Lec 16- Cardiac failure Flashcards
1
Q
What is HF
A
- HF is an inability of the heart to deliver blood and therefore O2 at a rate commensurate with the requirements of the metabolising tissue dispute normal or increased cardiac filling pressures
- May be chronic or acute
2
Q
Why might HF occur
A
- myocardial
- valvular
- pericardial
- endocardial
- electrical problems
- Or a combo of these
3
Q
How common is HF
A
- Incidence 1 new case/1000 people/ year (increases to 10/1000/1 in >85)
- Prevalence ranges from 3-20 cases/1000 (increases to 80/1000 in >75)
- Male to remale ratio 2:1
- Median age is 76
- Average GP will see 20 people a year with HF (4 will be admitted to hospital and 2 will die in next 4 years)
- HF accounts for more than 4% of all medical admission and more than 1% of NHS budget
- Prevalence of HF is increasing because of improved treatment of CHD and ageing population
4
Q
Risk factor
A
- Age
- Some viral infections
- Congenital heart defects
- Medical conditions; CHD;MI;HTN; sleep apnoea; valvular hearth disease
- Some medical conditions: rosiglitazone; pioglitazone; NSAIDS some HTN and chemotherapy
- Obesity
- Smoking
- Alcohol
5
Q
Pre-load
A
- Pre-load measures the pressure that drives the blood into the left ventricle, prior to contraction
- It depends on the venous pressure and the rate of venous return
- Pre-load is a measure of how much blood returns to the heart to pump
- Excessive preload damages the heart muscle
6
Q
Afterload
A
- After-load measures the pressure that the heart must overcome to pump blood out into the circulation
- i.e. to open the aortic and pulmonary artery valves
- It is largely dependant on aortic pressure
- The higher the after-load, the less blood the heart can pump
7
Q
Cardiac function curve
A
- How well can the heart pump blood out through the body
- Right atrial pressure (Pr measures blood returning to the heart
- (to the left is enhanced; to the middle is normal; to the right is depressed)
- These curves show the effects of increasing Pra (pressure Right Atria) on cardiac output (cardiac function)
- CO can be enhanced by increasing HR and inotropy or by decreasing after load
8
Q
What happens in HF
A
- Cardiac and systemic vascular curves combined. Point A is normal
- Changes in cardiac output (CO) and Pra in response to cardiac failure and compensatory increases in blood volume (vol) and SVR and decreased venous compliance (Cv)
- A normal operating point; B, decreased cardiac performance; C, compensatory increase in SVR coupled with increased Vol and reduced Cv
- The process of increasing CO damages the heart by expanding it, therefore CO will decrease, this acts in a vicious cycle
9
Q
Cardiac remodelling
A
- Increased number of myocytes in response to strain
- Initially some improvement in contraction
- As mass continues to increase, ventricle wall thickness increases, the heart changes shape and become less able to contract. Diastolic filling impaired
- Reduced by inhibitors of angiotensin and aldosterone
- An elarged heart may be seen on X-ray
10
Q
Cardiac remodelling
A
- Increased number of myocytes in response to strain
- Initially some improvement in contraction
- As mass continues to increase, ventricle wall thickness increases, the heart changes shape and become less able to contract. Diastolic filling impaired
- Reduced by inhibitors of angiotensin and aldosterone
- An elarged heart may be seen on X-ray
11
Q
HF, progressive worsening
A
-Poor ventricular function –>
-HF —>
-Decreased stroke volume and cardiac output –>
-Neurohormonal response –>
-Activation of sympathetic system and or RAAS –>
-Vasoconstriction: increase sympathetic tone; Angiotensin II; impaired NO release
Na and fluid retention: increased vasopressin and aldosterone –>
-Further stress on ventricular wall and dilation (remodelling) leading to worsening of ventricular function –>
-Further HF
12
Q
Actions of angiotensin
A
-Angiotensinogen -renin–>
Angiotensin I -converting enzyme—>
Angiotensin II –> aldersterone —> increased preload (via increased water and sodium retention)
