HF & Cardiomyopathy Flashcards
Effects of INCREASED Afterload result in:
Comment on ventricular pressure, ESV, SV
Increased Ventricular pressure
Increased ESV
Decreased SV
Effects of INCREASED PRELOAD
SV and ESV
Sequential increases result in
INCREASED SV, but constant ESV
Effects of INCREASED Contractility
result in:
SV/ ESV
- INCREASED SV
* DECREASED ESV
Systolic HF
HF with reduced EF
• Weakened, thinned heart wall muscle
– Decreased force of contraction (Decreased inotropy), decreased SV
Underlying causes of myocyte damage/death:
Cardiomyopathies (weakens muscle)
– CAD, MI (Decreased blood supply)
– Valve Ds. (Increased O2 demand)
– Arrhythmias (Increased O2 demand)
Increased work –>
Decreased pumping ability Increased Muscle death increased oxygen demand Increased work START OVER AGAINT (VICIOUS CYCLE)
SV formula
EDV- ESV
Decreased contractility = _____ESV & _____SV
Increased, Decreased
Normal venous return add to
Normal venous return adds to higher-than-normal ESV = INCREASED EDV
INCREASED EDV has compensatory function by partially elevating
SV toward normal via Frank-Starling mechanism (INCREASED Preload)
DIASTOLIC HF is
“HF with preserved EF”
In diastolic HF what is impaired?
EDV is ______and SV is _________
Reduced compliance =
– Impaired relaxation and filling
– Decreased EDV = Decreased SV
Underlying causes of enlarged, stiffened muscle:
COSH
– HTN
– SL Valve stenosis
– Cardiomyopathies
– Other (Age, CAD, etc)
Cycle of damage in diastolic HF
Increased pumping Resistance
Increased muscle
Increased oxygen demand
Increased cell death/stiffening
Normal EF
55-70%
EF less than 40
HF range
EF formula
SV/EDV
In diastolic HF, stiff wall leads to ? filling is ______, EDV is ______And SV is ________
Stiff wall = Decreased filling =Decreased EDV & Decreased SV
Curve is shifted upward ________ at
any diastolic volume, what pressure is higher?
ventricular pressure is higher than normal.
cor pulmonale”
Right-sided heart disease. that results from a PRIMARY
pulmonary process
Core pulmonale (RIGHT SIDED HF) is related to (systolic and diastolic) Pulmonary CIAC Cardiac (LPR) Respiratory (PP)
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
Compensatory Mechanisms
• Frank-Starling mechanism
• Neurohormonal alterations
• Ventricular hypertrophy and remodeling
• Natural compensatory mechanisms activated in
decreased C.O. to buffer HF and maintain BP &
organ perfusion
Compensatory Mechanisms
what are the (3)
- Frank-Starling mechanism
- Neurohormonal alterations
- Ventricular hypertrophy and remodeling
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 _____________
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
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
THE 3 MOST important for neurohormonal mechanism
-Sympathetic Nervous System
• Renin-angiotensin-aldosterone system
• ADH
Mainly neurohormonal will attempt to
INCREASE SV
SNS How does it regulate?
____________sensed by ________
It works by ___________
- Decreased CO sensed by baroreceptors
– increased sympathetic outflow
The RAAS is activated when __________leading to ____________ –>___________
There is decreased renal artery perfusion pressure–> stimulate release of RENIN –> Angiontensin II
ADH (Vasopressin) stimulates kidney to _______Via receptors _______
Reabsorb water ; receptor V2 ( think H2O)
ADH (Vasopressin) stimulates ________Via which receptors ?
Vasoconstriction (V1)
Neurohormonal activation initially ______overtime
Although initially beneficial, continued activation
proves harmful.
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.
Pattern of remodeling depends on
whether ventricle subjected to chronic volume or pressure
overload
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.
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.
TX Acute Pulmonary Edema (LMNOP)
Lasix • Morphine • Nitrates • Oxygen • Position
DILATED CARDIOMYOPATHY
LV (or bivent.) dilation with nearly normal wall thickness
• Systolic dysfunction present
DILATED CARDIOMYOPATHY ETIOLOGY
Etiology is genetic or assoc’d. with viral infection (coxsackie B) – normally self-limited. Myocardial
fibrosis from immune-mediated injury.
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
• Most common cardiac abnormality in young athletes who die suddenly with activity.
HYPERTROPHIC CARDIMYOPATHY
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.
Valvular disease associated with hypertrophic cardiomyopathy?
Mitral REGURGITATION
HYPETROPHIC CARdioMYOPATHY symptoms
SADS
Sudden cardiac death
Angina
Dyspna
Syncope
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:
Tx of dilated Cardiomyopahty (READ)
Treatment: – Similar to HF – General supportive measures – rest - Decreased physical activity
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
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 _______________
- Increase vol. and venous return = Increased pulmonary congestion.
