WARD 10 (heart failure)

Question 1

What is heart failure?

Answer 1

• A state where the heart can’t adequately pump enough blood to meet the body’s demands or receive blood effectively (leading to inadequate perfusion of organs and tissues) or can do so only at elevated filling pressures
• structural or functional impairment of
  ventricular filling or ejection of blood
• In pathophysiologic terms, HF has been defined as a syndrome characterized by elevated cardiac filling pressure and/or inadequate peripheral oxygen delivery, at rest or during stress, caused by cardiac
  dysfunction
• It is not a single disease entity but a clinical syndrome that represents the final pathway of multiple cardiac diseases

Question 2

What are the symptoms caused by heart failure based on mechanism?

Answer 2

• Low output (forward failure) causes
  fatigue, dizziness, muscle weakness, and shortness of breath, which is
  aggravated by physical exercise. = Increased filling pressure leads to congestion of the organs upstream of the heart (backward failure), clinically
  apparent as peripheral or pulmonary edema, maldigestion, and ascites.

Question 3

How are most patients with heart failure diagnosed?

Answer 3

Most patients with heart failure are diagnosed exclusively on the basis of
symptoms; that is, their heart function has never been directly measured
(e.g., by echocardiography)

Question 4

Types of heart failure

Answer 4

• Systolic failure (HFrEF)
• Heart failure with mildly reduced EF (HFmrEF)
• Diastolic failure (HFpEF)
• Left ventricular failure
• Right ventricular failure
  Note: Because most patients with HF (regardless of EF) have abnormalities
  in both systolic and diastolic function, the older terms of systolic heart
  failure and diastolic heart failure have fallen out of favor

Question 5

What is are reasons for systolic heart failure?

Answer 5

• Most commonly due to Ischemic heart disease causing either acute (myocardial infarction) or chronic loss of viable heart muscle mass
• Other reasons include chronic arterial hypertension and valvular diseases (both are decreasing in incidence due to improved therapy), genetically determined primary heart muscle defects (cardiomyopathies),
  viral infections (cytomegalovirus and possibly parvovirus),
  and toxins

Question 6

Toxins that can lead to heart failure

Answer 6

excessive alcohol, cocaine, amphetamines, and cancer drugs such as doxorubicin or trastuzumab

Question 7

Pathophysiology of heart failure

Answer 7

The pathophysiology of heart failure is
complex and involves four major interrelated systems:
* the heart itself
* the vasculature (increased peripheral stiffness)
* the kidney
* neurohumoral regulatory circuits

Question 8

Response to overload in the heart

Answer 8

• The usual response to overload is not myocyte division (since that stops in early postnatal period) but rather hypertrophy, growing in size and assembling more sarcomeres that can contribute to contractile force development.
• A direct consequence of cardiac myocyte hypertrophy is a reduced capillary/ myocyte ratio (i.e., less O2 and nutrient supply per myocyte), causing
  an energy deficit and metabolic reprogramming. Altered gene expression of ion channels, Ca2+-regulating proteins, and contractile proteins can be interpreted as partially beneficial, energy-saving adaptations; on the other hand, the adaptations also aggravate contractile failure and favor
  arrhythmias.
• Concurrently, fibroblasts proliferate and deposit increased
  amounts of extracellular matrix (e.g., collagen). This fibrosis in heart failure
  also favors arrhythmias, increases the stiffness of the heart, and interrupts
  myocyte-to-myocyte communication (coordinated conduction and
  force transmission). Finally, overload leads to cardiac myocyte death by
  apoptosis or necrosis. Collectively, these adverse adaptations are called
  pathological remodeling

Question 9

What influences heart alterations in heart failure?

Answer 9

Some of these alterations are direct, heart-intrinsic consequences of
overload (e.g., hypertrophy, altered gene expression); others are secondary
to neurohumoral activation and thereby susceptible to neurohumoral
blocking agents

Question 10

What is vascular compliance and what does it achieve and its correlation with pulse pressure

Answer 10

• The elasticity that permits vessels to extend in systole and contract in
  diastole.
• Good compliance reduces peak systolic pressure and increases
  diastolic pressure, which favors perfusion in diastole.
• It is negatively correlated with pulse pressure, that is, the difference between systolic and diastolic blood pressure, which is low in children and high in the elderly

Question 11

What is the main reason for reduced compliance?

Answer 11

Arterial hypertension and diabetes mellitus are the major reasons for
premature stiffening of blood vessels, which imposes increased afterload
to the heart and contributes to heart failure

Question 12

Summarized pathophysiology cycle in systolic heart failure

Answer 12

• Any major decrease in cardiac contractile function leads to activation of neurohumoral systems, including the SNS, the RAAS, and vasopressin (ADH) secretion, which acutely stabilize blood pressure and organ perfusion by stimulating cardiac output, constricting resistance vessels, decreasing kidney perfusion, and increasing Na+ and H2O retention.
• Unfortunately, these responses are maladaptive, causing chronic overloading and overstimulation of the failing heart.
• Direct hypertrophic, pro-apoptotic, fibrotic, and arrhythmogenic
  effects of NE and AngII further accelerate the deleterious process.
• Note that the concomitant activation of the ANP/BNP system is the consequence of stretch and increased wall stress in the heart and has opposite and beneficial effects.

