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Nursing - Bloomberg > 370: Cardiac Pathophysiology > Flashcards

370: Cardiac Pathophysiology Flashcards

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1
Q

What is the Frank-Starling Mechanism?

A

ncreased stretch of heart -> increased force of contraction.

Increased blood volume -> stretch of myocardium

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2
Q

What results in increased preload?

A

Increased stroke volume -> increased preload (EDV) -> increased stretch -> increased force of contraction

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3
Q

How do you calculate mean arterial pressure (MAP)?

A

(SBP + 2 x DBP)/3

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4
Q

Where are chemoreceptors found?

A
  1. Medulla oblongata
  2. Carotid body
  3. Aortic body
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5
Q

Where are baroreceptors found?

A
  1. Carotid sinus

2. Aorta

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6
Q

What is Laplace’s Law?

A

Wall tension = intraventricular pressure x internal radius

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7
Q

What happens to arterial pressure as radius increases?

A

As radius increases, so does tension but Pressure remains equal

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8
Q

What happens during cardiomyopathy?

A

Heart becomes significantly distended. Increased radius increases tension. Heart requires more energy to pump same amount of blood.

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9
Q

What happens during myocardial hypertrophy?

A

Thickening and stiffening of the heart muscle. Decreased elasticity, decreases compliance and contractility.

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10
Q

What are 4 factors affecting cardiac performance?

A
  1. Preload
  2. Afterload
  3. Heart rate
  4. Myocardial contractility
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11
Q

What 2 primary factors that effect preload?

A
  1. Amount of venous return to ventricle
  2. Blood left in the ventricle after systole or end-systolic volume (EDV)

Increased preload = increased cardiac output

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12
Q

What decreases preload?

A

Decrease in Venous return or filling

  1. Constrictive pericarditis
  2. Cardiac tamponade
  3. Hemorrhage
  4. 3rd spacing
  5. Vasodilators
  6. Diuretics
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13
Q

What is afterload?

A

Resistance to ejection during systole.

Force to eject blood from heart.

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14
Q

What are 2 main factors that effect afterload?

A
  1. Ventricular wall tension
  2. Peripheral vascular resistance

Increased afterload -> decreased cardiac output (CO)

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15
Q

What increases afterload?

A

Increased aortic pressure or increases SVR

  1. Aortic stenosis
  2. Severe HTN
  3. Vasoconstriction
  4. Vasopressors
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16
Q

What decreases afterload?

A
  1. Decreased SVR
  2. Vasodilation
  3. Sepsis
  4. Hyperthermia
  5. Decreases BP
  6. Nitrates
  7. Arterial dilators
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17
Q

What 3 factors effect contractility of the heart?

A
  1. Preload
  2. Innervation to ventricles
  3. Oxygen supply
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18
Q

What compromises intrinsic contractility of the heart?

A 
1. Poor myocardial perfusion 
(Secondary to atherosclerosis) 
2. Primary disease of myocardium 
3. Degenerative changes with aging 
4. Necrosis from MI
5. Negative ionotropic drugs
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19
Q

What drugs increase contractility of the heart?

A

Ionotropes (dobutamine, dopamine, digoxin)

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20
Q

What drugs decrease contractility of the heart?

A
  1. Beta blockers
  2. Calcium channel blockers
  3. Antiarrhythmatics
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21
Q

What are the effects of aldosterone?

A

Hormone that promotes sodium retention, which can increase H2O reabsorption, increased blood volume, and increased CO (HTN)

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22
Q

How is blood pressure calculated?

A

BP = CO x SVR

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23
Q

How is cardiac output calculated?

A

CO = stroke volume x HR

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24
Q

What are the 2 primary causes of sustained hypertension?

A
  1. Increased peripheral resistance

2. Increased blood volume

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25
Q

What are natriuretic peptides?

A
  1. Atrial natriuretic peptide (ANP)
  2. Brain natriuretic peptide (BNP)
  3. C-type natriuretic peptide (CNP)
  4. Urodilatin

Modulate renal sodium excretion

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26
Q

What do diuretics do?

