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SRNAAnatomy II > HF & Cardiomyopathy > Flashcards

HF & Cardiomyopathy Flashcards

1
Q

Effects of INCREASED Afterload result in:

Comment on ventricular pressure, ESV, SV

A

Increased Ventricular pressure
Increased ESV
Decreased SV

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2
Q

Effects of INCREASED PRELOAD

SV and ESV

A

Sequential increases result in

INCREASED SV, but constant ESV

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3
Q

Effects of INCREASED Contractility
result in:
SV/ ESV

A
  • INCREASED SV

* DECREASED ESV

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4
Q

Systolic HF

A

HF with reduced EF
• Weakened, thinned heart wall muscle
– Decreased force of contraction (Decreased inotropy), decreased SV

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5
Q

Underlying causes of myocyte damage/death:

A

Cardiomyopathies (weakens muscle)
– CAD, MI (Decreased blood supply)
– Valve Ds. (Increased O2 demand)
– Arrhythmias (Increased O2 demand)

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6
Q

Increased work –>

A 
Decreased pumping ability
Increased Muscle death
increased oxygen demand
Increased work 
START OVER AGAINT (VICIOUS CYCLE)
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7
Q

SV formula

A

EDV- ESV

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8
Q

Decreased contractility = _____ESV & _____SV

A

Increased, Decreased

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9
Q

Normal venous return add to

A

Normal venous return adds to higher-than-normal ESV = INCREASED EDV

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10
Q

INCREASED EDV has compensatory function by partially elevating

A

SV toward normal via Frank-Starling mechanism (INCREASED Preload)

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11
Q

DIASTOLIC HF is

A

“HF with preserved EF”

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12
Q

In diastolic HF what is impaired?

EDV is ______and SV is _________

A

Reduced compliance =
– Impaired relaxation and filling
– Decreased EDV = Decreased SV

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13
Q

Underlying causes of enlarged, stiffened muscle:

COSH

A

– HTN
– SL Valve stenosis
– Cardiomyopathies
– Other (Age, CAD, etc)

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14
Q

Cycle of damage in diastolic HF

A

Increased pumping Resistance
Increased muscle
Increased oxygen demand
Increased cell death/stiffening

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15
Q

Normal EF

A

55-70%

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16
Q

EF less than 40

A

HF range

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17
Q

EF formula

A

SV/EDV

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18
Q

In diastolic HF, stiff wall leads to ? filling is ______, EDV is ______And SV is ________

A

Stiff wall = Decreased filling =Decreased EDV & Decreased SV

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19
Q

Curve is shifted upward ________ at

any diastolic volume, what pressure is higher?

A

ventricular pressure is higher than normal.

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20
Q

cor pulmonale”

A

Right-sided heart disease. that results from a PRIMARY

pulmonary process

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21
Q 
Core pulmonale (RIGHT SIDED HF) is related to 
(systolic and diastolic) 
Pulmonary CIAC
Cardiac (LPR)
Respiratory (PP)
A

Pulmonary Parenchymal disease (CACI)

  • COPD
  • Insterstitial lung disease
  • Adult Resp distress syndrome
  • Chronic lung infection or bronchiectasis

Cardiac Causes

  • Left sided HF
  • Pulmonic Valve stenosis
  • RV infarction

Respiratory
Pulmonary embolism
Pulmonary HTN

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22
Q

Compensatory Mechanisms
• Frank-Starling mechanism
• Neurohormonal alterations
• Ventricular hypertrophy and remodeling

A

• Natural compensatory mechanisms activated in
decreased C.O. to buffer HF and maintain BP &
organ perfusion

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23
Q

Compensatory Mechanisms

what are the (3)

A
  • Frank-Starling mechanism
  • Neurohormonal alterations
  • Ventricular hypertrophy and remodeling
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24
Q

FRANK STARLING MECHANISM
________SV = Increased EDV higher than normal
What activates the Frank Starling? inducing ________and ________to preserve ________
What happens in Severe HF? _______which leads to _____________

A

Decreased SV = Increased EDV higher-than-normal
• Stretching LV activating Frank-Starling mechanism,
inducing greater contractility & Increased SV, preserving forward output
• Unfortunately, in severe HF, contractility is depressed, resulting in retrograde pressure to atria and pulmonary veins –> Pulmonary congestion and edema

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25
Q

NEUROHORMONAL MECHANISM
When is it activated?
What does it do to correct?

