Heart Failure Flashcards
Give some examples of causes of heart failure.
ISCHAEMIC HEART DISEASE (systolic heart failure)
Hypertension
Dilated cardiomyopathy
- infection
- toxins e.g. alcohol, drugs, poisons
- pregnancy (peri-partum and post-partum)
- idiopathic
Diabetes
(Congenital) valvular heart disease
Restrictive cardiomyopathy e.g. amyloidosis
Hypertrophic cardiomyopathy
Pericardial disease e.g. constrictive pericarditis
High-output heart failure (increased O2 requirement by body)
- anaemia
- pregnancy
- hyperthyroidism
- arteriovenous fistula
Arrhythmias
- AF
- heart block
Infection
- rheumatic fever —> calcification of valves
- Chagas’ disease
- HIV
- viral myocarditis
How does heart failure progress? What scale is used?
New York Heart Association
Class 1 = no symptomatic limitation of physical activity
Class 2 =
- slight limitation of physical activity
- ordinary physical activity results in symptoms
- no symptoms at rest
Class 3 =
- marked limitation of physical activity
- less than ordinary physical activity results in symptoms
- no symptoms at rest
Class 4 (very poor prognosis) =
- inability to carry out any physical activity without symptoms
- may have symptoms at rest
- discomfort increases with any degree of physical activity
What are the factors affecting cardiac output? How may these be affected in disease states?
Heart rate
e.g. chronic AF —> tachycardia; bradycardia
Venous capacity (LV preload) e.g. dehydration, fluid overload
Myocardial contractility
e.g. metabolic disturbances (hypo/hyperkalaemia, hypocalcaemia)
Aortic and peripheral impedance (afterload)
e. g. hypertension
e. g. hypertension
Describe the structural changes in the heart that occur in systolic heart failure. How can these inform about the cause of the heart failure?
Increased LV capacity but reduced LV output (less blood pumped put during systole)
- thinning of myocardial wall due to fibrosis and necrosis (e.g. MI) weakens heart muscle (cannot pump as well)
- dilatation pulls valve leaflets apart —> mitral valve regurgitation
Structural changes cause arrhythmias
Neuro-hormonal changes
Scar present = heart failure caused by MI
No scar present = heart failure caused by something other than MI
note: early revascularisation in MI will prevent/reduce extent of heart failure
note: heart can remodel around areas of fibrosis/necrosis to avoid rupture
Outline how sympathetic activation following myocardial damage contributes to heart failure.
Myocardial damage stimulates baroreceptors which cause sympathetic activation (initially improve cardiac output)
—> RAAS activation —> fluid retention —> increases wall stress —-> increased myocardial oxygen demand AND myocardial hypertrophy
—> Vasoconstriction —> increases wall stress —> increased myocardial oxygen demand AND myocardial hypertrophy
—> increased heart rate and contractility —> increased myocardial oxygen demand
—> direct cardiotoxicity —> myocyte damage
Increased myocardial oxygen demand —> decreased contractility
+ down-regulation/uncoupling of beta-receptors
+ NA induces cardiac hypertrophy, myocyte apoptosis, mycocyte necrosis
+ NA up-regulates RAAS
+ reduction in heart rate variability (reduced parasympathetic activity and increased sympathetic activity)
What hormones are activated in heart failure?
- RAAS
- natriuretic hormone
- ADH
- endothelin
- prostaglandins/nitric oxide
- kallikrein system (proteases)
- TNF-alpha
Reminder: outline the renin-angtiotension-aldosterone system
renin ACE
Angiotensinogen ——-> Angiotensin I ——> Angiotensin II
Angiotensin II
- –> AT1R (vasoconstriction)
- –> AT2R —> increased nitric oxide (vasodilatation)
Bradykinin —> BK2R —> increased nitric oxide (vasodilatation)
What are the effects of angiotensin II?
