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Pathophysiology I > Cardiac Pathophysiology > Flashcards

Cardiac Pathophysiology Flashcards

1
Q

What are the three branches off of the aorta?

A

Brachiocephalic artery
Left common carotid artery
Left subclavian artery

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2
Q

What two branches does the brachiocephalic artery divide into?

A

Right common carotid and the Right subclavian arteries

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3
Q

What is wall tension?

A

The tension in the LV wall must generate to eject the stroke volume

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4
Q

What components make up a person’s cardiac output?

A

CO = HR x SV (contractility and vascular tone)

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5
Q

How many segments is the aorta divided into?

A

Three: Ascending, aortic arch, descending aorta

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6
Q

What physiologic component has the greatest increase in myocardial O2 demand of the heart?

A

Increased LV wall tension

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7
Q

What is a hemodynamic consequence of cross clamping for cardiac bypass?

A

Elevated MAP –> HTN

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8
Q

Where is the tricuspid valve located?

A

Between the right atria and ventricle

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9
Q

Where is the mitral valve located?

A

Between the left atria and ventricle

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10
Q

In what direction does the heart normally pump?

A

In an elliptical fashion

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11
Q

What is the predominating ventricle when viewing an anterior approach of the heart?

A

RV

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12
Q

How many pulmonary arteries are there?

A

Two: Right and Left

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13
Q

How many pulmonary veins are there?

A

Four

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14
Q

What is the worse type of aortic aneurysm to have?

A

Ascending, when you clamp blood flow will cease to the brain

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15
Q

What is the artery of adamkiewicz?

A

artery that provides perfusion to the spinal cord

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16
Q

What is unique about the artery of adamkiewicz?

A

Its location varies in individuals

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17
Q

What coronary artery perfuses the inferior portion of the heart?

A

Right coronary artery

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18
Q

What coronary artery perfuses the anteroseptal portion of the heart?

A

LAD

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19
Q

What coronary artery perfuses the anteroapical portion of the heart?

A

Distal portion of LAD

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20
Q

What coronary artery perfuses the anterolateral portion of the heart?

A

Circumflex artery

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21
Q

What coronary artery perfuses the posterior portion of the heart?

A

Right coronary artery

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22
Q

What causes concentric hypertrophy?

A

Chronic pressure overload as occurs with chronic hypertension or aortic valve stenosis

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23
Q

How does concentric hypertrophy occur?

A

The ventricular chamber radius may not change; however, the wall thickness greatly increases as new sarcomeres are added in-parallel to existing sarcomeres.

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24
Q

What complications are associated with concentric hypertrophy?

A

This type of ventricle becomes “stiff” (i.e., compliance is reduced), which can impair filling and lead to diastolic dysfunction.

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25
Q

What causes eccentric hypertrophy?

A

Occurs when there is both volume and pressure overload.

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26
Q

How does eccentric hypertrophy occur?

A

Chamber dilation occurs as new sarcomeres are added in-series to existing sarcomeres.

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27
Q

What is the normal RA pressure?

A

4mmHg (Range 2-6mmHg)

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28
Q

What is the normal saturation of blood entering the RA?

A

75%

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29
Q

What is normal RV pressure?

A

25mmHg Ranges given for Systolic 15-30mmHg

0 mmHg Ranges given for Diastolic 2-8mmHg

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30
Q

What is the normal saturation of blood in the RV?

A

75%

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31
Q

What is normal PA pressure?

A

25 mmHg Ranges given for systolic 15-30mmHg

10 mmHg Ranges given for diastolic 8-15mmHg

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32
Q

What is the saturation of the blood in the pulmonary arteries before it has reached the lungs?

A

75%

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33
Q

What is the saturation of the blood in the pulmonary veins?

A

95%

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34
Q

What is the normal LA pressure?

A

6mmHg Range 4-12mmHg

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35
Q

What is the normal LV pressure?

A

100 mmHg

0 mmHg

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36
Q

What is the normal pressure in the aorta?

A

100mmHg

70 mmHg

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37
Q

What occurs in stable angina?

A

Lumen narrowed by plaque and inappropriate vasoconstriction

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38
Q

What occurs in unstable angina?

A

Plaque rupture, platelet aggregation, thrombus formation and unopposed vasoconstriction

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39
Q

What causes variant angina?

A

No overt plaques and intense vasospasm

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40
Q

What order does the ischemic cascade occur?

A

Occlusion of artery –> stiffness during filling –> reduced emptying –> Increased heart and lung pressure –> EKG changes –> Anginal chest pain

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41
Q

What causes pulmonary congestion during myocardial ischemia?

A

Decreased systolic function and decreased diastolic compliance

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42
Q

How is stroke volume represented in a cardiac pressure volume loop?

A

The area of the figure

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43
Q

What should occur normally in diastole?

A

The ventricles fill with blood

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44
Q

What should occur normally in systole?

