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Year 1: Patho/Pharm > Heart Failure_PATHO > Flashcards

Heart Failure_PATHO Flashcards

1
Q

Heart Failure
Definition

A

Change in heart structure results in dysfunction

Not able to pump

Decreased CO

Unable to meet metabolic demands of body, results in systemic symptoms (including pulmonary)

Clinical Syndrome

Chronic and progressive

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2
Q

Heart Failure
Incidence

A

increase with age

50% die in 5 years

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3
Q

Fomulae
Cardiac output

A

CO = HR x Stroke volume
4-8L/minute

HR (60-100bpm)
- SNS: beta 1 stimuli NE results in increased heart beat, contraction, conduction
- PNS: acetylcholine stimuli, decrease heart rate, beat, contraction

Stroke volume (70mL/beat)
- preload (blood return to heart, stretch at diastole)
- afterload (pressure pump against, PVR)
- contractility (myocardium force of contraction, Frank starling law)

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4
Q

Beta 1 receptors and HF
Heart and Kidney Compensation

A

HF: Decrease CO
- anaerobic metabolism = decrease pH = activation medulla = SNS activation
- decrease in BP = activation baroreceptors = SNS activation = NE release = beta 1 receptor activation

beta 1 receptors on heart and kidney
MOA
G protein activation
cAMP signal
Open calcium channels
influx calcium
depolarization

Heart:
increase contractility (phase II fast AP)
increase conduction and heart rate (phase 0 and 4 slow AP)
- increase CO

Kidney
increase renin release (RAAS)
angiotensin II: vasoconstriction, SNS stimuli, remodelling, aldosterone release
aldoesterone: Na/water reabsorption, higher baroreceptor setpoint, NE increased, heart remodelling
- increase preload (venous return)
- increase CO

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5
Q

Stroke Volume and HF
Contractility compensation

A

HF decrease CO
Decrease blood pressure
trigger activation baroreceptors (medulla)
activation SNS and release NE
activation beta 1 receptors

phase II fast AP
influx calcium
depoloarization and contraction of myocardium
increase force of contraction

Increase vasoconstriction alpha 1 (veins) and arteries; and angiotensin II vasoconstriction (veins) and arteries
- increase preload
- increase stretch, increase force of contraction (normal heart, Frank-starling Law)

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6
Q

Preload
Definition and factors that increase/decrease

A

Preload
- amount of cardiac stretch at the end of diastole
- venous return to the heart
- blood remaining in ventricles/atrium after contraction

Factors that increase preload
- blood products
- volume expanders
- ADH, aldosterone (absorption water, sodium)
- valvular regurgitation
* increase volume

Factors that decrease preload
- hemorrhages
- vasodilators (CCB), diuretics
*loss of volume

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7
Q

Afterload
Definition factors that increase / decrease

A

Afterload
- pressure heart has to pump against to eject blood

Factors that increase
- HTN
- stenosis
- vasoconstrictors (ex. dopamine)

Factors that decrease
- hypotension
- vasodilators
- ACE, ARB, nitrates

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8
Q

Frank Starling Curve
Heart Failure vs. Normal

A

Frank Starling Curve
- Y axis: CO or stroke volume
- X axis: Left ventricular end diastolic volume (preload, stretch)

Normal physiology
- increase stretch (preload), increase contractility, increase cardiac output (stroke volume)
- shift LEFT

Heart failure
- change in structure and function of heart (myocytes)
- increase stretch (preload), no increase/decrease contracitlity, no change/decrease in cardiac output (stroke volume)
- SHIFT RIGHT

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9
Q

Pathogenesis of Heart Failure
Systems involved

A
  1. Heart and vasculature
    - injury, inflammation
    - remodelling
    - change in structure and function
    - decrease CO
  2. Compensation: SNS, RAAS, ADH
    - CO = HR x SV
    - SNS: increase HR, conduction; increase contractility (SV)
    - RAAS: vasoconstriction (angiotensin II, SNS activation; increase preload/venous return), fluid volume retention (aldosterone release; increase preload)
    - ADH: fluid volume retention (preload; SV)
  3. Decompensation: SNS, RAAS, ADH
    - SNS: increased workload of heart = ischemia = inflammation = remodelling = damage = decrease CO
    - RAAS: vascular / heart remodelling (angiotensin II, aldosterone), increase afterload from vasoconstriction increases workload of heart ischemia, inflammation, remodelling (decrease CO), FVO, edema, back up blood pulmonary and systemic venous system
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10
Q