A

Activated in response to DECREASED C.O.
• Increase vascular resistance and intravascular volume
to preserve BP and organ perfusion

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26
Q

THE 3 MOST important for neurohormonal mechanism

A

-Sympathetic Nervous System
• Renin-angiotensin-aldosterone system
• ADH

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27
Q

Mainly neurohormonal will attempt to

A

INCREASE SV

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28
Q

SNS How does it regulate?
____________sensed by ________
It works by ___________

A
  • Decreased CO sensed by baroreceptors

– increased sympathetic outflow

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29
Q

The RAAS is activated when __________leading to ____________ –>___________

A

There is decreased renal artery perfusion pressure–> stimulate release of RENIN –> Angiontensin II

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30
Q

ADH (Vasopressin) stimulates kidney to _______Via receptors _______

A

Reabsorb water ; receptor V2 ( think H2O)

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31
Q

ADH (Vasopressin) stimulates ________Via which receptors ?

A

Vasoconstriction (V1)

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32
Q

Neurohormonal activation initially ______overtime

A

Although initially beneficial, continued activation

proves harmful.

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33
Q

Ventricular Hypertrophy and REMODELING (DSM)

A

Develop over time in response to hemodynamic burdens.
• Sustained Increased in wall stress stimulates hypertrophy and deposition of extracellular matrix = Increased mass of muscle fibers.
• Maintains contractile force; counteracts wall stress.

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34
Q

Pattern of remodeling depends on

A

whether ventricle subjected to chronic volume or pressure

overload

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35
Q

Volume overload causes “______________”Define

A

“eccentric hypertrophy”
– Results in synthesis of new sarcomeres in series with the old, causing myocytes to enlongate.
– Chamber radius enlarges in proportion to wall thickness.

36
Q

Pressure overload causes “____________” Think PC Define

A

concentric hypertrophy
– Results in synthesis of new sarcomeres in parallel with
the old, causing myocytes to thicken instead of elongate.
– Wall thickness increases without proportional chamber
dilation = substantially DECREASED wall stress.

37
Q

TX Acute Pulmonary Edema (LMNOP)

A 
Lasix
• Morphine
• Nitrates
• Oxygen
• Position
38
Q

DILATED CARDIOMYOPATHY

A

LV (or bivent.) dilation with nearly normal wall thickness

• Systolic dysfunction present

39
Q

DILATED CARDIOMYOPATHY ETIOLOGY

A

Etiology is genetic or assoc’d. with viral infection (coxsackie B) – normally self-limited. Myocardial
fibrosis from immune-mediated injury.

40
Q

HYPERTROPHIC Cardiomyopathy (ESEA)

AFFECT ______
ETIOLOGy _______

SX:

A

Excessive hypertrophy of ventricular wall.
Systolic contractile function is vigorous but thickened muscle is stiff = impaired relaxation and INCREASED diastolic pressures.
Affects 1 in 500 gen. pop.
Etiology: genetic

Sx –> all HF symptoms + systemic embolization from mural thrombi

41
Q

• Most common cardiac abnormality in young athletes who die suddenly with activity.

A

HYPERTROPHIC CARDIMYOPATHY

42
Q 
HYPERTROPHIC Cardiomyopathy (LVOTO) 
Why does obstruction develop?
A

LV outflow tract obstruction (LVOTO) develops from septal thickening and venturi effect that displaces anterior mitral leaflet during systole. Blocks outflow tract.
• Mitral regurgitation occurs.

43
Q

Valvular disease associated with hypertrophic cardiomyopathy?