A

The ventricles pump out about 60% of the blood

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45
Q

What occurs in diastole with systolic dysfunction?

A

The enlarged ventricles fill with blood

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46
Q

What occurs in systole with systolic dysfunction?

A

The ventricles pump out less than 40-50% of the blood

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47
Q

What occurs in diastole with diastolic dysfunction?

A

The stiff ventricles fill with less blood than normal

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48
Q

What occurs in systole with diastolic dysfunction?

A

The ventricles pump out about 60% of the blood but the amount may be lower than normal

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49
Q

What what decade of life does initial lesion and fatty streaks occur in formation of atherosclerosis?

A

From the first decade

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50
Q

What decade of life do intermediate lesions and atheromas occur in formation of atherosclerosis?

A

From third decade

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51
Q

In what decade does fibroatheroma and complicated lesions occur in formation of atherosclerosis?

A

From fourth decade

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52
Q

What is the main growth mechanism for atherosclerosis in the first three decades of life?

A

Growth mainly by lipid addition

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53
Q

What causes growth of atherosclerosis after the forth decade of life?

A

Increased smooth muscle and collagen

Thrombosis and or hematoma

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54
Q

What is considered an initial lesion in relation to atherosclerosis?

A

Histologically normal
Macrophage infiltration
Isolated foam cells

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55
Q

What causes the fatty streak in atherosclerosis formation?

A

Mainly intracellular lipid accumulation

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56
Q

What is considered an intermediate lesion in relation to atherosclerosis?

A

Intracellular lipid accumulation

Core of extracellular lipid

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57
Q

What causes an atheroma?

A

Intracellular lipid accumulation

Core of extracellular lipid

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58
Q

What is considered a complicated lesion in relation to atherosclerosis?

A

Surface defect
Hematoma Hemorrhage
Thrombosis

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59
Q

What causes a fibroatheroma?

A

Single or multiple lipid cores

Fibrotic/calcific layers

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60
Q

How do we calculate wall tension?

A

Pressure = Tension in wall

Radius

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61
Q

When does myocardial ischemia occur?

A

When oxygen demand exceeds oxygen supply

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62
Q

When myocardial ischemia occurs, what two factors cause pulmonary congestion?

A

Decreased systolic function and decreased diastolic compliance

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63
Q

What does myocardial ischemia cause?

A

Decreased systolic function
Decreased diastolic function
Papillary muscle dysfunction
Increased sympathetic tone

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64
Q

What is the most common type of HTN?

A

Essential, meaning there is no identifiable cause

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65
Q

What are the two main effects of systemic HTN?

A

Increased after load

Arterial damage

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66
Q

How does an increased after load affect the body?

A

Systolic dysfunction
LVH
Increased myocardial demand

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67
Q

How does arterial damage affect the body?

A

Accelerated atherosclerosis

Weakens vessel wall

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68
Q

What conditions can occur if there is weakening to the aorta as well as accelerated atherosclerosis?

A

Aortic aneurysm
Dissection
Stroke

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69
Q

What is congestive heart failure?

A

When the heart is unable to pump blood at rate to meet tissue metabolic requirements or do so only with elevated filling pressures

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70
Q

What is the end result of CHF?

A

The heart transforms into a neuroendocrine organ meaning catecholamines are depleted and bear hormones shifts the heart from responsive SNS to responsive to adrenal medulla

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71
Q

What type of symptoms are seen with left heart failure?

A

Pulmonary symptoms

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72
Q

What type of symptoms are seen with right heart failure?

A

Systemic symptoms

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73
Q

What are the evolutionally steps to CHF?

A

Cardiac injury –> neurohormonal activation –> cardiac remodeling –> fluid retention –> peripheral vasoconstriction –> contractile failure

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74
Q

What are the four factors that can be manipulated to improve CO?

A

HR
Preload
Afterload
Contractility

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75
Q

What conditions are known to cause heart failure?

A 
Ischemia
Valvular disease
Cardiomyopathy
Restrictive disease
Non cardiac causes
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76
Q

What non cardiac diseases can cause heart failure?

A

HTN, PE, High output states and thyrotoxicities

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77
Q

What is the most common cause of heart failure?

A

Ischemia

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78
Q

What hormone is known to be cardioprotective?

A

Estrogen, many post menopausal women develop cardiac issues

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79
Q

What is the problem associated with systolic dysfunction?

A

Problem with LV ejection which causes decreased contractility and SV at any given end diastolic volume

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80
Q

What is the problem associated with diastolic dysfunction?

A

Problem with LV filling due to decreased compliance, however contractility is normal
Impaired relaxation and restricted filling

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81
Q

How does the heart normal fill in diastole?

A

Energy dependent process requiring ATP to move Ca out

No O2 = no ATP = can’t relax heart

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82
Q

What pathologies are known to cause systolic HF?

