L30,32: Pharmacological treatment of cardiac disease

Question 1

Define heart failure

Answer 1

Despite adequate venous return, CO is insufficient to meet tissue demands

Question 2

Early heart failure is also known as…

Answer 2

Compensated heart failure

Question 3

What are clinical signs of heart failure

Answer 3

Poor exercise tolerance 
Shortness breath 
MM pallor/ cyanosis 
Slow CRT 
Cool extremities 
Cachexia 
Congestion

Question 4

How does the body attempt to make up for it’s heart’s failure?

Answer 4

Inc sympathetic stimulation
Renal effects –> Na, H20 retention
Frank starling –> INC EDV

Question 5

How does vasoconstriction contribute to compensating for heart failure?

Answer 5

Increasing TPR to maintain blood pressure

Question 6

What is an undesired effect of vasoconstriction during heart failure

Answer 6

Increased after load

Question 7

How does the heart attempt to make up for it’s failure?

Answer 7

Inc HR, Inc SV

Question 8

What is an undesired effect of cardiac inc HR/ SV?

Answer 8

Increasing CO also increases the hearts workload… “flogging a dead heart”

Question 9

How do the kidneys attempt to fix heart failure?

Answer 9

by increasing blood pressure via Na and H20 reabsorption in order to increase TPR and maintain BP.

Question 10

What is an undesired effect of RAAS activation during heart failure

Answer 10

Increased after load and preload

Question 11

How do Frank Starling forces help improve the heart failure situationononono?

Answer 11

Increase of EDV leads to increased CO

Question 12

How will the heart wall remodel subsequent of heart failure

Answer 12

Hypertrophy –> inc work/contraction

Question 13

How does early heart failure differ from chronic heart failure

Answer 13

Early= "compensated", heart attempts to cope with inadequate ventricular filling pressure. 
Chronic= "progressed", heart no longer can cope!

Question 14

What is an adverse effect of chronic activation of the sympathetic NS?

Answer 14

Baroreceptors reduce in sensitivity, so keep firing even when MAP is appropriate.
their set point is changed due to chronic increase in pressure.
B receptors in heart will be down regulated so have reduced capacity to respond to sympathetic stimulation.

Question 15

what is an adverse effect of chronic activation of RAAS?

Answer 15

Persistent vasoconstriction Increases preload and after load (also due to increase in BV)
angiotensin VERY potent vasoconstrictor and can cause myocardial toxicity.
Dec of baroreceptor sensitivity.

Question 16

What is an adverse effect of cardiac hypertrophy?

Answer 16

Capillary growth can’t match increase in muscle mass. Insufficient mitochondrial mass. Dec overall energy, less efficient contraction.

Question 17

What are the two ‘mechanisms’ by which the force of contraction is decreased in heart failure

Answer 17

DEC inotropy –> “weak” heart (systolic heart failure)

DEC lusitropy –> “stiff” heart (diastolic heart failure)

Question 18

Cardiac hypertrophy will increase the risk of what?

Answer 18

Arrhythmias

Question 19

What regulatory/compensatory mechanisms kick in during heart failure

Answer 19

ANP released to reverse toxic effects of angiotensin. Prostaglandins released to reverse vasoconstriction.

Question 20

How should we aim to treat heart disease guys?

Answer 20

By understanding the underlying pathophysiology to adequately supply the correct class of drug. We should ain to increase the responsiveness of the heart at any given amount of stretch.

Question 21

What does cardiac contractility depend on?

Answer 21

Ca++ from SR & membrane

Question 22

What are the 4 areas which we can target to modify contractility?

Answer 22

B receptor
Ca channel
Na/K ATPase
Contractile unit

Question 23

How does the sympathetic NS modify cardiac contractility

Answer 23

NA opens RO Ca++ by binding to B1 adrenoceptors.

Question 24

What is the action of positive inotropes

Answer 24

Increase cardiac contractility and CO