Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular System > Congestive Heart Failure > Flashcards

Congestive Heart Failure Flashcards

1
Q

What is Cardiac Failure

A

Failure of cardiac function to deliver oxygenated blood to tissue and the function defined as Cardiac Output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the aim of drug therapy in CHF

A

To relieve symptoms

To improve quality of life

To improve survival

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Determinants of Stroke Volume

A

Afterload

Preload

Contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Strategies to treat CHF

A
  1. Reduce Afterload-Artery dilators
  2. Reduce Preload-Remove water and Vein Dilators
  3. Increase contractility-Inotropes
  4. Inhibit RAAS system
  5. Inhibit Sympathetic NS activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Drugs used for the treatment of CHF

A

Artery Dilators: ACEI, Hydralazine and Minoxidil

Inotropes: Digoxin, Dobutamine and Milrinone

Diuretics: Furosemide
Vein Dilator: Nitrate(NTG) and ACEI-Captopril

ACEI

B-blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Drugs proven to improve Survival

A

Aspirin

B-blockers

ACE inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Classes of Drugs for CHF

A
  1. Inotropics
  2. Vasodilators
  3. Neurohormonal antagonists
  4. Diuretics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Inotropes:

Examples

A

Digoxin

Catecholamines

Phosphodiesterase III inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

_NEUROHORMONAL EFFECTS

A

Decreases Plasma Noradrenalin (Reduced Sympathetic tone)

Decreases Peripheral nervous system activity

Decreases RAAS activity (switches off)

Decreases Vagal tone or

Normalizes arterial baroreceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

_EFFECTs (SUMMARY)

A

Positive inotropia: Na K-ATPase inhibition

Negative chronotropia

Negative dromotropia

Increased Parasympathetic tone: Decreased AV conduction & heart rate

Decreased Sympathetic tone

A dromotropic agent affects the conduction speed in the AV node, and subsequently the rate of electrical impulses in the heart.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Digoxin:

Long Term Effects

A

Survival similar to placebo

Fewer hospital admissions

More serious arrhythmias

More myocardial infarctions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Digoxin:

Clinical Uses

A

Atrial Fibrillation with rapid ventricular response.

Congestive Cardiac Failure refractory to other drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Digoxin:

Contraindications

A
  • Digoxin toxicity• RELATIVE- Advanced A-V block withoutpacemaker- Bradycardia or sick sinus without PM- Extrasystoles- Marked hypokalemia- W-P-W with atrial fibrillation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Digoxin Side Effects/Toxicity:

Cardiac Manifestations

A

Arrhythmias:
Ventricular
Supraventricular

Blocks:
SA and AV blocks

Exacerbates cardiac failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Digoxin Side Effects/Toxicity:

Extracardiac

A

Gastrointestinal:
- Nausea, vomiting, diarrhea

Nervous System:
- Depression, disorientation, paresthesias

Visual:
- Blurred vision, scotomas and yellow-green vision

Hypoestrogenism:
- Gynecomastia, galactorrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Digoxin:

Drug Interactions

A

Antacids and Cholesteramine:
=> to reduced absorption of digoxin

Calcium Channel Blocker:
- Oppose the effect of digoxin on the heart

Drugs that cause Hypokalemia: Diuretics
- Cause digoxin arrhythmias

Drugs that block AV node: Quinidine
- worsen digoxin toxicity (bradycardia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Catecholamines:

A

B-adrenergic stimulants classification:

B1 Stimulants which Increase contractility:
Dobutamine

Mixed DA, B1 & B2:
Dopamine
DOPAMINE AND DOBUTAMINE
EFFECTS
Dopamine μg/kg/ml Dobutamine
<2 2-5 >5
Receptors DA1/DA2 β1 β1+α β1
Contractility ± ++ ++ ++
Heart rate ± + ++ ±
Arterial
pressure
± + ++ ++
Renal
perfusion
\++ + ± +
Arrhythmia - ± ++ ±
POSITIVE INOTROPES:
CONCLUSIONS
• May increase mortality
• Safer in lower doses
• Use only in cardiogenic shock
• NOT for use as chronic therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Conclusion of Positive Inotropes

A

May increase mortality

Safe in lower doses

Use only in cardiogenic shock

Not for us as chronic therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Vasodilators:

Drugs

A

ACE Inhibitors & AT-1 blockers

Nitrates

20
Q

ACEI:

Advantages

A

Inhibit left ventricular remodeling post-myocardial infarction

Modify the progression of chronic congestive heart
failure
-Increases Survival
- Decreases Hospitalizations
-Improve the quality of life

In contrast to others vasodilators, do not produce neurohormonal activation or reflex tachycardia

Tolerance to its effects does not develop

21
Q

ACEI:

Side Effects

A

Inherent in their mechanism of action

  • Hypotension
  • Hyperkalemia
  • Angioneurotic edema

Due to their chemical structure:

  • Cutaneous eruptions
  • Neutropenia, thrombocytopenia
  • Digestive upset
22
Q

ACEI:

Contraindications

A

Renal artery stenosis

Renal insufficiency

Hyperkalemia

Arterial hypotension

Intolerance (due to side effects

23
Q

AT1 Receptor Blockers:

Drugs

A

Losartan

Valsartan

Ibersartan
Competitive and selective
Inhibition of AT1 receptors

24
Q

Nitrates: Hemodynamic Effects

Types

A

Venous Vasodilation

Arterial Vasodilation

Coronary Vasodilation

25
Q

Venous Dilation:

A

Decrease Preload: When that happens:

It also decreases the following:

  • Pulmonary congestion
  • Ventricular size
  • Vent. Wall stress
  • MVO2
26
Q

Arterial Vasodilation

A

Decreases Afterload:

Thus decreasing:

  • Cardiac Output and
  • Blood Pressure
27
Q

Coronary Vasodilation

A

Increases myocardial perfusion:

28
Q

Nitrates:

Tolerance

A

” Decrease in the effect of a drug
when administered in a long-acting form”

Develops with all nitrates

Is dose-dependent

Disappears in 24 h. after stopping the drug

Can be avoided or minimized

  • Intermittent administration
  • Use the lowest possible dose
  • Intersperse a nitrate-free interval

Allow peaks and valleys in plasma levels

  • Vascular smooth muscle recovers its nitrate sensitivity during the nadirs
  • Patches: remove after 8-10 h
29
Q

Nitrates:

Contraindications

A

Previous hypersensitivity

Hypotension (< 80 mmHg)

1st trimester of pregnancy

WITH CAUTION in:

  • Constrictive pericarditis
  • Intracranial hypertension
  • Hypertrophic cardiomyopathy
30
Q

Nitrates:

Clinical Uses

A

Pulmonary congestion

Orthopnea and paroxysmal nocturnal
dyspnea

Congestive cardiac failure with myocardial
ischemia

Acute congestive cardiac failure and pulmonary
edema: TNT SL or IVI.

31
Q

Neurohormonal Antagonists:

B-blockers

A

Inhibit cardiotoxicity of catecholamines

Decreases Neurohormonal activation

Decreases Heart rate

32
Q

B-Blockers:

Clinical Uses

A

Suspected adrenergic activation

Arrhythmias

Hypertension

Angina

33
Q

ß-Adrenergic Blockers:

Contraindications

A

Hypotension: BP < 100 mmHg

Bradycardia: Heart rate < 50 bpm

Clinical instability

Chronic bronchitis, ASTHMA

Severe chronic renal insufficiency

34
Q

Diuretics:

Drugs

A

Thiazides

Loop diuretics

Potassium Sparing Diuretics

35
Q

Thiazides

A

Inhibit active exchange of Na-Cl in
cortical diluting segment of
ascending loop of Henle.

36
Q

Loop diuretics

A

Inhibit exchange of Na-Cl-K
in thick segment (ascending
loop of Henle)

37
Q

K- sparing

A

Inhibit reabsorption of
Na in distal convoluted
& collecting tubule

38
Q

Thiazides:

Mechanism of Action

A

Excrete 5 - 10% of filtered Na+

Increases Elimination of K+

Decreases Excretion of uric acid and Ca

Minimal dose - effect relationship

Some inhibit carbonic anhydrase: increase elimination of HCO3

39
Q

Loop Diuretics:

Mechanism of Action

A

Excrete 15 - 20% of filtered Na+

Increases Elimination of K+, Ca+ and Mg++

Decreases Resistance of afferent arterioles
– Increases Release renal PGs
– NSAIDs may antagonize diuresis

40
Q

K-Sparing:

Mechanism of Action

A

Eliminate < 5% of filtered Na+

Inhibit exchange of Na+ for K+ or H+

Spironolactone = competitive antagonist for the aldosterone receptor

Amiloride and triamterene block Na+ channels controlled by aldosterone

41
Q

Diuretic Effects

A

Volume and preload
– Improve symptoms of congestion

No direct effect on cardiac output, but excessive preload reduction may improve arterial distension.

Neurohormonal activation:
– Increased levels of renin and Angiotensin II
– Exception: Reduced with spironolactone

42
Q

Diuretics: Adverse Reactions:

Thiazides and Loop Diuretics

A

Changes in fluid balance and electrolytes:
– Reduce Volume
– Reduce Na+, K+, Mg++
– Metabolic alkalosis

Other changes:
– Increase blood glucose and uric acid
– Increase LDL cholesterol & Trigliserides

Cutaneous allergic reactions

Idiosyncratic effects:
– Blood dyscrasia, cholestatic jaundice and acute pancreatitis

Gastrointestinal effects

Genitourinary effects:
– Impotence and menstrual cramps

Deafness, nephrotoxicity
(Loop diuretics)

43
Q

Diuretics: Adverse Reactions:

K-Sparing

A

Changes in electrolytes:
– ↑ Na+, ↑ K+, acidosis

Musculoskeletal:
– Cramps, weakness

Cutaneous allergic reactions :
– Rash, pruritis

44
Q

Drugs used for Acute Heart Failure

A

In hospital: intravenous

Diuretics: Furosemide

Nitrates:

Inotropic agents: Dopamine/ dobutamine

Oxygen

45
Q

Drugs used for Chronic Heart Failure

A

Systolic dysfunction:

Diuretic + ACEI / ARB

Beta blocker

Spironolactone or eplerenone if needed

Digoxin if AF

Hydrallazine + nitrate

Anticoagulant/ antiplatelet drugs

46
Q

Drugs which may aggravate or induce Heart Failure

A

Drugs that increase fluid retention
– NSAIDs
– Rosiglitazone/ Pioglitazone
– High salt content: Fleet enema

Drugs with negative inotropic effect
– Betablocker
– Calcium channel blocker

Direct cardiotoxicity
– Cancer chemotherapy

Cardiovascular System (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions