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SRNAAnatomy II > HF & Cardiomyopathy > Flashcards

HF & Cardiomyopathy Flashcards

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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
NEUROHORMONAL MECHANISM When is it activated? What does it do to correct?
Activated in response to DECREASED C.O. • Increase vascular resistance and intravascular volume to preserve BP and organ perfusion
26
THE 3 MOST important for neurohormonal mechanism
-Sympathetic Nervous System • Renin-angiotensin-aldosterone system • ADH
27
Mainly neurohormonal will attempt to
INCREASE SV
28
SNS How does it regulate? ____________sensed by ________ It works by ___________
- Decreased CO sensed by baroreceptors | – increased sympathetic outflow
29
The RAAS is activated when __________leading to ____________ -->___________
There is decreased renal artery perfusion pressure--> stimulate release of RENIN --> Angiontensin II
30
ADH (Vasopressin) stimulates kidney to _______Via receptors _______
Reabsorb water ; receptor V2 ( think H2O)
31
ADH (Vasopressin) stimulates ________Via which receptors ?
Vasoconstriction (V1)
32
Neurohormonal activation initially ______overtime
Although initially beneficial, continued activation | proves harmful.
33
Ventricular Hypertrophy and REMODELING (DSM)
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.
34
Pattern of remodeling depends on
whether ventricle subjected to chronic volume or pressure | overload
35
Volume overload causes “______________”Define
“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
Pressure overload causes “____________" Think PC Define
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
TX Acute Pulmonary Edema (LMNOP)
``` Lasix • Morphine • Nitrates • Oxygen • Position ```
38
DILATED CARDIOMYOPATHY
LV (or bivent.) dilation with nearly normal wall thickness | • Systolic dysfunction present
39
DILATED CARDIOMYOPATHY ETIOLOGY
Etiology is genetic or assoc’d. with viral infection (coxsackie B) – normally self-limited. Myocardial fibrosis from immune-mediated injury.
40
HYPERTROPHIC Cardiomyopathy (ESEA) AFFECT ______ ETIOLOGy _______ SX:
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
• Most common cardiac abnormality in young athletes who die suddenly with activity.
HYPERTROPHIC CARDIMYOPATHY
42
``` HYPERTROPHIC Cardiomyopathy (LVOTO) Why does obstruction develop? ```
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
Valvular disease associated with hypertrophic cardiomyopathy?
Mitral REGURGITATION
44
HYPETROPHIC CARdioMYOPATHY symptoms | SADS
Sudden cardiac death Angina Dyspna Syncope
45
``` Restrictive CARDIOMYOPATHY (SAAC) MOST COMMON CAUSE ```
“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
Tx of dilated Cardiomyopahty (READ)
``` Treatment: – Similar to HF – General supportive measures – rest - Decreased physical activity ```
47
What are the end results of increased renin secretion?
Renin --> Angiotensin II leading to vasoconstriction Stimulates thirst response to increase water intake Stimulates aldosterone release from adrenal cortx
48
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 _______________
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
By what mechanism does ADH affect the CV system?
Vasopressin” • Stim. Kidney to reabsorb water (v2 receptors) • Stim. vasoconstriction (v1 receptors)
50
Chamber radius enlarges in proportion to wall thickness
ECCENTRIC
51
Wall thickness increases without proportional chamber | dilation
CONCENTRICL
52
CLASS I NYHA
NO limitation of physical activity
53
CLASS II NYHA
Slight limitation of activitly . Dyspnea and fatigue with moderate exertion (walking upstairs quickly)
54
CLASS III NYHA
Marked limitation of activity. DYSPNEA with minimal exertion (slowly walking upstairs)
55
CLASS IV NYHA
Severe limitation of activity. Symptoms are present even at rest.
56
Three major determinants of SV: (PAC)
Preload Afterload Contractility
57
Preload
Stretch on the ventricular fibers just before contraction , approximated by EDV
58
Contractility is
Property of heart that accounts for changes in the strength of contraction, independent of preload and afterload.
59
Afterload
The force that must be overcome for the ventricle to eject its contents
60
Stages of Chronic HF : Stage A
Patient at risk for developing HF not yet developed structural cardiac dysfunction (pt with CAD, HTN, family hx of cardiomyopathy)
61
Stages of Chronic HF : Stage B
The patient with STRUCTURAL heart disease with HF but NOT YET DEVELOPED SYMPTOMS
62
Stages of Chronic HF : Stage C
The patient with current or prior symptoms of HF associated with structural Heart disease
63
Stages of Chronic HF : Stage D
The patient with structural heat disease and REFRACTORY HF symptoms DESPITE MAXIMAL THERAPY requires advanced interventions.
64
Profile A : ______ means (WD)
``` 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
Profile B : ________means (WW)
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
PROFILE C is more ________ as there are (CW)
COLD and WET MORE SERIOUS 1. YES to ELEVATION of FILLING pressure 2. YES to signs of DECREASED CO and reduced tissue perfusion
67
PROFILE L__________ (CD)
COLD and DRY 1. NO LV filling pressure increase 2. YES to signs of decreased CO and reduced tissue perfusion
68
Pharmacological treatment for HF: Diuretics use B blockers with caution why?
•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
Pharmacological treatment for HF: Diuretics
•Diuretics: Decrease fluid & pulmonary congestion | overuse can cause decrease in C.O.
70
Pharmacological treatment for HF: VASODILATORS - 4 meds classes that Decrease preload, improve pulmonary congestion - Med class that DECREASE AFTERLOAD and increase SV
•Vasodilators and Venous (Nitrates) •ACE inhibitors •ARBs Arterial α blockers (Hydralazine) - Decrease afterload, Increase SV
71
Pharmacologic treatment of Inotropic Drugs: ___SV and C.O. | 3 classes
Increase •β agonists •Digitalis •Phosphodiesterase inhibitors
72
Pharmacologic treatment β blockers: use with caution –
blunts SNS
73
EF = example SV --> 70 EDV --> 120
SV/EDV | 70/120 --> 58% normal range
74
EF = example SV --> 70 EDV --> 120
SV/EDV 70/120 --> 58% normal range 46 ml/ --> 58% Diastolic HF 80 m
75
Vascular consequences of HF
Peripheral Edema & Hepatomegaly in RHF | VASCULAR CONGESTION
76
HF with reduced EF
SYSTOLIC
77
HF with preserved EF
DIASTOLIC
78
Conditions that causes Left side HF: Systolic dysfunction or _______EF heart failure
REDUCED Impaired contractility Increase afterload (Chronic pressure overload)
79
For left side HF, systolic dysfunction : Impaired contracitility caused by 3 things:
1. CAD (MI and Transient myocardial ischemia 2. Chronic volume overload (Mitral and aortic regurg.) 3. Dilated cardiomyopathies
80
For left side HF, systolic dysfunction : Increase afterload (Chronic pressure overload) caused y 2 things
1. Advanced Aortic Stenosis | 2. Uncontrolled Severe HTN
81
CAUSES of LEFT sided HF : Diastolic dysfunction or ________EF Heart failure caused
PRESERVED | Impaired Diastolic Filling
82
5 Conditions causing IMPAIRED DIASTOLIC FILLING are | LRMTP
1. LVH 2. Restrictive Cardimyopathy 3. Myocardial Fibrosis 4. Transient myocardial ischemia 5. Pericardial Constriction or tamponade
83
Abnormal EF range
40-55%
84
Restrictive cardiomyopathy tx (PISA)
poor prognoiss Iron Chelation (amyloidosis) Salt reduction Anticoagulation ( prone to IV thrombus)
85
MARKED LV hypertrophy
HYPERTROPHYIC CARDIOMYOPATHY
86
What causes dyspnea in Hypertrophic cardiomyopathy
Myocyte hypertrophy --> LVH --> Impaired relaxation (diastolic dysfunction)--> increased LVEDP
87
What causes ANGINA in Hypertrophic cardiomyopathy
Dynamic LDOVO --> increase Systolic pressure -->Increase MVO2 --> ANGINA

SRNAAnatomy II (16 decks)

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