management of heart failure Flashcards

1
Q

what physiological events occur during heart failure

A
  • activation of RAAS = salt/water retention
  • fluid build up in vessels
  • venous pressure rises
  • fluid pushed out of veins and capillaries
  • congestion and oedema
  • but CO and BP are restored

maintenance on BP is highest prority
other systems activated:
- increased production of anti-diuretic hormone = water retention
- natriuretic peptides triggered by arterial stretch, stimulate natriuresis (removal of salt and therefore water to reduce arterial stretch

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2
Q

what is decompensation

A
  • failure to compensate for functional overload caused by disease
  • eventually patient deteriorates
  • leading to congestive heart failure and disease progression
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3
Q

compare backward vs forward heart failure

A

backwards failure:
- congestion of veins (oozing out as oedema)
- most common in veterinary patients

forwards failure:
- poor perfusion
- less common (chronic, more compensation)

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4
Q

what occurs when you have left sided heart failure

A
  • congestion of pulmonary venous circulation
  • pulmonary venous circulation drains fluid from the lungs
  • if this does not work, leads to pulmonary oedema (seen as radiopaque lung fields)
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5
Q

what occurs in right sided heart failure

A
  • congestion of systemic venous circulation
  • systemic venous circulation drains fluid from body
  • leads to accumulation of fluid in abdominal cavity (ascites)
  • can see jugular vein without raising it due to increase in venous pressure
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6
Q

compare left and right heart failure

A
  • L sided heart failure is more common than R
  • diseases affect left more than right
  • L side of heart is high pressure = effects of disease more obvious and dramatic and accumulation of fluid in the lungs is life threatening
  • fluid in abdomin doesnt present with as dramatic life threatening clinical signs
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7
Q

how do patients with heart failure typically present

A
  • congestive heart failure
  • collapse
  • heart disease found by chance
  • non-specific malaise/weight loss

heart disease does not always equal heart failure

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8
Q

explain why congestive heart failure severity varies

A
  • clinical signs develop with time
  • patient compensates for disease intitally
  • gets progressively worse
  • clinical signs vary
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9
Q

what is the ACVIM consensus for scoring heart disease

A

stage A: patients at high risk of heart disease but have no identifiable structural disorder of the heart (breed risks)
stage B patients with structural disease (murmur) but no clinical signs
- B1: asymptomatic patients with no radiogrpahic or echocardiographic evidence of cardiac remodelling
- B2: asymptomatic patients with radiographic or echocardiographic evidence of left-sided heart enlargement

stage C: patients with past or current clinical signs of heart failure associated with structural heart disease. heart disease present evident of limited exercise intolerance that progressively worsens. signs evident with mild excersise = moderate
Stage D: patients with end stage disease with clinical signs of heart failure that are refractory to standard therapy. patient has obvious clinical signs with minimal exercise that worsens (maybe to point where they have clinical signs even at rest. progressively worsens, possibly until death

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10
Q

list factors that require consideration when considering treatment of patients with heart disease

A
  • primary causes of heart disease (can we treat it specifically? valve degeneration? cardiomyopathy? do we know cause?)
  • non-specific treatment of the primary disease
  • treatment of congestive heart failure
  • identify dysrhythmias and treat if indicated
  • identify complicating and co-existing factors (make sure kidney can take treatment and monitor for degradation of kidney function, dont send into kidney failure)
  • regular reassessment
  • what does the owner want
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11
Q

what drugs improve contractility

A

positive inotropes
- pimobendan (vetmedin)
- dobutamine
- digoxin

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12
Q

what drugs help relax heart (to treat hypertrophic disease)

A

positive lusitropes
- calcium channel blockers (diltiazem, verapamil)
- beta blockers (propranolol, atenolol)

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13
Q

how do you treat an animal in stage B1 heart failure

A
  • asymptomatic disease with no cardiac remodelling
  • no treatment but consider weight control, regular reassessment (q 6 mo) and client education (signs to look for in progression)
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14
Q

how do you treat an animal in B2 stage heart failure

A
  • asymptomatic disease with cardiac remodelling
  • same as B1, weight control, regular assessment and client education
  • EPIC study suggests giving pimobendan can be beneficial in slowing progression, increasing QOL and length of life (increases contractility)
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15
Q

how do you treat stage C heart failure

A
  • signs due to fluid accumultion
  • cough/breathing problems in LHF, fluid accumulation in body cavities in RHF)
  • problem with reversing or reducing clinical signs as stopping cycle can interrupt compensation of BP maintenance and perfusion leading to kidney failure
  • continue with pimobenden
  • excersise regime (consistent and within capacity)
  • aspirate fluid
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16
Q

what do diuretics do

A
  • remove fluid
  • act as kidney to increase urine output

examples:
- loop diuretics (furosemide and torasemide)
- aldosterone antagonsists (spironolactone)

17
Q

what do vasodilators do

A

dilate arteries, veins or both
act by:
- reducing arterial BP = afterload
- reducing venous pressure = preload
- reduction of load and therefore cardiac work
- treats cardiac failure
- has antihypertensive agents

venodilators
- increase venous capacity
- decrease preload
- reduce fluid build up
- decreas venous pressure
- reduce oedema formation

arterial dilators:
- reduce afterload (reduce resistance to flow)
- increase output
- reducuce valve leakage (blood follows path of least resistance)
- reduce work of heart

18
Q

how does the RAAS system work

A

system activated in heart failure
conversion of angiotensin I to II is done by ACE, blocking this prevents RAAS from occuring

19
Q

how do ACE inhibitors work

A
  • reduce level on angiotensin II (venous and arterial dilators)
  • reduce levels of aldosterone (reduces fluid accumulation
  • overall affect is decongestion (reduce oedema)

examples:
- imadipril
- enalapril
- benazepril (fortekor)
- ramipril

20
Q

how do you treat emegency CHF

A
  • if acute onset, L sided failure. patient likely in severe resp. distress.
  • cage rest and supply O2
21
Q

how do you treat dysrhythmias in heart failure

A
  • common in patients with heart disease
  • will require characterisation with ECG
  • specific antidysrhythmic therapy may be required
  • eg. beta blocker, calcium channel blocker, digoxin
  • few treatments licensed for vet use
22
Q

what should you assess for in your regular reassessment of patients with heart failure

A
  • efficacy of treatment (side effects, toxicity, etc.)
  • drug doses may need to be adjusted (rarely a standard does, needs to be adjusted with progression)
  • regular blood chemistries advisable (diuretics can lead to abnormailites in electrolyte values)
  • repeat investigations if needed (rads, U/s, echos)
  • weigh
23
Q

explain the therapeutic considerations in heart failure treatment and what can cuase therapy failure

A
  • aim is to resolve clinical signs (rarely a cure = lifelong treatment)
  • combination therapy is common (O needs to be invested in med regime, often several different meds at all times of day)

failure/adverse effects:
- Dose too low (indication for dosing by surface area rather than weight)
- administration failure (compliance)
- absorption if given by mouth (oedema in gut can decrease absorbancy)
- tachyphylaxis (progressive decrease in response to a given dose after repetitive administration of a drug)
- idiosyncratic reaction
- complicating factors (renal dysfunction)
- co-existing disease (liver dysfunction)
- effect of drug combinations( can drugs interact)