A

Increase renal excretion of Na+, H2O, Cl-, K+ by blocking reabsorption in distal tubule.
This decreases blood volume

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27
Q

What do Beta-Blockers do?

A

Blocks cardiac beta1-receptors to decrease HR and contractility.
This reduces cardiac output.

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28
Q

What do ACE inhibitors do?

A

Inhibit the enzyme that converts Angiotension 1 to Angiotension 2.
Blocks vasoconstriction and aldosterone mediated volume expansion.

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29
Q

What do calcium-channel blockers do?

A

Calcium channels regulate contraction of vascular smooth muscles. If blocked, contraction will be prevented and results in vasodilation.

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30
Q

What are complications of hypertension?

A
  1. Stroke, dementia
  2. Retinopathy-hemorrhage, blindness
  3. CAD, angina, MI, heart failure
  4. Aortic aneurysms or dissection
  5. Kidney injury, end stage renal disease
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31
Q

What are the roles of sympathetic nervous system in the circulatory system?

A
  1. Increase HR and contractility
  2. Vasoconstriction
  3. Releases renin from the kidneys
  4. Increased arterial pressure due to increased CO and SVR
  5. Increased insulin resistance
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32
Q

What are the primary risk factors of heart failure?

A
  1. CAD (Coronary artery disease)

2. Advanced age

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33
Q

What are contributing factors to heart failure?

A
  1. Hypertension
  2. Diabetes
  3. Tobacco use
  4. Obesity
  5. High cholesterol
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34
Q

What are the 2 types of heart failure?

A
  1. Acute

2. Chronic

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35
Q

What are the 4 compensatory mechanisms in heart failure?

A
  1. Frank-Starling Mechanism
  2. Sympathetic NS
  3. Neurohormonal responses
  4. Myocardial remodeling & hypertrophy
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36
Q

What are the effects of SNS on heart failure?

A
  1. Increase HR
  2. Increased contractility
  3. Vasoconstriction

Increase the workload of failing myocardium

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37
Q

What are the 4 neurohormonal responses that effect heart failure?

A
  1. RAAS system
  2. ADH
  3. Endothelin
  4. Proinflammatory cytokines
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38
Q

How does the RAAS system effect heart failure?

A

Angiotensin 2 causes adrenal cortex to release aldosterone. Causes sodium and water retention. Increased peripheral vasoconstriction, increases BP.

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39
Q

How does ADH effect heart failure?

A

Antidiuretic hormone causes increased H2O reabsorption in renal tubules, leading to H2O retention and increased blood volume.

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40
Q

How does endothelin effect heart failure?

A

Endothelin is stimulated by ADH, catecholines, and angiotensin 2. Causes

  1. Vasoconstriction
  2. Increase contractility
  3. Hypertrophy
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41
Q

How does proinflammatory cytokines effect heart failure?

A

Released in response to cardiac injury. Depressed cardiac function by causing cardiac hypertrophy, contractile dysfunction, and death of myocytes. Leads to cardiac wasting, muscle myopathy, and fatigue.

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42
Q

What are the 2 compensatory consequences of myocardial remodeling?

A
  1. Dilation

2. Hypertrophy

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43
Q

What happens during compensatory dilation?

A
  1. Elevated pressure of left ventricle
  2. Chambers of heart enlarge
  3. Eventually decreases CO
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44
Q

What happens during compensatory hypertrophy of the heart?

A

Increase muscle mass and cardiac wall thickness in response to chronic dilation. Results in:

  1. Poor contractility
  2. Higher O2 needs
  3. Poor coronary artery circulation
  4. Risk for ventricular dysrhythmias
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45
Q

What is another name for left-sided heart failure?

A

Congestive heart failure (CHF)

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46
Q

What causes left-sided heart failure?

A

Left ventricular dysfunction (MI HTN, CAD, cardiomyopathy) causes backup of blood into left atrium and pulmonary veins (pulmonary congestion, edema)

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47
Q

What are the subtypes of left-sided heart failure?

A
  1. Systolic: impaired contractile or pump function

2. Diastolic: impaired ventricular function

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48
Q

What is the primary causes of right-sided heart failure?

