CPT1: Heart Failure Flashcards
1
Q
What is chronic heart failure characteried by?
A
- Sudden death
- Progressive Cardiac dsyfunction
- Tiredness
- Breathlessness
- Neurohormonal disturbances
2
Q
What are alternative names for heart failure?
A
- Congestive heart failure
- Left ventricle Failure
- Congestive Cardiac Failure
3
Q
What is heart failure?
A
The inability of the myocardium to develop enough force to maintain a CO which meets the circulatory demands of the body
4
Q
What is heart faliure commonly cause by?
What happens with increasing age?
what are the stats?
A
- •Chronic heart failure
- affects 2-10% of the population
- Incidence rises with increasing age
- commonly due to coronary artery disease
- has a poor prognosis with a 5 year mortality of 50% rising to 80% in a year for some patients
5
Q
What are different forms of heart failure?
A
- Systolic - failure of contraction of the myocardium leads to reduced left ventricle ejection fraction
- Diastolic - Higher filling pressure required to maintain CO. Ejection fraction normal
- Left-side - inadeqoute out put from the left ventricle
- Right-side - Right ventricle failure. Secondary to left-side failure or pulmonary disease
6
Q
What underlying diseases can cause Congestive heart failure?
A
- •Congenital heart disease
- •Atherosclerosis
- •Rheumatic fever
- •Cardiomyopathy
- •Valve disorders
- •Ventricular failure
- •Left or right-sided failure
- •Hypertension
- •Prolonged alcohol or drug addiction
- •Previous heart attack
- •Diabetes
7
Q
What is rheumatic fever
A
•Strep throat from the streptococcal infection begins a disease process where the heart valves are damaged. This condition is called rheumatic fever and it affects the connective tissues of the body.
8
Q
What is Cardiomyopathy
A
The stretching and enlarging of the heart cavity making the heart weak so it does not pump correctly
9
Q
What is a type of cardiomyopathy?
A
takotsubo
10
Q
What is ventricular Failure
A
•Ventricular failure occurs when there are weak spots in the ventricular walls causing a bulge, or an aneurysm.
11
Q
What are symptoms of heart failure in terms of circulation?
A
- Cyanosis, or a bluish colour seen in the tips of fingers of lips due to a lack of oxygen
- Fatigue or weakness
- Fast or irregular heart beat
- Changes in behaviour e.g. restlessness, confusion and decreased attention span
12
Q
What are symptoms of heart failure in terms of congestion
A
- •Unexplained or unintentional weight gain
- •Chronic cough
- •Increased urination
- •Distended neck veins
- •Loss of appetite or indigestion
13
Q
What are symptoms involving gravity/ exertion?
A
- Orthopnea or Shortness of breath when lying down
- Shortness of breath during exertion
- Swelling of hands, legs, ankles
14
Q
What does clinical diagnosis involve?
A
Major Criteria
- Orthopnea/PND
- Venous distension
- Rales
- Cardiomegaly
- Acute pulm edema
- Elevated JVP
- HJR
Minor Criteria
- Ankle edema (see pic.)
- Night cough
- Exertional dyspnea
- Hepatomegaly
- Pleural effusion
- Tachycardia (>120)
- Decrease VC
- Weight loss with CHF tx
15
Q
Describe what NYHA classififcation system
A
New York Heart Association - Heart Failure classification.
- Class I - Symptoms with more than ordinary activity
- Class II - Symptoms with ordinary activity
- Class III - Symptoms with minimal activity
- Class IIIa - No dyspnea at rest (shortness of breath)
- Class IIIb - Recent dyspnea at rest
- Class IV - Symptoms at rest
Printed sheet has more depth
16
Q
What are the aims of Heart Failue management?
A
- To improve symptoms:
- Diuretics
- ACE inhibitors
- Digoxin
- To improve survival
- ACE inhibitors
- B-blockers
- Spironolactone
17
Q
Describe the management of Heart failure
A
18
Q
Describe symptomatic treatment
A
- Loop Diuretics
- The mainstay of symptomatic treatment
- Frusemide and Bumetanide
- Causes Diuresis (salt and water loss) but also has some vasodilatory effects
19
Q
Describe blocking detrimental hormonal changes treatment
A
- Sympathetic stimulation exacerbates heart failure
- B-blockers Carvediolol, Bisoprolol, Metoprolol are proven beneficial in CHF treatment
- Carvediolol mainly used. Only in small doses to start with. Reduces mortality in patients treated concomitantly with digoxin, diuretics and ACE inhibitors. Blocks both a and B receptrs
20
Q
Describe treatment in terms of RAAS
A
Angiotensin II
- Two groups of drugs available to block the effects of angiotensin II
- ACE Inhibitors (ENALAPRIL, CAPTOPRIL)
- Reduce symptoms, improve quality of life, reduce mortality with HF.
