Heart Failure Pathophysiology 1 Flashcards

1
Q

Define heart failure.

A

clinical syndrome resulting from the heart not being able to pump enough blood to adequately serve the body’s needs AND maintain normal pressures in the heart chambers and lung vessels

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2
Q

Contrast the two major type heart failure.

A

systolic heart failure is due to impaired contractile function of the heart

heart failure with preserved ejection fraction is a multifactorial disease where relaxation of the heart is often impaired

the resulting clinical syndrome is the same

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3
Q
  1. Discuss the two primary causes of heart failure in the US as well as several less common causes.
A

two primary causes are ischemic heart disease and HTN, less common causes include cardiomyopathy, infectious or inflammatory disease (or idiopathic- unknown cause)

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4
Q

Describe the general time course of systolic heart failure. What are this disease’s hallmark features?

A

chronic systemic disorder initiated by myocardial injury or damage and when untreated, characterized by progressive cardiac dysfunction and symptoms of fluid overload and in late stages fatigue characterized by fluid overload, vasoconstriction, and impaired perfusion

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5
Q
  1. Identify the processes responsible for the progression from an initial cardiac insult to overt heart failure.
A

an index event causes progressive heart remodeling (even in the absence of symptoms) and the vascular system develops compensatory mechanisms to reduce reduction in perfusion to critical systems, these compensatory mechanism can cause damage to the system into overt heart failure

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6
Q
  1. Discuss the clinical presentation of heart failure regarding respiratory distress.
A

increased wedge pressure causing transudate into lungs produces: exertion dyspnea, wheezing, orthopnea, paroxysmal nocturnal dyspnea and dyspnea at rest) leading to reduced exercise capacity

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7
Q
  1. Differentiate the different types of cardiac remolding an discuss the beneficial and harm a sects of theses structural changes
A

.

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8
Q
  1. Differentiate the beneficial short-term effects of neurohormonal compensatory mechanisms form the detrimental long-term effects.
A

the goals of compensatory mechanisms are to maintain stroke volume, stroke volume, vital organ perfusion and SBP, whereas the results of these mechanisms include vasoconstriction and fluid retention which can be detrimental

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9
Q

What systems are employed in increasing cardiac output during heart failure?

A

increased heart rate (CNS)
increased preload (volume increase via RAS)
increased contractile state (CNS-catecholamines)

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10
Q
  1. Discuss the clinical presentation of heart failure regarding fluid overload.
A

edema, abdominal bloating, early satiety, abdominal discomfort and solid weight loss (these symptoms reflect “right heart failure” which is most commonly caused by left ventricular dysfunction?)

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11
Q

Describe the symptoms of impaired perfusion.

A

fatigue
weakness
anorexia (cytokine induced possibly)
confusion (already a sign of cardiogenic shock)

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12
Q

Name 5 things you might expect to see on physical examination findings with heart failure.

A
elevated neck veins (right sided filling pressure and hepatic congestion)
hepatojugular reflux (increased preload)
edema
rales (increased wedge pressure)
S3 (during the y descent)

note hepatojugular reflex and orthopnea are the most sensitive signs (rales is not)

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13
Q

What is the appropriate treatment of a “warm and wet” patient with heart failure? What would you expect the PCWP and CI to be?

A

normal PCWP and perfusions, increased filling pressure can be addressed with natriuretic peptides (i.e.. nesiritide)

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14
Q

What is the appropriate treatment of a “cold and wet” patient with heart failure? What would you expect the PCWP and CI to be?

A

wedge pressure is elevated and perfusion is decreased, often as a result of high peripheral resistance and it is appropriate to give a vasodilator like nitroprusside or nitroglycerine

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15
Q

What is the appropriate treatment of a “cold and dry” patient with heart failure? What would you expect the PCWP and CI to be?

A

really the worst prognosis suffering from low perfusion yet low volumes/low congestion and is important to increase cardiac output with inotropic drugs like dobutamine and milrinone (a/B drugs until heart assist or transplant)

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16
Q

What is meant by “decompensated” heart failure?

A

patients with heart failure are unable to achieve simultaneous optimized volume perfusion resulting in symptoms

17
Q

Discuss common factors that leading to decompensation.

A
discontinued therapy
meds that worsen heart or renal function (NSAIDS)
dietary fluid or salt
alcohol
arrhythmias
fever or infection
myocardial ischemia or infarction
worsening hypertension or anemia
18
Q

Why is a a heart in heart failure unable to respond normally to excess preload?

A

in heart failure, heart does not respond normally to catecholamines that would increase contractility due to increased preload due to chronic adrenergic tone- B receptors are decoupled from G protein messenger systems and there is an overall down regulation of receptors (ultimately because of chronic vasoconstriction and fluid overload)

19
Q

Why is neurohormonal activation important to understand in heart failure?

A

in heart failure there is a fundamental hemodynamic imbalance where vasoconstriction actors out weigh vasodilation factors

20
Q

What neurohormones are particularly up regulated in heart failure leading to overwhelming vasoconstriction?

A
endothelin
angiotensin II
aldosterone
NE
(some elevated due to increase RAS response)