A
  1. Left-sided heart failure.
  2. Pulmonary diseases resulting in high pulmonary resistance
  3. Right ventricular infarction (ineffective R ventricular contractility)
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49
Q

What happens during right-sided heart failure?

A

Causes backflow of blood to the R atrium and venous circulation. Causes jugular distensión and hepatomegaly.

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50
Q

Which type of heart failure is pulmonary?

A

Right-sided (Lung Disease)

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51
Q

What are the symptoms of left-sided heart failure?

A
  1. Pulmonary Congestion (cough, crackles, wheezes, blood-tinged sputum, Dyspnea, orthopnea, paroxysmal nocturna dyspnea)
  2. Fatigue, activity intolerance, confusion, restlessness (reduces O2)
  3. Peripheral constriction (Cyanosis, cool, pale skin)
  4. Tachycardia (sympathetic stimulation)
  5. S3 (rapid ventricular filling)
  6. S4 (atrial contraction)
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52
Q

Lung disease and right-sided heart failure

A
  1. Increased force of RV contraction
  2. Increased RV oxygen demand
  3. RV hypoxia
  4. Decrease force of RV contraction
  5. Increase RV end-diastolic pressure
  6. Increased RV preload
  7. Increased RA preload
  8. Peripheral edema
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53
Q

What are the symptoms of right-sided heart failure?

A
  1. Venous congestion (jugular distension, hepatomegaly, splenomegaly)
  2. Congestion of liver and intestines (anorexia, fullness, nausea, RUQ pain)
  3. Fluid retention (ascites, dependent edema, weight gain)
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54
Q

What are the symptoms of left-sided heart failure?

A

(FORCED)

Fatigue
Orthopnea 
Rales/restlessness 
Cyanosis/confusion
Extreme weakness 
Dyspnea
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55
Q

What are the symptoms of right-sided heart failure?

A

(BACONED)

Bloating
Anorexia 
Cyanosis/cool legs
Oliguria
Nausea 
Edema 
Distended neck veins
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56
Q

What are complications of heart failure?

A
  1. Pleural effusion (from increased pressure of pleural capillaries)
  2. Atrial fibrillation (promotes thrombus/embolus formation, increased risk of stroke)
  3. Fatal dysrhythmias (ventricular tachycardia)
    Due to cardiac enlargement altering electrical pathways
  4. Hepatomegaly (congested with venous blood)
  5. Renal insufficiency/failure (due to decreased CO and perfusion to kidneys)
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57
Q

What are drug therapies for heart failure?

A
  1. Diuretics to reduce preload (thiazides/loop/potassium-sparing)
  2. Enhance contractility (digitalis, dopamine, dobutamine)
  3. Vasodilators to reduce preload (hydralazine, isosorbide dinitrate)
  4. Beta-blocking agents to reduce myocardial O2 demands
  5. ACE-inhibitors to suppress agiotensin2 (captopril)
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58
Q

Chronic heart failure is associated with activation of the:

A

Renin-angiotensin-aldosterone (RAAS) system

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59
Q

Heart rate is reduced by:

A

Stimulation of parasympathetic nervous system

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60
Q

A patient is diagnosed with pulmonary disease and elevated pulmonary vascular resistance. Which form of heart failure may result from pulmonary disease and elevated pulmonary vascular resistance?

A

Right-sided heart failure

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61
Q

In systolic heart failure, what effect does the RAAS have on stroke volume?

A

Increases preload and increases afterload (vasoconstriction)

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62
Q

Mechanism of coronary artery disease (CAD)?

A
  1. Decreased perfusion to myocardium due to occlusion (cholesterol, plaques, thrombi)
  2. Inadequate blood supply to meet myocardial O2 demand
  3. myocardial ischemia
  4. Myocardial death
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63
Q

Pathophysiology of atherosclerosis

A
  1. Blood lipids irritate or damage intima of arterial vessels
  2. Fatty substances enter vessels after damaging protective barrier, accumulate and for fatty streak formation
  3. Smooth muscle cells move to intima to engulf fatty substance
  4. Fibrous tissue formation and calcification
  5. Atheroma grows, causing vessel wall to become thick, fibrotic, and calcified
  6. Lumen narrows, impedes blood flow with risk for thrombosis
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64
Q

The hardening and narrowing of process of an artery

A

Atherosclerosis

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65
Q

What is the mechanism of atherosclerosis occlusion?

