Left ventricular dysfunction and failure Flashcards
Learning outcomes
Review physiology of control of cardiac output and circulation
•Discuss myocardial contractile function & its measurement (LVEF)
•Recognise the common clinical features of systolic heart failure & explain how they relate to the underlying pathophysiology
•Review the compensatory mechanisms which are activated by reduced cardiac output, describe how these contribute to the pathophysiology of heart failure, referring to the SNS, RAAS & counter-regulation by natriuretic peptides
•List the more common underlying causes of left ventricular dysfunction and systolic failure
•Describe common clinical investigations dysfunction including ECG, cardiac imaging and plasma biomarkers
•List the main aims of therapy in systolic heart failure and the main classes of drugs used, linkingrationale to pathophysiology
Normal physiology
Systemic circulation > right heart> pulm arteries > lungs > pulm veins > left heart > systemic arteries> capillaries (cyclical)
Phases of C. cyle - •Diastole (relaxation/ filling) isovolumic relaxation early filling diastasis late filling (Active) •Systole (contraction) isovolumic contraction ventricular ejection
Cardiac output
Cardiac output is the volume of blood pumped around the body in 1 minute
Cardiac output = stroke volume x heart rate
Stroke volume is determined by cardiac stretch and inotropic status (positive inotropic strengthens heart contraction) among other factors
LVEF (ejec.fraction) = End diastolic volume – end systolic volumeEnd diastolic volume
Using LV volume curve Ejection fraction (EF) = SV/EDV (%)
Other factors in cardiac performance
Cardiac output is affected also by the conditions into which the heart pumps
resistance to pumping (vascular resistance)arterial blood pressure
CO = arterial pressure / peripheral resistance
Heart failure and common causes
Systolic failure of left ventricle (pump failure)
– most common and best understood type
– reduced ejection fraction
- maintenance of cardiac output and BP is threatened
- cardiac / neural / hormonal mechanisms activated to compensate
Common causes of HF
Ischaemic heart disease/ myocardial infarction
•Undiagnosed/poorly controlled hypertension
•Valvular heart disease
•Heart muscle disease/loss (cardiomyopathy)
•Others: thyrotoxicosis, alcohol, infection, drug damage
Compensatory mechanisms activated in HF
CO = SV x HR
SV :↑ contractility ↑ heart rate
To increase CO, increase SV, heart rate or both
BUT cardiac work and oxygen demand increase
BP = CO x SVR
To increase blood pressure, systemic vascular resistance and blood volume are increased by neurohormonal mechanisms ( less constriction, more elasticity/changes in blood viscosity)
BUT: detrimental to cardiac function (pre/afterload
Consequences of pump failure
‘Forward’ failure– failure to provide adequate perfusion to tissues– hypoxia / tachycardia
• ‘Backward’ failure– pressure inside cardiac chambers increases– back pressure alters vascular haemodynamics– exudation of fluid from vulnerable beds
Neurohormonal hypothesis
• neurohormonal hypothesis of pathophysiology of chronic heart failure:
–failing heart misinterprets signal and sets in train a series of neural and hormonal responses to offset problem, but these ultimately become counter-regulatory causing further damage to myocardium and less efficient pumping
Baroreceptor reflex
Normally: ↑ BP, ↑ stretching ↑ firing rate of baroreceptors ↓sympathetic outflow from CNS vasomotor centre
HF: ↓ BP, ↓ stretching ↓ firing rate of baroreceptors ↑ sympathetic outflow from CNS vasomotor centre
Sympathetic activation
Initially
– Increase heart rate
– Increase cardiac contractility (inotropy)
– Increase vascular tone
– Increase blood pressure
– [Activation of RAAS]
• But requires increased work and oxygen
• persistent– heart muscle cell hypertrophy, apoptosis, necrosis, fibrosis, synthesis of extracellular matrix (scar tissue)
–↑contractile dysfunction, arrhythmias, sudden cardiac death
Noradrenaline levels predicts symptomatic HF and subsequent mortality
RAAS activation
Angiotensin > ( Renin- through BP (baroreceptors)renal hypoperfusion and ischaemia) angiotensin 1 > (angiotensin converting enzyme (ACE)) angiotensin 2 > angiotensin AT1 receptors (mediate majority of actions of ang 2)
- Aldosterone secretion (and vasopressin)
- salt/fluid retention(↑pre-load)
- vasoconstriction↑ after-load
RAAS activation in HF: actions of angiotensin II
- vasoconstriction, ↑BP, cardiovascular remodelling
- ↑ aldosterone, vasopressin secretion, Na+ /water retention
- ↑ noradrenaline release from SNS
- progressive glomerular and cardiac remodelling
- short-term adaptive↑ preload, cardiac output
- long-term chronic maladaptive ↑fluid retention, ↑after-load and remodelling, ↓EF Vasopressin levels also ↑ in severe CHF↑ water retention and oedema
Detection of HF
Clinical assessment symptoms signs • Evidence of systolic dysfunction Electrocardiograph (ECG) Brain Natriuretic Peptide (BNP) Echocardiogram (Echo)
Exudation of fluid from lung capillaries
Pulmonary oedema
Exudation of fluid from systemic capillaries
oedema, ascites
Starling Law- The Frank–Starling law of the heart represents the relationship between stroke volume and end diastolic volume. The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction, when all other factors remain constant.
Symptoms of HF
Symptoms of heart failure •dyspnoea •orthopnoea •paroxysmal nocturnal dyspnoea •exercise intolerance •fatigue •oedema / fluid accumulation
Clinical signs of HF
Left-sided failure– tachycardia– displaced apex beat (enlarged heart)– gallop rhythm (extra S3, S4 heart sounds)
– lung crepitations / rales due to oedema
• Right-sided failure– pleural effusion, ankle oedema, enlarged liver, ascites
Symptoms and signs
Increased venous pressure •Left ventricular failure -pulmonary venous pressure -pulmonary oedema -lung compliance Dyspnoea (exertional/at rest) orthopnoea/paroxysmal nocturnal dyspnoea bilateral basal crackles hypoxaemia/central cyanosis •Right ventricular failure -systemic venous pressure -elevated JVP -ankle oedema -ascites -tender hepatomegaly
Decreased cardiac output
- fatigue
- hypotension
- reduced peripheral perfusion (advanced stage)
- peripheral cyanosis (in absence of central cyanosis)
Ventricular dilatation/hypertrophy
Symptoms/signs
-displaced apex beat
Sympathetic compensation
Symptoms/signs
-tachycardia
