The Inotrope Workshop is required education to enable RNs  to care for patients with intractable heart failure requiring low dose inotropes on  the cardiology medical unit.

Through this education you will :

All education is  based on caring for the patient as per  NCS6235 Vasoactive Agents (Infusion) on Cardiology Ward (5A) and the infusion protocols in the Parenteral Drug Therapy Manual (PDTM). 

This online module is broken into five sections. Please familiarize yourself with the information in this module  in preparation for the classroom portion of the workshop. 

What is Heart Failure?

What is Heart Failure

Heart failure (HF) is a process where the heart weakens over the course of months or years until it is unable to pump out all the blood that enters the chambers. HF is usually the result of myocardial damage due to infarction, inflammation, toxic injury, or cardiomyopathy, and the body's compensation  for the injury. 

Heart failure can occur in a number of ways:

  • muscles of the ventricles become thin, weak, and stretched so they are no longer able to pump enough blood to meet the body's needs
  • muscles of the ventricles become stiff and/or thickened, losing their elasticity and ability to relax. Not enough blood is able to enter the ventricle so not enough can be pumped to the body to meet its needs
  • incompetent valves, narrowing or stiffening of valves, cause the regulation of flow to be hindered, or blood to flow back into the chamber 
  • the body's compensatory mechanisms to deal with decreased cardiac output can cause remodelling of the heart and further failure

What is not a primary cause of heart failure?

  • High blood pressure
  • Cardiomyopathy
  • Poliomyelitis
  • Coronary artery disease

Heart failure is a chronic condition which requires attention to diet, a reduction of stress, and daily medications. Which of the following would most increase the burden on an already weakened heart?

  • Narcolepsy
  • Consuming alcohol
  • Eating a hamburger
  • Obesity

Heart Failure Pathophysiology

Heart Failure Pathophysiology


Neurohormonal Activation

Any major injury that reduces cardiac pumping capacity activates neurohumoral mechanisms, including the sympathetic nervous system. Sympathetic activation of the adrenergic system leads to:

  • vasoconstriction which increased blood flow resistance and maintains arterial pressure when the cardiac output is low (epinephrine and norepinephrine increase heart rate and  speed of impulse conduction and contractile force)
  • increase myocardial workload and oxygen consumption.  Blood is redirected from skin, muscles, kidneys and the GI system to  perfuse the vital organs (heart, lungs, and brain)
  • activates the renin-angiotensin-aldosterone system (RAAS) causing systemic vasoconstriction and sodium and water retention
Though this initial compensatory response helps support cardiac output, continued activation causes detrimental effects  and accelerates the decline of the heart:
  • peripheral vasoconstriction increases the work on the heart (afterload) stressing the failing heart and further decreasing cardiac output.
  • continued stimulation of cardiac myocytes leads to cell death, fibrosis, increase in energy production, myocyte hypertrophy and arrhythmias. 
  • type B natriuretic peptide (BNP), a hormone,  is produced in response to atrial and ventricular distension leading to greater sodium excretion and vasodilation. BNP acts directly on blood vessels to cause vasodilation, salt, and water excretion and inhibit secretion of renin, aldosterone, and vasopressin. An elevated BNP is believed to be one of the first signs of HF and is used to monitor its progression. 

Ventricular Remodeling

Responses to reduced cardiac output lead to myocardial remodelling (increased myocardial volume and mass but a net loss of myocytes). In order to compensate for a reduced volume, the heart has the ability to change the strength of contractions and thus stroke volume. This is achieved by left ventricular enlargement; however, this cannot occur indefinitely. As the myocardial tissue grows, the interaction between contractile cells is reduced. 

The systemic response to a decrease in cardiac output accelerates heart rate, constricts arteries and veins, increases the ejection fraction, and increases blood volume through sodium and salt retention. A range of compensatory mechanisms respond to decreased circulation and lead to the clinical syndrome of heart failure. Two of the common compensatory mechanisms the module will discuss include neurohormonal activation and ventricular remodelling.

Heart failure is a syndrome defined as both structural heart changes and patient symptoms.

  • True
  • False

Heart Failure Classifications

Heart Failure Classifications

Heart failure can be classified according to the affected chambers of the heart, the affected side of the heart, or whether it is acute or chronic.

Chronic vs. Acute
The terms chronic and acute relate to time rather than acuity. As heart failure develops over the course of many years it can be considered a chronic condition. Once heart failure has been diagnosed, episodes of decompensation  (worsening signs and symptoms of heart failure) can occur frequently. These episodes of decompensation are often called acute, however, decompensated is the preferred term. 

In a small percentage of cases, a sudden onset of heart failure signs and symptoms in a person with no history of heart failure with a previous normal cardiac function may also be called acute. 

