Heart failure signs on X-ray
- Alveolar oedema (bat’s wings)
- kerley B lines (interstitial oedema)
- Dilated prominent upper lobe vessels
- Effusion (pleural)
Left Heart failure
common causes are ischaemic heart disease, valvular heart disease, and hypertension.
Affects the blood flow systemically to the brain and the rest of the body.
Left ventricular failure: Symptoms:
- Dyspnoea, poor exercise tolerance
- Paroxysmal nocturnal dyspnoea (pnd),
- Nocturnal cough (±pink frothy sputum)
- Wheeze (cardiac ‘asthma’)
- Muscle wasting
- Weight loss
- Cold peripheries
RV Heart Failure briefly
common causes are chronic left heart failure resulting in back pressure to the right side of the heart, pulmonary hypertension, chronic lung disease, infarction to the right side of the heart and adult congenital heart disease. Affects blood flow to the lungs.
- Peripheral oedema
- Pulsation in the neck, face
what is systolic heart failure?
Insufficient contraction of the heart i.e. reduced ejection fraction.
inability of the ventricle to contract normally, resulting ↓cardiac output. EF is <40%. Causes:IHD, MI, cardiomyopathy.
what is diastolic heart failure?
nsufficient relaxation of the heart muscles during diastole and hence decreased cardiac output. Patient has signs and symptoms of heart failure but ejection fraction is normal i.e. >45-50%. Common in elderly hypertensive patients
inability of the ventricle to relax and fill normally, causing ↑ filling pressures. ef is >50%. Causes: constrictive pericarditis, tamponade, restrictive cardiomyopathy, hypertension. NB: systolic and diastolic failure usually coexist.
SIGNS OF LEFT HF
paroxysmal nocturnal dyspnoea i.e. PND
bibasal crepitations - PLEURAL EFFUSION
laterally displaced apex beat - CARDIOMEGALY
RIGHT HEART FAILURE SIGNS
Peripheral pitting oedema,
Cellular mechnaisms of HF
Alterations in contractile properties of myocytes
Progressive loss of myocytes through apoptosis, necrosis, atophagic death
Abnormal myocardial energetics and metabolism
Reorganisation of structural collagen surroundings
Neurohormonal adaptations in HF
decreased CO in HF → “unloading” of high-pressure baroceptors in LV, carotid sinus, and aortic arch → afferent signals to the CNS →stimulate the release of ADH (AVP) from the posterior pituitary.
ADH is a powerful vasoconstrictor, ↑ permeability of renal collecting ducts, →↑reabsorption of water. These afferent signals to the CNS also activate efferent SNS pathways that innervate the heart, kidney, peripheral vasculature, and skeletal muscles.
SNS stimulation of kidney → release of renin → ↑ angiotensin II and aldosterone.
The activation of RAA system → salt and water retention & vasoconstriction of the peripheral vasculature, myocyte hypertrophy, myocyte cell death, and myocardial fibrosis.
While these neurohormonal mechanisms facilitate short-term adaptation by maintaining blood pressure, and hence perfusion to vital organs, these same neurohormonal mechanisms are believed to contribute to end-organ changes in the heart and the circulation, and to the excessive salt and water retention in advanced HF.
- Paroxysmal nocturnal dyspnea or orthopnea
- Neck vein distention
- Acute pulmonary edema
- S3 gallop
- Increased jugular venous pressure >16 cm H2O
- Circulation time >25 s
- Hepatojugulr reflux
- Ankle edema
- Night cough
- Dyspnea on exertion
- Pleural effusion
- Vital capacity decresed 1/3 from maximum
- Tachycardia (heart rate >120 beats/min)
Major or minor criterion
Weight loss >4.5 kg in 5 days in response to treatment
Definite congestive heart failure = 2 major criteria
or 1 major and 2 minor criteria
Cor pulmonale aetiology
Diseases Leading to Hypoxic Vasoconstriction
- Chronic bronchitis
- Chronic obstructive pulmonary disease
- Cystic fibrosis
- Chronic hypoventilation
- Neuromuscular disease
- Chest wall dysfunction
- Living at high altitudes
Diseases That Cause Occlusion of the Pulmonary Vascular Bed
- Recurrent pulmonary thromboembolism
- Primary pulmonary hypertension
- Venocclusive disease
- Collagen vascular disease
- Drug induced lung disease
Diseases That Lead to Parenchymal Disease
- Chronic bronchitis
- Chronic obstructive pulmonary disease
- Cystic fibrosis
- Idiopathic pulmonary fibrosis
COPD and cor pulmonale. Mechanism leading to pulmonary HTN
80% to 90% of cases of cor pulmonale are caused by COPD.
Mechanisms leading to pulmonary hypertension include:
1. Pulmonary vasoconstriction resulting from any condition causing alveolar hypoxia or acidosis
2. Anatomic reduction of the pulmonary vascular bed (e.g., emphysema, interstitial lung disease, pulmonary emboli)
3. Increased blood viscosity (e.g., polycythemia vera, Waldenström's macroglobulinemia)
4. Increased pulmonary blood flow (e.g., left-to-right shunts)
Systolic dysfunction HF
Heart failure caused by systolic dysfunction is defined as a ↓ EF (< 50%) and ↑ LV end-diastolic volumes.
