Heart Failure

Description

Mind Map on Heart Failure, created by kavi on 01/29/2014.
kavi
Mind Map by kavi, updated more than 1 year ago
kavi
Created by kavi about 11 years ago
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Resource summary

Heart Failure
  1. Intro
    1. Common
      1. 1-3% general population & 10% of elderly people
      2. Prognosis
        1. Poor; 25-40% 5Y mortality
          1. Higher BNP = higher CV and all-cause mortality. A/w sudden death.
            1. Persistent increased BNP despite vigorous Rx predicts adverse outcomes
        2. Definition
          1. Clinical syndrome that is characterised by inability of heart to maintain a CO that is sufficient for the body's needs
        3. Classification and corresponding causes
          1. Low output most common = low CO that fails to increase w/ exertion
            1. Pump failure
              1. Systolic dysfunction - <40% EF
                1. MI, IHD, CM
                2. Diastolic dysfunction - EF >50%
                  1. Constrictive pericarditis, restrictive CM, tamponade, HTN
                  2. Decreased HR
                    1. BB, MI, heart block
                    2. -vely inotropic drugs eg antiarrhythmics
                    3. Excessive preload
                      1. AR, MS, MR or fluid overload
                        1. More likely if renal impairment, or big volumes involved, or simultaneous cardiac insult, or elderly
                      2. Excessive afterload
                        1. AS, HTN
                        2. NYHA classification of sx severity
                        3. high output = CO high/normal but incr needs
                          1. Anaemia, pregnancy, paget's, hyperthyroidism, AVMs, beri beri
                        4. Investigations and diagnosis
                          1. If normal ECG and BNP then diagnosis unlikely
                            1. If either AN then echo required
                              1. Can indicate a cause ± presence of LV dysfunction
                              2. >100 then +ve, if <50 then -ve
                                1. Highest in those w/ syst + diastolic dysfunction.
                              3. Sx of HF and objective evidence of dysfunction at rest.
                                1. Framingham criteria for CCF
                                  1. 2 majors or 1 major and 2 minors
                                    1. Major
                                      1. PND, creps, S3 gallop, cardiomegaly, increased CVP (>16cmH20 in RA), >4.5kg w loss in 5/7 of treatment, Neck vein distension, acute pulmonary oedema, hepatojugular reflux
                                      2. Minor
                                        1. Bilateral ankle oedema, dyspnoea on ordinary exertion, tachycardia (>120), dec vital capacity by 1/3, nocturnal cough, hepatomegaly, pleural effusion.
                                    2. Other signs of HF
                                      1. Exhaustion, cool peripheries, cyanosis, low BP, narrow pulse pressure, pulsus alternans, displaced apex (LV dilatation), RV heave (pulmonary htn), murmurs of aortic or mitral valve disease, wheeze
                                    3. Routine Ix
                                      1. Bloods - FBC, U&E's, BNP
                                        1. CXR - classical features
                                          1. ECG - may indicate a cause eg LVH, MI, ischaemia. Rarely normal ECG in chronic HF.
                                        2. Management
                                          1. Acute - emergency mx
                                            1. ABC mx
                                              1. Airway - 100% oxygen unless COPD
                                                1. Breathing - ABG, CXR
                                                  1. Circulation - IV access, ECG, Temp, UO. Start IV diamorphine 2.5-5mg slowly (caution if liver disease or COPD).
                                                    1. Furosemide 40-80mg IV slowly, more if renal failure too.
                                                      1. If SBP >90mmHg then GTN SL, if SBP ≥100 and still breathless start ISDN infusion, keeping SBP > 90.
                                            2. Chronic mx
                                              1. Conservative
                                                1. Stop smoking, reduce salt, weight loss, nutrition etc
                                                  1. MDT
                                                    1. HF nurses, chest physio, OT
                                                  2. Medical
                                                    1. Treat any underlying causes, treat exacerbating factors eg thyroid disease, anaemia, infection, HTN
                                                      1. Drugs that improve prognosis
                                                        1. Diuretics
                                                          1. Loops reduce sx eg furos 40mg/day or bumet 1-2mg/day. SE = low K, renal impairment (requires large doses). ? thiazide if refractory oedema eg metolazone 5-20mg/day
                                                            1. Add K sparing if K<3.2, predisposed to arrhythmia, concurrent digoxin therapy (hypoK increases risk of dix toxicity), K losing condition.
                                                          2. ACEI
                                                            1. Dec mortality in proportion to LV dysfunction, dec risk of hospitalisation, provide sx relief in 1/52 approx.
                                                              1. AKI, K imbalances, cough, 1st dose hypotension, angiooedema (non-allergic)
                                                            2. B blockers
                                                              1. Start after ACEI and diuretic, start low and slow.
                                                                1. Cold peripheries, sleep disturbance, fatigue, impotence and loss of libido, loss of warning signs of hypoglycaemia can be lost
                                                              2. Sprinolactone (both)
                                                                1. In patients that are still sx despite other max therapy, prevents remodelling, and improves endothelial function. Little risk of hyperK even if taking ACEI.
                                                                2. Vasodilators (equal)
                                                                  1. Hydralazine (DI lupus) + ISDN if intolerant to ACEI and ARBs. Reduces mortality in black people with HF, in combo w/ standard therapy.
                                                                3. Drugs for sx relief only
                                                                  1. Digoxin
                                                                    1. Helps even in SR. ? if LV systolic dysfunction + signs and sx of HF despite standard therapy inc ACEI and BB. Or ? in AF.
                                                                      1. Maintain K 4-5. HypoK increases risk of toxicity.
                                                                        1. Sx of toxicity
                                                                          1. Dec cognition, yellow/green halos, arrhythmias, N, anorexia.
                                                                          2. If serious arrhythmia, correct hypokalaemia, and give Digibind - dig specific ab fragments taken from immunised sheep.
                                                                      2. Diuretics
                                                                    2. Surgical
                                                                      1. ICD
                                                                        1. Transplant
                                                                    3. Mechanism of disease
                                                                      1. Compensatory mechanisms that try to maintain perfusion and CO when the heart begins to fail.
                                                                        1. These become pathological as the failure progresses
                                                                          1. SNS activation
                                                                            1. Increased preload through venoconstriction. But increased after load due to arteriolar constriction.
                                                                            2. RAAS activation
                                                                              1. Increased fluid retention, with increased after load due to AII.
                                                                              2. Natriuretic peptides
                                                                                1. Released by atria, ventricles, and vasc endothelium
                                                                                  1. Water, salt loss, relaxes smooth muscle (dec preload). ?Compensatory mechanism but inadequate.
                                                                                    1. Sensitivity >90%, specificity 80-90%
                                                                                      1. Not raised in acute HF exacerbation. Low if no LV dysfunction or HF.
                                                                                    2. Secretion inc by glucocorticoids, tachycardia, thyroid hormones. Endothelin1 and AII influence secretion.
                                                                                  2. LV dilatation
                                                                                    1. Decreased ejection of blood - stretched ventricle. Over time starling response flattened and increased venous pressure.
                                                                                    2. Hypertrophy, loss of myocytes and increased fibrosis leading to irreversible pump failure.
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