19. Heart Failure Flashcards
Heart failure is a syndrome. What is it defined by?
Distinguish between acute and chronic heart failure.
Inability of the heart to generate sufficient cardiac output to meet the body’s demands without an increased filling pressure. This inability is 2o to an underlying cause. Incidence increases rapidly with age. Poor prognosis (25-50% die within 5 yrs of dx).
Chronic: most common feature = breathlessness with impaired exercise tolerence. Slowly progressive, periods of acute decompensation. State of fluid retention and overload. Venous congestion common, arterial presssure well maintained until late.
Acute: can be dramatic with flash pulmonary oedema (requring a participant e.g. ischaemia, arrhythmia, intercurrent infection), or gradual deterioration (fluid accumulation, falling exercise tolerance + fatigue, orthopnoea + paroxysmal nocturnal dyspnoea).
Distinguish between systolic and diastolic heart failure (incl. causes for both).
Systolic HF or HF with reduced ejection fraction or HF with mildly reduced EF. Inability of ventricle to contract normally = decreased CO. EF: <35% severe. 36-45% moderate. 46-55% mild. Causes: IHD, MI, cardiomyopathy.
Diastolic HF or HF with preserved EF. Inability of ventricle to relax and fill normally. Stiffness of vent. wall + increased filling pressure and reduced CO. EF: >50%. Echo = L vent hypertrophy, L atrial dilation, abnormal relaxation. Causes: constrictive pericarditis, tamponade, restrictive cardiomyopathy, HT.
NB systolic and diastolid HF usually coexist.
NB: S3 = after S2 (A + P valves closing), middle of diastole - blood rushing in so reverberates around ventricles. Hear more in diastolic HF b/c pressure higher and ventricle stiff.
S4: just before S1, because atria contracting into a cavity that’s already full.
Distinguish between right and left heart failure. List some symptoms.
Distinguish between low output and high output failure. List some causes.
RHF: fluid overload. 2o to L heart disease, pulmonary HT (cor pulmonale), cogenital heart disease and cardiomyopathy. R heart is a conduit to supply blood to lungs and can’t cope with elevated pressures. Symptoms: peripheral oedema, ascites, nausea, anorexia, facial engorgement.
LHF: common clinical syndrome of HFrEF. Symptoms: dyspnoea, poor exercise tolerence, fatigue, wheeze, muscle wasting.
Low output: common clinical syndrome, “low output state”. Causes: pump failure, excessive preload, chronic excessive afterload.
High output: heart is overworked, can be physiological. Pathophysiological due to metabolic derangement. Rare. Causes: anaemia, pregnancy, hyperthyroidism, Pagets.
What causese initial heart failure?
What causes further heart failure after this?
Describe how the RAAS contributes.
Poor ventricular function/myocardial damage (e.g. post MI), dilated cardiomyopathy.
(pic) NB: normally RAAS -> Na+ and H2O retention good b/c gives more blood to restore CO. Activation of sympathetic system activates RAAS and causes constriction of capacitance vessels to get blood back to heart. BUT these things are not good if HF!
Liver, vessels and brain -> angiotensinogen produced -> angiotensin I -> angiotensin II (which causes vasoconstriction and enhanced sympathetic activity) -> aldosterone release -> salt and water retention.
What specific heart modifications does myocardial damage cause via activation of sympathetic nervous system?
What is the formula for C.O?
What is Starling’s law of the heart?
(pic)
C.O = HR x stroke volume
Increase HR via autonomic NS, increase SV - more complicated and depends on ventricular performance.
Stroke volume increases with increased end diastolic volume. “Contractile function depends on velocity of muscle contraction, the load being moved, and the amount of stretch”. Pre-stretch improves relationship.
What are the main 3 causes of heart failure?
List some signs and symptoms of heart failure.
What is the NYHA classification for HF?
1) IHD (35-40%). 2)Dilated cardiomyopathy (30-35%). 3)Hypertensive heart disease (15-20%).
* Also valvular HD, arrhythmias (AF, bradycardia), COPD, infection (viral myocarditis), drugs (EtOH and chemo), infiltrative (amyloid, sarcoid), 1o heart muscle disease, metabolic (anaemia etc.)*
Symptoms: breathlessness (exertion/at rest/ orthopnoea/ paroxysmal noctural dyspnoea), tiredness and falling exercise tolerence, peripheral oedema, palpitations, depression, gout (uric acid = marker of prognosis, worse if high)
Signs: Raised JVP, 3rd heart sound, pulmonary crepitations, hepatomegaly, periphral/sacral oedema, cachexia (wasting syndrome).
