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PCOL 2 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

A cardiac disorder that impairs the
ability of the ventricle to deliver
adequate quantities of blood to
the metabolizing tissues during
normal activity or at rest.

A

Heart Failure

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2
Q

Sign and Symptoms of HF?

A

Shortness of breath
fatigue
limitation of exercise tolerance,
and fluid retention

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3
Q

What causes Heart
Failure? (most common)

A
  • ischemic heart disease
  • hypertension
  • diabetes
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4
Q

What causes Heart
Failure? (Less common)

A

cardiomyopathies,
valvular disease,
myocarditis,
infections,
systemic toxins
cardiotoxic drugs.

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5
Q

2 Pathophysiology of
Heart Failure

A

A. Compensation
B. Decompensation

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6
Q

HF and decreased cardiac output trigger a complex scheme of
______mechanisms designed to normalize cardiac output.

A

Compensation

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7
Q

4 mechanisms to have Compensation.

A
  1. Sympathetic responses
  2. Hormonal stimulation
  3. Concentric cardiac hypertrophy
  4. Frank-starling mechanism
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8
Q

Compensation: Inc. Norepinephrine

A

SNS ACTIVATION/Sympathetic responses

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9
Q

Compensation:Renin
Angiotension I
Angiotension II; Aldosterone (RAAS)

A

Hormonal stimulation

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10
Q

Results of Hormonal stimulation?

A

Vasoconstriction ->Inc. Afterload
Inc. salt ->Inc. Preload

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11
Q

is associated
with increased left ventricular wall
thickness

A

Concentric hypertrophy

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12
Q

a compensatory effect of the body to increase force of contraction in the heart ?

A

hypertrophy

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13
Q

is characterized by
dilatation of the left ventricular chamber.

A

eccentric hypertrophy

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14
Q

lesser force of the contraction of the heart =?

A

the lesser amount of blood being pump in the body

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15
Q

increased fiber dilation heightens the
contractile force, which then increases
the energy released.

it increase the stretch of the ventricle and contraction

A

Frank-starling mechanism

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16
Q

A combination of symptoms and signs that indicate that the
heart by reason of its abnormal condition no longer is able to
maintain an efficient circulation.

There is a mismatch between cardiac preload and
afterload.
- There is an inability to eject and/or accommodate blood
within physiological pressure levels.

A

Decompensation

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17
Q

force exerted on the ventricular muscle at the end of diastole that determines the degree of muscle fiber stretch.

“stretch”

A

Cardiac PREload

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18
Q

Cardiac PREload also known as ?

A

ventricular end diastolic
pressure

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19
Q

also a key factor in contractility and a way to fill heart with blood

A

ventricular end diastolic
pressure

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20
Q

too much increase of Cardiac PREload can cause ?

A

Heart Failure, mitral stenosis

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21
Q

a form of valvular heart disease characterized by the narrowing of the mitral valve orifice.

A

mitral stenosis

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22
Q

too much decrease of Cardiac PREload can cause ?

A

Hypovolemic shock,
hemmorhage

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23
Q

an emergency condition in which severe blood or other fluid loss makes the heart unable to pump enough blood to the body. This type of shock can cause many organs to stop working.

A

Hypovolemic shock

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24
Q

is bleeding from a damaged blood vessel.

A

hemmorhage

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25
Q

tension in ventricular muscles
during contraction. (squeeze)

It is the pressure or resistance the heart has to overcome to eject blood.

In the left ventricle, this tension is
determined by the amount of force
needed to overcome pressure in the
pulmonary artery.

to pump blood to the body

A

Cardiac AFTERload

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26
Q

Class of Heart failure: degree of effort necessary to elicit HF symptoms equals to those that would limit normal individuals.

A

CLASS I

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27
Q

Class of Heart failure: symptoms occurs with ordinary exertion

A

CLASS II

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28
Q

Class of Heart failure: symptoms occurs with less- than-ordinary
exertion.

A

CLASS III

29
Q

Class of Heart failure: symptoms occurs while at rest

A

CLASS IV

30
Q

Forms of Heart failure: most common type

metabolic demands are within normal limits but the heart is unable
to meet them. (depressed ejection fraction/ inability to eject blood
from the ventricles)

A

LOW OUTPUT Heart failure

31
Q

Can cause LOW OUTPUT Heart failure?

A

Dilated cardiomyopathy
chronic hypertension
valvular disease

32
Q

Forms of Heart failure: Rare type

have elevated cardiac output but has a low systemic vascular resistance and increase oxygen consumption

↑metabolic demands and the heart is unable to meet them

” unable to catch metal ball effect”

A

HIGH OUTPUT Heart failure

33
Q

Can cause LOW OUTPUT Heart failure?

A

Hyperthyroidism, severe anemia, pregnancy, beriberi (deficiency in Vit B1: thiamine)

34
Q

Forms of Heart failure:
when blood is not pumped from the ____ventricle, the fluid
portion of the blood backs up throughout the body=
Peripheral edema)

A

Right sided Heart failure

35
Q

the fluid portion of the blood backs up into pulmonary
alveoli, producing pulmonary edema.

A

Left sided Heart failure

36
Q

Sequence of Heart Flow ?

A
  1. Superior vena cava/ Inferior vena cava (enter of deoxygenated blood from the body)
  2. Right Atrium —> tricuspid valve
  3. Right Ventricle —> pulmonary valve
    —> Pulmonary artery to lungs ( to have a oxygenated blood)
  4. Pulmonary vein (w/ oxygenated blood)
  5. Left Atrium —> Mitral valve
  6. Left ventricle —> Aortic Valve
  7. Aorta— to the systemic circulation of the body.
37
Q

If the LV is unable to
pump= backflow to
lungs=?