A
  1. Plaques form in lining of artery
  2. Plaque grows, intima of artery damaged
  3. Plaque ruptures
  4. Blood clot forms, limiting blood flow
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66
Q

Why might CAD remain asymptomatic until it is far advanced?

A

Collateral circulation

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67
Q

Collateral circulation

A
  1. Anastomotic channels join small arteries

2. Smaller collateral vessels increase in size to provide alternative blood flow

68
Q

What are the non-modifiable risk factors of CAD?

A
  1. Age
  2. Sex (inc risk with menopause)
  3. Family history
  4. Ethnicity (lifestyle, SDH, awareness of risks)
  5. Genetics (familial hypercholesterolemia)
  6. Estrogen is cardio-protective
69
Q

What are the modifiable risk factors of CAD?

A
  1. Dyslipidemia (inc LDL, dec HDL, inc triglycerides)
  2. HTN(vascular inflammation, endothelial injury)
  3. Smoking (nicotine -> catecholamine release -> inc HR, peripheral vasoconstriction, inc BP -> inc cardiac workload and O2 consumption) (nicotine inc platelet adhesion; CO -> dec O2-carrying capacity of Hgb)
  4. Physical inactivity (cholesterol, HTN, diabetes, obesity)
  5. Diet (fat, cholesterol-> atherosclerosis)
  6. Obesity (dyslipidemia, insulin resistance, inflammation, endothelial dysfunction)
  7. Diabetes Melitis
  8. Co-morbidities (infection, renal insufficiency, HTN, insulin resistance)
  9. Lifestyle (alcohol, stress, drugs)
  10. SDH
70
Q

Which heart rhythms are shockable?

A

Ventricular tachycardia

Ventricular fibrillation

71
Q

What are the effects of acute and chronic cocaine use on the heart?

A
  1. Suppresses myocardial contractility
  2. Reduction of coronary blood flow
  3. Electrical abnormalities
  4. Increased HR and BP
  5. Increased platelet aggregation
  6. Acceleration of atherosclerosis
72
Q

What is the normal levels of LDLs?

A

< 2.6 mmol/L

73
Q

What are the normal levels for HDLs?

A

> 1.5 mmol/L

74
Q

What are the normal levels of cholesterol?

A

<5.0 mmol/L

75
Q

What are the normal levels of triglycerides?

A

< 1.7 mmol/L

76
Q

What are the effects of HDLs?

A

Reverse cholesterol transport. Extract excess cholesterol deposited in blood vessel walls and deliver to back to the liver for elimination through GI tract.

Also reduced BV injury through antioxidant and anti-inflammatory functions

77
Q

What are the conditions of metabolic syndrome?

A
  1. Waist circumference (men >= 102cm, women >= 88cm)
  2. Triglyceride levels >= 1.7 mmol/L
  3. HDL cholesterol (men < 1mmol/L; women < 1.3)
  4. BP (>= 130/85)
  5. Fasting glucose level (>= 5.6 mmol/L)
78
Q

What is a percutaneous transluminal coronary angioplasty?

A

Balloon on end of catheter fed through artery. Balloon inflates, flattening plaque to maintain patency of vessel.

Stent may be inserted afterwards

79
Q

What is coronary atherectomy?

A

Sheets off blockage in artery with Lazer, transluminal extraction, rayarían, directional catheter.

80
Q

What is coronary artery bypass grafting (CABG)?

A

Vessels from another part of body to help normalize blood flow in heart.

Adds alternative channels.

81
Q

Myocardial ischemia under 20 minutes

A

Ischemic attract (angina)

82
Q

Myocardial ischemia over 20 minutes

A

Myocardial infarction (MI)

83
Q

What are the 3 types of angina?

A
  1. Stable angina (angina pectoris)
  2. Unstable angina
  3. Variant (Prinzmetal) angina
84
Q

Which type of angina is under 10min, and characterized by precordial discomfort provoked by exertions or stress, and how would you treat it?

A

Stable angina (angina pectoris)

Tx: rest and nitrates

85
Q

Which type of angina is due to atherosclerosis?

A

Stable angina (angina pectoris)

86
Q

Which type of angina is characterized by anginal discomfort when resting or that awakens patient from sleep?

A

Unstable angina

87
Q

Which type of angina is caused by atherosclerosis with blood clot, and CAD?

A

Unstable angina

88
Q

Which type of angina is characterized by chest discomfort with atypical characteristics, often during rest, and follows a cyclic or regular pattern?

A

Variant (Prinzmetal) angina

Due to coronary artery spasm

89
Q

Sudden coronary obstruction caused by thrombus formation from

  1. Unstable angina
  2. Myocardial infarction
A

Acute Coronary Syndrome (ACS)

90
Q

What is caused by transient ischemia due to acute coronary syndrome?

A

Unstable angina

91
Q

What is due to sustained ischemia from acute coronary syndrome (ACS)?

A

Myocardial infarction and necrosis

92
Q

What are the manifestations of myocardial ischemia?

A
  1. Chest pain (May radiate)
  2. Shortness of breath
  3. Diaphoresis, pallor, cool clammy skin (SNS stimulation)
  4. Increased BP and HR
  5. Nausea and vomiting
  6. Fever
  7. Loss of consciousness
  8. Anxiety, sense of doom, denial
93
Q

Lethal ischemic injury to which myocardium zone due to MI

A

Zone of infarction

No ECG activity from this area

94
Q

Surrounding lethal ischemic injury if myocardium

A

Zone of injury (irreversible after 2-4 hours)

ST elevation on ECG

95
Q

Area of myocardium that do not have permanent effects from MI, but function erratically.

A

Zone of ischemia

  • reversible with perfusion
  • can cause T wave inversion
96
Q

What are the 7 classifications of myocardial infarctions?

A
  1. Transmural infarcts
  2. Subendocardial infarcts
  3. Anterior MI
  4. Inferior MI
  5. Septal MI
  6. Lateral MI
  7. Combination MI
97
Q

Which type of myocardial infarction involves all 3 layers of the ventricular wall?

A

Transmural infarction

98
Q

Which type of myocardial infarction involves the inner third to half of the ventricular wall?

A

Subendocardial infarct

99
Q

Which types of myocardial infarctions are due to left ventricular failure?

A
  1. Anterior MI

2. Septal MI

100
Q

Which blood vessel is occluded during an Anterior MI?

A

Left anterior descending artery (LAD)

101
Q

Which artery is occluded during an inferior MI?

A
  1. Right coronary artery (RCA)

2. Circumflex Coronary Artery

102
Q

Which type of myocardial infarction is a result of dysrhythmias or transient AV block?

A

Inferior MI

103
Q

Which artery is occluded during a Septal MI?

A

Left anterior descending (LAD) Coronary artery

104
Q

Which coronary artery is occluded during a lateral MI?

A

Circumflex Coronary Artery

105
Q

Which myocardial infarctions are due to occlusion of the left anterior descending (LAD) coronary artery?

A
  1. Anterior MI

2. Septal MI

106
Q

Which myocardial infarctions are due to the occlusion of the circumflex Coronary artery?

A
  1. Inferior MI

2. Lateral MI

107
Q

What does the arterial gas value HCO3 indicate?

A

The bicarbonate contents in the blood plasma which indicates alkaline reserve

108
Q

What is could arterial blood gas results indicate?

A
  1. Respiratory and lung problems
  2. Efficacy of oxygen therapy
  3. Acid-base levels (kidney failure, heart failure, uncontrolled diabetes, shock, etc)
109
Q

What is a state of low blood pH?

A

Acidemia pH < 7.35

110
Q

What refers to an excess of acid in the blood that causes pH to fall below 7.35?

A

Acidosis

111
Q

What is a state of high blood pH?

A

Alkalemia pH > 7.45

112
Q

What is the normal pH range for blood?

A

7.35 - 7.45

113
Q

Which 3 systems regulate normal acid-base levels?

