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
