnoea where large breath volumes after periods of apnoea increase the aortic root pressure hence
increasing the LV afterload, causing the left ventricle to dilate to work harder to contract and over time leading to systolic heart failure
(large dilated LV) similar to those with chronic hypertension.
Heart Lung interactions in spont breath…
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Pathophysiology of heart failure
Thompson, PL (ed.) 2011, Coronary care manual, 2nd edn, Elsevier, Australia. Chapter 12 ‘Pathophysiology of cardiac failure’, pp.
88-95 – Click here
Heart failure is frequently classified according to the section of the heart, or the aspect of cardiac function which is affected. In this way
definitions of forward and backward failure have been used as well as left and right sided, and systolic and diastolic failure. It is important
that you understand these definitions and can distinguish between different types of heart failure according to their pathophysiological
Systolic and Diastolic Heart Failure
The distinction between systolic (enlarged floppy ventricle) and diastolic heart failure (smaller, tighter and less elastic ventricle) is an
important one to understand as it impacts greatly on critical care nursing practice. Both systolic and diastolic heart failure result in an
inability of the heart to provide adequate blood flow to meet perfusion demand. While systolic heart failure results from impaired cardiac
contractility, diastolic heart failure results from impaired ventricular compliance resulting in impaired filling. Both systolic and diastolic heart
failure can occur simultaneously.
Use your resources to find the answers to the following questions.
Distinguish between the pathophysiology of left and right sided heart failure.
Describe the pathophysiology of systolic and diastolic heart failure.
Describe the effects of systolic and diastolic heart failure on preload, afterload and contractility of the heart.
What is meant by the term Left Ventricular Ejection Fraction (LVEF). How is this measured and what is the
normal value.
Distinguish between the clinical manifestations of left and right sides heart failure and systolic and diastolic
Diastolic Heart Failure diagnoisis and t…
Medical School – Heart Failure with Re…
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Lifespan considerations
As with adults, heart failure is a associated with a cardiac output that is inadequate to meet the metabolic needs of the body. In children,
congenital heart disease is the most common cause of heart failure. A congenital heart defect must be considered in any neonate or infant
who presents with circulatory or respiratory compromise.
Heart failure in children can be placed in 3 categories
Ventricular pump dysfunction – this will result in reduced contractility therefore imparing ventricular ejection. Causes may include
cardiomyopathy, myocarditis, arrhythmias and congenital heart disease.
Volume overload with preserved ventricular contractility – Increased preload may occur where there is a left to right shunt of blood
from the systemic to the pulmonary circulation. This may be due to septal defects, patent ductus arteriosus and aortapulmonary windows.
Pressure overload with preserved ventricular contractility – An increase in afterload may occur when there is a ventricular outflow
obstruction that impedes blood ejection, e.g, aortic and pulmonary stenosis.
Heart failure in children can also be caused by severe, chronic anaemia or inflammatory cardiac disease. The clinical signs of heart failure
may include lethargy, weakness and fatigue, tachycardia, decreased urine output and increasing peripheral vasoconstriction.
The link will provide you with a more detailed view of heart failure in the paediatric population. – Click Here (Singh, R.K
Older Adult
Several specific changes in cardiac structure and function are associated with cardiac ageing, and they may explain a number of
pathophysiological and phenotypic features typical of the elderly. Particularly important is the greater predisposition of the elderly to
develop HF, particularly HF with preserved ejection fraction.
Figure 1: Pathophysiological mechanisms predisposing to the development of diastolic dysfunction and heart failure in otherwise healthy ageing hearts. European Journal of
Heart Failure Volume 15, Issue 7,page 717.
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Pharmacological management of heart failure
Management of heart failure focuses on relief of symptoms and enhancement of cardiac performance. This includes correcting any
precipitating causes such as coronary artery disease hypertension and arrhythmias. In the critical care environment support of more than
one body system is frequently required in the patient with acute heart failure who presents with cardio-respiratory failure.
Cardiac performance is optimised in heart failure by correction of any precipitating causes such as coronary artery disease, hypertension
and arrhythmias. Preload, afterload and contractility are optimised using fluid and medication therapy. (Note that cardiogenic shock and
cardiac assist devices are covered in semester 2 )
Thompson, PL, (ed.) 2011, Coronary care manual, 2nd edn, Elsevier, Australia. – Click Here
Chapter 31 ‘Beta-blockers’, pp. 241-245.
Chapter 32 ‘Ace-inhibitors and angiotensin receptor blockers’, pp. 247-52.
Chapter 33 ‘Aldosterone blockade’, pp. 253-257.
Chapter 34 ‘Calcium channel blockers’, pp. 258-261.
Chapter 35 ‘Nitrate therapy’, pp. 263-266.
Review the actions of the following major pharmacological groups on cardiovascular function. Give and example of
each. Give consideration as to if they have an effect on preload, afterload, or contractility in heart failure.
Beta blockers.
Angiotensin-Converting Enzyme (ACE) inhibitors.
Angiotensin II receptors blockers.
Calcium channel blockers.
Cardiac glycoside, i.e. digoxin.
Define the terms agonist and antagonist.