OR (from angiotensin II) –>increased after load by causing vascular smooth muscle contraction (this action is direct from myocytes or indirect via stimulation of sympathetic nervous system)
13
Q
Cardiovascular reserve
A
- Degree to which CVS can increase performance in the face of increased circulatory demand and or increased after load or decreased contractility
- Max CO- resting CO = cardiac reserve
- Decreased exercise tolerance measures decreased cardiac reserve
14
Q
HF syndrome symptoms
A
-HF is a syndrome, not a diagnosis or a disease
Cardiac dysfunction leads to clinical syndrome
-Breathlessness and fatigue
-Cough and inability to sleep flat (Fluid accumulation in lungs)
-Fluid retention (peripheral oedema and elevated JVP)
-Reduced ejection fraction (EF) on echocardiogram
15
Q
clinical features
A
- The underlying diagnosis and aetiology must always be sought in patients presenting with HF syndrome
- This is the only way in which optimum treatment can be provided e.g. surgery; ACEI for LVSD
- It is also the reason why HF should not be recorded as the primary cause of death on a death certificate
16
Q
Forms of HF
A
- Acute
- Chronic divided into: left ventricular systolic dysfunction (LVSD) (50% of cases)
- HF with preserved left ventricular ejection fraction (HFPEF)- myocardium is ok but something is wrong with ventricles
- Others (valve disease, arrhythmias)
17
Q
Acute HF
A
- Often precipitated by MI
- Signs include: confusion
- severe breathlessness
- Frothy pink sputum
- Cold clammy skin
- Tachycardia
- Low BP
- Lung crepitations
- Raised JVP
- Third heart sound
18
Q
Acute HF: basic measures and initial drug treatment
A
BASIC MEASURES
-Sit patient upright
-Remove any implicated medications
-High flow O2 to correct hypoxia
INITIAL DRUG TREATMENT
-IV loop diuretic to remove fluid
-Nitrates only if there is ischaemia, severe HTN or valvular disease
IF HEART CANT MAINTAIN PERFUSION
-Dobutamine to increase contractility
-dopamine to increase contractility and renal perfusion
-Phosphodiesterase inhibitor to increase CO
19
Q
Specific treatments for causes of HF
A
Treat underlying conditions that may be implicated -Anaemia -Thyroid disorders -Arrhythmias Surgical corrections available: -Valve repair and replacements -Implanting pacemaker or defibrillator -structural congenital problems -Biomechanical pump (LVAD) operation -Heart transplant
20
Q
Chronic HF
A
- Making accurate diagnosis of HF and determining its cause can be difficult: often symptoms are non-specific; people may have not symptoms of HF; clinical diagnosis is confirmed to be accurate in approx 1/2 all cases when echocardiogram is used
- The likelihood of HF in the presence of suggestive symptoms and signs is increased is there is history of MI or angina, abnormal ECG or CXR showing pulmonary congestion
21
Q
Symptoms of chronic HF
A
- Shortness of breath on exertion
- Decreased exercise tolerance
- Paroxysmal nocturnal dyspnoea
- Orthopnoea (shortness of breath)
- Ankle swelling
22
Q
Compensated/ decompensated HF
A
- Compensated- patient maintains adequate CO at rest
- Decompensated- deterioration and patients unable to sustain adequate CO for normal activity or even breathlessness at rest
23
Q
Long term compensations
A
- Cardiac hypertrophy: increased contractility
- Polycythaemia more blood cells increased Hb in blood - increased O2 to tissue (this increases viscosity of the blood therefore makes the heart work harder which is negative)
- Renal compensation: fluid retention; vasoconstriction (Bad for the heart remodelling)
- All of these are ultimately damaging
24
Q
Complications and prognosis
A
- CHF has a prognosis worse than most cancers (average mortality rates range from 10-50%)
- Quality of life; if worse than with many other common medical conditions. Psychosocial functioning is impaired, with over 1/3 of people experiencing severe and prolonged depression
25
Q
Outcome measures
A
- Grade 1- no limitations of physical activity; ordinary physical activity doesn’t cause undue fatigue, palpitations of dyspnoea
- Grade 2- Slight limitations; comfortable at rest but ordinary physical activity results in fatigue, palpatations or dyspnoea
