Heart Failure & Thromboembolic Disorders Flashcards

1
Q

What are factors that affect cardiac output?

A

Cardiac Output = Heart Rate X Stroke Volume

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2
Q

What are factors affecting HR?

A
  • autonomic innervation
  • hormones
  • age
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3
Q

What are factors affecting SV?

A
  • heart size
  • contractility (force, duration) * preload (end diastolic volume)
  • afterload (vascular resistance)
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4
Q

What causes an ↑ in SV & CO?

A

↑contractility
↑preload
↓afterload

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5
Q

What causes a ↓ in SV & CO?

A

↓contractility
↓preload
↑afterload

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6
Q

Why athletes generally have lower heart rate?

A

↑muscle wall thickness (left ventricle - needs more profusion of blood & O2 b/c has thicker wall) → ↑contractility
→ ↑stroke volume → ↑tissue blood supply

↑ heart size → ↑end diastolic volume → stronger
contractility (left ventricle) → ↑stroke volume

↑SV → ↓HR (still in normal range) → maintain normal resting CO

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7
Q

Preload:

A

(stretch, filling)
* volume of blood in ventricles at end of diastole (EDP)

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8
Q

When does preload increase in?

A
  • hypervolemia
  • regurgitation of
    cardiac valves
  • heart failure
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9
Q

Afterload:

A

(vascular resistance)
* left ventricle must overcome resistance to circulate blood

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10
Q

↑afterload =

A

↑cardiac workload

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11
Q

When does afterload increase in?

A
  • hypertension
  • vasoconstriction
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12
Q

What are factors that affect preload, afterload, and contractility in heart?

A

Contractility
* SNS, PSNS stimulation
* hormones (e.g. epinephrine,
norepinephrine, thyroid)
* electrolytes (e.g. Ca2+,K+)
* hypoxia
* drugs

Preload
* venous return
* filling time
* electrolytes (Na+, K+, Ca2+) * hypoxia
* hormones (e.g. thyroid)
* drugs

Afterload
* vascular resistance
* valve damage

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13
Q

Ejection fraction:

A

The fraction of blood ejected from ventricle in each heart beat (contraction)

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14
Q

EF= SV/EDV =

A

(~70 ml) / (~140 ml) = (~ 50%)

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15
Q

↑end diastolic volume
–> ___ stretch in cardiac muscle –>
__ stroke volume

A


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16
Q

↑preload → __ stretch → __SV

A


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17
Q

What are determinants of ventricular function?

A
  • CONTRACTILITY
  • AFTERLOAD
  • HEART RATE
  • PRELOAD
    –> STROKE VOLUME
  • LV wall integrity
  • Valvular competence
    –> CARDIAC OUTPUT
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18
Q

In congestive heart failure (CHF), the heart:

A
  • fails to pump the blood efficiently
  • not able to maintain normal blood flow to organs
  • unable to provide adequate perfusion to meet metabolic needs of peripheral tissues
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19
Q

“ CHF represents a complex syndrome characterized by abnormalities of ____ _______ function and ____- ______ regulation, which are accompanied by ______ ______, ____ _______, and _______ ________”.
From Dr. Milton Packer

A

LEFT VENTRICLE

NEURO-HORMONAL

EXERCISE INTOLERANCE

FLUID RETENTION

REDUCED LONGEVITY

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20
Q

What are 2 major types of heart failure?

A

Systolic failure

Diastolic failure

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21
Q

Systolic failure:

A

The heart loses its ability to contract or pump blood
into the circulation.

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22
Q

Diastolic failure:

A

The heart loses its ability to relax because it becomes
stiff and cannot fill properly between each beat.

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23
Q

CHF is divided into 2 categories based on changes in EF:

A
  • heart failure with PRESERVED EF (≥50%)
  • heart failure with REDUCED EF (≤40%)
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24
Q

What are common causes of CHF?

A
  • heart attack (myocardial infarction)
  • coronary heart disease
  • hypertension
  • congenital heart defects
  • heart valve defects (mitral, aortic)
  • cardiac myopathy (heart muscle disease)
  • lung disease
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25
Q

What are the 4 compensatory mechanisms in CHF?