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Inotropes in acute heart failure
Inotropes are used extensively for patients with heart failure to maintain blood pressure and improve cardiac output. Sympathemometic
(catecholamine) inotropic agents include agents such as adrenaline, adrenaline and dopamine which are naturally occurring as well as
others such as dobutamine which is not. These agents act on the adrenergic receptors of the sympathetic nervous system. There are also
two major types of adrenergic receptors, alpha receptors and beta receptors. The beta receptors in turn are divided into beta and beta
receptors. Also, there is a division of alpha receptors into alpha and alpha receptors. The actions of these receptors are detailed in the
reading below.
Other positive inotropes fall into the category of phosphodiesterase inhibitors. The most commonly used of these in the Australian clinical
setting is milrinone.
Vasopressin often used in conjunction with noradrenaline, is often considered to be an inotrope as it increases blood pressure; however, it
is one of the most important endogenously released stress hormones, especially during shock. Vasopressin acts on vasopressin receptors
and not only vasoconstricts but also vasodilates some vascular beds making its action different to other vasoconstricting agents.
The drugs mentioned below can be used in acute heart failure. Organise them into a table defining them by group
and describe their action including any activation of adrenergic receptors where applicable. State whether each
drug is used for reduction in preload or afterload or both, or whether they are used for inotropic or chronotropic
support. Include the effect of different dose rates.
Glycerol Trinitrate (GTN)
Sodium Nitroprusside
1 2
1 2
Thompson, PL, (ed.) 2011, Coronary care manual, 2nd edn, Elsevier, Australia. – Click Here
Chapter 38 ‘Inotropic and vasoactive agents’, pp. 284-289.
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Acute pulmonary oedema
Patients with acute heart failure often present with symptoms of acute pulmonary oedema due to the influx of fluid from the circulation
across the alveolar capillary membrane and into the alveolar space. This causes a reduction in gas exchange, alveolar collapse and poor
ventilation perfusion relationship. Acute pulmonary oedema can be associated with both systolic and diastolic failure but leading to an
increase in hydrostatic pressure within the pulmonary capillaries. In acute heart failure diastolic heart failure (cramped heart) from
myocardial ischaemia is very common.
Thompson, PL (ed.) 2011, Coronary care manual, 2nd edn, Elsevier, Australia. Chapter 66 ‘Cardiac failure and acut pulmonary
oedema after acute coronary syndromes’, pp. 503 -508 – Click here
The typical patient with acute cardiogenic pulmonary oedema is pale; cool to touch and sweaty, reflecting intense sympathetic nervous
system activation, obviously breathless and sitting upright. Coughing up pink frothy sputum is relatively uncommon. Patients may have a
central or peripheral cyanosis and reduced oxygen saturations. The venous pressure is often clinically normal and the jugular venous
pressure hard to estimate but elevated in well hydrated patients (but most often they are dehydrated). Most patients do not have
peripheral oedema. Auscultation of the chest often reveals bilateral fine basal pulmonary crepitations that do not clear on coughing and
there may be high-pitched expiratory rhonchi.
Acute pulmonary oedema (APO) usually occurs in those with a history of hypertension. Hypertensive patients have a very sensitive
sympathetic nervous system (and accompanying neurohormonal compensation) so when chest pain or myocardial ischaemia stimulates
the sympathetic drive; there is extremely sudden and massive shunting of peripheral blood to the pulmonary bed causing fluid overload
that diffuses through to the alveolar hilum and space causing pulmonary oedema. One of the reasons for success of non-invasive
ventilation (NIV) in APO is that because NIV increases the positive pressure in the thorax; blood return to the thorax is impeded thereby
transferring blood to the systemic veins. Diuretics such as Frusemide which are commonly prescribed for APO are effective because they
vasodilate the venous bed also moving blood from the pulmonary bed to the peripheral venous bed. They also have a diuretic affect; often
not desired in a dehydrated APO patient without peripheral oedema who has blood in the wrong (pulmonary bed) compartment.
Cardiogenic Pulmonary oedema
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The use of continuous positive airway pressure in acute heart failure
Continuous Positive Airway Pressure, (CPAP) has been used successfully to treat patients with a sudden onset of acute pulmonary
oedema, as has other forms of non invasive ventilation such as bi level positive airway pressure (BiPAP). Both of these therapies improve
pulmonary gas exchange and reduce work of breathing as well as improving cardiovascular performance in the failing heart. This section
focuses on the cardiovascular effect of these therapies in acute pulmonary oedema. The nursing care of patients undergoing NIV is
covered in subsequent sections.
Positive pressure ventilation reduces preload and afterload in the failing heart
During systole, NIV increases the intrathoracic pressure (and the pleural pressure is much less negative)and reduces venous return, thus
decreasing the right and left ventricular preload; in diastole, NIV increases the pericardial pressure, reduces PTM, and thus decreases
afterload in the left ventricle wall as well as in the aortic root.
NIV also causes a decrease in the heart rate secondary to lung inflation and resultant increased parasympathetic tone (remember the
increased sympathetic tone that caused the sudden shift in fluid—this parasympathetic tone counteracts that). Recent evidence suggests
that the use of CPAP in patients with AHF decreases intubation rate and improves survival.
Flash Pulmonary Edema Emergency
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Acute heart failure and cardiogenic shock: a multidisciplinary practical guidance. Intensive Care Med 2015;42:147-63. – Click Here
Kee, K & Naughton, MT 2010, ‘Heart failure and the lung’, Circulation, vol. 74, no. 12, pp. 2507-2516.

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