- vasoconstriction (AT1R)
- LV hypertrophy and mycocyte dysfunction
- aldosterone release —> sodium and water retention —> volume overload —> hypertension
- ?stimulates thirst by central action
How can heart failure lead to renal failure?
Initially reduced renal blood flow activates RAAS (macula densa) to raise the blood pressure and maintain GFR
When this mechanism fails GFR falls, causing a raise in [urea]serum and [creatinine]serum
Exacerbated by ACE inhibitors and angiotensin receptor blockers (cause a 10%+ reduction in renal blood flow in normal individuals)
Describe the structural changes in the heart that occur in diastolic heart failure.
Reduced LV compliance impairing myocardial relaxation (stiff, thickened muscle cannot relax)
—> reduced diastolic LV filling —> reduced cardiac output AND increased pressure in left atrium —> increased pressure in pulmonary arteries
Neurohormonal activation
Concentric left ventricle hypertrophy
note: unable to compensate by increasing LV end-diastolic pressure
note: normal ejection fraction (50%-60%)
What is the aetiology of diastolic heart failure?
- frequently elderly females
- SYSTOLIC HEART FAILURE
- hypertension
- diabetes
- obesity (poor diastolic relaxation of the heart)
What is the aetiology of systolic heart failure?
- ISCHAEMIA
- dilated cardiomyopathy (idiopathic, viral, peri-partum, hypertension)
- valvular
What are the causes of right-sided heart failure?
Heart:
- LEFT-SIDED HEART FAILURE
- pulmonary/tricuspid valve disease
- left to right shunts
- isolated right ventricular cardiomyopathy
Lung:
- cor pulmonale
- chronic lung disease
- PE
- pulmonary hypertension
reminder: it is uncommon for one side of the heart to fail in isolation; usually have biventricular (congestive) heart failure
What are the symptoms of left-sided heart failure?
- fatigue
- exertional dyspnoea (severe heart failure: dyspnoea at rest)
- orthopnoea
- paroxysmal nocturnal dyspnoea (opening windows, sitting on the edge of the bed)
- ankle swelling (fluid retention)
- chest pain (due to cardiac ischaemia; increases resp. rate)
- anorexia (due to breathlessness whilst eating)
- dizziness
What are the signs of left-sided heart failure?
- overt breathlessness
- ?anaemia
- tachycardia
- blood pressure depends on aetiology
- cardiomegaly (displaced apex beat)
- gallop rhythm (3rd + 4th heart sounds)
- mitral regurgitation murmur
- basal pulmonary crackles (fluid overload)
- peripheral oedema (fluid overload)
What are the signs and symptoms of “pure” right-sided heart failure?
Distension and fluid accumulation in areas drained by systemic veins
- fatigue
- dyspnoea
- anorexia
- nausea
- raised JVP
- tender, smooth hepatic enlargement
- dependent pitting oedema
- ascites
- pleural effusion
What are the investigations for heart failure?
FBC
- ?anaemia exacerbating heart failure
- ?anaemia causing breathlessness mimicking heart failure
Renal function & electrolytes
- ?heart failure affecting GFR
- ?concomitant renal problems
Glucose & lipids
- ?diabetes
- ?hyperlipidaemia exacerbating heart failure
B-type natriuretic peptide
- increased in heart failure but not in COPD
- level indicates severity of heart failure (level falls when heart failure improves)
ECG
- ?MI
- ?signs suggestive of cardiomyopathy e.g. left bundle branch block
CXR
- ?cardiomyopathy
- ?fluid overload —> pulmonary oedema
Echocardiography
- compare left and right ventricles
- visualise valves
Chest CT
- ?evidence of lung disease
- ?cor pulmonale
What are Kerley B lines? What are they caused by?
Thickened subpleural interlobular septa (usually at lung bases)
Causes:
- pulmonary oedema
- lymphangitis carcinomatosis (lymphatic spread of cancer)
- pulmonary lymphoma
- pneumonia (viral, mycoplasma, PCP)
- interstitial pulmonary fibrosis
- pneumoconiosis
- sarcoidosis
Outline the management of heart failure.
