Heart Failure Flashcards
What is frank starlings law
The increased venous return would increase the contractility
How would frank starlings law change if there was heart failure
Would have the reduced cardiac stretch so would not have the increased contractility
so would have the higher EDV
What is acute heart failure
Rapid onset
What are the main causes of the acute heart failure
Pulmonary embolism
Drugs
Arrhythmias
Acute valvopathy
What is chronic heart failure
Progressive cardiac dysfunction
This can happen over a long time period
Normally would be die to the systolic or the diastolic issues
What is an ejection fraction
Fraction of blood that would be pumped out the heart compared to the volume of blood that would originally enter the heart
EF = SV/EDV
What is systolic heart failure
HFrEF (heart failure reduced ejection fraction)
Systolic dysfunction
Reduced contractility
MI
Dilated cardiomyopathy
So reduced ejection fraction
What is a dilated cardiomyopathy
Walls of the heart would be dilated
Could be due to viral infection
Heart cant generate enough pressure
Less blood pumped outwards
What is diastolic heart failure
HFpEF (heart failure preserved ejection fraction)
Diastolic dysfunction
Increased stiffness of the ventricle walls
Reduced preload (decreased filling)
Increased afterload (needs to work harder)
MI
Cardiac tamponade
Why would the EF be preserved with diastolic
The stroke volume would fall (less blood out) the end diastolic volume falls (less blood in to go out)
Ratio preserved
What happens in right sided heart failure
Reduced contractility (MI)
Increased afterload
Increased preload (pulmonary/tricuspid valve regurgitation)
Can develop FROM the leftsided heart failure
What factors would increase the afterload in right sided heart failure
Pulmonary stenosis
Pulmonary hypertension (From a PE)
Hypoxic vasoconstriction in pulmonary vessels (cor pulmonale)
What is hypoxic vasoconstriction
Perfusion and ventilation decreases
Preserve oxygen vessels vasoconstrict
Lead to pulmonary hypertension
What is low output heat failure
Heart cannot meet the cardiac demand of the body
Increased systematic vascular resistance to combat
Weak pulse and low BP
What is high output heart failure
CO > 8L/min
Heart cannot meet the demand of the cardiac function
Also
Increased demand due to the shunting of blood to the venous side (AV fistula, thymine deficiency)
What is AV fistula
Abnormal connection between the artery’s and the veins
Not enough time for the oxygen exchange
Can lead to heart failure
What happens in a thymine deficiency (chronic alcoholism)
Pyruvate ———— acetyl COA
Needs thymine
No thymine means no acetyl Co A
Build of lactate
Vasoconstriction
Blood goes from the artery’s to veins
Lack of oxygen transfer
What happens in left sided heart failure
Blood would normally accumulate in the left atrium
What are the symptoms of left sided heart failure
Dry cough
Dyspnea (shortness of breath)
Orthopnoea (difficulty lying flat fluid accumulation in the lungs and tissues)
Paroxysmal nocturnal Dyspnea (breathlessness that gets worse at night)
What are the signs of left sided heart failure
Bi basal crackles (both lungs on the base)
Tachycardia
Cardiomegaly
3rd and 4th heart sounds (additional due to the stiff and loose heart)
What are the symptoms of right sided heart failure
Dyspnea
Chest discomfort
Swelling
What are the signs of right sided heart failure
Jugular venous distension
Hepatic congestion
Peripheral odema
Ascites
(MAINLY FLUID BUILD UP)
What is congestive heat failure
The combination of the right and the left sided heart failures
What is the N-terminal pro-B-type Natriuretic peptide level and what does it show
Cardiac neurohormone
Made by the ventricle cardiomyocytes when have increased stress in the ventricles walls
Released with BNP (active) when increased pressure
Degradaes slower then BNP so better
What does a low level of NT-pro-BNP show
A strong negative predictive value
Levels <4000ng/L
What does eGFR do
Marks kidney function
Low renal perfusion would show a low cardiac output
What blood tests can be done to show heart failure
FBC and iron (shows anemias)
LFT (hepatic congestion, RSHF)
TFT (shows increased metabolic demand)
HbA1c and lipids (diabetes and hyperlipidemia shown)
What is the main investigative measure for the heart failure
Echocardiogram (transthoratic echocardiogram)
What are the three groups of heart failure
HFrEF = LVEF <40%
HFmrEF =LVEF 40-49%
HFpEF = LVEF >/~ 50%
How can you classify heart failure
Class 1
Class 2
Class 3
Class 4
What is class 1 heart failure
No symptomatic limitations to physical activity
What is class 2 heart failure
Slight limitations to physical activity. No symptoms at rest
What is class 3 heart failure (moderate)
Marked limitations to physical activity, no symptoms at rest
What is class 4 heart failure (severe)
Inability to carry out physical activity without symptoms. May have symptoms at rest
What do the ACE Inhibitors do
No conversion of Ang 1 to Ang 2
Reduced preload and afterload
Produced bradykinin
RAMIPRIL, LISIONPRIL, ENALAPRIL, CAPTOPRIL
What do the beta blockers do
Reduces heart rate
Longer time for the ventricles filling
Also increased force of heart contraction
PROPRANOLOL AND ATENOLOL
What do the mineralocorticoid receptor antagonists do
Reduce sodium reabsorption
reduces blood pressure and circulating volume
SPIRONOLACTONE AND EPLERENONE
What do the loop diuretics do
No effect on heart failure but can help with symptoms
Secretion of water from the kidney, reduces circulating volume and peripheral odema
FUROSEMIDE, BUMETANIDE
What are the second line treatments for heart failure
Digoxin (no channels working)
Hydralazine (would be able to increase the blood pressure of the system)
Ivabradine (channel blocker that would slow down the heart)
Sacubitril/valsartan
What are the device therapy’s
Implantable cardiac defibrillator
Cardiac resynchronisation therapy
What can be seen on an echocardiogram if the patient has heart failure
The heart would occupy more or equal to 50%of the window of view
(This could be because of the cardiomegaly in the LSHF)
What would happen to the after load and the preload in right sided heart failure
Increased afterload - pulmonary hypertension, pulmonary stenosis, hypoxic vasoconstriction
Increased preload - tricuspid/pulmonary valve regurgitation
What would happen to the preload and afterload in the HFpEF (diastolic)
Increased after load - cardiac tamponade, restrictive pericarditis
Decreased preload - aortic stenosis, coartication of the aorta
So would have the decrease in the stroke volume and the EDV (as less in)
Why would there be pulmonary edema in left sided heart failure
The increased venous pulmonary pressure as blood would pool in the left atrium
Backflow would lead to the pulmonary edema
What is Cor Pulmonale and when is it likely to happen
Respiratory disease
Most likely when have the left sided heart failure (would have the pulmonary oedema and the fluid would build in the lungs)
What is the normal EF
55-70%
What is Cor pulmonale
Blocked right bundle branch
This would normally come from left sided heart failure that would go to the right
What other factors can lead to Cor pulmonale
If right sided heart failure is caused by a respiratory disease
What does the stroke volume of the heart normally respond to
The preload of the heart
So when would have the effected stroke volume, would normally be an issue with the preload
What are the symptoms of the ACE inhibitors
Dry cough (excess bradykinin)
