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High Acuity > Cardiovascular Hemodynamics > Flashcards

Cardiovascular Hemodynamics Flashcards

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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
Preload
Filling Pressure/stretch in the myocardial fibers (ventricle muscle wall) at the end of diastole
26
Preload is the end ________ volume
Diastolic
27
When is preload increased>
Hypervolemia Valve Regurgitation Heart Failure
28
Contractility
Force/strength of the myocardial contraction Effected by size of muscle
29
Afterload
The pressure against which the ventricles pump to eject blood
30
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 ________
contracting systole
31
Pressure = _____ x ______
flow resistance
32
Afterload is increased in:
hypertension and vasoconstriction
33
Increasing afterload increases:
Cardiac workload
34
Ejection Fraction
the amount of blood expelled with each contraction (50-80%)
35
Frank Sterling Law
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.
36
What 2 systems regulate CO?
1. Autonomic Nervous System 2. RAAS
37
2 Receptors that monitor CO
1. baroreceptors 2. chemoreceptors
38
What do baroreceptors monitor?
Blood pressure/pressures changes/stretch
39
Location of baroreceptors
carotid sinus & aortic arch
40
When baroreceptors detect pressure changes/decreased CO, what occurs?
ANS compensation Increased HR
41
What do chemoreceptors monitor?
Chemical changes 2 types (peripheral and central)
42
Location of peripheral chemoreceptors and what they sense
carotid sinus & aortic arch PO2 and pH changes causing ANS compensation
43
Location of central chemoreceptors and what they sense
brain paCO2 and pH causing ANS compensaion
44
Goal of ANS and RAAS for CO regulation
Maintain CO through compensatory mechanisms (increase HR)
45
Neurotransmitter with sympathetic system
epinephrine and norepinephrine
46
Neurotransmitter with parasympathetic system
acetylcholine
47
Receptors with sympathetic system
alpha and beta adrenergic
48
Receptors with parasympathetic system
cholinergic 1. nicotinic (skeletal) 2. muscarinic (smooth)
49
Chronotropic effect of sympathetic stimulation
Increased HR
50
Chronotropic effect of parasympathetic stimulation
Decreased HR
51
Inotropic effect of sympathetic stimulation
increased strength of contraction
52
Inotropic effect of parasympathetic stimulation
no major effect
53
Dromotropic effect of sympathetic stimulation
Increased conduction velocity
54
Dromotropic effect of parasympathetic stimulation
Decreased conduction velocity
55
How do you measure afterload
Mean Arterial Pressure
56
Equation for measure MAP
MAP= Cardiac Output x Systemic Vascular Resistance Clinically… SBP + 2(DBP) 3
57
Normal MAP
70-100mmHg 60 necessary for adequate perfusion
58
Arterial Pressure Monitoring
Invasive, real time BP monitoring
59
Indications for Arterial Lines
* Need for continuous BP monitoring related to hemodynamic instability or vasopressor requirement * Frequent ABG draws
60
Complications of Arterial Lines
* Hemorrhage * Hematoma * Thrombosis * Proximal and distal embolization * Infection
61
How do you measure preload?
By assessing right atrial pressure
62
CVP/RAP
(central venous pressure/right atrial pressure): measurement of the amount of fluid in right side of the heart
63
CVP/RAP represents:
Right ventricular preload
64
How can CVP/RAP be monitored
central line or pulmonary artery catheter
65
Normal CVP/RAP
2-5mmHg
66
Normal PAP Values
* PAS: 20-30 mmHg (during systole) * PAD: 10 mmHg (during diastole)
67
Normal Pulmonary Artery Wedge Pressure (PAWP)/Pulmonary Artery Occlusion Pressure (PAOP) and what does it represent:
5-12mmHg Reflects pressure in the left side of the heart (left filling)
68
Signs and Symptoms of Decreased CO
* 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
Heart Failiure = _______ Failure
Pump
70
Systolic LSHF Pathophysiology
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
Diastolic LSHF Pathophysiology
The LV loses ability to relax; it is stiff, cannot fill
72
RSHF is a result of what 3 things?
1. LSHF 2. Pulmonary HTN 3. RV problem
73
When cardiac output is insufficient in meeting the body's the demands, how does the ANS respond?
Stimulates sympathetic nervous system Increases HR through beta 1 Increases BP by vasoconstriction alpha
74
When cardiac output is insufficient in meeting the body's the demands, how does the RAAS respond?
It is activated because decreased CO leading to decrease renal perfusion Aldosterone and angiotensin I are released Na/Fluid Retention and vasoconstriction
75
The body's compensatory mechanisms to decreased CO of vasoconstriction (RAAS and SNS) and fluid retention (RAAS) effect on HF:
Increase in afterload and preload; not helpful when the pump is the issue
76
What 2 compensatory mechanisms to decreased CO does the heart undergo itself and why each can be maladaptive?
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
LSHF Symptoms and why
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
RSHF Symptoms
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
Isolated RV failure not due to LSHF is called:
Cor Pulmonale
80
BNP Test Indicates
Protein released from ventricles with too much stretching; if not present can rule out HF
81
Why monitor electrolytes with HF?
