Chapter 279 - Heart Failure: Pathophysiology and Diagnosis Flashcards Preview

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Flashcards in Chapter 279 - Heart Failure: Pathophysiology and Diagnosis Deck (47)

How prevalent is heart failure in developped countries?

2% regarding global population. It increases with age, affecting 6-10% of people over 65 years of age.


How do you explain that almost half of the patients with heart failure are women, although this clinical syndrome is relatively less common in comparison to men?

"Although the relative incidence of Heart Failure (HF) is lower in women than in men, women constitue at least one-half of the cases of HF because of their longer life expectancy."


Normal or preserved ejection fraction heart failure affects approximately one-half of the patients with heart failure syndrome.
True or False?



What is the most frequent etiology for heart failure in developped countries?

Coronary artery disease (60-75%), aggravated by hypertension (75%).


Name two toxic causes of dilated cardiomiopathy.

Alcohol and chemotherapy.


It is known that an increasing number of cases of dilated cardiomiopathy are due to genetic defects affecting the cytoskeleton.
True or False?

Cytoskeleton's proteins mutations are associated with various hypertrophic aswell as dilated cardiomyopathy.


High output diseases usually cause heart failure in structurally healthy hearts.
True or False?



Name mutations associated with dilated cardiomiopathy. How are these syndromes inheredited?

"Most forms of familial dilated cardiomyopathy are secondary to specific genetic defects, most notably those in the cytoskeleton. Most forms of familial dilated cardiomyopathy are inherited in an autossomal dominant fashion. Mutations of genes that encode cytoskeletal proteins (desmin, cardiac myosin, vinculin) and nuclear membrane proteins (laminin) have been identified thus far. Dilated cardiomyopathy also is associated with Duchenne's, Becker's, and limb-girdle muscular dystrophies."


Name three causes of premature atherosclerosis.

Hypothyroidism, Hyperhomocysteinemia and Pseudoxantoma elasticum.


What is the most frequent cause of heart failure in south America?

Chagas' disease.


What is the mortality rate in a patient with class I functional classification (NYHA) heart failure in comparison to a patient with class IV (NYHA)?

5-10% instead of 30-70%, respectively.


Symptomatic heart failure (HF) has a poor prognosis.
True or False?

"Community-based studies indicate that 30-40% of patiensts die within 1 year of diagnosis and 60-70% die within 5 years, mainly from worsening HF or as a sudden event (probably because of a ventricular arrythmia."


How come patients with heart failure (HF) might be asymptomatic for years?

"one potential explanation is that a number of compensatory mechanisms become activated in the presence of cardiac injury and/or left ventricular (LV) dysfunction allowing patients to sustain and modulate LV function for a period of months to years. The compensatory mechanisms that ahve been described thus far include (1) activation of the renin-angiotensin-aldosteron (RAA) and adrenergic nervous systems, which are responsible, respectively, for maintaning cardiac output through increased retention of salt and water, and (2) increased myocardial contractility."


What might explain the transition from asympatomatic to symptomatic heart failure (HF)?

"Although the exact mechanisms that are responsible for this transition are not known (...), the transition to symptomatic HF is acocompanied by increasing activation of neurohormonal, adrenergic, and cytoine systems that lead to a series of adaptive changes within the myocardium collectively referred to as LV remodeling."


The pathogenesis of heart failure (HF) with preserved ejection fraction (HFpEF) is related to diastolic dysfunction, aswell as additional extracardiac mechanisms (such as increased vascular stiffness and impaired renal function).
True or False?



Name the main events that lead to left ventricle (LV) remodeling.

"LV remodling develops in response to a series of complex events that occur at the cellular and molecular levels. These changes include (1) myocyte hypertrophy; (2) alterations in the contractile properties of the myocyte; (3) progressive loss of myocytes through necrosis, apoptosis, and autophagic cell death; (4) beta-adrenergic desensitization; (5) abnormal myocardial energetics and metabolism; and (6) reorganization of the extracellular matrix with dissolution of the organized structural collagen weave surrounding myocytes and subsequent replacement by an interstitial collagen matrix that does not provide structual support to the myocytes."


Name the biologic stimuli for the left ventricle remodeling.

"The biologic stimuli for these profound changes include mechanical stretch of the myocyte, circulating neurohormones (e.g., norepinephrine, angiotensin I), inflammatory cytokines (e.g., tumor necrosis factor [TNF]), other peptides and growth factors (e.g., endothelin), and reactive oxygen species (e.g., superoxide)."


How do you explain higher concentrations of citosolic calcium in heart failure myocytes?

"The changes that regulate excitation-contraction include decreased function of sarcoplasmic reticulum Ca2+ adenosine triphosphatase (SERCA2A), resulting in decreased calcium uptake into the sarcplasmic reticulum (SR), and hyperphosphorylation of the ryanodine receptor, leading to calcium leakage from the SR."


Myocardial relaxation is an ATP-dependente process.
True or False?



Left ventrcile wall becomes thinner as its cavitiy dilates.
True or False?



What are the consequences of high end-diastolic wall stress?