Left vs. Right  
Right ventricular failure results in signs of inadequate peripheral circulation.  Blood flow from the right to the left side of the heart is insufficient causing poor blood flow to the left ventricle.  Left ventricular failure results in signs of pulmonary congestion/edema, and poor circulation to the vital organs and periphery.

Left-sided heart failure is more common than the right-sided failure and can be caused by abnormal systolic or diastolic action (see below). Left-sided heart failure can be further broken down into heart failure with reduced ejection fraction (HFrEF) or heart failure with preserved ejection fraction (HFpEF).

The following are common signs and symptoms associated with left-sided heart failure:

  • respiratory symptoms: may include dyspnea, tachypnea, dyspnea on exertion, increased work of breathing, orthopnea, paroxysmal nocturnal dyspnea, wheezing, cough, pulmonary crackles, pleural effusion
  • weakness, fatigue, decreased exercise tolerance
  • changes in mental status that may include restlessness, insomnia, nightmares, memory loss, anxiety, agitation, paranoia, confusion
  • diaphoresis, palpitations, tachycardia, S3, and S4, laterally displaced apical pulse, weight gain, pallor, cool extremities

Right-sided heart failure  is most often a result of left-sided failure. When the right ventricle fails blood received cannot be pumped out effectively and backs up. This  leads to congestion of systemic capillaries generating excess fluid accumulation, often in ankles, feet, legs and abdomen.  Increased pulmonary pressure or lung disease can also cause right-sided heart failure. 

The following are common signs and symptoms associated with right-sided heart failure: 

  • weight gain, peripheral edema, lower limb heaviness (usually, a substantial gain of extracellular fluid volume (ie, a minimum of 5 L in adults) must occur before peripheral edema develops) 
  • nocturia, diuresis at rest,  
  • ascites, abdominal distention, gastric distress, anorexia, nausea, constipation, hepatomegaly
  • neck vein distention
  • fatigue, shortness of breath

Heart Failure with Preserved Ejection Fraction (HFpEF)
Historically heart failure with a preserved or normal ejection fraction was referred to as diastolic heart failure as it was believed that there was  diastolic dysfunction (inability to relax/stiffness). However, recent research indicates that this may not always be the case and other aspects of pathophysiology may contribute to symptoms. Diastolic heart failure is now referred to as HFpEF. HFpEF is less well understood than HFrEF. 

HFpEF is a clinical syndrome characterized by clinical signs and symptoms of heart failure, normal EF (50%), and impaired diastolic function. HFpEF is almost always associated with co-morbidities including hypertension, coronary artery disease, diabetes, obesity, dyslipidemia, sleep apnea, lung disease, anemia and renal disease. 

Patients with HFpEF tend to be older (>65 yrs), female, have a higher body mass index, more likely to be obese, and have a below normal hemoglobin level. Some studies indicate that there is also a higher incidence of atrial fibrillation but less coronary artery disease or valve disease than HFrEF patients.  

During diastole, the myocardium relaxes and the ventricles stretch to allow the chambers to fill with blood. In patients with HFpEF, myocardial relaxation is impaired. This impacts the left ventricle's filling time and increases the chamber's stiffness. While the ejection fraction is preserved in HFpEF, systolic and myocardial function are abnormal. Below is a list of some of the causes of diastolic dysfunction. 

Heart Failure with Reduced Ejection Fraction (HFrEF)
The more common type of heart failure, occurring in about 50 % of patients,  is heart failure with a reduced ejection fraction, or HFrEF. With HFrEF, the left ventricle is dilated and enlarged with poor systolic function and an ejection fraction of less than 40%. The pump fails and is unable to contract sufficiently to circulate required blood to organs and tissues. 

HFrEF can occur following myocardial infarction when ventricular tissue death reduces the heart's pumping efficiency. HFrEF can also be caused by prolonged stress on the heart from hypertension, valve disease, dysrhythmias, coronary artery disease, or damage to the ventricular wall. 

What is systolic heart failure?

  • The inability of the heart to pump out blood
  • The inability of the heart to fill with blood
  • The body's inability to get rid of extra fluid
  • When fluid builds up in the lungs

HFrEF is another name for right-sided heart failure.

  • True
  • False

Heart Failure Symptoms and Complications

Heart Failure Signs And Symptoms

Signs and Symptoms

Often the symptoms patients experience are a result of the congestion from fluid build-up in the lungs and periphery. Other symptoms are a result of inadequate oxygen delivery to body tissues. Common signs and symptoms you may see include:

  • Fatigue: feeling tired
  • Dyspnea: generally occurs after exertion but can progress to shortness of breath with minimal exertion. Orthopnea occurs when the patient lies flat at night - the fluid that had accumulated in the lower legs and is returned to right ventricle and the left ventricle is unable to compensate for the increased volume resulting in pulmonary congestion
  • Peripheral edema: appears in the feet, legs, ankles, abdomen, sacrum
  • Cough: a wheezing or dry hacking cough that occurs a few hours after lying down
  • Loss of muscle mass: can occur over time due to reduced physical activity which is limited by their symptoms
  • GI symptoms: loss of appetite, nausea, abdominal pain - due to increased fluid retention in the abdominal region
  • Pulmonary edema: is fluid build up in the lungs; can occur suddenly or gradually; can be associated with a cough and pinkish sputum
  • Arrhythmia: can have abnormally fast or slow rhythms
  • Central sleep apnea: occurs in up to 50% of heart failure patients; the brain fails to signal the respiratory muscles to breathe

Complications of Heart Failure
Because the heart is the pump that supplies blood to the body and all its organs, failure of this pump can have a multitude of effects. 

  • Impaired kidney function: decreased kidney function is common in patients with heart failure due to the heart's inability to adequately perfuse the kidneys. 
  • Congestion: fluid builds up  in the lungs (left-sided failure) or periphery (right -sided failure) due to the impaired pumping of the heart. Congestion is usually treated with sodium and fluid restriction and diuretics. 
  • Arrhythmias: arrhythmias become more common when the electrical system of the heart is disrupted by remodeling or fluid accumulation from impaired pump function. Some of the more common arrhythmias include atrial fibrillation, left bundle branch block and ventricular arrhythmias.
  • Angina and heart attack: heart failure patients are a continued risk for these events.

What are physical signs of a patient who is hypoperfused?

  • tachycardia, diaphoresis, weakness, decreased urine output, hypotension
  • edema, orthopnea, high jugular venous pressure, hepatojugular reflux
  • hypertension, fluid retention, confusion, bradycardia,
  • increased urine output, tachypnea, lower leg edema, vomiting

Arrhythmias are a potential complication of heart failure.

  • True
  • False

Heart Failure Treatment

Heart Failure Treatment

Heart failure ranges from acute cardiogenic shock to compensated chronic heart failure. Treatment depends on the specific heart failure stage and symptoms.  

Let's look at the patient who is in acute decompensated heart failure.
Chronic stable heart failure may easily decompensate. This most commonly occurs from a concurrent illness (such as pneumonia), myocardial infarction, arrhythmias, uncontrolled hypertension, or failure/inability to maintain a fluid restriction, diet, or medication.  Medications that cause fluid retention, such as NSAIDs,  may also precipitate decompensation. Other precipitating factors include anemia and hyperthyroidism which place additional strain on the heart muscle.

In order to determine correct treatment, a patient's hemodynamic profile needs to be determined. 
  • Wet or dry refers to the patient's fluid volume status. "Wet" patients would have signs of volume overload (dyspnea, edema). "Dry" patients are those who do not have extra fluid volume or may be fluid depleted.
  • Warm or cold refers to the patient's cardiac output and peripheral perfusion. "Warm" patients have adequate cardiac output and peripheral perfusion. "Cold" patients have inadequate cardiac output and poor peripheral perfusion. 

Patients are profiled according to their volume status and perfusion (i.e. warm and dry, cold and wet, etc). Patients who are hospitalized are generally of the warm and wet profile and require diuresis and adjustments to their current medications. However, patients in the wet and cold profile are those patients who are often no longer responding to the first line medications, like diuretics, and will require inotropic agents. 

Goals of treatment for heart failure are to reduce symptoms, decrease the need for hospitalization and improve survival.  Factors which exacerbate or precipitate heart failure must be addressed to achieve these goals.  

Adrenergic Receptors
Adrenergic receptors are located in the cells of muscles, such as the heart, bronchiole walls, GI tract, urinary bladder, and ciliary muscle of the eye. Although there are many adrenergic receptors, the four main receptors are alpha1, alpha2, beta1, and beta2. 

Inotropes work on these receptors. When catecholamines (epinephrine and norepinephrine) or their precursors bind to adrenergic receptors the sympathetic nervous system is stimulated ( increase blood pressure,  bronchial tubes, and heart rate). 
Effects of Adrenergic Receptors:
Alpha1 – Force of heart contraction is increased; vasoconstriction increases blood pressure, dilation of pupils occurs; decreased secretion from salivary glands; increased urinary bladder relaxation and urinary sphincter contraction.

Alpha2 – Norepinephrine release inhibited; blood vessels dilate; produces hypotension; gastrointestinal motility and tone decreased.

Beta1 – Increases heart rate and force of contraction; renin secretion increases, which in turn, increases blood pressure.

Beta 2 – Bronchioles dilate; promotes gastrointestinal and uterine relaxation; promotes an increase in blood sugar through glycogenolysis in the liver; blood flow in skeletal muscles increases. 

