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.
4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failure
https://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585804 4/13
Review
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
dromotrophy
adrenergic receptor.
Lecture Notes – Click Here
Acute Heart Failure physiology and CP…
4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failure
https://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585804 5/13
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.)
4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failure
https://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585804 6/13
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…
4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failure
https://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585804 7/13
Pathophysiology of heart failure
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