Natriuretic Peptides
Physiological Antagonists

A

HF = decrease CO
= increase end diastolic volume (preload)
= atrial and ventricle stretch

release natriuretic peptides
ANP = atrial natriuretic peptide
BNP = bone natriuretic peptide (ventricles)

  1. excretion salt and water from distal tubules
  2. vasodilation

*BNP diagnostic for HF
*prognostic for HF
- use to determine therapeutic working
>30% increase from baseline BAD sign

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11
Q

Cycle of HF

A
  1. ischemia, injury, remodelling, dysfunction
  2. decrease CO
  3. Activation neuro-humoral system (baroreceptors carotid and aortic bodies, activation SNS)
  4. Activaiton SNS, ADH and RAAS
  5. Retention fluid, vasoconstriction, vascular and cardiac remodelling, increase SNS activity = self perpetuation
  6. INcrease cardiac demand, ischemia, necrosis, dysfunction

*self perpetuating
chronic
progressive

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12
Q

PHarmacological treamtnets for HF

A
  1. Block SNS
    - beta blockers
  2. Block ADH effects
    - diuretics
  3. Block RAAS effects
    - ACEi
    - ARB
    - MRA
    - CCB?
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13
Q

HF ejection fraction
Definitions

A

HFpEF
heart failure preserved ejection fraction
>/= 50%

HFrEF
heart failure reduced ejection fraction
< 40%

HFmEF
heart failure mid-range ejection fraction
heart failure recovered ejeciton fraction
between 41-49%

Refers to blood ejected from ventricle in 1 minute?

Normal ejection fraction is >/= 50%

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14
Q

Risk Factors
HF

A
  • age >40 years
  • gender (male > female; exception post-menopause)
  • HTN (hyptertension)
  • DM (hyperglycemia)
  • Smoking, alcohol, chemotherapy, radiation therapy (toxins)
  • obesity (dyslipidemia), elevated BMI, sedentary lifestyle
  • genetics (L hypertrophic cardiomyopathy, L dilated cardiomyopathy, arrhythmogenic R V cardiomyopathy)
  • acquired (myocarditis, takotsuba, toxins)
  • Valvular (stenosis, regurgitation)
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15
Q

2/3 of HF are due to…

A
  1. ischemic (CAD, MI)
  2. HTN
  3. Rheumatic fever (GAS) - valve
  4. COPD
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16
Q

Other causes of HF

A

Genetic
- cariomyopathy (hypertrophy, dilation LV; arrhythmogenic RV fattyscelerotic deposits)

Acquired
- myocarditis
- toxins
- takotsubo (broken heart syndrome)

17
Q

Symptoms of HF

A

Heart failure
- inability of the heart to pump
- decreased cardiac output and perfusion to the body…

Dyspnea
Fatigue
confusion
Orthopnea (difficulty breathing lying down)
paroxysmal dyspnea (wake up first 2 hours at night)
tachycardia and palpitations
nocturnal diuresis
coughing and wheezing (pulmonary congestion, edema)
Nausea, decreased appetite (blood congestion into venous system, liver, spleen, GI)

18
Q

Physical Exam findings
HF

A

Extra heart sounds
- S4 - diastolic HF (blood striking the non compliant ventricle)
- S3 - systolic HF (mitral valve regurgitation)
- regurgitations

Cardiomegaly
- shift in LV apex

JVP increased
HJ reflex
- increase venous distention
- hepatomegally

Hypotension
tachycardia
SpO2 low
pale, cold extremities

Rales, crackles, wheezing

peripheral edema and weight gain

19
Q

Left sided HF vs. Right sided HF

A

Left sided HF
- Left side of heart (ventricles)
1. systolic HF (reduced CO)
2. diastolic HF (loss of compliance, reduced perfusion)
- blood backs up into pulmonary circulation

Clinical signs and symptoms:
Dyspnea, fatigue, confusion
orthopnea, paroxismal nocturnal dyspnea, crackles/rales, cough
exercise fatigue

Right sided HF
- inability to pump blood into the pulmonary circulation
- blood backs up into the venous circulation (liver, spleen, GI)

Clinical signs and symptoms:
elevated JVP, HJ reflex
anorexia, nausea
hepatomegaly, splenomegaly
peripheral edema
ascites

  • can be caused by L sided HF
20
Q

NYHA Classification of HF

A

Class I - asymptomatic

Class II - mild, symptomatic with activity

Class II - moderate, symptomatic with normal ADL

Class IV - bed rest, symptomatic at rest

*Subjective rating
Patient report
determine if stable or getting worse

21
Q

AHA Classification HF

A

Stage A
Asymptomatic
no structure
just risk factors for HF

Stage B
Asymptomatic
structure changes present
LVEF reduced, LVH present

Stage C
Symptomatic
structural changes present
exercise intolerance

Stage D
Symptmatic
end stage
symptoms at rest
*transplant, LV assist device, end of life care

