L30,32: Pharmacological treatment of cardiac disease Flashcards Preview

Cardiovascular System > L30,32: Pharmacological treatment of cardiac disease > Flashcards

Flashcards in L30,32: Pharmacological treatment of cardiac disease Deck (24):
1

Define heart failure

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

2

Early heart failure is also known as...

Compensated heart failure

3

What are clinical signs of heart failure

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

4

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

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

5

How does vasoconstriction contribute to compensating for heart failure?

Increasing TPR to maintain blood pressure

6

What is an undesired effect of vasoconstriction during heart failure

Increased after load

7

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

Inc HR, Inc SV

8

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

Increasing CO also increases the hearts workload... "flogging a dead heart"

9

How do the kidneys attempt to fix heart failure?

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

10

What is an undesired effect of RAAS activation during heart failure

Increased after load and preload

11

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

Increase of EDV leads to increased CO

12

How will the heart wall remodel subsequent of heart failure

Hypertrophy --> inc work/contraction

13

How does early heart failure differ from chronic heart failure

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

14

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

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.

15

what is an adverse effect of chronic activation of RAAS?

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.

16

What is an adverse effect of cardiac hypertrophy?

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

17

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

DEC inotropy --> "weak" heart (systolic heart failure)
DEC lusitropy --> "stiff" heart (diastolic heart failure)

18

Cardiac hypertrophy will increase the risk of what?

Arrhythmias

19

What regulatory/compensatory mechanisms kick in during heart failure

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

20

How should we aim to treat heart disease guys?

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.

21

What does cardiac contractility depend on?

Ca++ from SR & membrane

22

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

B receptor
Ca channel
Na/K ATPase
Contractile unit

23

How does the sympathetic NS modify cardiac contractility

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

24

What is the action of positive inotropes

Increase cardiac contractility and CO