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High Acuity > Cardiovascular Hemodynamics > Flashcards

Cardiovascular Hemodynamics Flashcards

1
Q

The heart is between the lungs, in the:

Behind the:

A

mediastinum

sternum

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2
Q

The apex of the heart lies:

A

diaphragm pointing to the left

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3
Q

Pericardium

A

Outermost layer, protects the heart. Made of 2 layers fibrous and serous pericardium

Between 2 layers there is fluid to prevent friction/injury

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4
Q

Epicardium

A

visceral surface of the pericardium

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5
Q

Myocardium

A

Middle Layer. Thick muscular tissue. Responsible for major pumping action. Contains contractile fibers

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6
Q

Endocardium

A

Thin layer of the endothelium and connective tissue. Lines the valves and chambers

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7
Q

4 Layers of the Heart (outer to inner)

A
  1. Pericardium
  2. Epicardium
  3. Myocardium

4, Endocardium

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8
Q

Direction of Blood Flow through the heart with valves and chambers

A
  1. inferior and superior vena cava
  2. right atrium
  3. tricuspid atrium
  4. right ventricle
  5. pulmonic valve
  6. pulmonic artery
  7. lungs
  8. pulmonic veins
  9. left atrium
  10. mitral valve
  11. left ventricle
  12. aortic valve
  13. aorta
  14. systemic circulation
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9
Q

Function of the valves

A

Maintain forward flow of blood

Open and close with pressure & volume changes in the heart chambers

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10
Q

Function of coronary arteries

A

Supply and drain blood to the heart muscle (anterior and posterior surfaces) itself

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11
Q

When does coronary artery flow occur?

A

Diastole

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12
Q

3 Major Coronary Arteries

A
  1. right coronary artery
  2. Left coronary artery dissects into
    a) left anterior descending
    b) left circumflex
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13
Q

What does the RCA perfuse?

A

Perfuses right side of heart and inferior LV

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14
Q

What does the LAD perfuse?

A

left ventricle and left septum

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15
Q

What does the left circumflex perfuse?

A

Posterior surface and SA nose

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16
Q

Hemodynamics

A

the physical study of flowing blood and of all the solid structures (such as arteries) through which it flows

essentially the pressures and flows in circulatory sustem

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17
Q

Hemodynamic monitoring studies the relationship between what 4 variables?

A
  1. Heart rate
  2. Blood flow
  3. Oxygen delivery
  4. Tissue perfusion
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18
Q
A
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19
Q

2 components of successful delivery of oxygenated blood to tissues:

A
  1. Electrical impulse to stimulate a contraction
  2. Effective enough contraction to deliver appropriate cardiac output
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20
Q

Cardiac Output

A

The amount of blood the heart pumps each minute

CO = HR x SV

The delivery of oxygenated blood to tissues

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21
Q

Normal CO in adult

A

3-6L/min

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22
Q

3 Factors Effecting SV

A

preload + contractility + afterload

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23
Q

Stroke Volume

A

Amount of blood ejected from the heart (LV) with each pump

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24
Q

Normal stroke volume

A

60-70ml

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25
Q

Preload

A

Filling

Pressure/stretch in the myocardial fibers (ventricle muscle wall) at the end of diastole

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26
Q

Preload is the end ________ volume

A

Diastolic

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27
Q

When is preload increased>

A

Hypervolemia

Valve Regurgitation

Heart Failure

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28
Q

Contractility

A

Force/strength of the myocardial contraction

Effected by size of muscle

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29
Q

Afterload

A

The pressure against which the ventricles pump to eject blood

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30
Q

Afterload is t amount of resistance to the ejection of blood from the ventricle; amount of pressure that the heart needs to pump against when _________ during ________

A

contracting

systole

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31
Q

Pressure = _____ x ______

A

flow
resistance

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32
Q

Afterload is increased in:

A

hypertension and vasoconstriction

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33
Q

Increasing afterload increases:

A

Cardiac workload

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34
Q

Ejection Fraction

A

the amount of blood expelled with each contraction (50-80%)

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35
Q

Frank Sterling Law

A

The more the heart is filled during diastole (within limits – if overstretched, there will be decreased contractility; similar to rubber band), the more forcefully it contracts.

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36
Q

What 2 systems regulate CO?

A
  1. Autonomic Nervous System
  2. RAAS
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37
Q

2 Receptors that monitor CO

A
  1. baroreceptors
  2. chemoreceptors
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38
Q

What do baroreceptors monitor?

A

Blood pressure/pressures changes/stretch

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39
Q

Location of baroreceptors

A

carotid sinus & aortic arch

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40
Q

When baroreceptors detect pressure changes/decreased CO, what occurs?

A

ANS compensation

Increased HR

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41
Q

What do chemoreceptors monitor?

A

Chemical changes

2 types (peripheral and central)

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42
Q

Location of peripheral chemoreceptors and what they sense

A

carotid sinus & aortic arch

PO2 and pH changes causing ANS compensation

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43
Q

Location of central chemoreceptors and what they sense

A

brain

paCO2 and pH causing ANS compensaion

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44
Q

Goal of ANS and RAAS for CO regulation

A

Maintain CO through compensatory mechanisms (increase HR)

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45
Q

Neurotransmitter with sympathetic system

A

epinephrine and norepinephrine

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46
Q

Neurotransmitter with parasympathetic system

A

acetylcholine

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47
Q

Receptors with sympathetic system

A

alpha and beta adrenergic

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48
Q

Receptors with parasympathetic system

A

cholinergic
1. nicotinic (skeletal)
2. muscarinic (smooth)

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49
Q

Chronotropic effect of sympathetic stimulation

A

Increased HR

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50
Q

Chronotropic effect of parasympathetic stimulation

A

Decreased HR

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51
Q

Inotropic effect of sympathetic stimulation

A

increased strength of contraction

52
Q

Inotropic effect of parasympathetic stimulation

A

no major effect

53
Q

Dromotropic effect of sympathetic stimulation

A

Increased conduction velocity

54
Q

Dromotropic effect of parasympathetic stimulation

A

Decreased conduction velocity

55
Q

How do you measure afterload

A

Mean Arterial Pressure

56
Q

Equation for measure MAP

A

MAP= Cardiac Output x Systemic Vascular Resistance

Clinically…
SBP + 2(DBP)
3

57
Q

Normal MAP

A

70-100mmHg

60 necessary for adequate perfusion

58
Q

Arterial Pressure Monitoring

A

Invasive, real time BP monitoring

59
Q

Indications for Arterial Lines

A
  • Need for continuous BP monitoring related to hemodynamic instability or vasopressor requirement
  • Frequent ABG draws
60
Q

Complications of Arterial Lines

A
  • Hemorrhage
  • Hematoma
  • Thrombosis
  • Proximal and distal embolization
  • Infection
61
Q

How do you measure preload?

A

By assessing right atrial pressure

62
Q

CVP/RAP

A

(central venous pressure/right atrial pressure): measurement of the amount of fluid in right side of the heart

63
Q

CVP/RAP represents:

A

Right ventricular preload

64
Q

How can CVP/RAP be monitored

A

central line or pulmonary artery catheter

65
Q

Normal CVP/RAP

66
Q

Normal PAP Values

A
  • PAS: 20-30 mmHg (during systole)
  • PAD: 10 mmHg (during diastole)
67
Q

Normal Pulmonary Artery Wedge Pressure (PAWP)/Pulmonary Artery Occlusion Pressure (PAOP) and what does it represent:

A

5-12mmHg

Reflects pressure in the left side of the heart (left filling)

68
Q

Signs and Symptoms of Decreased CO

A
  • Decreased capillary refill
  • Compensatory of tachycardia
  • Decreased blood pressure
  • Weak pulses
  • Decreased urine output
  • Altered LOC (restlessness and confusion)
  • Cool extremities
  • Shortness of breath
  • Arrhythmias
  • Fatigue
  • Edema
69
Q

Heart Failiure = _______ Failure

70
Q

Systolic LSHF Pathophysiology

A

The LV loses ability to contract effectively and cannot pump with enough force to push enough blood into the system.
* ↓CO
* ↑afterload
* ↑ preload (blood “backs up” and pools into the pulmonary system)

71
Q

Diastolic LSHF Pathophysiology

A

The LV loses ability to relax; it is stiff, cannot fill

72
Q

RSHF is a result of what 3 things?

A
  1. LSHF
  2. Pulmonary HTN
  3. RV problem
73
Q

When cardiac output is insufficient in meeting the body’s the demands, how does the ANS respond?

A

Stimulates sympathetic nervous system

Increases HR through beta 1

Increases BP by vasoconstriction alpha

74
Q

When cardiac output is insufficient in meeting the body’s the demands, how does the RAAS respond?

A

It is activated because decreased CO leading to decrease renal perfusion

Aldosterone and angiotensin I are released

Na/Fluid Retention and vasoconstriction

75
Q

The body’s compensatory mechanisms to decreased CO of vasoconstriction (RAAS and SNS) and fluid retention (RAAS) effect on HF:

A

Increase in afterload and preload; not helpful when the pump is the issue

76
Q

What 2 compensatory mechanisms to decreased CO does the heart undergo itself and why each can be maladaptive?

A
  1. Left Ventricular Hypertrophy: increases oxygen needs of heart due to increased oxygen needs of muscle
  2. Left Ventricular DIlation: frank starling law to a limit - exceeds limit and decreases CO
77
Q

LSHF Symptoms and why

A
  1. wheezes/crackles (pulmonary congestion)
  2. decreased urine output (decreased perfusion)
  3. decreased LOC (decreased perfusion)
  4. cool extremities (diverting SV to vital organs)
  5. tachypnea (SNS activation and pulmonary congestion)
  6. tachycardia (SNS activation)
  7. diaphoresis (SNS activation)
78
Q

RSHF Symptoms

A
  1. systemic congestion (edema, weight gain, distended neck veins, hepatosplenomegaly)
  2. confusion (deoxy blood back up into brain)
  3. tachycardia
  4. S+S of LSHF (LSHF causes RSHF)
79
Q

Isolated RV failure not due to LSHF is called:

A

Cor Pulmonale

80
Q

BNP Test Indicates

A

Protein released from ventricles with too much stretching; if not present can rule out HF

81
Q

Why monitor electrolytes with HF?

A

with additional fluid volume, alterations to fluid status. Water accumulation and treated with diuretics themselves can cause shifts themselves

82
Q

Why monitor urea and creatinine with HF?

A

Kidney’s are highly effected by CO; indicate damage secondary to decreased CO

83
Q

Why monitor HgB/HcT in HF?

A

hemodilution effect; still may have normal RBC count but fluid conservation decreases ratio

84
Q

What would be seen on CXR of HF?

A

Cardiomegaly

85
Q

ABG of HF

86
Q

Acute Management of HF

A
  1. Airway and breathing
    - intubate if altered LOC
    - oxygenation PEEP to force fluid out of pulmonary system
    - diuresis to get fluid out of circulating volume
  2. Circulation
    - optimize hemodynamics
    - increase contractility
    - vasodilation
    - regulate HR
87
Q

How do you acutely manage circulation in HF (4 points)

A
  1. optimize hemodynamics (diuretics)
  2. increase contractility (digoxin and amiodarone)
  3. vasodilation
  4. regulate HR to decrease workload/oxygen needs of heart
88
Q

Goal of HF management and 2 ways this is done:

A

Reduce the workload of the heart

  1. Improve perfusion and CO
  2. Improve gas exchange
89
Q

How do you improve perfusion and CO of patient in HF?

A
  1. decrease preload (fluid management)
  2. decrease afterload
  3. improve quality of contraction
90
Q

How do you improve gas exchange in patient in HF?

A
  1. ventilation assistance/supplemental O2
  2. positioning to reduce SOB
  3. evaluate causes of fatigue
  4. reduce activity
91
Q

How is preload reduced in treatment of HF?

A

Fluid management

92
Q

4 Points of Fluid Management for patient in HF

A
  1. Fluid/salt restriction (1.5L/24 hours)
  2. Assessment of symptoms
    * Crackles
    * Edema
    * In’s and Out’s (want less coming in than going out)
    * Pulses
    * BP
    * Mental status
  3. Serum electrolytes/BUN/Creatinine
  4. Upright positioning
  5. Diuretics
93
Q

Rationale for use of anti-diabetics in fluid management

A

Increases excretion of glucose in urine

Glucose is large molecule. Water follows large molecules – mild diuretic effect

94
Q

ACE/ARB

A

Ramipril, enalapril; valsartan

  • Block RAAS
  • Decreased fluid retention and vasodilation
95
Q

Beta Blockers

A

Metoprolol, carvedilol
* Effect rate and contractility
* Block beta 1 receptors in heart to decrease rate and contractility

96
Q

Calcium channel blockers

A
  • Decrease heart rate
  • No effect on contractilityN
97
Q

Nitrates

A
  • Vasodilators to reduce afterload and secondary impact on preload
  • Nitroglycerin
  • Vasodilation in coronary arteries allows increased myocardial perfusion
98
Q

Inotropes

A

(PO = Digoxin  IV High Alert (ICU) = Dobutamine, Milrinone)
* Increased contractility

99
Q

Amiodarone

A
  • Anti-arrhythmic and rate control
  • Patients in HF can cause atrial fibrillation
100
Q

HCN channel blockers

A

(Ivabradine)
* Decrease spontaneous pacemaker activity
* Decrease HR

101
Q

What is Cardiac Resynchronization Therapy (CRT)

A

Biventricular pacing (if not contracting in unison)

Pacing: pace-making device (internal or external) sends electrical stimulation to stimulates contraction of ventricle

102
Q

Ventricular Assist Device

A

mechanically pumps the blood out of the heart. Bypass ventricle doing any work.