LIFESTYLE
- reduce salt intake
- reduce alcohol intake
- increase aerobic exercise
- reduce BP
PHARMACOLOGICAL
- ACE inhibitors (or angiotensin receptor blockers if not tolerated e.g. cough or nitrates if angiotensin receptor blockers not tolerated)
- Beta-blockers
- Spironolactone
+ loop diuretics (reduce fluid retention —> symptomatic relief)
+ antiarrhythmics (if req.)
Acute heart failure (heart failure causing cardiogenic shock)
- inotropes
- phosphodiesterase inhibitors
- digoxin/beta-blockers
CARDIAC SURGERY
- heart transplant (in suitable young patients with poor prognosis)
- mechanical assist devices (external pump)
- treat underlying cause e.g. valve surgery, revascularisation
IMPLANTABLE PACEMAKERS = biventricular pacing (left bundle branch block causes asynchronous contraction)
IMPLANTABLE DEFIBRILLATORS = if heart failure puts at risk of VT or VF
Reminder: define heart failure.
State in which the heart fails to maintain adequate circulation for the needs of the body despite an adequate filling pressure
Define the term systolic heart failure.
LV pump failure due to reduced cardiac contractility or fluid overload, although filling pressure is adequate.
Define the term diastolic heart failure.
Normal LV function but failure to adequately perfuse heart due to concentric LV hypertrophy (impaired relaxation)
Reminder: define contractility.
Extent to which a given increase in venous pressure leads to an increase in stroke volume at a given fibre length.
Reminder: define preload and afterload.
PRELOAD = end-diastolic filling pressure (stretch applied to single cardiac myocyte prior to contraction)
AFTERLOAD = pressure heart must work against to eject blood during systole (systolic pressure)
What compensatory mechanisms help support the cardiac output in heart failure?
Baroreceptor activation —> increased sympathetic stimulation —> tachycardia —> increased cardiac output
Reduced renal perfusion —> reduced GFR —> RAAS activation ——> vasoconstriction and venoconstriction —> increased total peripheral resistance —> increased BP
What are the main aims of the treatment of heart failure?
Reduce fluid overload (symptom management)
- diuretics (reduce Na+ and water retention)
- ACE-inhibitors/angiotensin II receptor blockers (reduce RAAS activation)
Increase inotropy
Reduce oxygen demand of the heart
- beta-blockers
How is central venous pressure estimated?
Estimate JVP (compare height of internal jugular vein to sternum at 45 degrees)
Cannulate internal jugular vein (central line)
Cannulate subclavian vein
What are crackles/crepitations? What can they be caused by?
Short interrupted breath sounds due to fluid build-up in the lungs
- fine crackles = high frequency, short duration
- coarse crackles = low frequency, long duration
Caused by abnormally closed airway opening during inspiration (INSPIRATORY)
OR abnormally closed airway closing during expiration (EXPIRATORY)
OR air bubbles moving through fluid
OR rapid equalisation of gas pressures —> pressure wave
- increased elastic recoil pressure
- inflammation/oedema in lungs —> narrows airways
Contrast the different timing of crackles and their different causes.
Early-mid inspiratory crackles (coarse) = large central airways affected
- e.g. bronchitis (early), bronchiectasis (mid)
- gravity independent (does not resolve with posture)
- associated with obstructive pathology
- resolve with coughing
Late inspiratory crackles (fine) = peripheral airways affected
- e.g. pneumonia
- gravity dependent (resolves with posture)
- associated with restrictive pathology
- does not resolve with coughing
What are the signs found in the respiratory exam in heart failure.
Late inspiratory fine crackles in posterior lung bases
Reduced breath sounds (pleural effusions)
+/- dullness to percussion