Question 13

Characteristics and physiology of the heart in systolic heart failure

Answer 13

In heart failure with reduced ejection fraction, the left ventricle enlarges and weakens, and the pressure-volume relationship reveals a reduction in stroke volume, an elevation in left ventricular end-diastolic pressure, and an increase in left ventricular end-diastolic volume.

Question 14

Which diseases is HFpEF associated with?

Answer 14

• HFpEF is typically associated with arterial hypertension, ischemic heart
  disease, diabetes mellitus, and obesity (metabolic syndrome);
• Also associated with atrial fibrillation, age-related cardiac changes, and underlying structural heart abnormalities such as hypertensive heart disease, and CKD

Question 15

Characteristics and physiology of the heart in diastolic heart failure

Answer 15

Heart failure with preserved ejection fraction is associated with hypertrophy and abnormal lusitropy, and the pressure-volume relationship indicates an elevation in end-diastolic pressure along with a reduction in stroke volume and left ventricular end-diastolic volume.

Question 16

What can heart failure be classified using?

Question 17

Chronic vs acute heart failure

Answer 17

Chronic heart failure describes patients with longstanding (e.g., months to years) symptoms and/or signs of HF typically treated with medical and device therapy
- Acute heart failure, previously termed acute decompensated HF, refers to the rapid onset or worsening of symptoms of HF.

Question 18

What are episodes of acute HF due to?

Answer 18

Most episodes of acute HF
result from worsening of chronic HF, but ~20% are due to new-onset
HF that can occur in the setting of acute coronary syndrome, acute valvular
dysfunction, hypertensive urgency, or postcardiotomy syndrome

Question 19

What is cardiotomy

Answer 19

a surgical procedure where an incision is made in the heart.

Question 20

What is acute pulmonary edema in the context of AF?

Answer 20

acute pulmonary edema in HF describes a clinical scenario in which a patient presents with rapidly worsening signs and symptoms of pulmonary congestion, typically due to severe elevation of left heart filling pressure.

Question 21

Prevalence and risk of AF based on age

Answer 21

The prevalence of HF increases significantly with age, occurring in 1–2% of the population aged 40–59 years and up to 12% of adults >80 years old (Fig. 257-1). The lifetime risk of HF at age 55 years is 33% for men and 28% for women.

Question 22

Which race is at higher risk of developing heart failure and why?

Answer 22

• blacks have the highest risk of developing HF, followed by Hispanic,
  white, and Chinese Americans
• These differences are attributed
  to disparities in risk factors (e.g., obesity, hypertension, diabetes),
  socioeconomic status, and access to health care.

Question 23

Mortality rate from HF

Answer 23

• In primary care, the overall 5-year survival following the diagnosis of HF is - ~50%. For patients with severe
  HF, the 1-year mortality may be as high as 40%.

Question 24

How often is HF seen on death certificates in USA?

Answer 24

In the United States,1 in 8 deaths list HF on the death certificate

Question 25

Ratio of HFrEF to HF

Answer 25

One-half of patients who develop HF have reduced left ventricular ejection fraction while the other half have near-normal or preserved EF

Question 26

Ejection fraction in different heart failure phenotypes

Answer 26

HFrEF ≤40%
HFmrEF 40-50%
HFpEF ≥50%

Question 27

Neurohormonal activation in HF

Answer 27

Activation of the sympathetic nervous
system (SNS) and renin-angiotensin-aldosterone system (RAAS)
plays a critical role in the development and progression of HF. Initially,
neurohormonal activation leads to increases in heart rate, blood
pressure, and cardiac contractility and retention of sodium and water
to augment preload and maintain cardiac output at rest and during
exercise. Over time, these unchecked compensatory responses lead
to excessive vasoconstriction and volume retention, electrolyte and renal abnormalities, baroreceptor dysfunction, direct myocardial toxicity, and cardiac arrhythmias. At the tissue level, neurohormonal activation contributes
to remodeling of the heart, blood vessels
(atherosclerosis), kidneys, and other organs and the development of symptomatic
HF
- Decreased cardiac output in heart failure (HF) results in an “unloading” of high-pressure baroreceptors (circles) in the left ventricle, carotid sinus, and
aortic arch, which in turn causes reduced parasympathetic tone. This decrease in afferent inhibition results in
a generalized increase in efferent sympathetic tone and nonosmotic release of arginine vasopressin from the
pituitary. Vasopressin is a powerful vasoconstrictor that also leads to reabsorption of free water by the kidney.
Afferent signals to the central nervous system also activate sympathetic innervation of the heart, kidney, peripheral vasculature, and skeletal muscles. Sympathetic stimulation of the kidney leads to the release of renin, with a resultant increase in circulating levels of angiotensin II and aldosterone. The activation of the renin-angiotensin aldosterone system promotes salt and water retention, peripheral vasoconstriction, myocyte hypertrophy, cell death, and myocardial fibrosis. Although these neurohormonal mechanisms facilitate short-term adaptation by maintaining blood pressure, they also result in end-organ changes in the heart and circulation

