CVS: Heart Failure Flashcards
What is the definition of heart failure?
Clinical syndrome, can result from structural or functional cardiac disorder, impairs ability of heart to fill or eject blood so insufficient blood flow for body’s demands
What are the 2 types of heart failure?
- Acute
- Chronic - 2 types of chronic
- HFrEF or Systolic HF - Heart failure with reduced ejection fraction
- HFpEF or Diastolic HF - Heart failure with preserved ejection fraction
Describe the 4 classes of heart failure, as per the New York Heart Association (NYHA) functional class
Class I - Symptoms not limiting daily activities, normal physical activity doesn’t cause fatigue, breathlessness, palpitation (Asymptomatic LV dysfunction included in this class)
Class II - Slight limitation of physical activity, patients comfortable at test. Normal physical activity results in fatigue, breathlessness, palpitation or angina pectoris (symptomatically ‘mild’ HF)
Class III - Marked limitation of physical activity. Patients comfortable at rest, but unordinary physical activity causes palpitation, fatigue, breathlessness (symptomatically ‘moderate’ HF)
Class IV - Inability to carry on physical activity w/o discomfort. Symptoms of congestive cardiac failure are present even at rest. Any physical activity increases discomfort (symptomatically ‘severe’ HF)
What are symptoms of HF?
- Tiredness
- Shortness of breath
- Coughing
- Pulmonary oedema
- Pumping of heart weaker
- Swelling in ankles + legs
- Pleural effusion
- Swelling in abdomen (ascites)
How does HF affect quality of life?
Causes:
- Nocturnal dyspnoea
- Dyspnoea on exertion
- Orthopnoea
- Rales/lung crackles
- Acute pulmonary oedema
- Neck vein distension
- Increased venous pressure
- Cardiomegaly
- Cough
- Ankle oedema
- Renal dysfunction
What are causes of HF?
- Impaired ventricular function (reduced pump function)
- MI or cardiomyopathy
- Pressure overload of ventricle (increased afterload)
- Systemic or pulmonary hypertension
- Inflow obstruction of ventricle (Reduced filling)
- Restrictive cardiomyopathy
- Mitral stenosis
- Diastolic HF
- Valvular disease
- Aortic, mitral or tricuspid stenosis/regurgitation
- Volume overload of ventricle
- Ventricular and Atrial Septal defect (VSD and ASD)
Why is HF progressive?
It’s not just reactive to hemodynamic change, it continues to worsen and is difficult to reverse
Describe stage 1, 2 and 3 of HF development
Stage 1: Insult or stimulus
- Myocardium injury/ ⬆️chronic pressure load etc.
- ⬇️Contractility (pumping capacity)
Stage 2: Compensated dysfunction
- Initial preserved function
- Myocardial hypertrophy and chamber dilation
- Moderate symptoms and treatment
Stage 3: Decompensated overt failure
- Gross change in heart shape → wall thinning, spherical, dilation
- Significant morbidity and mortality - Hospitalisation
Compare HFpEF and HFrEF
HFpEF (diastolic HF):
- Ventricle unable to adequately relax and fill at normal diastolic pressures/volumes to maintain stroke volume
- Pressure overload in ventricles e.g., hypertension, aortic stenosis
HFrEF (systolic HF):
- Inability of heart to maintain contractility producing reduction in ejection fraction and stroke volume
- Volume-overload in ventricles (e.g., MI, IHD)
Describe the compensatory mechanisms that arise due to HF
- Drop in SV through ventricular failure leads to compensatory mechanisms to maintain cardiac output
- Increase in SNS + RAAS + Vasopressin activities → Opposed via activation of ANP/BNP system
- This can be problematic, as excessive increase in neurohormonal compensation leads to changes in O2 demand, and long-term changes to the heart
What are the prolonged compensatory mechanisms due to HF?
- Continuous sympathetic activation
- B-adrenergic downregulation and desensitisation (less contractility/ inotropic response)
- Increased heart rate
- Increased metabolic demands and myocardial cell death
- Increased preload
- Beyond limits of Starling’s law, pressure transmitted to pulmonary vasculature leading to pulmonary oedema
- Increased total peripheral resistance
- Higher afterload leading to decreased SV/CO
- Continuous neurohormonal activation
- Chronically elevated RAAS, Ang II and aldosterone trigger inflammatory responses (cytokines → activate macrophages, fibroblasts) → Myocardial remodelling
Describe remodelling in HF
Genome expression, molecular, cellular and interstitial changes that manifest clinically as a change in size, shape, and function of heart
Concentric hypertrophy:
- Heart has thick walls + small cavities
- Sarcomeres added in parallel increase myocyte cell width
Eccentric hypertrophy:
- Heart has thin wall + large cavities
- Sarcomeres added in series, increase myocyte cell length
Describe the diagnostic algorithm for heart failure
HF suspected:
- Request NT-proBNP test
- Sensitive for HF, but is non-specific, also present with AF, hypertension
- BNP normal - Look for other causes of breathlessness
- BNP elevated - ECG to confirm/refute
- Gold standard, will confirm causes e.g. valvular, IHD, hypertensive
What is the rationale for treating HF?
- Reduce myocardial O2 demands and increase SV
- Surgical, e.g. valve replacement, coronary artery stents
- Pharmacological - reduce preload, afterload, e.g. ACEi/ARBs
- Reduce cardiac dilation
- Reduce 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. B-blocker
- Improve myocardial contractility
- B-blockers
Describe NICE guidelines (2018) for treatment of HF, including frontline pharmacological treatments
Lifestyle:
- Exercise
- Smoking
- Alcohol
- Sexual activity
- Driving
Pharmacological intervention:
- Loop diuretics - Reduce symptoms, remove excess fluid
Frontline: - Regulate compensatory mechanisms
- ACEi/ARB: Measure urea, creatinine, electrolytes, GFR
- B- blockers - Start low, measure HR/Blood pressure
Second line:
- Aldosterone antagonists (MRA), hydralazine with a nitrate, digoxin, ivadbradine (lower HR)
