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CVPR 312 Cardiac Pathophysiology > CVPR 312 Cardiac Pathophysiology / Lecture 2 / Ischemic Heart Disease > Flashcards

CVPR 312 Cardiac Pathophysiology / Lecture 2 / Ischemic Heart Disease Flashcards

1
Q

Ischemic Heart Disease (IHD) is Characterized by changes in the cardiac muscle that occur when ?

A

Coronary arterial oxygen supply is inadequate to meet myocardial metabolic demands.

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2
Q

Coronary sinus SvO2 =

A

30%

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3
Q

Inadequate blood supply (circulation) to a local area due to blockage of the blood vessels to the area.

A

Ischemia

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4
Q

An oxygen deficiency in body tissues

A

Hypoxia

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5
Q

Hypoxemia

A

Decreased PaO2

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6
Q

Anoxia

A

Absence of oxygen

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7
Q

Cyanosis

A

a bluish skin tint caused by inadequate oxygenation of the bloodstream.

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8
Q

Myocardial Ischemia (MI) can be du to the following 2 things?

A
  • Acute coronary thrombosis

- Coronary atherosclerosis

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9
Q

Most Common cause of death in the industrialized world

A
  • 500,000 die annually

- 12 million affected in US

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10
Q

Risk Factors for Myocardial Ischemia

A 
HTN
DM
Cigarette smoking
Hyperlipidemia …Cholesterol (LDL)
Obesity
Sedentary lifestyle
Psychological stress
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11
Q

Most frequent cause of coronary blood flow and myocardial ischemia ?

A

Atheromatous plaque

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12
Q

Coronary vasoconstriction / spasm Typically occurs at or near plaque and ?

A

damaged endothelium

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13
Q

Coronary emboli often results from ?

A

thrombi from LV or prosthetic valves

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14
Q

Severe hypotension

A

MAP < 45-55 mmHg = loss of coronary autoreg

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15
Q

In the precence of CAD pressure even higher than ___ may be needed to prevent ischemia.

A

70 mmHg

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16
Q

Causes of Myocardial Ischemia (cont.)

A
  • Aortic Valve stenosis
  • Hypertrophic cardiomyopathy
  • Inflammatory dz of coronary arteries
  • Congenital anomalies of the coronary circulation
  • Extremely raid heart rate
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17
Q

Imbalance between O2 Sypply & O2 demand

Predisposes patients to ?

A
  • Myocardial ischemia
  • Ventricular dysfunction
  • Electrical Instability
  • MI
  • Possible death from dysrhythmias or heart failure
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18
Q

At rest the myocardium extracts about ___________ of the O2 from coronary arterial blood

A

70-80%

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19
Q

Consequently, any increased O2 demand must be met by

A

increases in blood flow

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20
Q

In the myocardial oxygen supply - demand balance patients may develop myocardial ischemia if:

A
  1. ) Myocardial oxygen supply falls short of demand

2. ) Myocardial oxygen demand exceeds supply

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21
Q

In regards to the coronary arterial blood supply, the

LEFT coronary artery supplies what?

A

Anterior & Lateral portions of the LV

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22
Q

In regards to the coronary arterial blood supply, the

RIGHT coronary artery supplies what?

A

RV & posterior LV

80-90% of people

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23
Q

% of Coronary venous blood that comes from the LV to the Coronary Sinus ?

A

75% of total

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24
Q

From the RV to the > ________ > RA

A

anterior cardiac vein

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25
Q

_____ _____ empty directly into all chambers (very small amount)

A

Thebesian veins

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26
Q

Normal coronary blood flow at rest?

A

225 ml/min

4 - 5 %

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27
Q

Normal coronary blood flow

A
  • Phasic in nature esp. in LV
  • Low flow during systole (compression)
  • High flow during diastole (relazed state)
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28
Q

Normal coronary artery structure starting from the outside.