"(1) hypoperfusion of the subendocardium, with resultant worsening of LV function; (2) increased oxidative stress, with the resultant activation of families of genes that are sensitive to free radical generation (t.g., TNF and interleukin 1beta); and (3) sustained expression of stretch-activated genes (angiotensin II, endothelin, and TNF) and/or stretch activation of hypertrophic signaling pathways."


What are the cardinal symptoms of heart failure?

Fatigue and dyspnea.


How does one explain the mechanism for dyspnea in heart failure (HF)?

"The origin of dyspnea in HF is probably multifactorial. The most important mechanism is pulmonary congestion with accumulation of intersticial or intra-alveolar fluid, which activates juxtacapillary J receptors, which in turn stimulate the rapid, shallow breathing characteristic of cardiac dyspnea. Other factors that contribute to dyspnea on exertion include reductions in pulmonary compliance, increased airway resistance, respiratory muscle and/or diaphragm fatigue, and anemia."


Dyspnea may become less frequent with the onset of right ventricular failure and tricuspide regurgitation.
True or False?



Orthopnea is pathognomonic of cardiac disease.
True or False?

"Although orthopnea is a relatively specific symptom of heart failure, it may occur in patiensts with abdominal obesity or ascites and patiensts with pulmonary disease whose lung mechanics favor an uprigh posture."


How does one differentiate between proxysmal nocturnal dyspnea and cardiac asthma?

Paroxysmal nocturnal dyspnea (PND) "refers to acute episodes of severe shortness of breath and coughing that generally occur at night and awaken the patient from sleep, usually 1-3h after the patient retires. PNd may manifest as coughing or wheezing (...). Cardiac asthma is closely related to PND, is characterized by wheezing secondary to bronchospasm (...)"


How frequent is Cheyne-Stokes respiration in advanced heart failure?



What is the normal value of jugular venous pressure?

Less than or equal 8cm of water at 45º or less than 4,5cm of water at 30º.


How can one explain the fact that rales might be absent in chronic heart failure but are usually present in the acute setting?

"Importantly, rales are frequently absent in patients with chronic HF, even when LV filling pressures are elevated, because of increased lympathic drainage of alveolar fluid."


Which side would you expect a pleural effusion due to heart failure?

Most commonly, pleural effusion is bilateral and simmetric. When unilateral, they are most frequent in the right pleural space.


Which group of patients might have S3?

"S3 is most commonly present in patients with volume overload who have tachycardia and tachypnea, and it often signifies severe hemodynamic compromise."


Cardiac cirrhosis is associated with elevations of both direct and indirect bilirrubin.
True or False?



Where would you expect to find edema in a bedridden patient?

Sacral area (presacral edema) and scrotum.


What is the mechanism for cardiac cachexia?

"it is probably multifactorial and includes elevation of the resting metabolic rate; anorexia, nausea, and vomiting due to congestive hepatomegaly and abdominal fullness; elevation of circulation concentrations of cytokines such as TNF; and impairmnet of intestinal absorption due to congestion of the intestinal veins."


How does one explain the frequent absence of evidence of pulmonary hypertension, intersticial edema, and/or pulmonary edema?

"The absence of these findings in patiensts with chronic HF reflects the increased capacity of the lymphatics to remove intersticial and/or pulmonary fluid."


Name two functions of the echocardiography useful to evaluate patients with heart failure with preserved ejection fraction.

Tissue and wave-pulsed Doppler.


What is the most important index of left ventricular function?

Ejection Fraction.


Ejection Fraction has limitations has a measure of contractility since it might be affected by afterload and/or preload.
True or False?



Which type of heart failure demonstrates a great elevation of N-terminal pro-BNP and B-type natriuretic peptide?

Heart failure with reduced ejection fraction.


Which biomarkers might be used for the prognosis of chronic heart failure?

NT-proBNP, BNP, ST-2 and galectin-3.


Name the causes for NT-proBNP elevation not related do heart failure.

Age, renal impairment, right heart failure of any cause and falsely elevated in obese patients.


What is the cutoff of peak oxygen uptake that suggests a better prognosis for heart transplant rather than medical treatment?

VO2 less than 14mL/Kg.


Cor pulmonale never occurs without pulmonary hypertension.
True or False?



Name one group of diseases that is strongly associated with cor pulmonale, although they are rare as an absolute cause.

Primary pulmonary vascular disorders.


Name examples of acute decompensation causes for chronic cor pulmonale.

"Acute decompensation of previously compensated chronic cor pulmonale is a common clinical ocurrence. Triggers include worsening hypoxia from any cause (.e.g, pneumonia), acidemia (e.g., exacerbation of COPD), acute pulmonary embolus, atrial tachyarrythmia, hypervolemia, and mechanical ventilation that leads to compressive forces on alveolar blood vessels."


How does one explain lower-extremity edema in cor pulmonale?

"Lower-extremity edema may occur secondary to neurohormonal activation, elevated RV filling pressures, or incrased levels of carbon dioxide and hypoxemia, which can lead to peripheral vasodilation and edema formation."


Name one parameter for the evaluation of right ventricle function.

TAPSE (Tricuspide Annular Plane Systolic Excursion).