Unit 12 Week 4 Flashcards
Pitting oedema
Excessive interstitial fluid in which when pressure is applied leaves an indentation
Common causes of pitting oedema
Heart valve issues
Low protein levels
DVT
Congestive heart failure
Venous insufficiency
Infections
How does HF lead to pitting oedema
In heart failure with low CO state, kidneys are sensitive to changes in BP so macula densa cells of the juxtaglomerular apparatus detect a fall in BP, releases renin, renin leads to angiotensinogen –> ANG1 –> ANG2 via ACE. increases BP
Sodium is reabsorbed via various transporters in the nephron
As pressure builds up in the central venous system, ECF is forced out into the legs, abdomen, ankles and feet
How does a raised JVP relate to HF?
Jugular venous pressure provides an indirect measure for central venous pressure.
Low output HF leads to a reductio in the volume of blood ejected with each beat, leading to a rise in central venous pressure. This blood backs up into the vena cava, raising the pressure in the jugular vein subsequently.
Has a biphasic wavefront pattern
How does HF cause hepatomegaly?
Increased central venous pressure in the IVC leads to blood backing up into the hepatic veins, causing the liver to become congested and grow larger.
This is sometimes tender upon examination.
In severe cases might cause jaundice or ascites.
What is a gallop rhythm?
A third heart sound that occurs in HF- 3rd heart soundsoccur in early ventricular filling and represent the tensing of the chordae tendinae and atrioventricular ring.
Results in increased atrial pressure –> ↑ flow rates and large amounts of blood striking the compliant lect ventricle –> therefore often associated with ventricular dilation
Produces a sound like a galloping horse.
Symptoms of HF
Dyspnoea + orthopnoea (worse when lying down)
Fatigue
Fluid retention- peripheral oedema –> ascites
Nocturnal cough or wheeze
Light headedness or syncope
Anorexia
Signs of HF
Displaced apex or RV heave
Narrow pulse pressure
Raised JVP
Gallop rhythm
Inspiratory crackles
Tachypnoea
Pleural effusions
Cyanosed
Definition of heart failure
– complex clinical syndrome where the heart is incapable of maintaining a cardiac output that is adequate to meet metabolic requirements and accommodate venous return
It is the common end stage of many forms of chronic heart disease, developing from the cumulative effects of chronic cardiac work overload (e.g. valve disease or hypertension), or ischemic heart disease (e.g. following myocardial infarction)
Which acute haemodynamic stressors can precede HF
Fluid overload
Abrupt valvular dysfunction
Myocardial infarction
Symptoms of left ventricular heart failure
Symptoms of right sided heart failure
peripheral and abdominal fluid accumulation
Systolic HF
Heart is not able to eject enough blood in systole
Diastolic HF
Chambers aren’t filling sufficiently so therfore reduced preload and↓ contractility (frank-starling mechanism)
Stroke volume is too low - ejection fraction is preserved
Frank-starling mechanism
ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return
“strength of the heart’s systolic contraction is directly proportional to its diastolic expansion, with the result that under normal physiological conditions the heart pumps out of the right atrium all the blood returned to it without letting any back up in the veins”
A higher preload sufficiently stretches the walls of the ventricles meaning that there is more overlapping actin and myosin filaments. Therefore, more cross bridges can form and there is greater contractility.
If the walls are stretched too far- less overlapping filaments and therefore less contractility.
Means that CO=VR
Left sided heart failure
Usually due to systolic dysfunction
CO from the left ventricle does not match VR from pulmonary vein
Therefore blood backs up in the pulmonary circulation.
Can cause RSHF via cor pulmonale
Cause of LSHF: ischaemic heart disease
Artherosclerosis leads to emboli in coronary artery (most commonly LAD). Occludes artery and no perfusion to downstream cardiac tissue. Ischaemia that leaves a scar on the myocardium.
MI causes myocardial stunning, myocyte necrosis, decompensation of existing HF, restructuring of heart walls (thinning?) and acute mitral regurgitation due to papillary muscle dysfunction
Causes of left sided heart failure
Ischaemic heart disease (MI to myocardium of left V)
Long-standing hypertension
Dilated cardiomyopathy
Diastolic filling dysfunction
Restrictive cardiomyopathies
Cause of RSHF: Chronic hypertension
As arterial pressure in the systemic circulation increases it increases afterload.
To compensate left v hypertrophies so it can contract with more force.
This increase in muscle mass also means that there is a greater demand for oxygen.