A
  • Adventia
  • Media
  • Intima
  • Endothelium
  • Lumen
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29
Q

Angina Pectoris

A

Chest pain caused by fleeting deficiency in oxygen delivery to myocardium

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30
Q

Drug treatment of Angina Pectoris

A
  • Nitroglycerin = vasodilator
  • Beta blockers = block sympathetic beta adernergic
    receptors.
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31
Q

The degree of coronary intraluminal obstruction correlates with anginal presentation. If strenuous exercise or strong emotion = chest pain (clasical angina), then we can conclude what ?

A

Intraluminal Obstruction of > 50%

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32
Q

The degree of coronary intraluminal obstruction correlates with anginal presentation. If the patient often has angina at rest, then we can conclude what?

A

Intraluminal Obstruction of > 80%

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33
Q

Prinzmatal’s

A

Coronary vasospasm (no CAD) occurs typically at rest (morning hours)

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34
Q

Compensatory mechanisms for O2 supply/demand mismatch

A
  • Coronary arteriolar vasodilation
  • Coronary collateral circulation
  • Anerobic metabolism
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35
Q

What is the primary controller of Coronary arteriolar vasodilation:

A

Local Metabolism

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36
Q

Blood flow is regulated by local arteriolar

A

Vasodilation

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37
Q

What is the major factor that controls coronary blood flow?

A

Oxygen Demand

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38
Q

What percentage of oxygen is removed as it goes through the heart?

A

70%

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39
Q

Coronary blood flow is directly proportional to ?

A

Metabolic consumption

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40
Q

If there is a small occlusion in coronary blood flow, what happens?

A

collateral flow may double to affected area over several days.

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41
Q

If there is a GRADUAL occlusion in coronary blood flow, what happens?

A

Collaterals develop progressively with the disease.

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42
Q

What happens when sclerotic process overwhelms the collateral capacity?

A

Heart Failure

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43
Q

Under resting conditions, cardiac muscle normally consumes ____ ____ to supply most of its energy instead of carbohydrates .

A

Fatty Acids

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44
Q

What % of energy is derived from fatty acids?

A

70%

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45
Q

Under what conditions must cardiac metabolism call on glycolysis mechanisms for energy ?

A

Under ANAEROBIC or ISCHEMIC conditions.

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46
Q

Glycolysis consumes large amounts of ____ _____ and at the same time forms large amounts of LACTIC ACID in the cardiac tissue ?

A

BLOOD GLUCOSE

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47
Q

What is one of the causes of cardiac pain under cardiac ischemic conditions?

A

LACTIC ACID build up in the cardiac tissue

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48
Q

Vagal stimulation by Acetylcholine causes what DIRECT effect?

A

Vasodilation

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49
Q

Indirect stimulation is a far more important role. Sympathetic Stimulation causes what?

A

↑HR

↑Contractility = ↑ metabolic demand > sets off local blood flow regulatory mechanisms for DILATING

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50
Q

Sympathetic Stimulats and their receptors ?

A

Epi
Noepi
a & b receptors

51
Q

Vagal stimulation with its release of acetylcholine poduces:

A

↓HR
↓ contractility
> ↓ Cardiac Oxygen Consumption
= Indirectly constrict the coronary arteries

52
Q

Typical Angina evoked by:

A
  • Exertion
  • Emotions
  • Cold/heat exposure
  • Meals
  • Sexual Intercourse

Relieved by Rest

53
Q

Stable Angina

A
  • Reproducible and Predictable in onset
54
Q

Atypical Angina

A
  • No relationship to exertion
55
Q

Unstable Angina

A
  • New onset of typical angina

- Increasing in insensity or occurs at rest

56
Q

Type of Angina that varies in symptoms ?

A

Prinsmtal’s Angina

57
Q

ECG Evaluation of an MI ?

A
  • ST may be elevated or depressed

- T waves may be tall

58
Q

ECHO Evaluation of an MI ?

A

Wall motion abnormalities

59
Q

Thallium Scan Evaluation of an MI ?

A

Absence of thallium “cold spot” MI

60
Q

Lab Evaluation of an MI ?

A

Troponin

Creatine Kinase (CK-MB) 30 – 220 U/L.

Lactate dehydrogenase (LDH) 100 - 220 U/L

Myoglobin (Mb) 30 – 90 µg/mL

61
Q

Leading cause of death in industrialized countries?

