Pharmacology Ii- Introduction To Cardiogenic Shock And Congestive Heart Failure

Front 1

In cardiogenic shock preload would?

Back 1

increase due to vasoconstriction shifting blood to the heart from the vessels and icnreased water retention

Front 2

In cardiogenic shock venous hydrostatic pressure would?

Back 2

Increase causing edema

Front 3

In cardiogenic shock heart rate would?

Back 3

increase to try and increase cardiac output

Front 4

In cardiogenic shock afterload and resistance would?

Back 4

Increased due to vasoconstriction making it harder for the heart to pump out blood. In some types of heart disease afterload may also be increased due to a strictured valve (pressure overload)

Front 5

In cardiogenic shock contractility would>

Back 5

decrease due to toxins, drugs, and some acquried types of disease like DCM, contractility may be OK in other types of heart diease but due to increased resistance such as in pressures overload or poor diastolic function such as in hypertorphic cardiomyopathy cardiac output will be poor.

Front 6

In addition to the hemodynamic consequences of sympathetic stimulation, RAAS and vasopressin activation. What are other consequences?

Back 6

-Sympathetic system and RAAS release may be directly toxic to the heart

-They may contribute to cardiac muscle necrosis, fibrosis, and excessive hypertrohy in addition to other abnormalities such release of inflammatory mediators and ractive oxygen species formation all of which can also be toxic to the heart.

Front 7

What is the main goal in the treatment of most cases of cardiogenic shock and congestive heart failure and what type of drugs are used to accomplish this goal.

Back 7

Decrease preload with diuretics
Decrease afterload with vasodilators
Increase constractility with positive inotropes in appropriate types of heart disease
Block sympathetic and renin angiotensin aldosterone system to prevent direct toxic effects to the heart.

Front 8

How does treatment in emergency heart failure differ from stable heart failure

Back 8

Emergency Tx:
- fast acting, stronger drugs
- concerned about hemodynamic consequences of the sympathetic and RAAS and not the direct toxic effects
-Tx that decrease direct toxic effects may actually be harmful in the short term (for examples beta blockers are used in stable heart failure but not unstable because in emergency situations the decreased heart rate and contractility may decrease cardiac output even further thereby worsening blood pressure and blood flow
- vasodilators may also be used in emergency to decrease resistance thereby improving blood flow. However often it is difficult to determine if vasoconstriction is helpful or harmful so these drugs are not always used immediately. In particular very strong vasodilators like nitroprusside which can easily cause overdilation resulting in vasodilatory shock.
- in emergency positive inotropes are god in appropriate cases. Also because the patient is stable these drugs are less likely to decompensate the patient and they do not need to be as strong
- also many of these drugs also block excessive sympathetic, and RAAS pathways (eg. ACE inhibitors, beta blockers) leading to a improvemet in heart function over the long term, despite the possibility of decompensating the patient via vasodilation, decreased contractility and decreased heart rate

Front 9

what are some appropriate heart failure cases for positive inotropes?

Back 9

cases that cause a decrease in contractility in particular if cause is reversible. used in cases where decreased contractility due to heart disease.

Front 10

In what case might fluids or vasopressors be given to a patient in cardiogenic shock?

Back 10

in cases of systolic failure and concurrent vasodilatory shock or hypovolemia in which preload is low due to these concurrent processes (vasodilatory shock or hypovolemic shock).
-drugs such as anesthetic drugs or sepsis could create this situation
-vasoconstrictors and positive inotropes may be helpful in cases of vsodilatory and cardiogenic shock because in these patients resistance would be low.

Front 11

What drugs are used in emergency management of heart failure?

Back 11

Loop Diuretics: furosemide
Some Vasodilators: nitroglycerine, nitroprusside, hydralazine, isosorbide dinitrate
Some Positive Inotropes: dobutamine, dopamine, bipyridine, amrinone, miklrinone

Front 12

why are these drugs used in emergency management of heart failure and which are most commonly used>

Back 12

- They are quick and strong acting drugs with high activity in diruretic, vasodilatory, or inotropic effect
- Remember these patients need quick acting drugs with a strong effect to control their abnormalities
- Diuretics are often a first emerency heart failure drug used because the pulmonary edema is what is generally causing the most problems and they are least likely to destabilize the patient
- Nitroglycerine is mainly a venous dilator that is commonly used to help relieve edema formation. Sometimes it is difficult to tell if arterial vasodilation will be a good or bad thing. In addition some of the vasodilators like nitroprusside or so strong they may cause excessive vasodiation
-positive inotropes can overwork the heart and are harmful in some for heart disease such as HCM

Front 13

What is the goal of loop diuretics in emergency management of heart failure (ie. what is its cardiovascular pharmacological effect)?

Back 13

diuresis will reduce blood volume and therefore decrease preload/volume overload thereby improving heart function in an overloaded heart. They can also decrease vascular hydrostatic pressure thereby decreasing edema formation

Front 14

how do loop diuretics cause a diuretic effect?

Back 14

due to inhibition of Na-K-2Cl symporter (cotransporter) at the luminal membrane of the thick ascending loop of henle. This inhibition results in decreased sodium reabsorption thereby causing diuresis

Front 15

what effect do loop diuretic have on prostaglandins?

Back 15

they may increase prostaglandins causing increases in renal blood flow an increase in venous capitance (prostaglandins cause vasodilation

Front 16

What effect do loop diuretics have on prostaglandins?

Back 16

they may increase prostaglandins causing increases in renal blood flow an increase in venous capitance (prostaglandins cause vasodilation)

Front 17

How are loo diuretics given?

Back 17

Orally and parenterally (IV is best in emergency and it is one of the only fast acting diuretic that is injectible)

Front 18

What are the adverse effects of loop diuretics?