A

Mitral REGURGITATION

44
Q

HYPETROPHIC CARdioMYOPATHY symptoms

SADS

A

Sudden cardiac death
Angina
Dyspna
Syncope

45
Q 
Restrictive CARDIOMYOPATHY (SAAC)
MOST COMMON CAUSE
A

“Stiff” LV with impaired diastolic relaxation but normal systolic function. No wall thickening.
• Amyloidosis is most common cause. Results in fibrosis/scarring of myocardium.
• Amyloid fibrils deposit in the tissues, including the
heart.
• Congo red birefringence stain:

46
Q

Tx of dilated Cardiomyopahty (READ)

A 
Treatment:
– Similar to HF
– General supportive measures
– rest
- Decreased physical activity
47
Q

What are the end results of increased renin secretion?

A

Renin –> Angiotensin II leading to vasoconstriction
Stimulates thirst response to increase water intake
Stimulates aldosterone release from adrenal cortx

48
Q

Neurohormonal alteration eventually becomes harmful by
5 effects
1. Increase vol. and venous return =_________
2. Increased vasoconstriction = _______eventually impairs ________ = __________C.O.
3. INCREASED HR = ________________
4. Increased Epi/Norepi__________ and
___________= ________notropic response.
5. Increase ANGIOTENSIN II and Aldosterone provoke _______________

A
  1. Increase vol. and venous return = Increased pulmonary congestion.
  2. Increased vasoconstriction = Increased afterload, eventually impairs Stroke Volume = DECREASED C.O.
  3. INCREASED HR = INCREASED Oxygen demand.
  4. Increased Epi/Norepi down regulates β-receptors and
    up-regulates inhibitory G proteins = Decrease inotropic response.
  5. Increase ANGIOTENSIN II & Aldosterone provoke inflammatory cytokines, macrophages, fibroblasts fibrosis & adverse remodeling of heart wall.
49
Q

By what mechanism does ADH affect the CV system?

A

Vasopressin”
• Stim. Kidney to reabsorb water (v2 receptors)
• Stim. vasoconstriction (v1 receptors)

50
Q

Chamber radius enlarges in proportion to wall thickness

A

ECCENTRIC

51
Q

Wall thickness increases without proportional chamber

dilation

A

CONCENTRICL

52
Q

CLASS I NYHA

A

NO limitation of physical activity

53
Q

CLASS II NYHA

A

Slight limitation of activitly . Dyspnea and fatigue with moderate exertion (walking upstairs quickly)

54
Q

CLASS III NYHA

A

Marked limitation of activity. DYSPNEA with minimal exertion (slowly walking upstairs)

55
Q

CLASS IV NYHA

A

Severe limitation of activity. Symptoms are present even at rest.

56
Q

Three major determinants of SV: (PAC)

A

Preload
Afterload
Contractility

57
Q

Preload

A

Stretch on the ventricular fibers just before contraction , approximated by EDV

58
Q

Contractility is

A

Property of heart that accounts for changes in the strength of contraction, independent of preload and afterload.

59
Q

Afterload

A

The force that must be overcome for the ventricle to eject its contents

60
Q

Stages of Chronic HF : Stage A

A

Patient at risk for developing HF not yet developed structural cardiac dysfunction (pt with CAD, HTN, family hx of cardiomyopathy)

61
Q

Stages of Chronic HF : Stage B

A

The patient with STRUCTURAL heart disease with HF but NOT YET DEVELOPED SYMPTOMS

62
Q

Stages of Chronic HF : Stage C

A

The patient with current or prior symptoms of HF associated with structural Heart disease

63
Q

Stages of Chronic HF : Stage D

A

The patient with structural heat disease and REFRACTORY HF symptoms DESPITE MAXIMAL THERAPY requires advanced interventions.

64
Q

Profile A : ______ means (WD)

A 
WARM and DRY
NORMAL hemodynamics 
CV symptoms due to other than HF
1. NO elevation of LV filling pressure
2. No signs of Decreased CO and reduced tissue  perfusion
65
Q

Profile B : ________means (WW)

A

WARM and WET
WET lungs But PRESERVED TISSUE PERFUSION
1. YES elevation of LV pressure
2. NO signs of decreased CO and reduced tissue perfusion

66
Q

PROFILE C is more ________ as there are (CW)

A

COLD and WET
MORE SERIOUS
1. YES to ELEVATION of FILLING pressure
2. YES to signs of DECREASED CO and reduced tissue perfusion

67
Q

PROFILE L__________ (CD)

A

COLD and DRY

  1. NO LV filling pressure increase
  2. YES to signs of decreased CO and reduced tissue perfusion
68
Q

Pharmacological treatment for HF: Diuretics

use B blockers with caution why?