- Grade 3- Marked limitations; comfortable at rest but less than ordinary activity causes fatigue, palp or dysp
- Grade 4- unable to carry out physical activity without discomfort; symptoms of cardiac insufficiency at rest
26
Q
Drugs treatment and advice
A
- Diuretics: offer a low to med dose of loop diuretic to patients with HFPEF
- CCB- consider amlodipine for combed HTN or angina but avoid verapamil, dlitiazem
- Amiodarone (antidysrrythmic)
- Anticoagulants- sinus rhythm, VTE or TE
- Aspirin- atherosclerotic arterial disease
- Inotropic agents- only IV for short term
- ACEI- DON’T initiate in patented with valve disease until assessed by specialist
27
Q
General principles for drug use
A
- Therapy will probably involve multi-drug regimes
- Careful monitoring of renal function is essential
- Multi-disciplinary management programmes achieve better control: up-titration; monitoring
28
Q
ACEI
A
- 1st line for all patients with LVSD
- Unless contra-indicated should be considered mandatory
- Unequivocally reduce morbidity and mortality (20-25% risk reductions)
- Caution in use in patients with significant renal disease
- Monitor potassium
29
Q
ACEI mechanism
A
- ACEI prevents angiotensin 1-converting enzyme from turning agiotensin 1 –> angiotensin 2
- Angiotensin II increases aldosterone; salt and water retention; vasoconstriction; sympathetic nervous stimulation
- By stopping all of these factors (which increase BP) we are decreasing BP
30
Q
ACEI clinical trial evidence
A
- Captopril- SAVE
- Enalapril- CONSENSUS; SOLVD
- Lisinopril- ATLAS
- Ramipril- AIRE
- Trandolapril- TRACE
31
Q
Angiotensin receptor blockers ARB’s
A
- RAAS is not completely blocked by ACEI
- Angiotensin || is produced through pathways other than ACE
- Antagonists could more completely inhibit the adverse effects of angiotensin || through the AT1- receptor
- Leave the desirable effects of the AT-2 receptor stimulation
- Not all unopposed effects of AT-2 receptor stimulation are desirable
32
Q
AT1 and AT2 receptor stimulation outcomes
A
AT1- receptor stimulations -Vasoconstriction -Na+ water retention -Aldosterone synthesis and secretion -Increased vasopressin secretion -Cardiac hypertrophy AT2-receptor -Inhibition of cell growth -Vasodilation -Apoptosis -Modulation of extracellular matrix -Cellular differentiation
33
Q
BB in CHF- deleterious effects of B-agonists in CHF
A
- Increase HR
- Increase contractility
- Electrical instability
- Apoptosis
- Myocardial toxicity
- LV dilation/hypertrophy
- Renin release
34
Q
BB in CHF- mechanism of BB in CHF
A
Reduction in -Renin release -Angiotensin || and aldosterone (following decrease in renin) -Myocardial O2 demand -Catecholamine- induced free fatty acid release from adipose tissue -Myocardial oxidative stress Improvement in cardiac function -Anti-dysrhythmic effect
35
Q
BB in LVSD
A
BB 1st line treatment with ACEI
- including patients with: erectile dysfunction; diabetes; COPD;
- Start low dose- this is because if you block all of the B1 receptors you stop all sympathetic stimulation which is controlling the heart this can cause acute HF and death
- Switch stable patients already on BB to a BB licensed for HF
36
Q
Sacubitril-vasartan
A
- Sucubitril is a prodrug of LBQ657 which inhibits neprilysin (neutral endopeptidase; NEP) that would normally degrade peptides such as natriuretic peptides
- Symptomatic chronic HFEF: NYHA class || to |V; LVEF (Left ventricular ejection factor) of 35% or less; already on stable dose of ACEI or ARB
- Monitor: renal function; BP; K+
- BNP is nto suitable biomarker
- Side effects: anaemia; hypotension; diarrhoea; gastritis; hyperkalaemia
37
Q
Aldosterone antagonists
A
- Spironolactone blocks aldosterone receptors
- prevents aldosterone-mediated Na+ absorption in DCT of kidney
- Also prevents cardiac remodelling
- In RALES trial, 30% reduction in death in patients taking spironolactone
- 2nd line in LVSD
- Monitor: renal function for declines; Na (may reduce); K (may increase)
38
Q
Aldosterone antagonists
A
- Spironolactone blocks aldosterone receptors
- prevents aldosterone-mediated Na+ absorption in DCT of kidney