with additional fluid volume, alterations to fluid status. Water accumulation and treated with diuretics themselves can cause shifts themselves
82
Why monitor urea and creatinine with HF?
Kidney's are highly effected by CO; indicate damage secondary to decreased CO
83
Why monitor HgB/HcT in HF?
hemodilution effect; still may have normal RBC count but fluid conservation decreases ratio
84
What would be seen on CXR of HF?
Cardiomegaly
85
ABG of HF
Hypoxemia
86
Acute Management of HF
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
How do you acutely manage circulation in HF (4 points)
1. optimize hemodynamics (diuretics) 2. increase contractility (digoxin and amiodarone) 3. vasodilation 4. regulate HR to decrease workload/oxygen needs of heart
88
Goal of HF management and 2 ways this is done:
Reduce the workload of the heart 1. Improve perfusion and CO 2. Improve gas exchange
89
How do you improve perfusion and CO of patient in HF?
1. decrease preload (fluid management) 2. decrease afterload 3. improve quality of contraction
90
How do you improve gas exchange in patient in HF?
1. ventilation assistance/supplemental O2 2. positioning to reduce SOB 3. evaluate causes of fatigue 4. reduce activity
91
How is preload reduced in treatment of HF?
Fluid management
92
4 Points of Fluid Management for patient in HF
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
Rationale for use of anti-diabetics in fluid management
Increases excretion of glucose in urine Glucose is large molecule. Water follows large molecules – mild diuretic effect
94
ACE/ARB
Ramipril, enalapril; valsartan * Block RAAS * Decreased fluid retention and vasodilation
95
Beta Blockers
Metoprolol, carvedilol * Effect rate and contractility * Block beta 1 receptors in heart to decrease rate and contractility
96
Calcium channel blockers
* Decrease heart rate * No effect on contractilityN
97
Nitrates
* Vasodilators to reduce afterload and secondary impact on preload * Nitroglycerin * Vasodilation in coronary arteries allows increased myocardial perfusion
98
Inotropes
(PO = Digoxin  IV High Alert (ICU) = Dobutamine, Milrinone) * Increased contractility
99
Amiodarone
* Anti-arrhythmic and rate control * Patients in HF can cause atrial fibrillation
100
HCN channel blockers
(Ivabradine) * Decrease spontaneous pacemaker activity * Decrease HR
101
What is Cardiac Resynchronization Therapy (CRT)
Biventricular pacing (if not contracting in unison) Pacing: pace-making device (internal or external) sends electrical stimulation to stimulates contraction of ventricle
102
Ventricular Assist Device
mechanically pumps the blood out of the heart. Bypass ventricle doing any work. Bridge to Transplant
103
If HF progresses to pulmonary edema, what cues would you see and what is the treatment?
* Pink frothy sputum * Acute respiratory deterioration * Inability to exchange gases: decreased sats, SOB * Treatment= IVP furosemide (plus increase supply, decreased demand)
104
How does the process of infective endocarditis begin?
with damage to endothelium of a valve
105
Pathophysiology of Infective Endocarditis
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
What 2 conditions commonly occur as a result of IE
Aortic stenosis and mitral regurgitation
107
3 Types of Valvular Disease
1. stenosis 2. insufficiency 3. Prolapse
108
Treatment of valvular disease is based on:
Symptom Severity
109
Valvular Stenosis
tissue thickening narrows valve opening causing poor delivery of blood throughout the chambers
110
Valvular Insufficiency/Regurgitation
incomplete valve closure. Opposite to stenosis, blood can flow from atria to ventricle, but incomplete closure sends blood backwards and forwards (decrease CO)
111
Mitral valve prolapse can progress to
Mitral regurgitation
112
What occurs in mitral valve prolapse
Leaflet (half of valve) bends opposite direction leading to backflow/regurgitation
113
Symptoms seen in mitral valve prolapse
* Often called “click-murmur syndrome” * May have palpitations or chest pain
114
Mitral Regurgitation
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
Aortic Regurgitation
Valve doesn’t close completely during diastole, so blood flows back from aorta into LV * Diastolic murmur
116
Treatment of Regurgitation/Insufficiency
medications for symptom relief (HF); valve repair/replacement
117
Mitral stenosis and S+S
* L atrial pressure increases; L atrium dilates; pulmonary artery pressure increases; right ventricle hypertrophies * Signs & Symptoms: right HF, diastolic murmur
118
Aortic stenosis and S+S
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
Bicuspid Aortic Valve
* 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
Cues of Infective Endocarditis
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
Diagnosis of IE
1. +BC 2. New murmur 3. echo to see structural defect
122
3 Points of IE Treatment
1. aggressive antibiotics (bacteremia and valve infection) 2. manage complications associated with decreased CO/HF 3. Surgery
123
Describe biologic valves
1. last shorter (8-10 years) 2. no anticoagulation 3. no click
124
Describe mechanical valves
1. last over 20 years 2. lifelong anticoagulation (warfarin) 3. click
125
Priorities of care of IE
1. infectin 2. HF symptoms 3. systemic embolization
126
Complications of IE
1. Cardiac: valve damage, HF, emboli, pericarditis, myocarditis, AV blocks, cardiogenic shock 2. stroke 3. systemic embolization

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