A

Ischemic damage/dysfunction
Chronic pressure overload
Chronic volume overload
Non ischemic cardiomyopathy

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83
Q

What are majority of CHF cases the result of?

A

Impair contractile function (EF

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84
Q

What mechanism is used to compensate for the increased preload in systolic HF?

A

Frank Starling, however limited

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85
Q

What are characteristics of diastolic HF?

A

Reduced compliance with normal contractility (EF > 40-45%)

Increased preload = increased LVEDP

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86
Q

What pathologies are known to cause diastolic HF?

A

Pathological myocardial hypertrophy
Restrictive cardiomyopathy
Aging
Ischemic fibrosis

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87
Q

What are the primary compensatory mechanisms when heart failure occurs?

A 
Increased preload
Increased SNS tone
RAAS activated
AVP released 
Ventricular remodeling
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88
Q

How does the SNS impact the heart?

A

Augments myocardial contractility
Increases HR and TPR (after load)
Arterial constriction

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89
Q

What occurs when chronic SNS activation is necessary for HF?

A

Decreased response to catecholamines (down regulated) predominately B receptors

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90
Q

Why is anesthesia so challenging in HF patients?

A

Catecholamine dependent, anesthesia causes a withdrawl of the SNS

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91
Q

How is the RAAS activated in HF patients?

A

Macula densa of kidney sense low sodium from decreased blood flow to kidneys causing the JG cells to release renin

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92
Q

What is the role of renin in the RAAS system?

A

It acts upon a circulating substrate, angiotensinogen, that forms angiotensin I.

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93
Q

Where is ACE located?

A

Predominately in the lungs, however found in the kidneys

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94
Q

What is the role of ACE in the RAAS?

A

Converts angiotensin I to angiotensin II

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95
Q

How does Angiotensin II contribute to HF?

A 
Cardiac and vascular hypertrophy
Systemic vasoconstriction
Increases blood volume
Stimulates the release of aldosterone
Sodium and fluid retention
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96
Q

What causes the release of vasopressin?

A

SNS
Angiotensin II
Decreased atrial receptor firing
Hyperosmolarity

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97
Q

What effects does vasopressin have on the heart?

A

Agonizes V1 receptors which causes vasoconstriction and increases after load
Agonizes V2 receptors of the kidney which reduces free water clearance (hyponatremia)

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98
Q

How does vasopressin affect the heart?

A

Causes remodeling of the heart

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99
Q

What is ventricular remodeling?

A

Increased size of individual cells without increasing the quantity

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100
Q

What type of hypertrophy is seen in HF with pressure overload?

A

Concentric Hypertrophy

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101
Q

What are the properties of concentric hypertrophy?

A

Increased systolic wall stress
Large increase in wall thickness, decreased area for volume
Thickening of individual myocytes
Parallel replication of myofibrils

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102
Q

What type of hypertrophy is seen in HF with volume overload?

A

Eccentric hypertrophy

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103
Q

What are the properties of eccentric hypertrophy?

A

Increased diastolic wall stress
Mild increase n wall thickness
Myocyte elongation
Replication of myofibrils in series

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104
Q

What New York Hear Association classification is a person that ordinary physical activity does not cause symptoms?

A

Class I

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105
Q

What New York Hear Association classification is a person that symptoms occur at rest?

A

Class IV

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106
Q

What New York Hear Association classification is a person that less than ordinary activity causes fatigue, palpitations or dyspnea

A

Class III

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107
Q

What New York Hear Association classification is a person that ordinary activity causes fatigue, palpitations or dyspnea

A

Class II

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108
Q

What are indications seen on physical assessment that a patient has poor ventricular function?

A

S3 heart sound
EKG abnormalities
EF 15mmHg
ECHO shows hypokinesis, akinesia, aneurysm of ventricle dyskinesia

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109
Q

What physical assessment finding has the greatest predictive accuracy of HF?

A

S3 heart sound

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110
Q

What tool is used to assess the extent of HF without imaging or tests?

A

Metabolic score based on activities

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111
Q

How many mets are given to a patient that is able to play tennis, swim, partake in strenuous sports and had normal exercise tolerance?

A

> 10 mets

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112
Q

How many mets are given to a patient that is able to climb stairs, have sex, gold, push a vacuum and jog with a moderate level of exercise tolerance?

A

4-10 mets

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113
Q

How many mets are given to a patient that is able to only eat, dress and walk around the house with minimal exercise tolerance?

A

1-4 mets

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114
Q

What is shock?

A

Abnormality of the circulatory system in which there is inadequate tissue perfusion because of relatively low or absolutely inadequate cardiac output

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115
Q

What are the four types of shock?

A

Hypovolemic
Distributive
Cardiogenic
Obstructive

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116
Q

How does increased levels of lactate affect the body?

