Pathophysiology of cardiac failure Flashcards
Systolic ventricular dysfunction
– impaired cardiac contractility
↓ ejection fraction
– (<40%; normal ~50-65%)
Diastolic ventricular dysfunction
– normal ejection fraction but impaired diastolic ventricular relaxation and decreased filling
– ↓in SV and CO
Systolic Dysfunction commonly results from conditions that effect:
1. contractility – e.g. IHD, cardiomyopathy 2. volume overload 3. pressure overload – valvular stenosis; hypertension
this results in ↑EDV (preload), ventricular dilation, ↑ventricular wall tension
Diastolic Dysfunction
Normal contraction; impaired relaxation
causes of diastolic dysfunction
1. impedance of ventricular expansion – constrictive pericarditis etc. 2. increased wall thickness – hypertrophy etc. 3. delayed diastolic relaxation – aging; ischaemia 4. ↑heart rate
Right Ventricular Dysfunction: Causes
Conditions impeding flow into the lungs
– Pulmonary hypertension
– Valve damage/stenosis/incompetence
Pumping ability of right ventricle
– Cardiomyopathy
– Infarction
Left ventricular failure
Congenital heart defects
Left Ventricular Dysfunction: Causes
Hypertension (↑TPR)
Acute myocardial infarction
Aortic or mitral valve stenosis or regurgitation
Increase in pulmonary pressure can lead to right ventricular failure
Compensatory Mechanisms
In the early stages of heart failure, compensatory mechanisms (i.e. those involved in hypovolemia) maintain cardiac output
Longer-term, they contribute to the worsening of the condition
Problems with the Compensatory Mechanisms: 1. Frank-Starling
↑ in vascular volume leads to ↑EDV
↑ in muscle stretch and O2 consumption
Problems with Compensatory Mechanisms: 2. Sympathetic activity
Initially, sympathetic activity can be helpful; long-term it is not:
– Tachycardia, vasoconstriction, ↓ perfusion of tissues, cardiac arrhythmias, renin release
– ↑ the workload of the heart
• ischaemia, damage to myocytes, ↓ contractility
– Desensitisation of b but not a receptors
Problems with Compensatory Mechanisms: 3. Renin-Angiotensin
↓ in renal blood flow s9mulates release of renin
↑ renin release
therefore ↑ angiotensin II formation
– Vasoconstrictor, plus stimulates aldosterone release
therefore sodium and water reabsorp9on is ↑ both directly (decreased flow rate through the kidney) and indirectly (via aldosterone)
Angiotensin II and aldosterone are also involved inflammatory responses leading to
deposition of fibroblasts and collagen in the ventricles
↑ the stiffness and ↓ the contrac9lity of the heart, leading to myocardial remodelling and progressing dysfunction
Strategies for treatment
↑ cardiac contractility
↓ preload and/or afterload to ↓ cardiac work demand
– By relaxing vascular smooth muscle
– By reducing blood volume
Inhibit the RAAS
Prevent inappropriate ↑ in heart rate
New York Heart Association Classification of Heart Failure (NYHA) 1
No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea (shortness of breath).
New York Heart Association Classification of Heart Failure (NYHA) 2
Slight limitation of physical activity. Comfortable at rest. Ordinary
II physical activity results in fatigue, palpitation, dyspnea (shortness of
breath).