- Also prevents cardiac remodelling
- In RALES trial, 30% reduction in death in patients taking spironolactone
- 2nd line in LVSD
- Monitor: renal function for declines; Na (may reduce); K (may increase)
39
Q
Other diuretics in CHF
A
- Loop diuretics cornerstone treatment in patients with fluid retention
- Addition of thiazide may augment diuresis (possibly overcome diuretic resistance often seen with high dose loop diuretics)
- Patients requiring diuretics should commence on a salt and fluid restriction (1.5L/day)
- Counsel patients on fluid balance and monitoring daily weight
40
Q
Diuretics resistance
A
- Patients with oedema may exhibit apparent resistance to oral diuretics; decreased intestinal drug absorption
- Patients with renal insufficiency may exhibit another type of diuretic resistance markedly decreased diuretic response- when GFR <30ml/min little filtered Na and water reach the distal nephron
41
Q
Who should receive diuretic treatment
A
- Patients with signs of Na and water retention: peripheral oedema; pulmonary oedema or an elevated jugular venous pressure; should receive diuretic therapy
- Breathless patients withought signs probably also get a better symptomatic response to diuretics than any other treatment
42
Q
Vasodilators
A
Hydralazine -Arteriolar dilator- uncertain mechanism -Decreased after load -Increased CO BUT -Increased reflex; increased HR -Increased fluid retention -Headache -Lupus syndrome (autoimmune disease)
43
Q
Hydralazine/nitrate combination
A
- In afro-carribbeans, treatment with hydrazine and nitrates vs placebo resulted in reduced mortality and morbidity, better quality of life but with more headaches
- Alternative 1st line treatment or option for 2nd line treatment for LVSD
- Seek specialist advice and consider for patients who are intolerant of ACEI and ARB’s
- Seek specialist advice and consider as an option for 2nd line treatmen , especially in people of African or Caribbean origin with moderate to severe HF
44
Q
Cardiac glycosides- Digoxin
A
- Increased force of myocardial contraction
- Decreased conductivity in the AV node
- Blocks Na/K ATPase –> Increased Na+ i –> Increased Ca2+(i) –> increased contractility
- CO increased residual volume –> heart less distended, cardiac fibres decrease in length
- Mild sympatholytic action- increased baroreceptor sensitivity in HF: after load and decreased HR
45
Q
Digoxin-cardiac glycosides
A
- Role in CHF not clear
- Current recommendations
- Use digoxin in patients remaining symptomatic with LVSD despite max medical therapy
- Use in patients for rate control in those with AF
- Consider age and renal function when dosing due to narrow therapeutic range
- Monitoring: pulse; signs and symptoms of toxicity (see clinical pharmacy toolkit)
46
Q
Ivabradine
A
- Slows firing of the SA node (blocks If current, which regulates pacemaker activity thus HR)
- Reduces HR without affecting contractility
- Used if EF <35% and HR >75 BPM
- Contraindiacted if HR <60
- Side effects- Visual disturbances; bradycardia; hearth block; headache
47
Q
Lifestyle advices
A
- Diet
- Exercise
- Compliance
- Smoking
- Alcohol
- Sexual activity
- Vaccination
- Air travel
- Driving regulation
48
Q
How easy is it for the heart to fill with blood
A
- Venous compliance (opposite of venous tone)
- Systemic vascular resistance
- If there is high Pra than the heart won’t be filling properly because the pressure in the venous will be low, this can be changed by increasing blood volume (so increasing pressure) or constriction of the venous system
49
Q
Atrial and brain type nature tic factors (should be after actions of angiotensin)
A
- Atrial and brain naturetic factors are released when the walls of the atria of blood vessels are stretched
- These peptides are released by vasodilation so BP decreased
- Inhibit renin therefore decreased fluid retention
50
Q
NICE
A
-HF due to LVSD –>
-Offer both ACEI and BB (ARB if intolerance to ACEI) –>
-Consider hydrazine in combination with nitrate if intolerant of ACEI and ARB –>
-Specialist advise consider:
CRT (Pacemaker)
Digoxin
-HF due to HFPEF treat comorbidities and seek specialist advice