It is caused by inadequate left ventricular contractility or ↑ afterload.
The heart compensates for low EF and ↑ preload through hypertrophy and ventricular dilation (Frank-Starling law), but the compensation ultimately fails, leading to ↑ myocardial work and worsening systolic function.
Diastolic dysfunction HF
Defined by ↓ ventricular compliance with normal systolic function.
The ventricle has either impaired active relaxation (2° to ischemia, aging, and/or hypertrophy) or impaired passive filling (scarring from prior MI; restrictive cardiomyopathy).
LV end-diastolic pressure ↑, cardiac output
remains essentially normal, and EF is normal or ↑.
Treatment of acute HF
■ Correct underlying causes such as arrhythmias, myocardial ischemia, and drugs (e.g., CCBs, antiarrhythmics, NSAIDs, alcohol, thyroid and valvular disease, high-output states).
■ Diurese aggressively with loop and thiazide diuretics
■Give ACEIs to all patients who can tolerate them. If a patient cannot tolerate ACEIs, consider an angiotensin receptor blocker (ARB).
β-blockers should not be used during decompensated CHF but should be started once the patient is euvolemic.
■ Treat acute pulmonary congestion with LMNOP:
Causes of Cardiac Failure
- Ischaemic heart disease (35-40%)
- Cardiomyopathy (dilated) (30-34%)
- Hypertension (15-20%)
- Cardiomyopathy (undilated): hypertrophic, restrictive (amyloidosis, sarcoidosis)
- Valvular heart disease (mitral, aortic, tricuspid)
- Congenital heart disease (ASD, VSD)
- Alcohol and drugs (chemotherapy - trastuzumab, imatinib)
- Hyperdynamic circulation (anaemia, thyrotoxicosis, haemochromatosis, Paget's disease)
- Right heart failure (RV infarct, pulmonary hypertension, pulmonary embolism, (COPD))
- Tricuspid incompetence
- Arrhythmias (atrial fibrillation, bradycardia (complete heart block, the sick sinus syndrome))
- Pericardial disease (constrictive pericarditis, pericardial effusion)
- Infections (Chagas' disease), e.g. myocarditis
Epidemiology of heart failure
Epidemiology: >10% of >65 y/o,
2% overall population
Management of chronic cardiac failure
Stop smoking. Eat less salt. Optimize weight & nutrition.
• Treat the cause (eg if dysrhythmias; valve disease).
• Treat exacerbating factors (anaemia, thyroid disease, infection, ↑BP).
• Avoid exacerbating factors, eg nsaids (fluid retention) and verapamil (–ve inotrope).
- ACEI: Consider in all those with LV systolic dysfunction; improves symptoms and prolongs life
- Diuretics for symptomatic relief, also reduce risk of death. Loop, potassium sparing.
- β-blockers (eg carvedilol) decrease mortality in heart failure. Initiate after diuretic and ACEI.
- Spironolactone: Spironolactone (25mg/24h po) ↓mortality by 30% when added to conventional therapy.Use in those still symptomatic despite optimal therapy as listed above. It improves endothelial dysfunction (↑nitric oxide bioavailability) and prevents remodelling
- Digoxin helps symptoms even in those with sinus rhythm;Should be considered for patients with lv systolic dysfunction who have signs or symptoms of heart failure while receiving standard therapy
- Vasodilators: The combination of hydralazine (SE: drug-induced lupus) and isosorbide dinitrate should be used if intolerant of ACEI and ARBs as it reduces mortality
causes of intractable heart failure and what to do next??
Intractable heart failure:
Reassess the cause. Are they taking the drugs?—at maximum dose? Switching furosemide to bumetanide (one 5mg tab≈200mg furosemide) might help: absorption may be better. Consider admitting for:
• Strict bed rest ± Na+ & fluid restriction (≲1.5L/24h po).
• Metolazone (as above) and iv furosemide
• Opiates and iv nitrates may relieve symptoms
• Weigh daily.
Do frequent u&e (beware K+↓).
•DVT prophylaxis: heparin + ted stockings
•Cardiac resynchronisation therapy: biventricular pacing improves outcomes in EF<35%
Describe dilated cardiomyopathy
Typical ECG features
Is a syndrome of global ventricular dysfunction and dilatation.
Aetiology often unconfirmed, more common in males.
Often LBBB and poor R wave progression on ECG.
Anticoagulation may be necessary: incidence of AF and ventricular thrombus is high
Causes of dilated cardiomyopathy
- Undiagnosed HTN
- Autoimmune disease
- Nutritional deficiency: thiamine
- Muscular dystrophies
- Drugs (doxorubicin)
- Infiltration (haemochromatosis, sarcoidosis)
Produces symptoms identical to constrictive pericarditis.
The ventricles are excessively rigid and impede diastolic filling.
AF may occur
- Connective tissue disease
- Metabolic and storage disease
- Malignancy or radiotherapy