Cardiac haemodynamics and heart failure

Question 1

Equation for cardiac reserve

Answer 1

Cardiac Reserve = Maximal CO- CO at rest

Question 2

What is preload?

Answer 2

Preload is the level of stretch that a cardiomyocyte is exposed to before ventricular ejection
– LV end-diastolic volume

Question 3

What is after load?

Answer 3

Afterload is the pressure against which the heart is contracting when it ejects blood
– e.g. increased afterload in hypertension

Question 4

What does a reduced CO mean?

How does the body sense it?

Answer 4

Reduced CO = reduced organ perfusion

Body senses it via baroreceptors and juxtaglomerular apparatus in kidneys.

Question 5

What happens when mean systemic arterial pressure is decreased?

Answer 5

If mean systemic arterial pressure decreased, baroreceptor firing would decrease, sympathetic tone would increase and parasympathetic tone would decrease.

Question 6

What happens when mean systemic arterial pressure is increased?

Answer 6

If mean systemic arterial pressure increases, baroreceptors fire more, sympathetic tone will decrease and parasympathetic tone will increase.

Question 7

In the ANS where doe the baroreceptor reflex occur? What does it reduce? How does is it augment vagal tone?

Answer 7

•	Arterial stretch sensed
•	Afferent loop ends in nucleus tractus solitarius and rostral ventrolateral medulla
•	Reduces sympathetic tone
•	Augments vagal tone
–	Reduced HR (β)
–	Reduced SV (β)
–	Vasodilatation (α)

Question 8

How does juxtaglomerular apparatus work?

Answer 8

• Renal perfusion pressure sensed at glomerulus
• Sodium concentration sensed in fluid surrounding distal convoluted tubule
• If either reduced, renin is released
• Inactive prorenin  renin + active prorenin

Question 9

What are the two types of myocardial dysfunction?

Answer 9

• Diastolic dysfunction
– Known as heart failure with preserved ejection fraction (HFPEF)
• Systolic dysfunction
– Known as heart failure with reduced ejection fraction (HFREF)

Distinguish important- reduced ejection fraction gives a larger chance of mortality than preserved ejection fraction

Diastolic- stiffen ventricle
Systolic-damage so can’t pump properly

Question 10

What are the symptoms of heart failure?

Answer 10

Oedema- swelling
Dyspnoea- breathlessness from exercise and orthopnea (lying flat)
Paroxysmal nocturnal dyspnea- an attack of severe shortness of breath and coughing that generally occur at night

Question 11

What is heart failure of the LV? What does it cause?

Answer 11

• Back pressure in LV causes raised pressure in pulmonary circulation
• Increased hydrostatic pressure forces fluid outside vascular compartment
• Interstitial space in lungs fills with fluid
• Pulmonary oedema / Pleural effusions
• Patient becomes breathless, oxygen sats drop
• Lying flat worsens symptoms (orthopnoea)

Question 12

What is heart failure of the RV? What does it cause?

Answer 12

• Back-pressure transmits to venae cavae
• Internal jugular venous pressure rises
• Jugular venous pressure raised
• Gravity and raised orthostatic pressures force fluid from vascular compartment to peripheral tissue
• Ankles / sacrum swell- still affects LV
• Hepatomegaly / ascites

Question 13

What are the causes of heart failure?

Answer 13

• MI
• Atrial fibrillation
• Alcohol
• HTN
• Myocarditis (virus or anything causing myocardial infection)
• Increased BP
• Genetic factors

Question 14

What is anterolateral infarct?

Answer 14

Anterolateral infarct- Anterior wall myocardial infarction is often caused by occlusion of the left anterior descending coronary artery.

Question 15

What is posteroinferior infarct?

Answer 15

Posterior inferior cerebellar artery (PICA) occlusion may cause infarction of any part of the vascular territory of the PICA, namely the posterior inferior cerebellum, inferior cerebellar vermis and lateral medulla.

Question 16

What happens when ejection fraction drops?