22
Q

Work up for HF

A
  1. past medical history
    - Risk factor assessment
    - DM, HTN, obesity, inactivity, alcohol, smoking, toxins, radiation, chemo, genetics, vavular, MI, age, gender, etc.
  2. presenting illness
    - clinical signs and symptoms
    - L sided HF: dyspnea, exercise tolerance decreased, fatigue, confusion, tachycardia, orthopnea, paroxysmal nocturnal dyspnea
    - R sided HF: anorexia, nausea, hepatomegaly, splenomegaly, edema, ascites
  3. Physical findings
    - Vital signs: hypotension, tachycardia, SpO2 reduced, pale periphery, cold
    - PVS: edema, weight gain, increased JVP, HJ reflex present
    - ABDO: hepatomegaly or splenomegaly, ascites
    - RESP; crackles lungs
    - CARDIO: displaced apex, S3 or S4
  4. Diagnostics or laboratory values

Blood work
- CBC and diff (anemia, infectious causes)
- electrolytes (Na, K, Ca, Mg, P)
- FPG and A1C
- lipid profile
- TSH (hypo increased DBP? hyper increased SBP?)
- Cr and BUN
- LFTs (AST, ALT)
- BNP (dx. HF)

  1. Diagnostic BNP

BNP > 400pg/mL (likely)
BNP < 100pg/mL (unlikely)

out of hospital
BNP > 50pg/mL
N-pro-BNP > 125pg/mL
- proceed with imaging below:

  1. Imaging

ECG
1. rate
2. rhythm
3. ischemia or infarct
4. hypertrophy

Echocardiogram
1. wall motion
2. hypertrophy / diameter
3. valvular regurgitation / stenosis
4. ejection fractions

Chest X ray
1. cardiac sillouette (hypertrophy)
2. pulmonary edema (vascular redistribution (upper), kerly B lines (lower))
3. pleural effusions

Cardiac perfusion studies
1. Stress echocardiogram
2. vasodilator echocardiogram (nuclear perfusion studies)
3. angiogram
4. CT / MRI (better imaging of heart - genetic, acquired causes)

23
Q

SV =

A

SV
1. preload = EDV + venous return
2. afterload = PVR + aortic pressure
3. contractility = SNS, EDV, oxygen supply to heart

24
Q

HR

A

CNS
SNS
baroreceptors
atrial receptors
hormones (NE, cortisol, thyroid)

25
Q

Hypertensive hypertrophic cardiomyopathy

A

Triggers
- Angiotensin II
- catecholamines
- ischemia, inflammation (TNF alpha)
- aldosterone

Pathological remodelling
1. dilation
2. hypertrophy
3. increased ECM, fibrosis
4. thickening

26
Q

Cycle HF with HFrEF

A

Mi –> reduced contractility

  1. decreased ejection fraction
    increased LVEDV
    increased preload
    decreased contraction
  2. decreased ejection and cardiac output
    increase SNS, increase RAAS
    increase afterload
    hypertension
27
Q

HFrEF vs. HFpEF

A

HFpEF
- female
- normal EF >. 50%
- no cardiomegaly
- no dilation
*hypertrophy
*decreased chamber size
- S4

HFrEF
- male
- reduced EF < 40%
- cardiomegaly
- dilation
- normal to increase hypertrophy
- increased chamber size
- S3

28
Q

Etiology
HFpEF

A
  • chronic activation SNS and RAAS
  • diastolic dysfunction
  • remodelling: thickening, hypertrophy, decreased compliance
29
Q

Right Ventricular HF

A

Causes
- Pulmonary pressure
- ARDs (acute respiratory disease)
- COPD
- pulmonic valvular stenosis
-left sided heart failure (increased EDP; blood left in ventricles after pumps)

30
Q

Pathophysiology
Right ventricular HF

A

increased pulmonary pressure (HTN)

increased workload of R ventricle

increased oxygen demand

unable to contract and pump

increase RVEDV and Pressure

back up blood into systemic cirucaltin

  • increase RVEDP (RVEDV)
  • increase RV preload
  • increase back up of blood
31
Q

High output heart failure

A

Trigger:
Increase in tissue hypoxia / oxygen demand

Causes:
Sepsis
Hyperthyroidism
Anemia
BeriBeri (thyamine deficiency)

Result:
Turns on SNS and catecholamine release
increase HR, conduction, contractility and CO increases

Year 1: Patho/Pharm (39 decks)

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