CVS: Heart Failure Flashcards
What is heart failure?
The heart’s can’t properly fill or eject blood. Hay insufficient blood flow to meet the body’s needs
How is chronic heart failure classified?
Two types of Chronic HF:
Heart failure w reduced ejection fraction (HFrEF)/Systolic HF
Heart Failure w preserved ejection fraction (HFpEF)/Diastolic HF
HF can also be classified into I, II, III and IV. As the number increases, the severity of the HF also increases
Outline differences between HFrEF and HFpEF
HFrEF (systolic HF)
Inability of heart to maintain contractility, reducing ejection fraction and SV. Caused by volume-overload e.g. MI, IHD
HFpEF (diastolic HF)
Ventricle can’t adequately relax and thus fill at normal diastolic pa/volumes to maintain SV. Caused by pa-overload e.g. hypertension, aortic stenosis
How do you know which one is which?
Give symptoms of heart failure
- Nocturnal dyspnoea
- Dyspnoea on exertion
- Lung crackles linked to acute pulmonary oedema
- Neck vein distension
- Cardiomegaly
- Cough
- Ankle oedema
- Renal dysfunction
What are the causes of HF?
Impaired ventricle function bc of MI or cardiomyopathy/remodelling
Increased afterload. Caused by hypertension- heart needs to overcome extra wall stress
Reduced ventricular filling. Caused by restrictive cardiomyopathy, Mitral stenosis (inability of LA to fill LV), diastolic HF
Describe the development of heart failure
Stage 1 :Insult or stimulus, eg myocardium injury, pressure/volume load etc which decreases contractility (pumping capacity)
Stage 2 :Compensated dysfunction. Initial preserved function, myocardial hypertrophy and chamber dilatation. Moderate symptoms and treatment
Stage 3:Decompensated overt failure. Gross change in heart shape - wall thinning, spherical, dilatation. Significant morbidity and mortality, hospitalisations
Explain compensatory mechanisms during heart failure
Ventricular failure causes a drop in SV. This leads to compensatory mechanisms to maintain CO, including: Increase in sympathetic + RAAS + Vasopressin activities to increase heart activity.
This then activates ANP/BNP systems which try to switch off these compensatory mechanisms
Describe the Effects of Prolonged Compensatory Mechanism
- Continuous sympathetic activation means β-adrenoreceptors get desensitised (less inotropic response)
- Increased HR means increased metabolic demands and myocardial cell death
- In**reased preload gets beyond limits of Starling’s law, pressure is transmitted to pulmonary vasculature leading to pulmonary oedema
- Increased TPR causes higher afterload leading to decreased SV/CO
- Continuous neurohumoral activation: chronically elevated RAAS, Ang II and aldosterone trigger inflammatory responses causing myocardial remodelling
Draw a diagram to explain remodelling in heart failure
Draw a diagram to describe the way in which heart failure is diagnosed
What is the main rationale in the treatment of heart failure?
Reduce myocardial O2 demands and increase stroke volume. Done surgically by valve replacement, coronary artery stents OR drugs to reduce preload, afterload, e.g. ACEi/ARBs
Reduce cardiac dilation, by reducing blood volume to reduce preload, e.g. diuretics and prevent/reverse remodelling, e.g. ACEi/ARBs
Prevent arrhythmias – reduce sympathetic nervous system activity, e.g. β-blockers
Improve myocardial contractility – β-blockers
B1 adrenoreceptors actually increase ionotropic effect and is good for contractility. Why then, do we use β-blockers in chronic heart failure?
- Slowing HR pevents overworking of a failing heart and increases diastolic time - increases coronary perfusion
- Reducing contractility reduces O2 demand - makes failing heart work more efficiently
- Prevents desensitisation of β-adrenoceptors caused by excess compensatory sympathetic nerve activity in heart failure . Therefore more β-adrenoceptors available for contractility
- Prevent β-adrenoceptor-associated arrhythmias
