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Drug Action I > Block 2 - CHF Physiology > Flashcards

Block 2 - CHF Physiology Flashcards

1
Q

What is HF?

A

Inability of heart to pump adequate amount of blood to meet metabolic needs

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2
Q

What are the primary HFs?

A
  1. Muscular contraction problem (decreased ejection)
  2. Muscular relaxation problem (inadequate filling)
  3. Combination of contraction and relaxation
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3
Q

What is CO?

A

Amount of blood pumped out of the heart in L/min

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4
Q

What are the systems affected by HF?

A

RAAS and SNS

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5
Q

What causes volume overload and fatigue?

A

Response to compensatory mechanism triggered by decreased CO for long term maintenance

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6
Q

What mechanisms can exacerbate HF?

A
  1. Fluid retention
  2. Vasoconstriction
  3. Myocardial stimulation
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7
Q

What are the symptoms of HF?

A
  1. Fatigue
  2. SOB
  3. Inability to exercise
  4. Swelling in extremities (edema)
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8
Q

How is HF diagnosed?

A

Increased BNP levels with HF

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9
Q

What is BNP?

A

Secreted cardiomyocytes in response to excess stretching from increased ventricular blood volume

PreproBNP → ProBNP → BNP + NT-proBNP

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10
Q

What does BNP do?

A
  1. Vasodilation → decrease resistance
  2. Naturesis and diuresis → reduced BV
  3. Decrease CO and pressure
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11
Q

What are the concepts of HF that reinforce it being a progressive disorder?

A
  1. Initial cardiac injury
  2. Compensatory mechanisms
  3. Secondary damage
  4. Cardiac decompensation
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12
Q

What kind of cardiac injury leads to HF?

A
  1. Damages of heart
  2. Impairs heart ability to contract
  3. Reduce pumping capacity of heart
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13
Q

What are the compensatory mechanisms used to control HF?

A
  1. Activate with reduction in pumping capacity
  2. Maintaining near-normal left ventricle functions (SNS, RAAS, Inflammatory mediators)
  3. Maladaptive over time
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14
Q

What are secondary damages that caused by HF?

A
  1. End organ damage (ventricle)
  2. Left venatricular remodeling
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15
Q

What are classifications of HF?

A
  1. Chamber affected
  2. Type of HF
  3. Clinical sequelae
  4. Type and timing of symptoms
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16
Q

What is left-sided HF? Outcomes?

A

Causes volume overload and venous congestion in lungs → Na+ and H2O retention → pulmonary venous congestion → Fatigue and SOB

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17
Q

What is the difference between forward and backward failure LHF?

A

F: Fails to put enough out (decreased urine, palpitations, fatigue)
B: Fails to relieve enough in (congestion, fluid buildup)

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18
Q

What is Right sided HF? Pathophys?

A
  1. Caused by LVF
  2. More vulnerable to volume overload than LV
  3. When LV fails, pulmonary venous congestion increases RV work → Generating more force → venous congestion
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19
Q

What are the results in RHF?

A
  1. Elevated jugular pressure
  2. Liver congestion
  3. Peripheral edema
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20
Q

What are the results of isolated RV failure?

A
  1. Incomplete LV filling
  2. Decreased CO
  3. Contributes to HF
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21
Q

T or F: Reduced CO is always caused by reduced contractility

A

False

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22
Q

What is SV?

A

Amount of blood pumped out of the heart with each beat

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23
Q

What is EF?

A

Percentage of blood ejected from the ventricles with each contraction

EF = SV/EDV

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24
Q

What is the difference between systolic and diastolic HF?

A

S: HF with reduced EF
D: HF with preserved EF

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25
Q

What kind of HF is a majority of cases?

A

low output HF

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26
Q

What is low-output HF?

A

Heart can’t pump a sufficient amount of blood

CO is reduced
Tissue perfusion decreases
Cells don’t receive sufficient O and nutrients

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27
Q

T or F: HF is chronic

A

True

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28
Q

How can patients manage their HF?

A
  1. Meds
  2. Low sodium
  3. Symptom monitoring
  4. Weight and vital sign monitoring
  5. Health status decision making
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29
Q

Individuals with chronic HF may develop ______ requiring ______

A

Acute decompensated HF; hospitalization

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30
Q

What are the causes of ADHF?

