Lec 16- Cardiac failure Flashcards
What is HF
- 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
Why might HF occur
- myocardial
- valvular
- pericardial
- endocardial
- electrical problems
- Or a combo of these
How common is HF
- 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
Risk factor
- 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
Pre-load
- 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
Afterload
- 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
Cardiac function curve
- 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
What happens in HF
- 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
Cardiac remodelling
- 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
Cardiac remodelling
- 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
HF, progressive worsening
-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
Actions of angiotensin
-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)
Cardiovascular reserve
- 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
HF syndrome symptoms
-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
clinical features
- 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
Forms of HF
- 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)
Acute HF
- 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
Acute HF: basic measures and initial drug treatment
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
Specific treatments for causes of HF
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
Chronic HF
- 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
Symptoms of chronic HF
- Shortness of breath on exertion
- Decreased exercise tolerance
- Paroxysmal nocturnal dyspnoea
- Orthopnoea (shortness of breath)
- Ankle swelling
Compensated/ decompensated HF
- Compensated- patient maintains adequate CO at rest
- Decompensated- deterioration and patients unable to sustain adequate CO for normal activity or even breathlessness at rest
Long term compensations
- 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
Complications and prognosis
- 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