A
  1. Chemical Buffer System
  2. Respiratory system
  3. Renal system
114
Q

What are the 3 major chemical buffer systems in the body?

A
  1. Carbonic acid-bicarbonate buffet system (extracellular)
  2. Phosphate buffer system (intracellular)
  3. Protein buffer system (intercellular)
115
Q

What is a limitation to the carbonic acid-bicarbonate buffer system?

A

Only functions when the respiratory system is functioning normally

116
Q

What happens to the blood pH if the respiratory system is not functioning properly?

A
  1. Excess CO2 combines with H2O to make carbonic acid (H2CO3)
  2. Increase in H2CO3 cause increase depth and rate of respiration, reducing carbonic acid and increasing blood pH (alkalosis)
  3. Decreased H2CO3 causes decrease and shallow respiration, thereby retaining CO2, increasing carbonic acid and decreasing blood pH (acidosis)
  4. Activation of the lungs to compensate occurs within 1 to 3 minutes
117
Q

What is the effect of the renal system on blood pH?

A
  1. Kidneys retain or excrete bicarbonate ions (HCO3-) which neutralices excess acid in the blood
  2. As blood pH decreases, kidneys compensate by retaining HCO3-
  3. As pH rises, kidneys excrete HCO3-
  4. Kidneys can also generate additional bicarbonate ions or Elina te excess H+ to compensate during acidosis
  5. This takes hours to days to correct the imbalance
118
Q

What blood pH values are fatal?

A

pH < 6.8

pH > 7.8

119
Q

What are the manifestations if acidosis?

A
  1. pH < 7.35
  2. CNS depressions through decreased synaptic transmission
  3. Increased rate and depth of respiration
  4. Weakness and disorientation
  5. Seizures
  6. Coma and death
120
Q

What are the manifestations of alkalosis?

A
  1. pH > 7.45
  2. Over-excitability of CNS and PNS
  3. Numbness
  4. Irritability, lightheaded, nervousness
  5. Muscle spasms/tetany
  6. Cramping
  7. Convulsions
  8. Loss of consciousness and death
121
Q

What is the normal range of PaO2?

A

80 - 100 mmHg

Decreases with age:
PaO2 = 102 - 1/3age

Healthy lungs = oxygen% x 5

122
Q

What is the normal range for PaCO2?

A

35 - 45 mmHg

Elevated = acidity 
Reduced = alkalinity
123
Q

What is the normal range for HCO3- arterial blood gas values?

A

22-26 mmol/L

Increased = alkalinity
Decreased = acidity
124
Q

Condition of lowered blood pH due to decreased respiratory rate (hypoventilation) or volume

A

Respiratory Acidosis

125
Q

Condition of lowered blood pH due to reduction in bicarbonate

A

Metabolic Acidosis

126
Q

A condition of increased blood pH due to increase in bicarbonate (HCO3-)

A

Metabolic Alkalosis

127
Q

What does PaO2 represent?

A

The saturation of oxygen to hemoglobin in arterial vessels.

Correlated with O2 Sats.

128
Q

What does SvO2 represent?

A

The saturation of oxygen once delivered to the tissues.
If cardiac output is low, tissues try extracting more oxygen.

75%

129
Q

Hypoxemia

A

Decreased amount of oxygen in the arterial blood

130
Q

Hypoxia

A

Decreased oxygen at the tissue level

131
Q

What are the normal value ranges for cardiac output?

A

4-6L/min

132
Q

What is the ejection fraction?

A

The volumetric fraction of fluid ejected from a chamber with each contraction.

As heart gets weaker, only able to pump out less blood (Grades 1-4)

133
Q

What are some interventions to stabilize the hemodynamic status?

A
  1. Inc/dec preload (ex. dec BP)
  2. Inc/dec afterload
    (Keeps BP up)
  3. Improve heart function or contractility (ex. Digoxin)
  4. Ensure sufficient oxygenation
  5. Fluid and medication management
134
Q

What are some interventions that effect preload?