A
  1. Elevated heart rate (activation of SNS)
  2. Elevated preload
  3. Ventricular hypertrophy (enlarged heart)
  4. Vasoconstriction (endothelin, RAAS, SNS)
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26
Q

Describe the elevated HR (activation of SNS) pros and cons

A
  • Pros: helps maintain cardiac output
  • Cons:↓filling time, ↑O2 demand, ↑risk of arrhythmias
    (b/c heart is beating faster, therefore resting/filling time is shorter)
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27
Q

Describe the elevated preload pros and cons

A

↑renin/angiotensin/aldosterone system → Na+ and water retention
- Pros: ↑stroke volume; ↑cardiac output
- Cons: pulmonary/peripheral edema, ↑O2 demand

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28
Q

Describe the ventricular hypertrophy (enlarged heart) pros and cons

A
  • Pros: helps to maintain cardiac output
  • Cons: ↑risk of ischemia, arrhythmias, fibrosis
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29
Q

Describe the vasoconstriction (endothelin, RAAS, SNS) pros and cons

A
  • Pros: maintains BP, recruit blood to heart and brain - Cons: ↑afterload (resistance) → ↓stroke volume
30
Q

Norepinephrine mechanism of action:

A

↑heart rate (tachycardia), ↑contractility, vasoconstriction

31
Q

Angiotensin II (RAAS) mechanism of action:

A

vasoconstriction, Na+ retention in kidney, aldosterone release

32
Q

Aldosterone mechanism of action:

A

Na+ and water retention in kidney

33
Q

Anti-diuretic hormone mechanism of action:

A

↑water retention,↑vasoconstriction

34
Q

Natriuretic peptides atrial (ANP), brain (BNP) mechanism of action:

A

diuretic (hypotensive) effects
- released from atrium & ventricles

35
Q

Where are Natriuretic peptides atrial (ANP) RELEASED from?

A

atria

36
Q

Where are Natriuretic peptides brain (BNP) RELEASED from?

A

ventricles

37
Q

What are the signs & symptoms of CHF?

A
  • Fluid retention and edema (peripheral/pulmonary)
  • Shortness of breath (dyspnea, orthopnea, cough) - b/c of buildup of fluid in lungs & decrease O2 b/c of edema
  • Fatigue (especially with activity) - can’t get to 2nd floor as easily as before
  • Cyanosis (insufficient oxygen in blood)
  • Confusion (if blood flow to brain is reduced)

(need more pillows at night to feel comfortable)

38
Q

What are signs of Fluid retention and edema (peripheral/pulmonary) in CHF?

A

– WEIGHT GAIN (mainly due to edema)
– PITTING EDEMA (squishy feet/ankles) - indent stays there after you release finger
– ELEVATED JVP (jugular venous pressure)
– CRACKLING SOUNDS IN LUNGS (on auscultation)

39
Q

What do symptoms of CHF depend on?

A

Symptoms depends on the type of heart failure (left-sided or right-sided).
- might see in both

40
Q

What are symptoms of CHF mostly related to?

A

Symptoms are mostly related to compensatory mechanisms to improve reduced cardiac output.

41
Q

What are the 2 types of CHF?

A
  • Left-sided CHF
  • Right-sided CHF
42
Q

Left-sided CHF:

A

left side of heart (mainly left ventricle) fails; blood back up in lungs

(enough blood isn’t leaving heart)

43
Q

Right-sided CHF:

A
  • also called “Cor Pulmonale”
  • right side of heart fails; blood back up in (areas that are easier to have fluid build-up like…) abdominal organs and peripheral tissues
44
Q

What are the signs/symptoms of LEFT-sided CHF?

A
  • paroxysmal nocturnal dyspnea
  • ↑pulmonary capillary wedge pressure
  • ↑pulmonary congestion
  • cough
  • crackle
  • wheeze
  • blood-tinged sputum
  • tachypnea (b/c can’t get enough O2 exchange, so they try to compensate with increase HR)
  • restlessness
  • confusion
  • orthopnea
  • exertional dyspnea
  • tachycardia
  • fatigue
  • cyanosis - ending of toes, fingers, lips get darker –> indication of decrease O2 levels in blood
45
Q

What is the diagnosis of CHF using the PHYSICAL ASSESSMENT?

A
  1. Assessment of JVP
    * indirect measure of central venous
    pressure
    * normal <4 cm above sternal angle
    * ↑JVP indicates VOLUME OVERLOAD (doesn’t indicate HF - but commonly seen in volume overload)
  2. Presence of ascites (fluid accumulation in peritoneal space)
    - b/c abdominal has more room
  3. Peripheral edema (pitting edema)
46
Q

What is the diagnosis of CHF using IMAGING?

A
  1. Chest X-ray (CXR):
    * evaluate heart size and pulmonary edema
    * cardio-thoracic ratio >50% indicates enlarged heart
    (ratio of heart:chest is increased in those patient)
  2. Echocardiogram (ECHO):
    CHF heart chest
    * ultrasound waves used to image heart
    * detect heart structural & functional abnormalities
    * assess left ventricular EF (normal = 55-70% ; HF = <40%)
    (never gets 100% or close to that)
47
Q

What are strategies used to improve CHF?