Dobutamine is a direct-acting inotropic agent used for short-term treatment of HF decompensation. Dobutamine acts primarily on the beta 1 adrenoreceptors of the heart  and increases contractility and cardiac output. It has weak beta 2 effects which make it useful as a vasodilator. 
Low doses  provide mild arterial vasodilation by reducing afterload and increasing preload.

  • Side Effects The major side effects of dobutamine include tachycardia, especially in patients with atrial fib, and atrial and ventricular arrhythmias. The overall effect on blood pressure is variable, depending on the effects on vascular tone and cardiac output achieved.  A 10-20 mmHg increase in systolic blood pressure and an increase in heart rate of 5-15 bpm have been noted in most patients. About 5% of patients will have increased PVCs during infusion. Dobutamine does not act on the dopamine receptors (which cause the release of norepinephrine) so is less likely to cause hypertension than dopamine. 

A sudden drop in blood pressure can occur occasionally with dobutamine. As well, dobutamine may cause a marked increase in heart rate (30 bpm or more) or blood pressure (50 mmHg or greater) in about 10% of patients. Decreasing the dose or stopping the infusion typically results in a rapid return to baseline blood pressure and heart rate. 

Less common side effects include nausea, headache, angina, palpitations, shortness of breath and a mild drop in serum potassium.

Milrinone causes inotropic/vasodilator effects by working on the phosphodiesterase enzyme. It is used for the short-term treatment of patients with decompensated HF. Milrinone increases the heart's contractility, vasodilation by decreasing afterload and pressure on the heart, and improving the heart's pumping action. 

  • Side Effects Ventricular arrhythmias (SVT, nonsustained VT) and ectopy (PVCs) can occur with milrinone infusions. Those with atrial fib can have increased ventricular response rates. Hypotension, angina, headaches, hypokalemia, rash, and tremor are less common but potential side effects. Blood pressure typically drops 5% at doses between 0.375 to 0.5 mcg/kg/min. 

Dopamine is a natural catecholamine and neurotransmitter in the CNS. Dopamine produces positive chronotropic  and inotropic effects through beta-adrenoceptors and  resulting in increased heart ´╗┐rate and contractility. Dopamine at low doses is used to treat HF decompensation by increasing cardiac output and decreasing systemic vascular´╗┐ resistance.  Effects are dose dependent. At low rates of infusion (0.5-2 mcg/kg/min) dopamine causes vasodilation that is presumed to be due to a specific agonist action on dopamine receptors (distinct from alpha and beta adrenoceptors) in the renal, mesenteric, coronary, and intracerebral vascular beds.

  • Side Effects Tachycardia, ectopy, angina, palpitations, vasoconstriction, hypotension, dyspnea, nausea, headache are potential side effects of dopamine. Local reactions at infusion site can cause skin necrosis, therefore dopamine requires infusion through a central line. 

What is inotropy?

  • The force of muscle contraction
  • The speed of electrical conduction through the heart
  • An increase in the heart rate
  • Rapid uncoordinated contractions of the ventricles

Patients typically require inotrope therapy when they are in the "wet & warm" category.

  • True
  • False

Check Your Knowledge

Cardiac output is determined by:

  • Stroke Volume X Heart Rate
  • Stroke Volume X contractility
  • Heart rate X contractility
  • Ejection fraction X preload

What is the name for the volume of blood in the ventricle immediately before it is ejected?

  • Preload
  • Afterload
  • Contractility
  • Automaticity

Stimulation of the sympathetic nervous system produces which of the following responses?

  • Bradycardia
  • Tachycardia
  • Hypotension
  • Decreased myocardial contractility

Which of the following is a neurohormonal change due to heart failure?

  • Activation of the parasympathetic nervous system
  • Activation of the sympathetic nervous system
  • Inhibition of the renin-angiotensin-aldosterone system
  • Inhibition of the anti-diuretic hormone

Which of the following symptoms is most commonly associated with left-sided heart failure?

  • Crackles
  • Arrhythmias
  • Hepatic engorgement
  • Hypotension

Shortness of breath that causes one to wake up at night is called:

  • Paroxysmal nocturnal dyspnea
  • Sleep apnea
  • Night-time dyspnea
  • Respiratory intolerance

Which of the following symptoms might a client with right-sided heart failure exhibit?

  • Adequate urine output
  • Polyuria
  • Oliguria
  • Polydypsia

Which of the following conditions is most closely associated with weight gain, nausea, and a decrease in urine output?

  • Angina
  • Cardiomyopathy
  • Left-sided heart failure
  • Right-sided heart failure

Which of the following classes of medications maximizes cardiac performance in clients with heat failure by increasing ventricular contractility?

  • Beta blockers
  • Calcium channel blockers
  • Diuretics
  • Inotropic agents

Which of the following foods should the nurse teach a patient with heart failure to avoid or limit when following a 2-gram sodium diet?

  • Beef tenderloin
  • Apples
  • Whole wheat bread
  • Tomato juice