A

•Diuretics: Decrease fluid & pulmonary congestion
(overuse can cause decrease in C.O.)

•Arterial α blockers (Hydralazine) -
Decrease afterload, Increase SV
•ACE inhibitors
•ARBs

  • Inotropic Drugs: increase SV and C.O.
  • β agonists
  • Digitalis
  • Phosphodiesterase inhibitors
  • Aldosterone antagonists (spironolactone)
  • β blockers: use with caution – blunts SNS
69
Q

Pharmacological treatment for HF: Diuretics

A

•Diuretics: Decrease fluid & pulmonary congestion

overuse can cause decrease in C.O.

70
Q

Pharmacological treatment for HF: VASODILATORS

  • 4 meds classes that Decrease preload, improve pulmonary congestion
  • Med class that DECREASE AFTERLOAD and increase SV
A

•Vasodilators and Venous (Nitrates) •ACE inhibitors
•ARBs
Arterial α blockers (Hydralazine) - Decrease afterload, Increase SV

71
Q

Pharmacologic treatment of Inotropic Drugs: ___SV and C.O.

3 classes

A

Increase
•β agonists
•Digitalis
•Phosphodiesterase inhibitors

72
Q

Pharmacologic treatment β blockers: use with caution –

A

blunts SNS

73
Q

EF =
example SV –> 70
EDV –> 120

A

SV/EDV

70/120 –> 58% normal range

74
Q

EF =
example SV –> 70
EDV –> 120

A

SV/EDV
70/120 –> 58% normal range
46 ml/ –> 58% Diastolic HF
80 m

75
Q

Vascular consequences of HF

A

Peripheral Edema & Hepatomegaly in RHF

VASCULAR CONGESTION

76
Q

HF with reduced EF

A

SYSTOLIC

77
Q

HF with preserved EF

A

DIASTOLIC

78
Q

Conditions that causes Left side HF: Systolic dysfunction or _______EF heart failure

A

REDUCED
Impaired contractility
Increase afterload (Chronic pressure overload)

79
Q

For left side HF, systolic dysfunction : Impaired contracitility caused by 3 things:

A
  1. CAD (MI and Transient myocardial ischemia
  2. Chronic volume overload (Mitral and aortic regurg.)
  3. Dilated cardiomyopathies
80
Q

For left side HF, systolic dysfunction : Increase afterload (Chronic pressure overload) caused y 2 things

A
  1. Advanced Aortic Stenosis

2. Uncontrolled Severe HTN

81
Q

CAUSES of LEFT sided HF : Diastolic dysfunction or ________EF Heart failure caused

A

PRESERVED

Impaired Diastolic Filling

82
Q

5 Conditions causing IMPAIRED DIASTOLIC FILLING are

LRMTP

A
  1. LVH
  2. Restrictive Cardimyopathy
  3. Myocardial Fibrosis
  4. Transient myocardial ischemia
  5. Pericardial Constriction or tamponade
83
Q

Abnormal EF range

A

40-55%

84
Q

Restrictive cardiomyopathy tx (PISA)

A

poor prognoiss
Iron Chelation (amyloidosis)
Salt reduction
Anticoagulation ( prone to IV thrombus)

85
Q

MARKED LV hypertrophy

A

HYPERTROPHYIC CARDIOMYOPATHY

86
Q

What causes dyspnea in Hypertrophic cardiomyopathy

A

Myocyte hypertrophy –> LVH –> Impaired relaxation (diastolic dysfunction)–> increased LVEDP

87
Q

What causes ANGINA in Hypertrophic cardiomyopathy

A

Dynamic LDOVO –> increase Systolic pressure –>Increase MVO2 –> ANGINA

SRNAAnatomy II (16 decks)

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