A

pulmonary edema

38
Q

If the RV is unable to pump= backflow to circulation= ?

A

peripheral edema

39
Q

Forms of Heart failure: The ventricles cannot pump enough BLOOD.
(pumping problems)

A

Systolic Heart Failure

40
Q

Forms of Heart failure: The ventricles cannot fill
enough BLOOD. (Filling problem)

A

Diastolic Heart Failure

41
Q

Forms of Heart failure:
▷The heart works well enough that you either don’t notice
any problems.
▷Compensatory mechanism works Although initially beneficial in the
early stages of heart failure, all of these compensatory mechanisms eventually
lead to a vicious cycle of worsening heart failure.
▷The symptoms are easy to manage.

A

COMPENSATED HF

42
Q

Forms of Heart failure:

▷the heart by reason of its abnormal condition no longer is able to
maintain an efficient circulation.
- There is a mismatch between cardiac preload and afterload.
- There is an inability to eject and/or accommodate blood within physiological
pressure levels.
▷a syndrome defined by worsening fatigue, dyspnea, or edema
that results from deteriorating heart function
▷usually leads to hospital admission or unscheduled medical
intervention.

A

DECOMPENDATED HF

43
Q

Treatment Goals for
Heart Failure:???

A
  1. Remove or mitigate the underlying causes or risk factors
  2. Eliminating ingestion of certain drugs or other substances
    (Ex: NSAIDs, OHAs, Calcium channel blockers, Clonidine, Nasal
    decongestants)
  3. Relieve symptoms (Ex: Inotropic agents- increase heart
    contraction, diuretics to manage edema)
  4. Reduce the need for emergency room visits and
    hospitalization and Improve patient’s QoL.
44
Q

An ion that is responsible for initiating action potential & triggered contraction of heart muscle.

A

Na+ / Sodium Ion

45
Q

an ion that is responsible for the termination of action potential & contraction (Relax) initiating Repolarization

A

K+/ Potassium Ion

46
Q

This causes depolarization of the resting
membrane potential=

A

Heart Contraction (Inotropic effect)

47
Q

Most known Na+/K+ ATPase inhibitors drug classsification ?

A

INOTROPIC AGENTS

48
Q

used in conjunction with diuretics, ACE inhibitors, βadrenergic blockers to improve the symptoms and clinical
status of patients with HF

Digitalis lanata/purpurea (Foxglove)

A

Digoxin (Lanoxin)

49
Q

Digoxin Dec. absorption with?

A

Sulfasalazine, Neomycin

50
Q

Digoxin inc. absorption with?

A

Erythromycin, Tetracycline

51
Q

Digitalis Glycoside:
Effects of antibiotic: Can be affected.
Pathway of Excretion: Kidneys (renal clearance, water solubility)
Renal impairment: Adjust dosage

A

Digoxin

52
Q
A
53
Q

Digitalis Glycoside:
Effects of antibiotic: Not affected
Pathway of Excretion: Biliary excretion
Renal impairment: does not
significantly prolong
the half-life of ______

A

Digitoxin

54
Q

MOA: inhibit Na+/K+ ATPase, the
membrane-bound transporter often
called the sodium pump.

A

Digitalis Glycoside:
Pharmacodynamics

55
Q

Mechanical Effects
* Increase contractility of the heart muscle
* by increasing the free calcium
concentration
* (+) inotropic effect
Digitalis Glycoside
The increase in calcium concentration is
the result of a two-step process:
1. Na+/K+ ATPase inhibition
2. reduction of calcium expulsion

A

Digitalis Glycoside: Cardiac
Effects

56
Q
  • mixture of direct and autonomic actions.
  • decrease in action potential
  • as a result of increased potassium
    conductance that is caused by increased
    intracellular calcium.
    **Shortening of the action potential contributes
    to the shortening of atrial and ventricular
    refractoriness
A

Electrical Effects of Digitalis Glycoside

57
Q

Digitalis Glycoside: Effects on other organs-GIT- gastrointestinal tract

A

V.A.N.D
*Anorexia
* Nausea
* Vomiting
* Diarrhea

58
Q

Digitalis Glycoside: Effects on other organs- CNS- central nervous system

A
  • vagal and chemoreceptor zone
    stimulation.
  • disorientation and hallucinations —
    especially in the elderly
  • visual disturbances
  • Agitation and con
59
Q

rare effect of digitalis
it is not certain whether this
effect represents a peripheral
estrogenic action of these
steroid drugs or a
manifestation of hypothalamic
stimulation.

A

Gynecomastia

60
Q

Therapeutic effects of Digoxin:

A
  1. Positive inotropic effects
  2. DEACTIVATION OF renin-angiotensin-aldosterone compensation
61
Q

Dosage Form of Digoxin: Therapeutic plasma concentration

A

0.5–1.5 ng/mL

62
Q

Dosage Form of Digoxin: Toxic plasma concentration

A

> 2 ng/mL

63
Q

Dosage Form of Digoxin: Daily dose (slow loading or maintenance)

A

0.25 (0.125–0.5) mg

64
Q

Dosage Form of Digoxin: Rapid digitalizing dose
(rarely used)

A

0.5–0.75 mg every 8 hours
for three doses

65
Q

Precautions and Monitoring: POTASSIUM- dec. potassium levels
favor digoxin binding to cardiac cells and increase its effect

A

inc. digitalis toxicity

66
Q

Precautions and Monitoring:
Inc potassium levels

This is likely in patients taking potassium, or a ______ like agent.

A

decrease digoxin binding and effect.
(2) captopril

67
Q

Precautions and Monitoring:
act synergistically with digoxin
it inc force______ of myocardial contraction.

A

CALCIUM IONS

68
Q

Precautions and Monitoring:
inversely related to digoxin activity.

A

PCOL 2 (2 decks)

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