Class I: no symptoms. Class II: symptoms on exertion. Class III: symptoms on minimal exertion. Class IV: symptoms at rest. (Symptoms = fatigue/palpitations/dyspnoea).
What investigations are done for heart failure and why?
What does this ECG show?
a) Normal
b) STEMI
c) LBBB
d) RBBB
FBC and iron studies (anaemia), U+Es, glucose (kidneys, diabetes), cholesterol, LFTs (liver), TFTs (thyroid), BNP (marker of atrial stretch, increases with HF), uric acid (prognostic), ferritin (haemochromatosis), CK, immunoglobulins, (myeloma) autoimmune profile, viral titres. Genetics. ECG.
c) LBBB b/c RSR is lateral. Can see RSR complex in V6. Broad QRS complex in V3 = BBB. W in V1 - WiLLiaM.
What does this ECG show?
L axis deviation + RBBB = L anterior vesicular block.
Partial RBBB because QRS < 3 small squares but not broad enough to be RBBB. I and aVL +ve so L axis deviation.
What do these CXRs show?
L: Huge hilum! Cardiomegaly. Beginnings of pulmonary oedema. Increased shadowing; hazy appearance to lung fields. More BVs at top of lung fields than bottom: upper lobe diverson of BVs - blood diverted up to top where getting more O2.
R: Lots of shadowing, more upper lobe diversion of vessels.
What do these transthoracic echocardiograms show?
What other investigations could you do (apart from CXR, EXG and echo)?
L: normal heart
R: septum thicker, mitral valve doesn’t move much (when looking at the moving img)
Holter monitoring, lung function tests (for COPD/SoB cause), cardiopulmonary exercise testing, cardiac catheterisation, perfusion iimaging, cardiac MRI (pic - Top L = 4 chambers, top R = 2, bottom = 3)
How is acute pulmonary oedema due to HF managed?
(pic = lots of pulmonary oedema)
Medical emg! High flow O2, morphine and anti-emetic, IV GTN (decreases stress on heart + vasodilation), furosemide if fluid overload. ECG monitoring. May need ventilatory support. Understand the cause.
How is chronic heart failure managed by a multidisciplinary team?
What types of therapy are carried out in heart failure management?
Nurses: hospital, community. Psychologists. Rehab: physiotherapists, occupational therapists. Social workers. Doctors: GP, heart failure specialist, interventional cardiology, electrophysiology, renal physicians.
Remove exacerbating factors, drug therapy (start with low doses and slowly up titrate. Best prognotic drug = β-blocker (pic)), device therapy, surgical therapy, exercise training through cardiac rehabilitation, palliaton.
What does this ECG show?
a) Sinus rhythm
b) Atrial fibrillation
c) VT
d) VF
If a pt has heart failure and is at risk of a life-threatening abnormal rhythm, what can be given?
c) VT
ICD (implantable cardiac defibrillator). Implicated if QRS 120-149ms. CRT if no LBBB (pic).
ICD - can have 1 or 2 wires (leads) depending on what the heart needs. One lead goes in R ventricle, and if 2nd lead needed, it will be placed in R atrium.
CRT-D system adds a 3rd, attaching a lead to the L ventricle so it can help both sides beat in synch and thus pump more efficiently. If a pt has experienced heart failure, they’ll most likely get a CRT-D.
What management option do these CXRs show?
Cardiac resynchronisation therapy. Can see pacemaker on L and ICD coils on R.
What are some surgical options for managment of heart failure?
What is are LVADs?
What is ECMO (extracorporeal membrane oxygenation)? (pic)
Valve surgery. Revascularisation. Stem cells. Heart transplants (200/yr).
L. ventricular assist devices - mechanical pump implanted inside a person’s chest to help a weakened heart pump. Unlike a total artificial heart, the LVAD doesn’t replace the heart (pic).
Extracorporeal technique (outside body) of providing prolonged cardiac and respiratory support to pts whose heart and lungs can’t provide adequate gas exchange or perfusion. The technology is largely derived from cardiopulmonary bypass, which provides shorter-term support.