62
Q

Ischemic heart disease leads to what

A
  • Angina
  • MI
  • Sudden Cardiac Death
  • Chronic Heart Failure
63
Q

Arteriosclerosis

A

Natural changes in the following:

  • INTIMA
  • CONNECTIVE TISSUE
  • DIAMETER of ARTERY.
64
Q

Atherosclerosis

A

pathologic phenomenon occurring in the following:

  • coronary
  • carotid
  • iliac
  • femoral arteries
  • aorta.
65
Q

Narrowing and hardening of the arteries leads to imbalance between what?

A

Supply and Demand which leads to ISCHEMIA.

66
Q

Ischemic Heart Disease is a result of what

A

CAD (atherosclerosis)

67
Q

How is Ischemia detected?

A
  • Symptoms (angina)

- ECG (indirectly)

68
Q

Cross Section of an artery on how atherosclerosis develops, starting from the inside?

A
  • Endothelium
  • Internal Elastic Tissue
  • Smooth Muscle Cells
  • External Elastic Tissue
  • Connective Tissue
69
Q

Inflammatory response is the result of

A

proliferation of tissue within the arterial wall which may result in obstruction of blood flow.

70
Q

What are the causes of atherosclerosis?

A 
↑ cholesterol 
↑ triglycerides
↑ BP - turbulent blood flow
- tobacco smoke 
- glycosylated  substances
71
Q

Response to injury hypothesis ?

A

Endothelium is injured > Platelets & monocytes adhere to endothelium > Release growth factors.

Monocytes become Macrophages & take up LDL & SMC’s.

Smooth muscle proliferation & migrate from medial to intimal layer.

72
Q

Migration to the intima smooth muscles with lipids form fatty streaks AKA ?

A

Foam Cells

73
Q

Fibromuscular layer with cholesterol core ?

A

Fibromuscular plaque

74
Q

Atherosclerosis affects what vessels?

A

Intermediate and Large arteries

75
Q

Fatty lesions that develop on the inside surface of the artery.

A

Atheromatous plaque

76
Q

Results of atheromatous plaques ?

A

↓ Lummen Size

↓ Blood Flow

77
Q

How do atheromatous plaques begin?

A

they begin by deposition of cholesterol crystals in the intima and smooth muscle.

78
Q

Minimal intrusion into vessel lumen ?

A

Fatty Streak

79
Q

Artherosclerosis can result in ?

A
  • Hypertensive Heart Disease
  • Coronary Artery Occlusion
  • ↑ cholesterol
  • ↑ LDL
80
Q

Good Cholesterol

81
Q

Muscle cells die after

A

1 hour of ischemia

82
Q

↑ in Cardiac Output results mostly from ?

A

Sympathetic Stimulation

83
Q

Circulatory response to exercise challenge causes an increase in arterial pressure by ?

A
  • Vasoconstriction of arterioles
  • ↑ contractility of the heart
  • ↑ filling pressures
84
Q

A MASS Sympathetic discharge causes what ?

A

↑ Arterial pressure
↑ in rate & strength = ↑ Cardiac Output

Muscle walls of veins are contracted = ↑ venous return / preload.

85
Q

SVR formula ?

A

80 X (MAP-RAP)
_____________
CO

86
Q

Platelet aggregation and thrombus formation is secondary to what ?

A

Atherosclerosis

87
Q

Coronary vasospasm can lead to what ?

A

Rupture of plaque

88
Q

What can cause a vasospasm ?

A

Platelet activation

89
Q

Area of the myocardium that is affected as a result of an MI?

90
Q

The percentage of heart attacks that are fatal?

91
Q

Neutorphils that cause tissue damage are activated by ?

A

Lack of O2

92
Q

Damaged myocardial tissue is replaced by what ?

A

Connective Tissue

93
Q

Often the origin of infarct moves from endocardium to epicardium. This is know as what?

A

Subendocardial myocardial infarction

94
Q

Decreased cardiac output causes death because ?

A
  • Systolic Stretch

- Cardiogenic Shock

95
Q

Daming of venous blood causes death because?

