Origin of Symptoms in Heart Failure Flashcards

1
Q

Circulation, 1993

A

In 1993, one year survival rates for Congestive Heart Failure were 60%

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2
Q

CONSENSUS Trial, 1987

A

Trial of Enalapril versus placebo showed that Enalapril reduced one year mortality in heart failure by 44%

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3
Q

RALES Trial, 1999

A

Trial of Spironolactone showed that it reduced one year mortality in Heart failure by 33%

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4
Q

CIBIS II Trial, 2002

A

Trial of Bisoprolol showed that it reduced one year mortality from heart failure by 13%

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5
Q

Ribner, 1990 and Cleland, 1993

A

Consistently show that ACE Inhibitors improve exercise capacity, symptoms and quality of life

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6
Q

Packer, 1996 and Witte, 2005

A

Beta blockers are shown to inconsistently improve exercise capacity, symptoms and quality of life

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7
Q

Van Thielen, 2008 and Larsen, 2013

A

Cardiac resynchronisation therapy is shown to inconsistently improve exercise capacity, symptoms and quality of life

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8
Q

Clark, 2015

A

Showed that treatments traditionally used for the treatment of breathlessness aren’t actually very effective.
Loop Diuretics improved congestion but showed no benefit to people without congestion and there was no prognostic benefit
Oxygen was found to improve long term survival but made no difference to breathlessness
Opiates meant that patients scored higher on the Borg Scale (a measure of quality of life) but there was no improvement in breathlessness.

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9
Q

Coats and Witte, 2004

A

Exercise intolerance in heart failure is not related to cardiac function. Chronotropic incompetence is not the cause of exercise intolerance.
Increasing heart rate showed no change in pVO2, exercise time, VeVCO2 or Respiratory Exchange Ratio

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10
Q

Jamil, 2016

A

Reducing heart rate using Ivabradine made no difference to exercise intolerance

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11
Q

Witte, 2004

A

Withdrawal of Beta-blockers made no difference to exercise time, pVO2 or VO2 Max

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12
Q

Heart, 2001

A

Symptomatic heart failure patients show much lower quadriceps strength and peak leg blood flow than asymptomatic LVSD patients and controls.
Increased lean muscle mass is shown to predict increased VO2, so muscle dysfunction in HF could be a cause of exercise intolerance

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13
Q

Anker, 1997

A

Showed that skeletal muscle wasting is an independent predictor of quality of life and mortality.
People with muscle wasting and exercise intolerance had much lower survival than people with either or none.

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14
Q

Witte, 2005

A

Showed that as NYHA class increases, maximal inspiratory pressure decreases, so peak oxygen intake is lower. This is because there is considerable diaphragmatic weakness in heart failure

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15
Q

Witte, 2005

A

Showed that there is considerable airways resistance in heart failure and that as resistance increases, peak oxygen intake is lowered-NEGATIVE ASSOCIATION

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16
Q

Clark, 1996

A

Showed that training with a tight cuff around the leg caused a bigger increase in ventilation than exercising without. Because restricted blood flow forces muscles to work harder which is detected by ergoceptors that then increase ventilation

17
Q

Witte, 2008

A

Showed that as Muscle Sympathetic Nerve Activity (a measure of systemic sympathetic activity) increases, minute ventilation and VCO2 also increase.

18
Q

Witte, 2004

A

Beta blockers improve echocardiographic variables and prognosis, but make no difference to maximal or submaximal exercise capacity. BUT beta blockers are shown to REDUCE ventilation.

19
Q

Witte, 2004 and 2008

A

These findings taken together show that heart failure is a state of sympathetic over-activity which results in an increase in ventilation