- Increased vasoconstriction = Increased afterload, eventually impairs Stroke Volume = DECREASED C.O.
- INCREASED HR = INCREASED Oxygen demand.
- Increased Epi/Norepi down regulates β-receptors and
up-regulates inhibitory G proteins = Decrease inotropic response. - Increase ANGIOTENSIN II & Aldosterone provoke inflammatory cytokines, macrophages, fibroblasts fibrosis & adverse remodeling of heart wall.
By what mechanism does ADH affect the CV system?
Vasopressin”
• Stim. Kidney to reabsorb water (v2 receptors)
• Stim. vasoconstriction (v1 receptors)
Chamber radius enlarges in proportion to wall thickness
ECCENTRIC
Wall thickness increases without proportional chamber
dilation
CONCENTRICL
CLASS I NYHA
NO limitation of physical activity
CLASS II NYHA
Slight limitation of activitly . Dyspnea and fatigue with moderate exertion (walking upstairs quickly)
CLASS III NYHA
Marked limitation of activity. DYSPNEA with minimal exertion (slowly walking upstairs)
CLASS IV NYHA
Severe limitation of activity. Symptoms are present even at rest.
Three major determinants of SV: (PAC)
Preload
Afterload
Contractility
Preload
Stretch on the ventricular fibers just before contraction , approximated by EDV
Contractility is
Property of heart that accounts for changes in the strength of contraction, independent of preload and afterload.
Afterload
The force that must be overcome for the ventricle to eject its contents
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)
Stages of Chronic HF : Stage B
The patient with STRUCTURAL heart disease with HF but NOT YET DEVELOPED SYMPTOMS
Stages of Chronic HF : Stage C
The patient with current or prior symptoms of HF associated with structural Heart disease
Stages of Chronic HF : Stage D
The patient with structural heat disease and REFRACTORY HF symptoms DESPITE MAXIMAL THERAPY requires advanced interventions.
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
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
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
PROFILE L__________ (CD)
COLD and DRY
- NO LV filling pressure increase
- YES to signs of decreased CO and reduced tissue perfusion
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
Pharmacological treatment for HF: Diuretics
•Diuretics: Decrease fluid & pulmonary congestion
overuse can cause decrease in C.O.
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
Pharmacologic treatment of Inotropic Drugs: ___SV and C.O.
3 classes
Increase
•β agonists
•Digitalis
•Phosphodiesterase inhibitors
Pharmacologic treatment β blockers: use with caution –
blunts SNS
EF =
example SV –> 70
EDV –> 120
SV/EDV
70/120 –> 58% normal range
EF =
example SV –> 70
EDV –> 120
SV/EDV
70/120 –> 58% normal range
46 ml/ –> 58% Diastolic HF
80 m
Vascular consequences of HF
Peripheral Edema & Hepatomegaly in RHF
VASCULAR CONGESTION
HF with reduced EF
SYSTOLIC
HF with preserved EF
DIASTOLIC
Conditions that causes Left side HF: Systolic dysfunction or _______EF heart failure
REDUCED
Impaired contractility
Increase afterload (Chronic pressure overload)
For left side HF, systolic dysfunction : Impaired contracitility caused by 3 things:
- CAD (MI and Transient myocardial ischemia
- Chronic volume overload (Mitral and aortic regurg.)
- Dilated cardiomyopathies
For left side HF, systolic dysfunction : Increase afterload (Chronic pressure overload) caused y 2 things
- Advanced Aortic Stenosis
2. Uncontrolled Severe HTN
CAUSES of LEFT sided HF : Diastolic dysfunction or ________EF Heart failure caused
PRESERVED
Impaired Diastolic Filling
5 Conditions causing IMPAIRED DIASTOLIC FILLING are
LRMTP
- LVH
- Restrictive Cardimyopathy
- Myocardial Fibrosis
- Transient myocardial ischemia
- Pericardial Constriction or tamponade
Abnormal EF range
40-55%
Restrictive cardiomyopathy tx (PISA)
poor prognoiss
Iron Chelation (amyloidosis)
Salt reduction
Anticoagulation ( prone to IV thrombus)
MARKED LV hypertrophy
HYPERTROPHYIC CARDIOMYOPATHY
What causes dyspnea in Hypertrophic cardiomyopathy
Myocyte hypertrophy –> LVH –> Impaired relaxation (diastolic dysfunction)–> increased LVEDP
What causes ANGINA in Hypertrophic cardiomyopathy
Dynamic LDOVO –> increase Systolic pressure –>Increase MVO2 –> ANGINA