A
  1. control diet
    - salt (Na+) restriction
    - fluid restriction (~2L/day) (will increase fluid build-up in body)
  2. modify lifestyle:
    - stop smoking
    - weight loss in obese patients (b/c will be less work on heart)
    - exercise (after symptoms are controlled)
    Note: rapid weight gain maybe due to water/salt retention (build-up of fluid)
    (asking what they eat (diet) wouldn’t be appropriate b/c not due to food
  3. pharmacotherapy: treatment is chosen based on underlying problem, type, and severity of CHF
48
Q

What is rapid weight gain maybe due to? What should we ask the patient?

A

rapid weight gain maybe due to water/salt retention (build-up of fluid)
- asking what they eat (diet) wouldn’t be appropriate b/c not due to food

49
Q

Thrombosis:

A

Formation of blood clot comprised of platelets, fibrin, & entrapped RBCs in the vascular system which is attached to vascular endothelium.

50
Q

Embolism:

A

A small portion of the clot breaks off, travels, and becomes trapped in a small vessel, causing occlusion leading to ischemia and infarction.

51
Q

What is the Virchow’s Triad?

A

Three factors that promote venous thrombosis:

  1. Venous Stasis
    - abnormality of blood flow
  2. Endothelial Injury
    - abnormality of surfaces in contact with blood
  3. Hypercoagulability
    - abnormality in clotting components
52
Q

What is a thrombosis in heart like?

A

Thrombus on the wall of a heart chamber (ventricle or atria) is called MURAL THROMBUS.

53
Q

What is a thrombosis in arterial system like?

A

Common locations (of clot formation) include:
* cerebral
* coronary
* mesenteric
* renal arteries

54
Q

What is a thrombosis in venous system like?

A

Common locations include:
* large deep veins of pelvis & lower extremities
* is referred to as deep venous thrombosis (DVT)
* may result in pulmonary embolism

55
Q

What is a thrombosis in venous system like?

A

Common locations include:
* large deep veins of pelvis & lower extremities
* is referred to as deep venous thrombosis (DVT)
* (consequence) may result in PULMONARY EMBOLISM

56
Q

Arterial thrombosis disease:

A
  • It usually results from endothelial injury & platelet activation
    (main cause: atherosclerosis)
57
Q

What are the complications of Arterial thrombosis disease?

A
  • vessel occlusion
  • ISCHEMIC INJURY
  • ORGAN INFRACTION (myocardial infarction,
    cerebrovascular accident)
    (cause major damages in tissue)
58
Q

Venous thrombosis disease:

A
  • Common sites:
    It usually develops in large veins of pelvis & lower
    extremities.
59
Q

What are the complications of Venous thrombosis disease?

A

Pulmonary embolism, is the most significant consequence of venous thrombosis.

60
Q

Explain Pulmonary embolism

A
  1. Blood clot (or fat, air, tumor) forms in a vein and breaks free from vessel wall.
  2. Embolus travels through the bloodstream to the heart.
  3. Embolus travels through the heart & blocks blood vessels in the lung.
61
Q

What are the clinical features of Deep Vein Thrombosis?

A
  • pain
  • edema
  • diaphoresis (lot of sweating b/c SNS system is activated and is trying hard)
  • erythema
62
Q

What are the clinical features of Pulmonary embolism?

A
  • shortness of breath
  • chest pain
  • cough
  • syncope (can be severe enough that patient can’t breathe anymore)
  • hemoptysis
63
Q

What are ways you can diagnosis deep vein thrombosis?

A
  • Ultrasonography
  • Duplex ultrasonography
  • Ventilation-Perfusion Scan (see if it’s traveled into pulmonary system)
    A) Ventilation scan: INHALATION of radioactive compound (should get to all areas of blood)
    B) Perfusion scan: INJECTION of radioactive compound (colour will change if there or not)
64
Q

What is the treamtent of pulmonary embolism?

A
  • anticoagulants
  • vena cava filters
  • thrombolysis (try to lyse clot)
  • embolectomy (surgery to remove clot if can’t lyse or anything else)
  • prevention strategies for high risk patients (ex: anticoagulants)
65
Q

CO regulatory mechanisms

A

on slide 37

66
Q

What are consequences of impaired LV function?

A
  • Impaired LV function
  • ↓cardiac output
  • neurohumoral imbalance
  • ↑systemic vascular resistance
  • ↑ afterload
67
Q

Thrombosis:

A

Formation of blood clot attached to the vascular endothelium.

68
Q

Embolism:

A

Clot breaks off, travels, and becomes trapped in small vessels causing ischemia / infarction.

69
Q

What is Thrombosis caused by?

A

abnormalities in blood flow, blood vessel surfaces, or blood clotting process.

70
Q

Where can Thrombosis occur in?

A

in heart, arteries, veins.

71
Q

What does Arterial thrombosis usually result from?

A

endothelial injury (antherosclerosis)