Heart Failure and CRT Flashcards
Describe heart failure syndrome, its incidence and global impact
Heart failure result when the heart is unable to provide enough blood supply to meet the metabolic demands of the body.
It is estimated that 5 million people suffer from HF in USA, 6 million people in Europe and 400000 are newly diagnosed each year.
1st year mortality from HF is 20-30%
5 year mortality 50%
80% of patients with HF have at least 2 hospital admissions per year
HF has a progressively worsening trajectory with periods of stability and periods of exhacerbation/ worsening of symptoms. The main causes of mortality in HF are due to pump failure and SCD.
What are the sings and symptoms of heart failure?
Typical symptoms are breathlessness, ankle swelling, fatigue, paroxysmal nocturnal dyspnoea, orthopnoea. Typical sings are increased jugular venous pressure, pulmonary crackles, peripheral oedema.
Describe the pathophysiological mechanism of dyspnoea in HF.
The LV dysfunction results in increased end systolic volume (amount of blood after contraction) and increase in end diastolic volume (amount of blood left in the ventricle just before a contraction). The increase in systolic and diastolic volumes leads to increase in LVEDP which causes elevation of the left atrial pressure which causes increased pulmonary capillary pressure. As the pressure in the vessels increases, fluid is pushed into the alveoli of the lungs. Fluid reduces the normal oxygen flow in the lungs leading to dyspnoea.
What are the main compensatory mechanisms in HF? Explain each of them.
Neurohormonal activation: there are 3 neurohormonal compensatory reactions:
* Sympathetic Nervous System (SNS) -> inreases HR&ejection
* Renin –Angiotensin – Aldosterone System (RAAS) -> salt&water retention -> augments preload
* Antidiuretic hormone (Vasopressin) -> vasoconstriction -> maintains BP and perfusion of vital organs
Frank-Starling mechanism: compensatory increase in venous return -> temporary increase in stroke volume -> increase in contractility
Ventricular remodeling: left ventricular hypertrophy
Describe the types of heart failure.
Chronic vs acute HF:
Acute HF:
* Develops rapidly (hours/days)
* Can be immediately life-threatening
* Dramatic drop in cardiac output
* May be new (e.g. acute MI, sepsis) or an exacerbation of chronic disease.
Chronic HF:
* Long-term condition (months/years)
* More insidious
* Associated with the heart undergoing adaptive responses (e.g. dilation, hypertrophy) to a precipitating cause.
Left-sided vs right-sided:
Left-sided HF:
Most often heart failure begins with the left ventricle (the heart’s primary pumping chamber).
There are two types of left-sided heart failure:
* Preserved ejection fraction, also called diastolic heart failure
* Reduced ejection fraction, also called systolic heart failure.
Right-sided HF:
- Due to failure of the right ventricle
- Often a consequence of LV systolic dysfunction
- Can be secondary to pulmonary disease (i.e. pulmonary hypertension in which the right
ventricle will hypertrophy).
Systolic vs diastolic:
Systolic:
- Inability of the heart to contract effectively
Approximately two-thirds of heart failure patients have systolic dysfunction.
The heart muscle does not contract effectively and less oxygen-rich blood is pumped out to the body.
Diastolic:
- Impaired filling/relaxation.
The heart muscle contracts normally but the ventricles do not relax as they should during ventricular filling (or when the ventricles relax).
What are the causes of HF?
In the developed world, ischaemic heart disease and hypertension are the leading causes of HF. In developing countries, rheumatic heart disease leading to valvular dysfunction is more likely.
Systolic LV dysfunction results from primarily four underlying diseases:
1. Heart muscle disease (cardiomyopathies)
2. Ischaemic heart disease
3. Valvular diseases
4. Arrhythmias
What are the main factors that contribute to systolic HF.
Systolic LV dysfunction results from primarily four determinants:
1. Volume overload (due to valvular disease)
2. Pressure overload (excessive pressure overload due to uncontrolled HTN)
3. Loss of myocardium (ICD)
4. Impaired contractility (toxins)
Explain the general pathophysiology of HF.
Unloading of the high pressure barroreceptors in the LV, carotid sinuses and aortic arch generate signals that stimulates the cardioregulatory centre in the brain resulting in the activation of the sympathetic nervous system. This leads to an increased HR even at rest and an increase in peripheral vascular resistance. Activation of the renal sympathetic nerves stimulate the release of the hormone vasopressin causing an increase in peripheral vasocontriction. Sympathetic activation also causes renal vasoconstriction as does Angiotensin II. Angiotensin II constricts the blood vessels and stimulates the release of Aldosterone from the adrenal gland which decreases sodium excretion and causes remodeling of cardiac myocites.
What are the main factors that contribute to diastolic HF?
- Hypertrophy -> stiffer muscles due to fibrous connective tissue -> less myocardial compliance -> reduced reservoir
- Secondary disease (chronic HTN, Aortic stenosis, cardiomyopathies - hypertrophic and restricitve)
Explain the importance of the activation of the sympathetic nervous system as a compensatory mechanism in HF.
With the decrease in CO there is an increased necessity to maintain adequate perfusion of vital organs.
Mean arterial pressure= Cardiac output x Total peripheral resistance.
A decrease in CO leads to a decrease in mean arterial pressure (MAP). Decrease in MAP leads to activation of the sympathetic nervous system and release of catecholamines (adrenaline and noradrenalin). These cause increase in HR, contractility and vasoconstriction -> which increase stroke volume and total peripheral resistance and in turn increase MAP.
What are the BNP levels and how do they correlate to likelihood of CHF?
BNP<100 pg/ml - CHF very unlikely (2%)
BNP 100-500 pg/ml - baseline LV dysfunction, underlying cor pulmonale or acute pulmonary embolism
BNP >500 pg/ml - CHF very likely (95%)
What are the main goals of treatment for HF?
Reduce heart workload
Improve cardiac efficiency
Slow down progression
Prevent sudden cardiac death
How is the heart workload reduced?
Control of high blood pressure (Vasodilator)
Decrease peripheral vascular resistance (ACE-inhibitor or ARB)
Reduced sodium and fluid retention (Diueretic)
How is the cardiac efficiency improved?
Reduce the heart rate (Beta-blocker)
Prolong the diastolic filling time (Beta-blocker)
Increase effective myocardial blood flow
Increase end-systolic elastance (Inotrope)
Increase stroke volume
How is the progression of HF slowed down?
Block nerve and hormone activation (ACE-inhibitor or ARB)
Stop progression of ventricular dilatation
Protect cardiac myocytes from cardiotoxic effects of catecholamines and angiotensin (Beta-blocker)
