Please enable JavaScript.
Coggle requires JavaScript to display documents.
Heart Failure- inability of CO --> physiologic demands Atrial…
Heart Failure- inability of CO --> physiologic demands
Atrial Fibrillation- chaotic, irregular atrial rhythm at 300-600bpm
uncoordinated atrial activity on surface ECG - temporal, paroxysmal, persistent, permanent
Epi
age - 2in 1000 UK - 23 mill worldwide
Signs/Symptoms
Left
SOB (orthopnea) - when supine (increased venous return from redistribution of blood - gravity effect - exacerabates pulmonary vascular congestion)
paroxysmal nocturnal dyspnea - breathless awakening from sleep - increased venous return from redistibution of blood, reabsorption of peripheral edema
cough
confusion
decreased urine output
nocturia
pulmonary edema- incresed pulmonary venous pressure --> pulmonary venous distention and transudation of fluid- presence of hemosiderin-laden macrophages (HF cells in lungs)
Signs:
pul. crackles
accenuated P2
mitral regurgitaiton murmur
pulse alterations
Right
peripheral edema/sacral/ascites
hepatosplenomegaly - increased central venous pressure --> increased resistance to portal flow
anorexia
Signs:
increased JVP/Kausmal signs (increased JVP with insipration)
tricuspid regurgitation
palpable right ventricle
Aetiology/Pathophysiology
Causes
:
IHD, cardiomyopahty, hypertension, valvular HD- mitral/aortic/tricuspid
congenital HD
alcohol/drugs
hyperdynamic circulation
tricuspid incompetence
arrhythmias
pericardial disease
Systolic - inadequate myocardial contractile function - consequence of IHD/hypertension
Diastolic dysfunction - inability of heart to adequately relax and fill - massive left ventricular hypertrophy, myocardial fibrosis, amyloid deposition, contrictive pericarditis
Pathophysiology
- compensate for reduced myocardial contractility:
Frank-Starling
increased EDV filling --> stretch cardiac myofiber --> increasing CO --> compensation
ventricular dilation - expense of increased wall tension --> amplifies o2 requirements --> decompensation
Activation of neurohumoral systems:
NE by ANS --> increase HR + contractility + vascular resistance
activation of RAAS --> water and salt retention --> increases vascular tone
release of ANP - acts to balance RAAS through diuresis ans vascular SM relaxation
Myocardial structural changes:
cardiac myocytes cannot proliferate --> adapt to increased work by increasing no. of sarcomeres (hypertrophy)
pressure overload states - hypertension or valvular stenosis - new sarcomeres added parallel to myocytes (concentric hypertrophy)
volume overload states - valvular regurgitation or shunts - new sarcomeres added in series with existing --> muscle fiber lenght increases - ventricle dilate - wall thickness - increased, normal or decreased
Diagnosis
serum BNP (100-400) or N-terminal pro-BNP (<300)
if BNP >400 - refer immediately
transthoracic doppler echo
ECG/CXR/blood - electrolytes/U&E/eGFR
TFT/LFT/fasting lipid/FBC
Management
Acute
diuretics
morphine
Nitrate (people with concomitant MI, severe HTN, regurgitant aortic or mitral valve disease)
oxygen
Chronic
lifestyle - exercise, smoking, alcohol, sexual activity, vaccination (influenza, pneumococcal disease), air travel, driving
ACEi + beta blockers
aldosterone antagonist
ARB
hydralazine + nitrate (African/Caribbean descent)
Digoxin - worsening or severe HF
All types:
diurectics (congestive symptoms and fluid retention)
CCB - amlodipine - comorbid HTN (avoid verapamil/dilitiazem or short acting dihydropyridine)
amiodarone
Anticoagulants - thromboembolism, LV aneurysm, intracardiac thrombus
Aspirin - HF + artherosclerosis (CAD)
inotropic agents - dobutamin, milrione, enoximone - short term treatment of acute decompensation of CHF
Epi/Risk factors
0.5-1% , increasing age,
HTN, CAD, CHF, age, DM
rheumatic valvular --> mitral stenosis
alcohol --> cardiomyopathy
arrhythmias --> reentrance
smoking
thyroid
Aetiology
HF, HTN, valve disease - mitral stenosis, regurg, hyperthyroidism, alcohol induced, familial, electrolytes
Pathogenesis- pul veins --> dysfunction of cardiac electrical signalling, atria no longer in contract in coordinated manner, atria fall to empty adequately (no longer coordinated contraction)
Signs/Symptoms
incidental/none, chest pain, palpitations, dyspnea, faintness, stroke/TIA, syncope/dizzyness
Signs- irregularly irregular pulse, apical pulse rate > radial, 1st HS- variable
Diagnosis
ECG- P waves - absent, irregular QRS complex (RR intervals), narrow QRS
Blood - U/E - cardiac enzymes, thyroid function, echo --> atrial enlargement/ mitral valve disease
Management
Thromboprophylaxis
Assessment of stroke: CHA2DS2VASc - age, sex, CHF, HTN, stroke hx, vascular disease hx, DM hx
Assessment for major bleeding risk - HAS BLED - HTN, Renal disease , Liver disease, stroke, prior major bleeding or predisposition to bleeding, age >65, medication (antiPLT/NSAIDs), alcohol or drug use > 8 drinks
Anticoagulation (men with score >1, people >1)
apixaban, dabigatran etexilate, rivaroxaban or Vit K antagonist
Apixaban (AF + 1 risk factor - stroke/TIA, >75, HTN, DM, HF)
Dabigatran etexilase - non valvular AF + 1 RF (previous stroke, TIA/embolism, LVEF <40%, class II HF, >75, >65 + DM, CAD, HTN)
Rivaroxaban - AF + 1 RF (CHF, HTN, >75, DM)
Vit K antagonists - calcular TTR
Rate and Rhythm Control
Rate (give as 1st line except when reversible, HF caused by AF, new onset AF, atrial flutter)
Beta blocker (except sotalol) or Rate limiting CCB
Digoxin - monotherapy with non paroxysmal AF + sedentary
Combination therapy (2 of)
beta blocker
diltiazem
digoxin
Rhythm - pharm/electrical- AF whose symptoms continue after HR controlled or rate control not successful
Cardioversion
AF > 48h
amiodarone - starting 4 weeks before and continuing upto 12 months after electrical cardioversion to maintain sinus rhythm
Transosophageal echocardiography (TOE) and conventional cardioversion
-
Long term
beta blockers
Drondedarone (sinus rhythm after cardioversion in paroxysmal or persistent AF)