A

Myocardial depressant, decreased peripheral response to catecholamine and can cause coma

117
Q

What are the bodys compensatory mechanisms to shock?

A

Tachycardia, Vasoconstriction, Tachypnea, Restlessness, interstitial movement of fluid int capillaries, RAAS, vasopressin, plasma protein synthesis

118
Q

What is the progression of shock?

A

Decreased pulse pressures or MAP
Decreased input to baroreceptors
Increased vasomotor discharge
Generalized vasoconstriction except to heart and brain
Tachycardia, water retention, decreased GFR, norepi, angiotensin II, carotid and aortic chemoreceptors

119
Q

What is refractory shock?

A

Occurs when the patient does not die immediately but they do not get better
Eventually no response to vasopressors or volume

120
Q

What factors can lead to refractory shock?

A

Decreased cerebral perfusion
Myocardial failure
Pulmonary damage –> ARDs

121
Q

What is the cause of hypovolemic shock?

A

Inadequate blood volume

122
Q

What are the four types of hypovolemic shock?

A

Hemorrhagic
Traumatic
Surgical
Burn

123
Q

At what amount of blood loss is considered hemorrhagic hypovolemia?

A

5-15mL/kg

124
Q

How long does it take for an increase in erythropoietin to occur?

A

4-8 weeks to restore RBC to normal

125
Q

What is the cause of traumatic hypovolemia?

A

Damage to muscle and bone

126
Q

Where is a common place that blood can hide in traumatic hypovolemia?

A

The thigh 1L may only increase diameter by 1cm

127
Q

What is crush syndrome?

A

When pressure is relieved from previously crushed skeletal muscles, the muscles are reperfused and free radicals ae generated
Calcium, potassium, myoglobin and fat

128
Q

What is surgical shock?

A

A combination of external hemorrhage bleeding into tissues and dehydration

129
Q

What is cardiogenic shock?

A

When the pumping action go the heart is impaired to the point that tissue perfusion needs are not met

130
Q

What are common causes of cardiogenic shock?

A

Dysrhythmias
Acute valvular dysfunction
Ruptured ventricle
Pump failure

131
Q

What type of shock is considered warm shock?

A

Distributive shock

132
Q

What is the cause of distributive shock?

A

Massive peripheral vasodilation

133
Q

What is neurogenic shock?

A

An interruption in the transmission of autonomic activity results in vasodilation and peripheral pooling of blood

134
Q

What is obstructive shock?

A

Congestion prevents blood from being distributed appropriately

135
Q

What are common causes of distributive shock?

A 
Cardiac tamponade
Massive PE
Tension pneumothorax
Pericardial disease
Cardiac tumor
136
Q

When is recall most likely to occur in a compromised patient?

A

During times of HoTN and shock

137
Q

Define cardiomyopathy?

A

A heterogenous group of diseases of the myocardium associated with mechanical or electrical dysfunction that usually exhibit inappropriate ventricular hypertrophy or dilation and are due to a variety of causes that are frequently genetic

138
Q

What are the three types of cardiomyopathies?

A

Dilated
Hypertrophic
Restrictive

139
Q

How does dilated cardiomyopathy occur?

A

There is myocardial injury that causes a decrease in contractility and SV
Results in increased ventricular filling pressures, LV dilation and decreased CO

140
Q

What part of the cardiac cycle does dilated cardiomyopathy affect?

A

Problem with systole

141
Q

What are common symptoms seen with dilated cardiomyopathy?

A 
Pulmonary congestion
Systemic congestion
Low CO, fatigue weakness
HoTH, tachycardia, tachypnea
A-fib and complex PVC
142
Q

What is the treatment for dilated cardiomyopathy?

A

Limit activity
Salt/fluid restriction
Pharmacology –> ACE inhibitors, diuretics, digoxin, anticoagulants

143
Q

What are some poor prognosis indicators in dilated cardiomyopathy?

A

EF 20mmHg

Cardiac index

144
Q

What is the primary reason a patient required an immediate heart transplant?

A

Dilated cardiomyopathy

145
Q

What is peripartum cardiomyopathy?

A

Enlargement of the heart due to preegnancy

146
Q

What are risk factors for peripartum cardiomyopathy?

A

Obesity, smoking, ETOH abuse, multiple pregnancies, poor nutrition, personal history of myocarditis and age greater than 30

147
Q

What drugs are desirable to use in peripartum cardiomyopathy?

A

After load reducing drugs
Inodilators
Nitrates

148
Q

What is the most common genetic CV disease?

A

Hypertrophic cardiomyopathy

149
Q

What is the presentation of hypertrophic cardiomyopathy?

A

Hypertrophy of the LV particularly the ventricular septum, in the absence of other causes

150
Q

Why is there varying clinical manifestation seen in hypertrophic cardiomyopathy?

A

Morphologic and hemodynamic abnormalities

151
Q

How does low stroke volume occur with hypertrophic cardiomyopathy?