Question 28

Vasodilatory hormones in HF

Answer 28

While RAAS
and SNS activation contributes to disease
progression in HF, a number of counterregulatory
hormones are upregulated and exert
beneficial effects on the heart, kidney, and
vasculature. These include the natriuretic
peptides (atrial natriuretic peptide [ANP]
and B-type natriuretic peptide [BNP]),
prostaglandins (prostaglandin E1 [PGE1]
and prostacyclin [PGI2]), bradykinin, adrenomedullin,
and nitric oxide. ANP and BNP
are stored and released primarily from the
atria and ventricles, respectively, in response
to increased stretch or pressure. Beneficial
actions are mediated through stimulation of
guanylate cyclase and include systemic and
pulmonary vasodilation, increased sodium
and water excretion, inhibition of renin and
aldosterone, and baroreceptor modulation.

Question 29

Renal dysfunction in HF

Answer 29

Traditionally, this relationship was deemed to be a consequence of an
impairment in forward flow (cardiac output) leading to a decrease in
renal arterial perfusion, worsening renal function, and neurohormonal
activation with release of arginine vasopressin, resulting in water and
sodium retention. However, evidence has emerged that renal dysfunction
may not be adequately explained simply by arterial underfilling
and a decline in cardiac output. Systemic venous congestion in HF
with increased backward pressure may be operative in determining the
development of the cardiorenal syndrome, and relief of venous congestion
is associated with significant improvement in renal function
in HF

Question 30

What can symptoms of heart failure be divided into?

Answer 30

• Symptoms of congestion: Pulmonary venous congestion (seen in left HF) versus systemic (right HF)
• Symptoms of reduced perfusion
• Other symptoms (nocturia, mood disturbances, poor sleep)
• Generally: Shortness of breath, orthopnea, paroxysmal nocturnal dyspnea, Persistent cough or wheezing
  . Edema (generalized or lower extremity).
  Fatigue and Tiredness, Lack of appetite and nausea (because some patients develop right upper quadrant pain related to stretching of the hepatic capsule), Confusion and impaired thinking, Palpitations

Question 31

Symptoms of congestion in HF

Answer 31

• The most common symptoms of HF are related to volume overload with
  elevation in pulmonary and/or systemic venous pressures. Shortness of
  breath is a cardinal manifestation of left HF and may arise with increasing
  severity as exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and dyspnea at rest
• Weight gain and lower extremity edema may be the initial
  manifestations in right HF followed by a range of gastrointestinal symptoms due
  to edema of the bowel wall and hepatic congestion. Abdominal bloating,
  anorexia, and early satiety are common.

Question 32

Mechanism of dyspnea in HF

Answer 32

Mechanisms of dyspnea include pulmonary venous congestion and transudation of fluid into the interstitium
and/or alveoli, leading to decreased lung compliance, increased airway
resistance, hypoxemia, and ventilation/perfusion mismatch

Question 33

What is orthopnea and why does it occur

Answer 33

dyspnea that occurs in the recumbent position and is due to redistribution of fluid from the abdomen and lower body
into the chest, increased work of breathing due to decreased lung compliance, and, in patients with ascites or hepatomegaly, elevation of the
diaphragm

Question 34

What is paroxysmal nocturnal dyspnea?

Answer 34

Paroxysmal nocturnal dyspnea (PND) refers to episodes of shortness
of breath that awaken a patient suddenly from sleep with feelings
of anxiety and suffocation and require sitting upright for relief.

Question 35

Acute pulmonary edema symptoms

Answer 35

Severe shortness of breath and pink, frothy sputum

Question 36

Symptoms of reduced perfusion HF

Answer 36

Some patients with advanced
HF present with symptoms related to decreased CO, sometimes
referred to as low-output syndrome. Fatigue and weakness, particularly
of the lower extremities, are nonspecific symptoms that can occur with
exertion or at rest

Question 37

symptoms and survival of patients with HFpEF and HFrEF

Answer 37

Patients had typical heart failure symptoms, including acute decompensation with pulmonary edema and a survival prognosis not much better or even identical to patients with reduced EF (systolic heart failure or HFrEF).

Question 38

Signs of heart failure

Answer 38

Pulses alternans
Cyanosis
Elevated jugular venous pressure
Displaced LV apex beat
Cardiac cachexia
Pallor
Sinus tachycardia
Right ventricular heave
Bilateral rales/ crepitations or a cardiac wheeze on lung exam
Presence of S3
Pitting edema in dependent areas
Tender hepatomegaly
Ascites
Cool extremities and cyanosis (

Question 39

What is pulsus alternans

Answer 39

an arterial pulse with alternating strong and weak beats