Heart Failure Flashcards

(68 cards)

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
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
Cardiac AFTERload
26
Class of Heart failure: degree of effort necessary to elicit HF symptoms equals to those that would limit normal individuals.
CLASS I
27
Class of Heart failure: symptoms occurs with ordinary exertion
CLASS II
28
Class of Heart failure: symptoms occurs with less- than-ordinary exertion.
CLASS III
29
Class of Heart failure: symptoms occurs while at rest
CLASS IV
30
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)
LOW OUTPUT Heart failure
31
Can cause LOW OUTPUT Heart failure?
Dilated cardiomyopathy chronic hypertension valvular disease
32
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"
HIGH OUTPUT Heart failure
33
Can cause LOW OUTPUT Heart failure?
Hyperthyroidism, severe anemia, pregnancy, beriberi (deficiency in Vit B1: thiamine)
34
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)
Right sided Heart failure
35
the fluid portion of the blood backs up into pulmonary alveoli, producing pulmonary edema.
Left sided Heart failure
36
Sequence of Heart Flow ?
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
If the LV is unable to pump= backflow to lungs=?
pulmonary edema
38
If the RV is unable to pump= backflow to circulation= ?
peripheral edema
39
Forms of Heart failure: The ventricles cannot pump enough BLOOD. (pumping problems)
Systolic Heart Failure
40
Forms of Heart failure: The ventricles cannot fill enough BLOOD. (Filling problem)
Diastolic Heart Failure
41
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.
COMPENSATED HF
42
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.
DECOMPENDATED HF
43
Treatment Goals for Heart Failure:???
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
An ion that is responsible for initiating action potential & triggered contraction of heart muscle.
Na+ / Sodium Ion
45
an ion that is responsible for the termination of action potential & contraction (Relax) initiating Repolarization
K+/ Potassium Ion
46
This causes depolarization of the resting membrane potential=
Heart Contraction (Inotropic effect)
47
Most known Na+/K+ ATPase inhibitors drug classsification ?
INOTROPIC AGENTS
48
used in conjunction with diuretics, ACE inhibitors, βadrenergic blockers to improve the symptoms and clinical status of patients with HF Digitalis lanata/purpurea (Foxglove)
Digoxin (Lanoxin)
49
Digoxin Dec. absorption with?
Sulfasalazine, Neomycin
50
Digoxin inc. absorption with?
Erythromycin, Tetracycline
51
Digitalis Glycoside: Effects of antibiotic: Can be affected. Pathway of Excretion: Kidneys (renal clearance, water solubility) Renal impairment: Adjust dosage
Digoxin
52
53
Digitalis Glycoside: Effects of antibiotic: Not affected Pathway of Excretion: Biliary excretion Renal impairment: does not significantly prolong the half-life of ______
Digitoxin
54
MOA: inhibit Na+/K+ ATPase, the membrane-bound transporter often called the sodium pump.
Digitalis Glycoside: Pharmacodynamics
55
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
Digitalis Glycoside: Cardiac Effects
56
* 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
Electrical Effects of Digitalis Glycoside
57
Digitalis Glycoside: Effects on other organs-GIT- gastrointestinal tract
V.A.N.D *Anorexia * Nausea * Vomiting * Diarrhea
58
Digitalis Glycoside: Effects on other organs- CNS- central nervous system
* vagal and chemoreceptor zone stimulation. * disorientation and hallucinations — especially in the elderly * visual disturbances * Agitation and con
59
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.
Gynecomastia
60
Therapeutic effects of Digoxin:
1. Positive inotropic effects 2. DEACTIVATION OF renin-angiotensin-aldosterone compensation
61
Dosage Form of Digoxin: Therapeutic plasma concentration
0.5–1.5 ng/mL
62
Dosage Form of Digoxin: Toxic plasma concentration
>2 ng/mL
63
Dosage Form of Digoxin: Daily dose (slow loading or maintenance)
0.25 (0.125–0.5) mg
64
Dosage Form of Digoxin: Rapid digitalizing dose (rarely used)
0.5–0.75 mg every 8 hours for three doses
65
Precautions and Monitoring: POTASSIUM- dec. potassium levels favor digoxin binding to cardiac cells and increase its effect
inc. digitalis toxicity
66
Precautions and Monitoring: Inc potassium levels This is likely in patients taking potassium, or a ______ like agent.
decrease digoxin binding and effect. (2) captopril
67
Precautions and Monitoring: act synergistically with digoxin it inc force______ of myocardial contraction.
CALCIUM IONS
68
Precautions and Monitoring: inversely related to digoxin activity.