Heart Failure Flashcards by Amy Nyarko

What is frank starlings law

The increased venous return would increase the contractility

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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

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What is acute heart failure

Rapid onset

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What are the main causes of the acute heart failure

Pulmonary embolism
Drugs
Arrhythmias
Acute valvopathy

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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

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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

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What is systolic heart failure

HFrEF (heart failure reduced ejection fraction)
Systolic dysfunction
Reduced contractility
MI
Dilated cardiomyopathy
So reduced ejection fraction

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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

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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

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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

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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

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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)

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What is hypoxic vasoconstriction

Perfusion and ventilation decreases
Preserve oxygen vessels vasoconstrict
Lead to pulmonary hypertension

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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

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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)

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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

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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

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What happens in left sided heart failure

Blood would normally accumulate in the left atrium

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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)

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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)

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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)