Pathophysiology Of Heart Failure Flashcards
What is heart failure
What enables the heart to work effectively as a pump?
Inability of the heart to meet the demands of the body - i.e. deliver a blood volume that allows body tissues to function as required
Functioning muscle, chamber size, one way valves - conditions that affect/impair these potentially lead to impairment of cardiac function - as well as the input and the output
Aetiology of heart failure
Most common cause of HF is IHD (CHD) - this leads to myocardial dysfunction e.g. through fibrosis (scarring) and remodelling of the muscle
Rarely, other disorders can cause HF if a grossly elevated demand is placed on the CO e.g. sepsis, severe anaemia, thyrotoxicosis (High CO heart failure), Aortic stenosis, Hypertension, Arrhythmias
How to measure ability of heart to meet body’s demand?
What influences stroke volume?
Frank starlings law?
CO = cardiac output = volume expelled per ventricle /min
CO = Stroke volume x heart rate
SV is only a fraction of the total volume within the ventricle at the end of diastole (EDV)
SV/EDV=fraction ejected (ejection fraction)
What influences stroke volume?
I.e. the volume of blood a ventricle can eject in a single beat
Pre-load (volume in the ventricle at the end of diastole = EDV) - which is effected by the stretch on ventricle just before contraction - hence SV is affected by Myocardial contractility
After load (total peripheral resistance) - hypertension at the peripheries - too much pressure at peripheries means its harder for heart to push blood through them
Frank Starling’s law - More ventricular distension during diastole = Greater volume ejected (SV) during systole
Called the intrinsic property of cardiac myocytes - the greater they are stretched the greater their force of contraction (up to a certain point - if end diastolic volume/distension during diastole increases too far then heart doesnt have the muscle to pump that amount of blood therfore CO decreases)
Frank starling Curves vary depending on inotropic state of the heart
Contractility of the heart can increase with increased sympathetic activity (curve shifted upwards and left) - Greater CO for a given LV EDP (more volume is forced out) - this occurs because greater SNS stimulation leads to more adrenaline binding to heart, therefore more calcium entering therefore increasing force of contraction
Whi is cardiac output reduced in heart failure
Stroke volume can be reduced due to -
Reduced pre load (reduced EDV) - Impaired filling of ventricle during diastole - this can occur due to, chambers are too stiff (not relaxing) or the chamber walls thickened - due to excess hypertrophy
Reduced myocardial contractility - Muscle not able to produce same force of contraction (systole) for a given volume within ventricle - this could be due to muscle walls thinned/fibrosed, chambers have enlarged to far (overstretched sarcomers), abnormal or uncoordinated myocardial contraction (which could have come about due to over-stretching) - Afib Increased afterload - increased pressure against which ventricle contracting e.g. aortic stenosis, chronic severe hypertension
Classifying heart failure - according to ejection fraction
Heart failure with reduced ejection fraction (HFrEF) - i.e. the % of blood exiting the ventricles compared to normal has decreased -
usually due to systolic dysfunction - i.e. contractility problem - heart cant contract enough to get the blood out
most common type - known as systolic heart failure
Heart failure with preserved ejection fraction (HRpEF) - the % you will eject is the same as before - just will be operating with lower volumes -
Usually due to Diastolic dysfunction - i.e. a Filling problem - ventricle size on relaxation is not large enough to cope with the body’s needs - could be due to LV hypertrophy preventing the LV from distending and relaxing normally
Known as diastolic heart failure
Ejection fraction - measurement on echocardiogram
Normally >50/>60%
Reduced <40%
How can a heart be
Classifying heart failure according to ventricles involved
Left or right ventricle ?
Left ventricle most commonly involved - But this comes with subsequent involvement of the right ventricle
Therefore you get Involvement of both ventricles - called Biventricular (congestive) heart failure
Right ventricular heart failure can occur isolation, secondary to chronic lung diseases (cor pulmonale)
Much less common than left ventricular heart failure
Note that the most common cause for RV heart failure is LV heart failure
Frank-starling’s curve in heart failure
Reduced CO for given level of ventricular filling (contractility impaired)
Increased LV filling in a healthy heart leads to big increase in CO (gradient of curve)
Increased LV filling in failing heart leads to a very little increase in CO…(gradient of curve) and eventually with failing heart, the CO worsens (curve dips down)
This can spiral out of control - due to the lack of CO, the body may stimulate SNS more, therefore increasing SV to try and rescue the falling CO, but this leads to a Markedly increased LVEDP [in attempts to increase SV] result in further falling of CO and development of pulmonary congestion
Drop in CO triggers a number of phsyiological mechanisms - to try and correct the falling CO
2 pathways - Baroreceptors in carotid sinus and aorta and activation of RAAS pathway
Baroreceptors are quick short term response - when low BP is detected (due to lack of CO) there is an increase in SNS which increases HR and TPR - therefore increasing after load
RAAS pathway is a more long term solution - angiotensin 2 also causes vasoconstriction and increased SNS activity (increasing afterload), but also stimulates ADH and aldosterone to increase uptake of Na+ and water which increases circulating blood volume (increasing pre load)
These mechanisms, however, ultimately lead to an increased cardiac demand and a further reduction in stroke volume (further deterioration in cardiac output and the condition)
Clinical signs and symptoms of heart failure
Symptoms will often include
Fatigue/ lethargy,
Breathlessness
+/-leg swelling - oedema due to the increase in pressure
Many signs (and symptoms) due to increased interstitial fluid (oedema) in Pulmonary tissues and Peripheral tissues (dependent areas i.e. lower limbs)
Formation of tissue fluid and tissue oedema
Gradient between hydrostatic and oncotic pressure governs movement of fluid out of or back into capillaries - too much hydrostatic and not enough oncotic leads to fluid leaking out of the blood vessels
Returning to right side of the heart (RA—>RV) from systemic circulation
Returning to left side of the heart (LA—>LV) from pulmonary circulation
Formation of Tissue Oedema - Increased capillary hydrostatic pressures leads to less fluid being drawn back intravascularly at venule end
If right or left ventricle is failing, it will cause a backlog of higher pressures in venous circulation
Similarities between right and left ventricular failure
Raised JVP
Similarities - both will see fatigue and lethargy in patients
Will also see breathlessness in both patients
Differences - in LV failure you will see - orthopnea (shortness of breath when lying flat), paroxysmal nocturnal dyspnoea (shortness of breath/coughing during sleep), basal pulmonary crackles (excess fluid in airways), cardiomegaly (displaced apex beat-indicating enlarged LV)
In RV failure you will see - Peripheral odema, raised jugular venous pressure and tender smooth enlarged liver (due to liver congestion)
Raised Jugular Venous pressure (JVP) - Measurement of the pressure in the right internal jugular vein can be used as a direct reflection of pressure in the right side of the heart
