Heart failure Flashcards
Heart failure signs on X-ray
- Alveolar oedema (bat’s wings)
- kerley B lines (interstitial oedema)
- Cardiomegaly
- Dilated prominent upper lobe vessels
- Effusion (pleural)
briefly:
Left Heart failure
common causes
symptoms
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
- Fatigue
- Orthopnoea
- Paroxysmal nocturnal dyspnoea (pnd),
- Nocturnal cough (±pink frothy sputum)
- Wheeze (cardiac ‘asthma’)
- Nocturia,
- Muscle wasting
- Weight loss
- Cold peripheries
RV Heart Failure briefly
common cuases
symptoms
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
- Ascites
- Hepatomegaly
- Nausea
- Anorexia
- Pulsation in the neck, face
- epistaxis
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
- Tachypnoea,
- orthopnoea
- paroxysmal nocturnal dyspnoea i.e. PND
- bibasal crepitations - PLEURAL EFFUSION
- PULMONARY OEDEMA
- laterally displaced apex beat - CARDIOMEGALY
- gallop rhythm,
- murmurs,
- cyanosis
RIGHT HEART FAILURE SIGNS
- Peripheral pitting oedema,
- hepatomegaly,
- increased JVP,
- parasternal heave,
- ascites.
- gallop
Cellular mechnaisms of HF
- Myocyte hypertrophy
- Alterations in contractile properties of myocytes
- Progressive loss of myocytes through apoptosis, necrosis, atophagic death
- Beta-adrenergic desensitizaation
- 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.
Farmingham criteria
Major criteria
- Paroxysmal nocturnal dyspnea or orthopnea
- Neck vein distention
- Rales
- Cardomegaly
- Acute pulmonary edema
- S3 gallop
- Increased jugular venous pressure >16 cm H2O
- Circulation time >25 s
- Hepatojugulr reflux
Minor criteria
- Ankle edema
- Night cough
- Dyspnea on exertion
- Hepatomegaly
- 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
- Obesity
- 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
- Bronchiectasis
- Cystic fibrosis
- Pneumoconiosis
- Sarcoid
- 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:
-
Pulmonary vasoconstriction resulting from any condition causing alveolar hypoxia or acidosis
- Anatomic reduction of the pulmonary vascular bed (e.g., emphysema, interstitial lung disease, pulmonary emboli)
- ** Increased blood viscosity** (e.g., polycythemia vera, Waldenström’s macroglobulinemia)
- 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 ↑.