A

Systolic anterior motion of the mitral valve leaflet created by LV ejection velocity during systole as blood is ejected into the aorta can cause obstruction of the LV outflow

152
Q

What can make the CO worse in hypertrophic cardiomyopathy?

A

Obstruction is worse if preload is low

153
Q

What part of the cardiac cycle does hypertrophic cardiomyopathy affect?

A

A disease of diastolic dysfunction

154
Q

In hypertrophic cardiomyopathy, what does the heart depend on for ventricular filling?

A

Atrial kick, isn’t able to passively fill during diastole

155
Q

What is often the first sign of hypertrophic cardiomyopathy?

A

Sudden death from arrhythmias

156
Q

What is the predominate cause of hypertrophic cardiomyopathy?

A

Genetic, myofibrils are not arranged appropriately

157
Q

What are the variations of hypertrophic cardiomyopathy?

A

Symmetric hypertrophy
Atypical hypertrophy
Asymmetric septal hypertrophy without obstruction
Asymmetric septal hypertrophy with obstruction

158
Q

What are the characteristics of symmetric hypertrophy?

A

Symmetric or concentric hypertrophy

159
Q

What are the characteristics of atypical hypertrophy?

A

Atypical hypertrophy

Small cavity remains

160
Q

What are the characteristics of asymmetric septal hypertrophy without obstruction?

A

Cavity size reduced but mitral valve in appropriate position

161
Q

What are the characteristics of asymmetric septal hypertrophy with obstruction?

A

Mitral valve presses against septum causing obstruction Systolic anterior motion of mitral valve (SAM)
Mitral regurgitation

162
Q

What can cause an increase in LVOT obstruction with hypertrophic cardiomyopathy?

A 
Increased contractility
Beta stimulation
Decreased preload/vasodilators 
Tachycardia 
Positive pressure ventilation
163
Q

What can cause a decrease in LVOT obstruction with hypertrophic cardiomyopathy?

A

Beta blockers/ CCB
Increased after load/ alpha stimulation
Volatile anesthetics
Increase preload

164
Q

What drugs should be avoided in patients with hypertrophic cardiomyopathy?

A

Nitroglycerin, sodium nitroprusside

165
Q

What is the definitive treatment for patients with hypertrophic cardiomyopathy?

A

Heart transplant
May have palliative procedures such as myomectomy (resection of septum) and septal ablation to decrease the outflow obstruction

166
Q

What occurs in restrictive cardiomyopathy?

A

The walls of the ventricles become still but not necessarily

167
Q

What part of the cardiac cycle does restrictive cardiomyopathy affect?

A

Problem with diastole

168
Q

What is the main cause of restrictive cardiomyopathy?

A

Amyloidosis –> infiltrative

169
Q

What is the pathophysiology of restrictive cardiomyopathy?

A

Rigid myocardium causes increased diastolic ventricular pressure and decreased ventricular filling

170
Q

How does restrictive cardiomyopathy typically present?

A

Heart failure without cardiomegaly, the chambers are still and non compliant

171
Q

Why aren’t patients with restrictive cardiopathy typically a candidate for a heart transplant?

A

Due to the systemic nature of the disease, even if receive new heart the process will reoccur with the new heart

172
Q

What is the treatment for restrictive cardiomyopathy?

A

Diuretics to treat pulmonary and systemic congestion, supportive measurements

173
Q

What are some anesthetic considerations for patients with restrictive cardiomyopathy?

A

Maintain NSR because stroke volume is fixed

Maintain venous return and IV fluid volume

174
Q

What structure supports the heart and limits displacement?

A

Pericardial Ligamentous

175
Q

What structures protect the heart from external friction?

A

Pericardial Membranous

176
Q

What encloses the heart in a relatively fluid filled envelop which prevents acute cardiac dilation and preserves normal ventricular compliance?

A

Pericardial Mechanical

177
Q

How much fluid is usually in the pericardial sac?

A

10-20mL, up to 100mL can enter before symptoms are seen

178
Q

What are common causes of cardiac tamponade?

A

Trauma
Post open heart surgery
Enlarging pericardial effusion

179
Q

How can cardiac tamponade be life saving if blunt force trauma to the chest occurs?

A

Prevent exsanguination when heart/great vessels are traumatized

180
Q

What are some common causes of a slowly enlarging pericardial effusion?

A 
Bacterial/viral infections
Malignancy and Radiation
Uremia
Connective tissue disorder
Bleeding from anticoagulants
181
Q

What is the best tool to determine if cardiac tamponade is present?

A

TEE

182
Q

How is the transmural pressure affected in cardiac tamponade?

A

There is an increase in transmural pressure

(pressure inside - pressure outside) the pressure inside becomes greater

183
Q

Why does HoTN occur in cardiac tamponade?