A
  1. Stress
  2. Infection
  3. Diet and med nonadherence
  4. Poor health
  5. High BP
  6. MI
  7. Alcohol and endocrine disorders
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31
Q

ADHF can range from ___ to ___

A

Volume overload to cariogenic shock

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32
Q

T or F: Acute HF can NOT be isolated.

A

False

Patients can recover from event but must take inotropic meds or have mechanical support

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33
Q

Classifications of heart disease are based on _____ according to the _____

A

Functional capacity; NY Heart Association

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34
Q

Describe the classes for staging HF according to NYHA?

A

Class I: Heart disease does not affect daily activities.
Class II: Heart disease causes slight activity limitations but does not cause problems at rest.
Class III: Heart disease causes marked activity limitations but does not cause problems at rest.
Class IV: Heart disease causes symptoms with any level of activity and sometimes at rest.

35
Q

What are the pros and cons of having the system based on NYHA?

A
  1. Subjective and prone to bias
  2. Difficult to define what constitutes normal activity
  3. Effective in predicting mortality
36
Q

How do ACC/AHA differ from NYHA classification of HF?

A

Based on evolution of disease

Staging can only advance and patient can’t move back

37
Q

Describe the classes for staging HF according to ACC/AHA? How is it treated?

A

A: At high risk for HF but without structural heart diseaseor symptoms of HF. Lifestyle modifications. Treatment of underlying disorder.
B: Structural heart disease but without signs or symptoms of HF. ACE inhibitors, ARBs, beta blockers, blood pressure control.
C: Structural heart disease with prior or current symptoms of HF. Diuretics, aldosterone blockers, vasodilators.
D: Refractory HF requiring specialized interventions. Heart transplantation, LV assist devices, continuous IV inotropes.

38
Q

NYHA is based on ____
ACC/AHA is based on ____
Killip classificaction is based on ____

A
  1. Functional capacity
  2. Evolution of disease
  3. Hemodynamic ability
39
Q

How does Killip differ from other stagings?

A
  1. Severity of MI in the presence of HF
  2. Based on seerity of HF symptoms that occur as a result of depression of heart muscle function
40
Q

Describe the classes for staging HF according to Killip? How is it treated?

A

I: No HF.
II: HF.
III: Severe HF.
IV: Cardiogenic shock.

41
Q

The higher the Killip class, the ___ severe ______

A

More: burden of HF

42
Q

What is used by Killip to determine the risk of death after MI?

A
  1. TIMI-RS
  2. GRACE-RS
  3. CADILLAC-RS
43
Q

What impariments does systolic HF cause? What does it effect?

A
  1. Decreased CO and BP
  2. Triggers compensatory mechanisms
  3. HF with reduced EF

Right, left, or both sides

44
Q

What are some of the causes of dilated cardiomyopathy for Systolic HF?

A
  1. Idiopathic
  2. Ischemic
  3. Familial
45
Q

What are the principles of normal heart function that are affected by systolic HF?

A
  1. CO
  2. Cardiac index
  3. Preload
  4. Afterlead
  5. Contractility
  6. Systemic vascular resistance
46
Q

How do you calculate CO?

47
Q

What is cardiac index? Normal value?

A

Obtained when CO is divided by body surface area
2.5-4.3 L/min/m^2

48
Q

What is preload?

A

The amount of blood in the ventricle before contraction

Influenced by BFV, venous return, and EF

49
Q

What is afterload?

A

The amount of pressure the heart must generate to pump blood out of the ventricle

50
Q

Right ventricle is to ____ circulation as the left ventricle is to ____ circulation

A

Pulmonary; Aortic and systemic

51
Q

What is contractility?

A

The strength of muscular contraction in the heart muscle

52
Q

T or F: Decreased contractility decreases SV.

53
Q

What is systemic vascular resistance? Normal value?

A

The resistance to forward flow of blood

800-1200 dynes/sec/cm^3

54
Q

DIfference between low and high SVR?

A

Lower: Lower pressure needed for forward flow of blood
Higher: More difficult for heart to provide forward flow

55
Q

What is a pulmonary artery catheter used to measure?

A
  1. Preload
  2. Afterload
  3. CO
56
Q

As CO decreases ___ ___ and ____ response occurs

A

EF decreases; neurohumoral

57
Q

EF decrease → ___

A
  1. Ventricular preload increases
  2. Cardiac muscle stretches
  3. Increase contractility when heart in normal (no increase if abnormal)
58
Q

What occurs in neurohumoral response?