Bridge to Transplant

103
Q

If HF progresses to pulmonary edema, what cues would you see and what is the treatment?

A
  • Pink frothy sputum
  • Acute respiratory deterioration
  • Inability to exchange gases: decreased sats, SOB
  • Treatment= IVP furosemide (plus increase supply, decreased demand)
104
Q

How does the process of infective endocarditis begin?

A

with damage to endothelium of a valve

105
Q

Pathophysiology of Infective Endocarditis

A
  1. Some form of damage occurs to valve attracting platelets
  2. Some bacteria enters bloodstream from various source
  3. bacteria settle on valve and form vegetation, which are similar to emboli
  4. alteration to valve function as vegetations grow
106
Q

What 2 conditions commonly occur as a result of IE

A

Aortic stenosis and mitral regurgitation

107
Q

3 Types of Valvular Disease

A
  1. stenosis
  2. insufficiency
  3. Prolapse
108
Q

Treatment of valvular disease is based on:

A

Symptom Severity

109
Q

Valvular Stenosis

A

tissue thickening narrows valve opening causing poor delivery of blood throughout the chambers

110
Q

Valvular Insufficiency/Regurgitation

A

incomplete valve closure. Opposite to stenosis, blood can flow from atria to ventricle, but incomplete closure sends blood backwards and forwards (decrease CO)

111
Q

Mitral valve prolapse can progress to

A

Mitral regurgitation

112
Q

What occurs in mitral valve prolapse

A

Leaflet (half of valve) bends opposite direction leading to backflow/regurgitation

113
Q

Symptoms seen in mitral valve prolapse

A
  • Often called “click-murmur syndrome”
  • May have palpitations or chest pain
114
Q

Mitral Regurgitation

A

Valve doesn’t close completely during systole– blood flows back through the valve into LA when LV contracts
* Systolic murmur: hearing blood going the wrong way

115
Q

Aortic Regurgitation

A

Valve doesn’t close completely during diastole, so blood flows back from aorta into LV
* Diastolic murmur

116
Q

Treatment of Regurgitation/Insufficiency

A

medications for symptom relief (HF); valve repair/replacement

117
Q

Mitral stenosis and S+S

A
  • L atrial pressure increases; L atrium dilates; pulmonary artery pressure increases; right ventricle hypertrophies
  • Signs & Symptoms: right HF, diastolic murmur
118
Q

Aortic stenosis and S+S

A

narrowed valve opening obstructs blood flow from LV to aorta during systole
* Most common cardiac valve dysfunction – “wear and tear”
* Signs & Symptoms: left HF, systolic murmur

119
Q

Bicuspid Aortic Valve

A
  • Most common congenital cardiac malformation
  • Usually has 3 leaflets; only 2 in this condition
  • Usually benign, if develop HTN later in life can cause issues due to high pressure state of aorta
  • Often not diagnosed until adulthood
120
Q

Cues of Infective Endocarditis

A
  1. fever (infection)
  2. new murmur (different associated murmur with aortic/mitral stenosis/regurgitation_
  3. acute fatigue due to decrease in CO
  4. evidence of systemic embolization (bursting of tiny capillaries)
  5. positive BC if bacterial
121
Q

Diagnosis of IE

A
  1. +BC
  2. New murmur
  3. echo to see structural defect
122
Q

3 Points of IE Treatment

A
  1. aggressive antibiotics (bacteremia and valve infection)
  2. manage complications associated with decreased CO/HF
  3. Surgery
123
Q

Describe biologic valves

A
  1. last shorter (8-10 years)
  2. no anticoagulation
  3. no click
124
Q

Describe mechanical valves

A
  1. last over 20 years
  2. lifelong anticoagulation (warfarin)
  3. click
125
Q

Priorities of care of IE

A
  1. infectin
  2. HF symptoms
  3. systemic embolization
126
Q

Complications of IE

A
  1. Cardiac: valve damage, HF, emboli, pericarditis, myocarditis, AV blocks, cardiogenic shock
  2. stroke
  3. systemic embolization

High Acuity (20 decks)

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