A

Decreased pulmonary blood flow leads to a decrease in return to the LV
Decreased end diastolic volume

184
Q

What is the end result of cardiac tamponade?

A

All chambers will equal outside of the heart leading to limited movement of blood

185
Q

How can cardiac output be maintained during cardiac tamponade?

A

If CVP exceeds right ventricular end diastolic pressure

186
Q

What does increased intrapleural pressure lead to?

A

Impaired diastolic filling of the heart, decreased stroke volume and HoTN with extreme SNS activation

187
Q

What are telltale signs go advanced tamponade?

A

HoTN
Tachycardia
JVD
Pulsus paradoxes of > 10mmHg

188
Q

What are the components of bucks triad and when does this occur?

A

Quiet heart sounds
Increased jugular venous pressure
HoTN
This occurs in advanced cardiac tamponade

189
Q

What is the treatment for cardiac tamponade?

A

Surgery or a pericardial fluid removal

Volume expansion and inotropic therapy are temporary measures

190
Q

What should the provider anticipate treating after the cardiac tamponade has resolved?

A

HTN from extreme SNS activation

191
Q

What anesthetic consideration should be made for a patient with cardiac tamponade?

A

Stable induction (Etomidate) extremely HoTN
Positive pressure ventilation can cause life threatening HoTN
Correct metabolic status and infuse catecholamines

192
Q

What is known to cause acute pericarditis?

A

Viral infection or post infarction

193
Q

Why symptoms are typically seen with acute pericarditis?

A

Chest pain aggravated by deep breathing, lying supine or coughing
Tachypnea
EKG changes –> ST elevation and T wave inversion

194
Q

What is the treatment for acute pericarditis?

A

Aspirin

Avoid steroids

195
Q

What is known to cause constrictive pericarditis?

A

Usually idiopathic, but can be caused by previous cardiac surgery or radiation therapy, TB and calcifications

196
Q

What symptoms are associated with constrictive pericarditis?

A

Increased CVP and low CO

Decreased exercise tolerance, fatigue, JVD, hepatic congestion, ascites and peripheral edema

197
Q

What other cardiac ailment can constrictive pericarditis be confused for?

A

Mimics RV failure without pulmonary congestion

198
Q

What is the end result of constrictive pericarditis?

A

Eventually RA = RVEDP = LVEDP

As pericardial pressure increases so does RAP in parallel

199
Q

What is the treatment for constrictive pericarditis?

A

Pericardectomy

200
Q

What is the square root signs and what cardiac ailment is it associated with?

A

A pressure contour recorded by cardiac catheterization, which consists of an elevation of the right ventricular diastolic pressure with early filling and a subsequent plateau, a finding suggestive of chronic constrictive pericarditis

201
Q

What is regurgitation?

A

Leaking or back flow of blood across valve

202
Q

What is stenosis?

A

Obstruction of forward flow across an opened valve

203
Q

What occurs during systole?

A

The aortic valve and the pulmonic valves are open and the mitral and tricuspid valves are closed

204
Q

What valvular disease is seen in systole?

A

Mitral regurgitation

Aortic stenosis

205
Q

What occurs during diastole?

A

Aortic and Pulmonic valves are closed while the tricuspid and mitral valves are closed

206
Q

What valvular diseases occurs in diastole?

A

Aortic regurgitation

Mitral stenosis

207
Q

What is the issue in mitral stenosis?

A

Increased left trial after load results in impaired LV filling and reduced SV and CO

208
Q

What is the result of mitral stenosis?

A

Problem with pressure = concentric hypertrophy of LA and atrophy of the LV

209
Q

What type of symptoms are seen with mitral stenosis?

A

Pulmonary, blood backs up from LA to pulmonary vaculature

210
Q

What is typically the cause of Rheumatic fever?

A

Group A strep

211
Q

What are normal LA pressures?

A

8-10mmHg

212
Q

What are anesthetic considerations for mitral stenosis?

A

Keep HR

213
Q

What drugs are good to give to patients with mitral stenosis?

A

Opioids
Small dose of BB
Phenylephrine

214
Q

What drugs are bad to give to patients with mitral stenosis?

A

Potent vasodilators

Ketamine, etomidate, ephedrine and pavulon

215
Q

What is an appropriate level to keep SVR in a patient with mitral stenosis?

A

SVR 800-1200mmHg

216
Q

What is important to remember with mitral stenosis?

A

Sinus, slow and tight

217
Q

When does mitral regurgitation occur?

A

During Systole

218
Q

What is a major cause of acute mitral regurgitation?

A

Posterior papillary muscle ischemia

219
Q

What occurs in mitral regurgitation?

A

Reduced forward SV, reduced backward flow from the LV into the LA

220
Q

How does the heart initially respond to mitral regurgitation?

A

The CO increases due to FS and SNS however eventually contractility is less

221
Q

What type of LV hypertrophy occurs with mitral regurgitation?

