5. Heart failure Flashcards
Heart failure general definition
Heart failure = the cardiac output is not enough to deliver the necessary amount of blood to the tissues
- A generally chronic process
- Body will compensate with neurohormonal and inflammatory reactions
- Will react with cellular a macroscopic remodelling
- Leads to abnormal mechanical and electrical disturbances
- Progressions, prognosis usually guarded
Types of cardiovascular insufficiency
- Heart failure → can lead to cardiogenic shock i.e. central shock
- Peripheral circulatory failure → peripheral shock
➔ Important to distinguish, life-saving fluid therapy in peripheral shock is contraindicated in cardiogenic shock
Cardiac Output (CO)/ cardiac performance/ stroke volume = heart rate x ejection volume … in l/min
Cardiac output is determined by:
- Preload = initial stretching of the cardiac myocytes → left ventricular end-diastolic volume
Preload ↑ → CO ↑ (→ congestion and incr. oxygen demand) - Afterload = the load to which the heart must pump against → determined by vascular resistance (vasoconstriction/ vasodilation), also called ventricular wall stress
Afterload ↑ → CO ↓ (→ hypertrophy and incr. oxygen demand) - Contractility = ability of the heart to contract (change in rhythm influences contractility → arrhythmias influence CO)
Contractility ↑ → CO ↑ (→ incr. oxygen and energy demand); arrhythmias generally CO ↓ - Heart rate
Heart rate ↑ → CO ↑ … but consequently CO ↓ - Distensibility = ability of the heart to be stretched
Distensibility ↑ → CO ↑ (→ pathological dilation, incr. oxygen and energy demand) - Synchronisation of heartbeats
Backward heart failure
ventricle fails to pump out all its blood that got in → ventricular filling pressure → congestion → systemic (right side) or pulmonary (left side) oedema
Forward heart failure
not enough blood delivered to the tissues
Frank starling law
strength of the contraction increases parallel with the original length of the cardiac muscle cell
heterometric auto regulation of the strength of the heartbeat
the lengthening of cardiac cells are increasing the myofibrils sensitivity to calcium and may increase the amount of calcium released from the sarcoplastic reticulum
(basically, describes the relationship between stroke and diastolic volume → Cardiac Output increases in response to an increase in volume of blood in ventricles during diastole, i.e. larger volume of blood stretches the cardiac muscle fibres and leads to an increase in the force of contraction)
Laplace rule
increasing pressure during ejection is caused by decreasing volume
during dilation of the heart wall tension should be increased (to the cost of higher energy and oxygen consumption)
Hypertrophy due to training doesn’t induce increased wall stress
wall stress creates wall tension/wall thickness (law applicable after afterload)
Cardiac insuffiency
Cardiac insufficiency:
- Bradycardia, tachycardia, arrhythmia
- Myocardial dysfunction (heart disease)
-
Failure of systolic mechanical function (pump function) of the heart, due to
• Pressure overload (→ concentric hypertrophy)
➢ From primary heart disease
• Volume overload (→ will lead to dilated myopathy)
➢ From primary heart disease, infusion overdose or peripheral arteriovenous shunt
- Failure of diastolic distension
➢ From primary heart or pericardial disease - Hyperkinetic (high output) circulation
➢ From fever, gravidity, anaemia, hyperthyroidism
Cardiac failure types
- Course of disease:
• Acute or chronic - Signs during what level of circulatory demand:
• Absolute or relative (only during exercise) - Anatomy:
• Left-sided or right-sided - Function:
• Systolic (can’t contract sufficiently) or diastolic (can’t distant sufficiently)
• Systolic e.g. mitral regurgitation, DCM
• Diastolic e.g. myocardial fibrosis, hypertrophic cardiomyopathy, restrictive cardiomyopathy, pericardial disease - Direction:
• Forward or backward (see above) - Grad of heart failure:
• Compensated or decompensated (can be originally compensated in chronic HF)
Compensation of the heart failure
in order to keep the blood volume, stroke volume and arterial pressure on an optimal value
A) elevated heart rate (but:decreased diastolic filling, decreased coronary filling)
B) increased myocardial activity (increased oxygen and energy consumption - myocardial hypertrophy
C) peripheral vasoconstriction (but: increased afterload!)
D) increased blood volume renio-angiotensin-aldosteron sytem - elevated preload -> pathological overcompensation
Sympathetic tone goes up due to decreased blood pressure (baroreceptors)
and later due to angiotenzin II
→ + inotropic, + lusitropic, + chronotropic effects
→ vasoconstric;on
→ arrhythmias
→ increased renin synthesis
Parasympathetic tone ↓
Chronic sympathetic activation (decreased baroreceptor
sensitivity)
Β-receptor density and sensi;vity ↓ (especially β1), α ?
Priorities of the body in heart failure
- To sustain systemic arterial blood pressure in the most important organs (= brain, heart, kidneys)
- To sustain systemic arterial blood pressure in other organs
- To keep systemic venous blood pressure (preload) on a reasonable low level
➔ For these the body needs to keep optimal blood volume, CO and arterial pressure
A. Elevated heart rate
➢ But leads to decreased diastolic filling a decreased coronary flow
B. Increased myocardial activity
➢ But leads to increased oxygen demand and energy consumption due to myocardial hypertrophy
C. Peripheral vasoconstriction
➢ But leads to increased afterload
D. Increased blood volume with RAA system
➢ But acts at loss of third priority (keeping venous pressure low) elevated preload → signs of overcompensation
Mechanism of compensation
neural compensation - → increased sympathetic tone
• Due to 2 mechanisms:
➢ Decreased blood pressure detected by baroreceptors (early)
➢ Angiotensin II (later)
• Leads to: ➢ Increased inotropic, lusitropic and chronotropic effects ➢ Vasoconstriction ➢ Arrhythmias ➢ Increased renin synthesis
- Decreased parasympathetic tone!
- Chronic sympathetic activation will lead to decreased baroreceptor sensitivity → baroreceptor sensitivity and density decreases (especially beta1)
Renin-Angiotensin-Aldosteron System (RAAS)
Angiotensin→ Angiotensin I → Angiotensin II (vasoconstrictor)
• Angiotensin II → Aldosterone → Na and water retention
→Arginine Vasopressin (ADH) → Vasoconstrictor and water retention
• Effects:
➢ Sodium and water retention, potassium excretion
➢ Vasoconstriction
➢ Sympathetic tone increased
➢ Myocardial fibrosis, necrosis and hypertrophy
➢ Cardiac remodeling → left ventricular hypertrophy
➢ Arrhythmias
Endothelin?
- Most potent vasoconstrictor
- Synthetized by endothelium and myocardium
- Endothelium converting enzyme converts it into its active form
- Receptors at the endocardial layer of the heart and in heart valves
- Leads to vasoconstriction and myocardial hypertrophy
Consequences of heart failure
Heart failure will lead to an increase in inflammatory mediators → myocardial fibrosis, necrosis, apoptosis
- Paracrine molecules
- Origin from mononuclear cells, myocardium, endotoxins from the gut (?)
- Interleukins
- TNF-alpha
➔ Cardiac cachexia, catabolic processes, anorexia
➔ Myocardial contractility decreased
➔ Myocardial hypertrophy, fibrosis
➔ Increase in free radicals
➢ Reactive molecules with unpaired electrons
➢ Formed in hypoxic environment
➢ Inflammatory mediators
➢ Decreased contractility
➢ BUT important physiological role as messengers, antibacterial actions etc.