A
  1. SNS release NE and E for BP and CO
  2. SNS activation of RAAS
59
Q

Natural responses can ____ HF by decreasing ____ ____
Neurohumoral responses lead to ____ ____ in the heart with chronic HF

A

Worsen; myocardial contractility

Physical changes

60
Q

Systolic HF doesnt affect the ____ but ____ ventricle

A

Circulation to ventricle; back up blood behind ventricle

61
Q

What are the general symptoms of systolic HF?

A
  1. Fatigue
  2. Sleep disturbances
  3. Weight loss
  4. Anorexia
  5. Dyspnea
62
Q

What are the clinical signs of SHF?

A
  1. Peripheral edema
  2. Diminished distal pulses
  3. Hypotension
  4. Tachycardia
63
Q

Pulmonary edema and hepatic congestion may develop ___

A

Cough
Frothy sputum
Right upper quad pain

64
Q

How do you diagnose Systolic HF?

A
  1. Transthoracic echocardiography
  2. Chest X-ray
  3. PRemature artial contraction
  4. Biopsy of heart muscle
  5. Coronary arteriography
65
Q

What are the goals of systolic HF?

A

Decrease fluid retention and counteract neuorhumoral effects to reduce symptoms

66
Q

What is the first line for Systolic HF?

A

ACEI

ARB for those who can’t use ACEIs

67
Q

What are the treatments for systolic HF

A
  1. Beta blockers
  2. Vasodilator
  3. Diuretic
  4. Aldosterone antagonists
68
Q

What are non pharms for Systolic HF?

A
  1. Self care
  2. Education
  3. Ca
69
Q

What is diastolic heart failure?

A

Abnormal relaxation of the heart with normal contractility
HFpEF (presevered EF)

70
Q

What are the characteristics of HFpEF?

A
  1. SIgns and symptoms of HF
  2. Normal left ventricular EF
  3. Difficulty with ventricular relaxation that decreases diastolic ventricular filling
71
Q

What are some of the outcomes of HFpEF?

A

Failure in relaxation caused by stiffness of muscle cells

Decreased ventricle filling → Decreased CO → HF

72
Q

What are soem risk factors that lead to HFpEF?

A
  1. Obesity
  2. HTN
  3. Metabolic syndrome
  4. DM
73
Q

What are clinical manifestations of diastolic HF?

A
  1. Decreased CO activates RAA
  2. Renal insufficiency
74
Q

How is Diastolic HF diagnosed?

A

None

Diagnosis by exclusion

75
Q

What are treatment with HFpEF?

A

No therapy to improves

Cautions use of diuretics

76
Q

What are the causes of LVHF?

A
  1. Cardiomyopathy
  2. CAD
  3. ALcohol
  4. HTN
  5. HFpEF
  6. Systolic HF and HFpEF
77
Q

What are the clinical manifestations of LVHF?

A
  1. Decreased BP
  2. Enlarged cardiac muscle
  3. Decreased CO
  4. Preload increase and pressure in lungs
  5. COugh
  6. Extra heart sounds
  7. Pulmonary edema
  8. Decreased tissue perfusion and hypotenstion
78
Q

How do you diagnos LVHF?

A
  1. ECG
  2. Pulmonary artery catheterization (PAC)
  3. Lab exams
79
Q

Treatment for LVHF?

A
  1. Diuretic
  2. ACEI
  3. ARB
  4. Aldosterone antagonists
  5. Beta blockers
  6. Self care
  7. Surgery
80
Q

What are the causes of RVHF?

A
  1. increased RV afterload due to left-sided HF

Pulmonary HTN → increased afterload → RV failure

Ischemia or MI

81
Q

What are the clinical manifestations of RVHF?

A
  1. Reduced CO → SNS and RAAS
  2. Mesentery edema
  3. Liver enlargement
  4. Neck vien distend and jugular pressure increase
  5. Ascites and peripheral edema
82
Q

How do you diagnose RVHF?

A
  1. MRI
  2. Transthoracic echocardiography
  3. PAC
83
Q

Treatment for RVHF?

A
  1. Treatment of RV failure
  2. Low sodium diet
  3. Diuretics
  4. Direct acting pulmonary vasodialtors
  5. Inotrope support
  6. IV inotropes
  7. Surgery

Drug Action I (32 decks)

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