Extra muscle also squeezes down on the coronary arteries, meaning that even less blood is delivered to the myocardium.
Ultimate result is that the myocardium has weaker contractions.
Dilated cardiomyopathy as a cause of LSHF
In hypertension, myocardium undergoes concentric hypertrophy
concentric hypertrophy
new sarcomeres are generated in parallel with the old ones
As the ventricular wall enlarges, it therefore crowds into the ventricular chamber space, leaving less room for filling.
can also be caused by aortic stenosis (narrowing of the aortic lumen) and by hypertrophic cardiomyopathy (abnormal ventricular wall thickening often from a genetic cause).
Cause of LSHF: restrictive cardiomyopathies
Myocardium becomes stioffer and less compliant and therefore, can’t easily stretch and fill.
Role of RAAS in symptoms
With a lower CO, detected renal baroreceptors and activates the RAAS
Causes a gretaer BV –> more pressure in vessels –> water forced out into peripheral tissues
Ultimately causes increased fluid retention via sodium retention
Compensatory sytem as increased BV –> increased filling and preload –> increased contractility
Signs of LSHF
Inability to pump blood means it backs up into the pulmonary circulation via the pulmonary vein. Increased P over cap beds and pul artery.
Water forced out of caps into pulmonary interstitium and alveoli making gas exchange slower –> blood not as high oxygen content –> detected in brain –> tachypnoea
Fluid is heard as crackles and pops
Enough fluid can rupture these caps and bleed into alveoli
Treatment for left sided heart failure
Medications to increase blood flow
e.g. ACE inhibitors to heklp dilate blood vessels
Diuretics reduce fluid build up
Prevent hypertension from making hF worse
Right sided heart failure
Often caused by left sided HF (biventricular HF)
Increased pulmonary BP makes it harder for the RSH to pump.
Causes of right sided heart failure
left sided heart failure
Left to right cardiac shunt (isolated RSHF)
Chronic lung disease (isolated RSHF)
Cause of isolated RSHF: left to right cardiac shunt
May be an atrial or ventricular defect allowing blood to flow from the higher pressure left side to the lower pressure right side
This ↑ volume on the right side of the heart, leads to concentric hypertrophy
Makes it more prone to ischaemia, a systolic dysfunction
and also a smaller volume, a diastolic function
Cause of RSHF: chronic lung disease
Makes it hard to exchange oxygen. In response to hypoxia, the pulmonary arterioles constrict, increasing pulmonary BP and causing hypertrophy and heart failure—– this is COR PULMONALE
Right sided congestion
Jugular venous distension
Hepatosplenomegaly- painful
Liver congestion can cause cirrhosis
Exces fluid near organ surface–> peritoneal space–> ascites
Leg –> oedema
Sacrum –> oedema
3 determinants of stroke volume
myocardial contraction
preload
afterload
Frank-starling mechanism and laplace law influence these factors
laplace law
pressure insde an inflated elastic container with a curved face (e.g., blood vessel or chamber) is inversely proportional to the radius
Wall stress
(cavity pressure x radius) / (2 x wall thickness)
increase to ventricular wall stress and therefore increased oxygen demand:
increased LV pressure
increased LV radius
increased LV wall thickness
myocardial infarction
Causes of HF general
Corronary heart disease
hypertension
valvular heart disease
obesity
high output states (e.g., thyrotoxicosis)
Volume overload (end stage chornic kidney disease)
obesity
drugs (e.g., cocoaine, alcohol)
Stages of heart failure
by fucntional limitation
class 1- No limitation. Normal physical exercise does not cause fatigue, dyspnea or palpitations.
class 2- Mild limitation. Comfortable at rest but normal physical activity produces fatigue, dyspnoea or palpitations.
class 3- marked limitation. comfortable at rest but gentle physical acitivity produces marked symptoms of heart failure
class 4- Symptoms of HF occur at rest and are exacerbated by any physical activity.
Types of heart failure
biventricular
congestive
left sided
HF w reduced ejection fraction
HR w preserved ejection fraction
HPmrEF - mid range
Right sided
cor-pulmonale
low output
high output
valvular
arrhythmic
acute
Arrhytmic HF
Prolonged period od your heart pumping ineffectively die to bradycardia or tachycardia (like atrial fibrillation) can lead to heart failure.
valvular heart failure
one or more of valves in your heart doesn’t work properly (don’t open or close properly). This can cause the blood flow through your heart to your body to be disrupted.