Back 18

-Excessive administration can cause excessive volume depletion. This may worsen blood flow due to excessive decreases in preload resulting in decreased cardiac output and blood pressure (in other words this can cause hypovolemia

-electrolyte imbalances such as hyonatremia, hypkalemia, hypomagnesema

-systemic alkalosis

- other minor effects include hyperglycemia, cardiac arrythmias, hyperurecemia, ototoxicity, gastrointestinal disturbance, and hemotologic abnormalities (anemia, leukopenia)
-most likely of diuretics to cause dehydration and electrolyte abnormalities

Front 19

What benefit do vasodilators have in emergency management of heart failure (what is the pharmacological effect on hemodrynamics)?

Back 19

-arterial dilators reduce afterload allowing the heart to more effectively pump blood
- venous dilators reduce preload (may improve cardiac output in volume overloaded heart) and venous hydrastitics pressure (will reduce edema formation)

Front 20

Does nitroglycerine mainly dilate veins or arteries?

Back 20

veins

Front 21

What is the mechanism of action of nitroglycerine?

Back 21

causes the formation of nitric oxide (nitric oxide is a natural endogenous vasodilator)

Front 22

How is nitroglycerine given?

Back 22

topically

Front 23

What are the main adverse effects of nitroglycerine?

Back 23

Excessive vasodilation can decrease blood pressure/blood flow due to excessive decrease in preload and therefore decreased cardiac output and decreased resistance

Sometimes it is difficult to tell if vasoconstriction in heart failure is a good or bad thing (you may not want to block the vasodilation). Nitroglycerine is relatively safe however compared to balance strong vasodilators like nitroprusside

Front 24

Does nitroprusside mainly dilate the veins or arteries?

Back 24

both it is a balanced vasodilator

Front 25

How does nitroprusside cause vasodilation?

Back 25

increased formation of nitric oxide

Front 26

How is nitroprusside given?

Back 26

IV

Front 27

what is an important metabolite of nitroprusside?

Back 27

metabolized to cyanogen (cyanide radical) which is converted to thiocyanate which can than eliminated in urine feces and exhaled

Front 28

what are adverse effect of nitroprusside?

Back 28

excessive vasodilation can decrease arterial blood pressure and blood flow due to excessive decreases in resistance and pooling of blood in capillaries will decrease preload causing a decrease in cardiac output and therefore decreased blood pressure and blood flow.
-Prolonged use can cause cyanide toxicity and tolerance to vasodilatory effect

Front 29

What drug is more likely to cause excessive vasodilation nitroprusside or nitroglycerine?

Back 29

Nitroprusside is more likely because it is a much better vasodilatory in cases of severe heart failure but when giving you need continuous monitoring to avoid hypotension

Front 30

Hydralazine is mainly an arterial or venous dilator?

Back 30

arterial
less often used likely b/c it give no venodilation and is given orally which may be difficult to give and adjust when given to heart failure patients.

Front 31

What is isosorbide dinatrate?

Back 31

vasodilator like nitroprusside. it is mainly a venodilator

Front 32

On what adrenergic receptors does dobutamine act on and which receptor causeas the positive inotrope effect?

Back 32

It is a beta 1 agonist resulting in increased ionotrophy and chronotropy. It has very little to no beta 2 and alpha activity

Front 33

Why does dobutamine have minimal effect on blood vessels and is this good in heart failure treatment?

Back 33

It has no beta 2 and alpha activity so it has very little effect on blood vessels. This may be good in heart disease if you want to avoid vasodilation and vasoconstriction

Front 34

How is dobutamine given?

Back 34

IV can't be given orally degraded in GIT

Front 35

in what type of heart disease is it best to use dobutamine?

Back 35

heart disease associated with systolic heart failure like dilated cardiomyopathy

Front 36

In what type of heart disease it is best not to use dobutamine (or any postive ionotrope)

Back 36

heart disease assoicated with decreased contractility. it is not good in heart failure where systolic failure is normal such as hypertrophic cardiomyoptathy or stenosis
it may also wrosen heart failure i ncases of valvulr regurgitation

Front 37

What are the adverse effects of dobutamine?

Back 37

Tachyarrhythmia
may be helpful in short term but in long term increased oxygen consumption due to positive ionotropic and chronotropic effects may worsen heart disease

Front 38

Why is dobutamine a first line agent as an inotrope in heart failure and what limits its use?

Back 38

because it has mainly BETA1 activity with little effect on blood vessels and is least likely of the catecholamines to cause arrhythmias. The adverse effects mentioned above and need for continuous monitoring due to potential arrhythmias limit the use of dobutamine in general practice

Front 39

what is another catecholamine that can be used as a positive ionotrope?

Back 39

dopamine

Front 40

is dopamine used at its low, mid, or high dose in heart disease?

Back 40

mid dose is dose with beta activity thereby increasing cardiac contractility and rate

Front 41

Adverse effects and uses of doapmine are similar to what other catecholamine and what is the main difference in receptor activity?

Back 41

dobutamine. The difference is that dopamine has BETA 2 effect at mid dose along with BETA 1 effects and has ALPHA activity at higher doses. It also causes vasodilation due to dopamine receptor activiation. Vasodilation could potentially be a good thing in heart failure but it is sometimes hard to tell.

Front 42

What other drugs can be used as positive ionotropes in emergency heart failure. Also what is the mechanism of action, pharmacological effect and adverse effects of these drugs?

Back 42

Bipyridines (amrinone and milrinone)
They are phosphodiasterase inhibitors an can increase contractility and cause vessels dilations. Best in heart failure associated with poor contractility and should not be used if systolic function is not the problem.
Adverse effects are similar to catecholmines- arrhytmias