- Irritates airway - cough
- Angiotensin antagonists (LOSARTAN) but these are not as effective
- Less liable to cough
- Reduce mortality
Aldosterone
- Effects blocked by SPIRONOLACTONE
- Produces a significant reduction in morbidity
21
Q
Describe treatment in terms of enhancement of cardiac function
A
Positive Inotropes
- Current positive inotropic drugs act by one of two mechanisms. The first is to elevate cAMP levels as a result of agonism at β1 adrenoceptors, or indirectly by phosphodiesterase inhibition (PDEI). The latter drugs inhibit phosphodiesterase, the enzyme that breaks down cAMP. Elevated cAMP increases calcium currents making more calcium available for contraction. Cardiac glycosides act by a different mechanism to elevate calcium levels.
- B-agonists
- Cardiac glycosides
Vasodilators
22
Q
Describe the use of Cardiac glycosides
A
- These drugs improve the ability of the heart to pump and so improve cardiac status
- DIGOXIN is the only drug in common use.
- all glycosides have the same basic molecular mechanism of action in inhibiting the Na/K ATPase enzyme in the cell membrane after binding to an extracellular site on the enzyme. Such enzyme inhibition occurs in all tissues. In the heart it results in therapeutic and toxic effects, whereas in other tissues only toxicity occurs. The glycoside used in clinical practise is digoxin. It can be given i.v., or orally (70% absorbed), and has a half-life of 30 hours.
- A variety of tissue responses result from digoxin’s basic molecular mechanism of action. In the heart, Na/K ATPase inhibition results in intracellular accumulation of sodium. This results in reduced extrusion of Ca, and makes increased intracellular Ca available for excitationcontraction coupling. However, such a beneficial action is limited since toxic actions intervene if therapeutic actions are pursued too far.
- As a result of its basic molecular action digoxin can poison all tissues. Digoxin excites the afferent limb of vagal reflexes thereby producing indirect parasympathomimetic actions (bradycardia and depression of AVN conduction). In the gastrointestinal tract it induces nausea and vomiting. Despite the toxic actions on other tissues, the major lethal action is arrhythmias
23
Q
Describe the use of B-agonists
A
- Beta agonists (used only rarely in acute/emergency situations). β1 adrenoceptors are cardiac adrenoceptors whose activation results in increased rate and force, together with oxygen wasting. β2 adrenoceptor activation relaxes smooth muscles (bronchial, vascular, uterine and gastrointestinal). The +ve inotropic effect of cardiac β1 stimulation is accompanied by excessive oxygen consumption and is thus is oxygen wasting (inefficient inotropism).
- Noradrenaline is not used clinically, and adrenaline is used only in life threatening emergencies. Dobutamine is a selective β1 agonist (stimulant) which is useful, while dopamine is also used since it also stimulates dopamine receptors and thereby preserves kidney function.
24
Q
A
- Nitroglycerin (or NO drugs) can be used acutely to treat acute cardiac failure, especially when there is ischaemic pain. By virtue of venodilation it reduces pre-load while concomitant ateriolar dilation will reduce after-load. Both improvr cardiac function.
- Other vasodilators that have been used include hydralazine in conditions where ACE inhibitors cannot be used.
25
What is the problem with treatement?
Mortality remains high
* •ACEI
* Risk reduction 35% (mortality and hospitalizations)
* •b Blockers
* Risk reduction 38% (mortality and hospitalizations)
* •Oral nitrates and hydralazine
* Benefit vs. placebo; inferior to enalapril (mortality)
**However: 4-year mortality remains ~40%**
26
Describe the monitoring of benefit/ disease progression?
* Symptomatic relief
* SOB, tiredness, lethargy
* Clinical relief
* Peripheral oedema, ascites, weight
* Monitor weight regularly
* Patient performs daily weight assessment
* Increase medication according to symptoms or weight
* Patient education
* BNP NT proBNP levels.
27
Describe monitoring of BNP levels
* High levels BNP \> 400 pg/ml (116 pmol/litre) or NTproBNP \> 2000 pg/ml (236 pmol/litre)
* Raised levels BNP 100-400 pg/ml (29-116 pmol/litre) or NTproBNP 400-2000 pg/ml (47-236 pmol/litre)
* Normal levels BNP \< 100 pg/ml (29 pmol/litre) or NTproBNP \< 400 pg/ml (47 pmol/litre
28
Describe the use of loop diuretics
•Loop Diuretics (FRUSEMIDE)
–The main stay of treatment
–It is essential to remove excess salt and water before introducing other agents
–The loop diuretics induce profound diuresis
–Act by inhibiting the NA-K-Cl transporter in the Loop of Henle
–Work at very low glomerular filtration rates
–Prevent the reabsorption of 20% of filtered sodium and water
29
In severely effected patients or resistant patients what should be done?
* In the most severely affected patients or in resistant patients they can be used in combination with thiazide diuretics
* This combination is very powerful and may induce a diuresis of 5-10 litres a day
30
What are adverse effects of this
–Dehydration
–Hypotension
–Hypokalaemia, Hyponatraemia
–Gout
–Impaired glucose tolerance, diabetes
31
Describe drug interactions
**Frusemide** and...
* aminoglycosides = aural and renal toxicity
* lithium = renal toxicity
* NSAIDs = renal toxicity
* Antihypertensives = profound hypotension
* vancomycin = renal toxicity