High output HF
normally functioning heart can’t keep up with an unusually high demand for blood to one or more organs in the body. The heart may be working well otherwise, but it cannot pump out enough blood to keep up with this extra need. o High output
Low output HF
decreased CO accompanied by end organ hypoperfusion.
o Heart failure with reduced ejection fraction (HFrEF)
also called systolic failure when LV loses ability to contract normally. Heart cant pump with enough force to push enough blood into circulation.
Heart failure with preserved ejection fraction
also called diastolic failure = LV loses its ability to relax normally (because muscle become stiff). Heart cant properly fill with blood during resting period between each beat.
Link between atrial fibrillation + tachycardia to heart failure
Risk factor for HR, stroke and sudden MI
Improper filling of atria means that ventricles don’t fill properly and therefore CO drops transiently.
Cardiac remodelling
1) pathopysiological stimuli (e.g. cardiac injury, neurohormonal stim.)
2) Remodelling pathways
a) CMs loss- autophagy, necrosis, apoptosis
b) CMs hypertrophy- Ca2+ influx stimulates hypertrophic response
c) myocardial fibrosis- MIs cause release of DAMPS that bond to PRR’s that cause fibrosis
3) Cardiac remodelling- changes in geometry of the ventricles from eliptical to spherical
Neurohormonal response to heart failure
SNS
RAAS
ADH
Endothelin system
natriuretic peptides
Role of SNS in heart failure
Activated in HF via low and high-pressure baroreceptors
Provides inotropic support and maintains cardiac ouput
chronic activation is harmful
activates RAAS–> increased venous and arterial tone, reabsorption of salt and increasing noradrenaline concs
gradual desensitisation to catecholamines
Role of RAAS in heart failure
Ang II is a vasoconstrictor and stimulates the release of noradrenaline from sympathetic nerve terminals and inhibits vagal tone (therefore increasing HR)
leads to sodium and therefore water retention and increased potassium excretion
Aldosterone, ang II and SNSN are potent stimulants for myocardial hypertrophy and fibrosis as well as vascular remodelling
ADH levels are increased in severe chronic HF
HF = paradoxical increase in ADH
contributes to the enhanced renal retention of fluid
Endothelin system
endothelin is secreted by vascular endothelial cells and is a potent vasoconstrictor peptide, especially on renal vasculature so promotes retention of sodium
Natriuretic peptides
3 of them and they lead to the excretion of sodium in urine:
Atrial NP- released from atria, responds to stretch –> natriuresis and vasodilation
Brain NP- released from the ventricles
C-tyoe NP- limited to vascular endothelium and CNS- limited effects on. natriuresis
ANP ans BNP both increase in response to volume expansion and pressure overload of the heart and act as antagonists to the effects of ANG II on vascular tone, aldosterone secretion and renal-tubule reabsorption
As HF progresses, NPs fail to compensate
Digestive link to HF
Splanchnic circulation receives nearly 25% of CO
High SNS concentration
Even small reductions in splanchnic perfusion leads to intestinal iscahemia
BNP
nowadays measure the NT-proBNP
increases GFR- filtered laod of sodium and water via dilatinf afferent and constricting efferent
Decreases sodium reabsorption
inhibits renin secretion
promotes urination
inhibits effects of catecholamines
Basal crepitations
Crepitous sounds caused by excess fluid in the airaways having a bubbling/ crackling sound
can either be exudate or infection
Cardiothoracic ratio
Allows you to confirm cardiomegaly (enlargement of the heart) on CXR.
CT ratio: A=B/C
Possible causes of a ratio greater than 50% include:
cardiac failure
pericardial effusion
left or right ventricular hypertrophy
A doctor might use echocardiograms in HF to find out:
The size of your heart. An enlarged heart might be the result of high blood pressure, leaky heart valves, or heart failure. Echo also can detect increased thickness of the ventricles. Increased thickness may be due to high blood pressure, heart valve disease, or congenital heart defects.
- Heart muscles that are weak and aren’t pumping well. Damage from a heart attack may cause weak areas of heart muscle. Weakening also might mean that the area isn’t getting enough blood supply, a sign of coronary heart disease.
- Heart valve problems, can show whether any of your heart valves aren’t operating normally (regurgitation ect)
- Problems with your heart’s structure. Echo can detect congenital heart defects, such as holes in the heart.
- Blood clots or tumors.
Heart failure clinics
Aims to reduce symptom trouble
each patient has their own plan
often works with heart failure specialist nurses
patient education
pathway to get involved in research