A

It is an issue with volume overload so eccentric LV hypertrophy occurs

222
Q

What does the EF look like in patients with mitral regurgitation?

A

The EF is overestimated since blood is being ejected and flows in two directions

223
Q

How do we calculate EF and what is a normal value?

A

EF = SV/ EDV x 100 = percentage

Normal is > 60%

224
Q

What are common causes of mitral regurgitation?

A 
Annular calcifications
Papillary muscle rupture or dysfunction
Chordae tendonae rupture 
Endocarditis
Rheumatic disease
MVP
225
Q

What causes mitral valve prolapse?

A

Myxomatous degeneration of the posterior mitral valve leaflet which leads to systolic prolapse of the MV leaflets into the left LA

226
Q

What can be used to diagnose mitral valve prolapse?

A

Murmur, mild systolic click and ECHO

227
Q

What does MVP look like on an ECHO?

A

Valve leaflets balloon upward as the ventricle contracts

228
Q

Which artery feeds the posterior leaflet of the MV?

A

Posterior descending artery

229
Q

What arteries perfuse the anterior leaflet of the MV?

A

LAD and circumflex

230
Q

What artery is perfusing if right dominance is noted in the chart?

A

A branch of the right coronary artery

231
Q

What artery is perfusing if left dominance is noted in the chart?

A

A branch of the circumflex coronary artery

232
Q

What artery is perfusing if co dominance is noted in the chart?

A

Anastomosis of the left and right coronary artery

233
Q

What symptoms are typically seen with mitral regurgitation?

A

Low CO
Severe pulmonary congestion
A-Fib (remodeling of LA)

234
Q

What are determinants of the amount of volume regurgitated?

A 
Size of office
HR
LA-LV pressure gradient during systole
SVR
LA compliance
235
Q

What is the treatment for mitral regurgitation?

A

Maintain contractility
Avoid Tachycardia and increased SVR
Relieve wall stress

236
Q

What drugs are beneficial for mitral regurgitation?

A 
Digoxin
Diuretics
Anticoagulation (A fib)
Vasodilators
ACE inhibitors
237
Q

What should the provider remember about mitral regurgitation?

A

Fast Full and forward
Fast HR 80-100
Full beyond normal
Forward Avoid acute increases in after load

238
Q

What should be avoided in mitral regurgitation?

A

Anything that will decrease HR and LV contractility

Anything that will increase SVR

239
Q

What is seen with PAC monitoring that can tell the degree of mitral regurgitation?

A

V waves

240
Q

How does atrial compliance affect the symptoms a patient presents with mitral regurgitation?

A

Low atrial compliance will cause vascular congestion and edema
High atrial compliance will cause signs of decreased CO

241
Q

What is the most beneficial intervention for patients with mitral regurgitation?

A

After load reducers, it increases SV and decreases the amount regurgitated

242
Q

If what phase of the cardiac cycle is aortic stenosis a problem?

A

During systole

243
Q

What type of LV hypertrophy occurs with aortic stenosis?

A

There is an issue with pressure, concentric hypertrophy occurs

244
Q

What is the normal AO valve area compared to critical stenosis?

A

Normal: 3.5-4cm

Critical stenosis:

245
Q

Why is the atrial kick so important in aortic stenosis?

A

When the LA pressures are equal to the LV pressure there won’t be any passive filling, the atrial kick is what allows blood to pass into the LV

246
Q

Why might angina be the first sign that a patient has aortic stenosis?

A

Left ventricular end diastolic pressure increases causing the LAP to increase and O2 demand increases

247
Q

What findings may indicate aortic stenosis on physical examination?

A

S4 mid systolic murmur and carotid pulses that come and go

The intensity of the pulses vary

248
Q

What is a poor indicator in the prognosis of aortic stenosis?

A

A-fib

249
Q

What are considered the big three symptoms in aortic stenosis?

A

Angina
Syncope
CHF

250
Q

What is the benefit of developing concentric hypertrophy in aortic stenosis?

A

Enables the LV to maintain SV by generating transvalvular pressure needed to cross the valve

251
Q

Why does contractility progressively worse in patients with aortic stenosis?

A

Reduced LV compliance due to LVH and diastolic dysfunction

252
Q

What is LV filling dependent on in aortic stenosis?

A

Atrial systole (atrial kick)

253
Q

Why does Afib cause death in aortic stenosis?

A

Loss of atrial kick causing blood stasis in the heart

254
Q

Why isn’t bradycardia tolerated in aortic stenosis?

A

SV is fixed thus the only way to increase CO is HR

255
Q

What are anesthetic considerations in patients with aortic stenosis?

A

Maintain NSR, SVR

Avoid tachycardia and intravascular volume

256
Q

What anesthetic should be avoided in patients with aortic stenosis?