Answer 16

• Reduced CO
• Reduced systolic BP
• Reduced arterial stretch
• Reduced renal perfusion

Question 17

What is a CV maladaptation in sarcomere?

Answer 17

• Increased preload lengthens sarcomeres
• Raise in end-diastolic pressure of LV
• Augments stroke volume, i.e. CO
• Works for a while but will result in compensation

Question 18

What happens when LV stretch is exceeded?

Answer 18

• LV stretch eventually exceeds physiological levels  Decompensation
• We move to the descending limb of the sarcomere tension curve
• Small rises in LVEDP (i.e. fluid retention) cause large drops in sarcomere tension, i.e. LV contractility and stroke volume
• Reduces CO, further impact on ANS and RAS

Question 19

Adverse remodelling- what is the law of Laplace?

Answer 19

Laplace’s Law: for any given LV cavity pressure (P), the wall stress will be directly proportional to the LV cavity size or radius (R) and inversely proportional to the LV thickness (T)

Question 20

Adverse remodelling-what happens to the left cavity?

Answer 20

Scar causes thinning and stretching of the left cavity

Doesn’t cause hypertrophy because of the thinning.

Question 21

How can we assess patients with heart failure?

Answer 21

• Assessment of severity
• ≥55% is normal
• 45-54% is mildly impaired
• 36-44% is moderately impaired
• ≤35% is severely impaired

LVEF %= Stroke Volume/ End Diastolic Volume

Question 22

What acute therapy is there?

Answer 22

• Oxygen- If have bad pulmonary oedema- force oxygen in lungs to push fluid out of lungs
• Optimise alveolar ventilation
• May need to increase pressure in airways to oxygenate blood
 Non-invasive or invasive ventilation

Question 23

What does morphine do?

Answer 23

• We could relax her pulmonary vessels
• This would reduce her preload and take the strain off the LV
• Morphine would help her breathing and any pain too

Question 24

What do diuretics do and how does it affect the LC and the position along the Starling curve?

Answer 24

Diuretics limit reabsorption of fluid
– Offloads the ventricles
– Moves us back along the Starling curve
– Can maximise LV contractility

Question 25

What are the side effects of diuretics?

Answer 25

– Renal dysfunction- if give too much
– Reduces Na, K, Mg- excreting salt so if too low v dangerous
– Can induce diabetes (thiazides- type of diuretic)

Question 26

What are drugs for chronic therapy?

Answer 26

Drugs for Symptomatic Benefit- diuretics

Drugs for Prognostic Benefit:

ACEI and A2RBs- Give them Rampiril ACEI stops the action of AgII thus no actions of RAAS

Question 27

What responses are beta-receptors involve in? Blocking of them does what?

Answer 27

• Beta-receptors are involved in myocardial and renal responses to reduced CO
• Blockade of these can reduce HR
– Moves back along the Bowditch curve
– Allows LV more relaxation time, so better filling
• Also blunts RAAS overactivation
– Concomitant effects on fluid retention
• Cautions: asthma, low HR, heart blocks

Question 28

What are other rate modifiers in the body?

Answer 28

• SA node- Ivabradine

* AV node- Digoxin- reduces HR slows conduction through AV node and re-introduces depolarization- positively ionotropic

Question 29

What does sacubitril and valsartan do?

Answer 29

• Valsartan is an ARB
• Sacubitril is a neprilysin inhibitor
– Enhances action of natriuretic peptides
– Promotes sodium/water excretion
• Combination has good evidence above ACEI/ARB

Question 30

What device therapy is there?

Answer 30

ICD- If someone has cardiac arrest- give defibrillator, patients has internal cardiac defibrillator- shocks you to prevent you have an irregular heart rhythm

CRT- one side of the heart moving well and one isn’t- desynchrony- this therapy helps this
Into RA- SVC and IVC and coronary sinus- CRT goes through coronary sinus- can now put heart back into sync

Implantable cardioverter-defibrillator (ICD)
Cardiac resynchronisation Therapy (CRT)