heart failure Flashcards
defintion
inability of the heart to sustain adequate circulation of blood to the tissue
arterial blood pressure =
systemic vascular resistance x CO
stroke volume =
LVEDV- LVESV
LVEDV = left ventricular end diastolic volume
LVESV = left ventricular end systolic volume
normal stroke volume
70ml ( 110-40)
normal cardiac output
5 litre/min
the proportion of LVEDV that is ejected is the what
what is the formula
ejection fraction - normal 70%
Ejection fraction is a measure of how effectively the heart is pumping.
EF (ejection fraction) = (SV/EDV) x 100. Normally over 60% and can be over 90% in exercising trained athletes.
EF can be compromised by systolic heart failure.
heart failure is influenced by what
pump function and state of circulation
the heart has two circulations
right side pumps to the lungs - lower resistance and shorter pulmonary circulation and left side pumps blood through systemic tissues and organs so has
higher resistance and long systemic circulation
left side fails more often as works 5 times harder
COCO
valves
left ventricle will fill up to 120ml with hardly any pressure after this is will be restricted due to stretching of what
pericardium
The heart muscle is like an elastic band = the more you stretch the myocardium by filling the more it will recoil back and the more effectively it will eject blood.
the frank-starling relationship assumes that aferload is constant up until point
what 2 factors explain this
2 factors explain this:
Greater contact of actin/myosin interaction
Increased sensitivity of myofibrils to Ca2+ (from SR)
heart failure can result from systolic or diastolic dysfunction
Systolic - HFrEF (heart failure with reduced ejection fraction)
Impaired myocardial contraction
Heart cannot empty properly
flabby weak ventricle due to systolic contraction reducing therefore reducing SV
Diastolic - HFpEF (heart failure with preserved ejection fraction)
Impaired myocardial relaxation
Heart cannot fill properly
stiff fibrotic ventricle so diastolic compliance decreases to LVEDP rises to SV falls
heart failure like pump to garden - garden no longer supplied and the tank build up and overflows
effects of HR
inability to keep up with venous return therefore increasing the upstream pressure in the circulation
inadequate perfusion of vital organs especially the kidney making the problem worse - RAAS system - renin related in low blood volume to lead to vasoconstriction and sodium retention ( aldosterone)
in HF RAAS activated and make the situation worse as ADH increases too to retain water
in the kidney inadequate perfusion is sensed by what
junta-glomerular apparatus - interprets this as hypovolamic shock
angiotensin 2 causes what
vasoconstriction
aldosterone causes what
sodium and therefore water retention
What is the result of an increase in SVR(afterload) resulting from vasoconstriction?
The hydrostatic (physical) pressure in the circulation is a major determinant of fluid movement at the capillary level
in the blood vessels hydrostatic pressure gradient pushed fluid out what happens on the interstitial side
osmotic pressure gradient pulls fluid in
overall slightly more fluid leaves the capillary than is reabsorbed - returns via lymphatic system
how is pulmonary oedema caused
rise in hydrostatic pressure forcing fluid out
if (odemea and increased JVP) fluid congestion and hypo perfusion ( low BP and low renal function) what does the patient present like
cold and wet
if no hypo perfusion and no fluid congestion present as
warm and dry
if hypo perfusion and no fluid congestion
cold and dry
if no hypo perfusion with fluid congestion present present as
warm and wet
causes of heart failure
ischaemic heart disease valvular disease fluid overload arrhymais intra-cardiac shunts cardiomyopathy hypertension drugs
what infections is someone with HF prone to
Because heart failure causes volume overload, she will be more prone to chest and leg infections secondary to pulmonary and peripheral oedema, respectively.
chest infectious and ulcerated celleuritic leg
first line treatment for heart failure
The first-line treatment for all patients is both an ACE-inhibitor and a beta-blocker
Second-line treatment is an aldosterone antagonist
Third-line treatment should be initiated by a specialist. Options include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy
ivabradine
criteria: sinus rhythm > 75/min and a left ventricular fraction < 35%
sacubitril-valsartan
criteria: left ventricular fraction < 35%
is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs
should be initiated following ACEi or ARB wash-out period
digoxin
digoxin has also not been proven to reduce mortality in patients with heart failure. It may however improve symptoms due to its inotropic properties
it is strongly indicated if there is coexistent atrial fibrillation
hydralazine in combination with nitrate
this may be particularly indicated in Afro-Caribbean patients
cardiac resynchronisation therapy
indications include a widened QRS (e.g. left bundle branch block) complex on ECG