A

Spinal anesthesia

257
Q

Why do patients with aortic stenosis have a poor response to CPR?

A

It is difficult to generate enough pressure for forward flow

258
Q

What occurs in aortic regurgitation?

A

Failure of the aortic leaflet to coapt causing SV to leak back into the LV

259
Q

In what part of the cardiac cycle does aortic regurgitation occur?

A

Diastole

260
Q

What type of LV hypertrophy is associated with aortic regurgitation?

A

Eccentric hypertrophy, there is a problem with volume into the LV

261
Q

What problem develops after time in aortic regurgitation?

A

Initial volume overload of the LV then pressure overload develops

262
Q

What population is aortic regurgitation most common in?

A

Males 30-60years old

263
Q

What is the difference between chronic and acute aortic regurgitation?

A

Chronic occurs over time FS law to compensate at first, enlarge LA develops
Acute is not compatible with life, the patient has a normal size LA and fluid immediately backs up into the lungs causing HF

264
Q

What are usually the causes of acute aortic regurgitation?

A

Trauma

Aortic dissection

265
Q

What pathologies have been known to cause aortic regurgitation?

A 
Infective endocarditis
Rheumatic fever
Bicuspid aortic valve (supposed to be tricuspid)
Marfans syndrome
Syphilis
HTN
Aortic root dilation
Weight loss drugs
266
Q

What are clinical signs of aortic regurgitation?

A 
Enlarged and displaced apex
Widened pulse pressures
Austin flint murmur
Bounding pulses
Aortic diastolic murmur
267
Q

How does the aortic diastolic murmur change with severity?

A

Length correlates with severity

Acute AR the murmur shortens as aortic DP = LVEDP and mitral pre-closure occurs

268
Q

What is the pathology of acute AR?

A

Normal size LV is suddenly overloaded, high LAP causes pulmonary edema

269
Q

What is the pathology of chronic AR?

A

Primarily LV dilation and LV hypertrophy

Low aortic diastolic BP and widened pulse pressures are seen

270
Q

What can be seen on a chest X-ray in patients with chronic AR?

A

Enlarged ventricular silhouette

271
Q

What is the treatment for symptomatic AR?

A

Preserve LV function and aferload reduction

272
Q

When is surgical intervention required in aortic regurgitation?

A

When the EF is

273
Q

What makes up the total stroke volume in aortic regurgitation?

A

It is both the forward and the regurgitant volume combined

274
Q

How should a patient with aortic regurgitation be managed?

A

Fast HR 80-100- deceases time in diastole
Full maintain preload
Forward avoid drugs that increase SVR and depress the myocardium

275
Q

What drug can be used to maintain coronary perfusion?

A

Phenylephrine to maintain coronary perfusion pressure however over use can increase SVR and cause more regurgitation

276
Q

What patient population require prophylactic antibiotics for dental care?

A

Prosthetic heart valve
Valvular repair
History of endocarditis
Congenital heart abnormalities ecept PFO

277
Q

What are the three layers of the blood vessel?

A

Intimia
Media
Adventisia

278
Q

What are characteristics of a true aneurysm?

A

The entire wall balloons out (all three layers)

279
Q

What do we call true aneurysm that are symmetrical?

A

Fusiform aneurysms

280
Q

What do we call true aneurysms that only dilate on one side?

A

Saccular aneurysms, one side has been exposed to chronically high BP than the other side
Also known as Beri aneurysms

281
Q

What are characteristics of a pseudo aneurysm (false)?

A

Occur from a puncture to one of your vessels such as with an arterial injection and blood leaks outside of the vessel wall
Not actual dilation of the vessel, does have similar shape

282
Q

What are major risk factors associated with aneurysm development?

A

Atherosclerosis
Smoking (directly damages blood vessel wall)
COPD
HTN
Male
Age > 65y/o (stiffened aorta)
Genertics –> connective tissue disorder or family Hx

283
Q

What symptoms may be seen in an intact aneurysm?

A

Compression of structures (RLN, VC, trachea, esophagus)

Pain in region

284
Q

What symptoms may be seen in a ruptured aneurysm?

A

HoTN
Syncope
Hemypotysis
Vomiting blood

285
Q

What is an aortic dissection?

A

When you develop a tear between your intima and media in your aortic wall
It tears the layers away from each other

286
Q

What is a type A dissection?

A

The tear occurs in the ascending part of the aorta, before left subclavian artery

287
Q

What is the goal of a Type A dissection?

A

To replace the affected aorta

288
Q

How are type B dissections treated?

A

Conservative therapy

Don’t get as invasive because surgery is a larger risk that pharmacological management

289
Q

What drugs are used to manage a type B dissection?

A

Low BP
SNP –> vasodilator decreased BP
BB –> beta receptors can’t be activated to decrease HR
CCB –> vasodilates

Pathophysiology I (4 decks)

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