A
  • It increases capillary hydrostatic pressures

- Leads to Edema and Congestion

96
Q

Fibrillation can cause death and is most often the result of what?

A
  • Depletion of K+
  • Injury Current
  • Sympathetic reflexes
  • Abnormal conduction pathways
97
Q

Hemodynamic alterations can be a result of?

A
  • shock
  • hemorrhage
  • anesthesia induced hypotension
98
Q

Ischemic Heart Diseases that are Non-Atherosclerotic ?

A
  • Lupus
  • Traumatic injury
  • Kawasaki Disease
  • Cocaine-Induced Vasospasm
99
Q

Treatments of CAD

A
  • Clot dissolving drugs
  • Shock for fibrillation
  • IABP
  • Angioplasty / Stents
  • Coronary Bypass on CPB or Op-CAB
  • Cardiomyoplasty
  • Heart Transplant
100
Q

CAD patients tend to be

A

Hypovolemic with increased SVR

101
Q

CPB Considerations: Hypovolemia

When anesthesia removes vosoconstriction during induction, what is needed?
Keep track of how much crystalloid is given before bypass; check HCT just before going on CPB if concerned.

A
  • Volume Expansion
102
Q

The lower the EF (<40%), the greater the likelihood of the patient to be in CHF, therefore the patient may be ?

A
  • Normal or hypervolemic
103
Q

CPB Considerations: ECG

Be alert for any ectopic or Eschemic changes. When going on CPB, be especially observant for

A
  • ST Elevations
  • Bradycardia (no vent yet)
  • PA Pressures
104
Q

The change from pusitile pressure to non - pulsitile pressure decreases the following:

A
  • ABP
  • hemodilution
  • Cooling
  • Surgical manipulation

Increase flow and pressure to optimize flow to coronaries.

105
Q

With myocardial protection in mind what should be considered with a patient that has AI?

Should retrograde carioplegia be considered ?

A
  • Suction with LV Vent

- Depends on the extent and location of legions.

106
Q

Why is the time during cross-clamp removal so critical ?

A
  • We want to prevent distention of the heart
107
Q

Mortality risk of a redo CABG?

108
Q

Risk of entering a patant IMA graft during sternotomy approaches what percentile?

109
Q

Blood flow in muscles during strenuous exercise can increase by how much ?

110
Q

Rate of blood flow through the muscles is ?

A

Intermittent during contraction due to mechanical compression of the vessels.

111
Q

Capillaries open (vasodilate) during exercise do to ?

A

Decreased O2 in the tissues.

112
Q

Drop in Oxygen content in muscle tissues causes what ?

A

Local arteriolar dilation

113
Q

Sympathetic vasoconstrictor nerves secrete

114
Q

Adrenal glands secrete

A

norepi (a) and Epi (B)

115
Q

Vasodilation is due to:

A
  • ↓ O2 in the tissues
  • Adenosine
  • H+
  • Lactic Acid
  • CO2
116
Q

Sympathetic vasoconstrictor nerves secrete the following?

A

Norepinephrine at their nerve endings

117
Q

When the Sympathetic vasoconstrictor nerves are maximally activated, they can secrete enough norepinephrine to cause what?

A

Decrease in blood flow through the resting muscles to as little as 1/2 to 1/3 of the normal flow.

118
Q

Mass Sympathetic discharge causes what ?

A
  • Increase in Arterial Pressure

- Increase in C.O.

119
Q

Increase in Arterial Pressure causes what ?

A
  • Vasoconstriction of arterioles
  • Increased contractility of the heart
  • Increased filling pressures
120
Q

During Mass Sympathetic discharge, the heart is stimulated which causes what?

A
  • Increased HR

- Increased in contractility

121
Q

During Mass Sympathetic discharge, the arterioles of the PVS are strongly contracted which causes what ?

A
  • Active muscles are strongly dilated

- No vasoconstriction in coronary & cerebral circulation

122
Q

During Mass Sympathetic discharge, the muscle walls of the veins are contracted which causes what ?

A
  • Increase in venous return / preload
123
Q

Increase in C.O. results mostly from

A
  • Sympathetic stimulation

CVPR 312 Cardiac Pathophysiology (15 decks)

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