A

Fluid Volume Excess:
1. Diuretics (ex. Lasix)
2. Venous dilators (ex. Nitroglycerine, nitroprusside)
Fluid deficits:
3. Volume expanders (ex. Pentaspan, voluven)
4. NS, blood

135
Q

What medications effect contractility of the heart?

A

Positive ionotropes (ex. Dopamine, dobutamine, milronone)

136
Q

What does Central Venous Pressure (CVP) measure?

A

Measures the mean right atrial pressure, which provides estimates of right ventricular preload

Normal: 2-8mmHg

137
Q

What are the 2 shockable heart rhythms?

A
  1. Ventricular tachycardia (Vtach)

2. Ventricular fibrillation

138
Q

What is the P wave indicate on an ECG?

A

Electrical pulse coming from SA node

139
Q

What does the PR interval indicate on an ECG?

A

Time electrical impulse travels from SA node to AV node

140
Q

What does the QRS complex indicate on an ECG?

A

Time to depolarize and contraction of ventricles

O.04-0.02

141
Q

What are premature ventricular contractions?

A

PVC= extra ventricular contraction consisting of wide and bizarre QRS complex that originated in an ectopic pacemaker in the ventricles

142
Q

What do the ECG waves of V-tach look like?

A

Wide QRS because beats from ventricles.

Like sinusoidal smooth wave

143
Q

What is synchronized cardioversion?

A

When defibrillator machine decides when to shock the heart in line with heart beat (R wave).

Can otherwise go into V-fib

144
Q

What are interventions for V-tach?

A

Stable (with pulse):

  1. Anti-arrhythmias (ex. Adenosine, Ami Oda robe)
  2. Vagas maneuvers
  3. Synchronized cardioversion

Unstable:
3. Synchronized cardioversion (100J and higher)

Pulseless:
4. Defibrillation

145
Q

What is ventricular fibrillation?

A

Twitching of the ventricles, no pulse, no organized contractions

Can only shock

146
Q

What are treatments for asystole?

A
  1. CPR
  2. Epinephrine

CANNOT SHOCK

147
Q

What is atrial fibrillation?

A

Loss of effective atrial contraction, characterized by disorganized atrial electrical activity due to multiple ectopic foci

148
Q

What are the 3 types of AFib?

A
  1. Paroxysmal
    - temporary, resolved within 24 hours
  2. Persistent (>7 days)
    - requires medical or electrical intervention
  3. Permanent (>1 year)
    - required blood thinners to prevent thrombus
149
Q

What are the differences between controlled and uncontrolled AFib?

A

Controlled < 100 bpm

Uncontrolled > 100 bpm

150
Q

What are pharmacological treatments of AFib?

A

Rate control:

  1. CCBs (ex diltiazem)
  2. B-blockers (ex metoprolol)
  3. Anti-arrhythmics (ex. Amiodarone, procaiamide)
  4. Anticoagulants (ex. Warfarin, NOACs)
  5. Cardioversion
151
Q

What is Acute Coronary Syndrome (ACS)?

A

Deterioration of atherosclerotic plaque ruptured and thrombus is formed, resulting in unstable lesion. Develops when ischemia is prolonged and not immediately reversible.

152
Q

What are the types of Acute Coronary Syndrome (ACS)?

A
  1. ST Elevation Myocardial Infarction (STEMI)
  2. Non-ST Elevation ACS (NSTE-ACS)
    A. Unstable Angina
    B. Non-STEMI
153
Q

What are complications of ACS?

A
  1. Dysrhythmias
  2. Heart failure
  3. Cardiogenic shock
  4. Sudden death
  5. Refractory Angina
154
Q

What are the molecular markers after an MI?

A
  1. Triponin 1 and Tropinin 2
  2. CK-MB
  3. Myoglobin
155
Q

What does Tropinin levels indicate?

A

Released during cardiac cell death.

Cardiac specific, but not useful for reinfarction (remain elevated for 10 days)

156
Q

What does CK-MB levels indicate?

A

Creatinine kinase with MB isoenzyme.

High specificity for myocardial injury

157
Q

What do myoglobin levels indicate?

A

Cell death.

Low cardiac specificity. Most sensitive early marker.

158
Q

What are the 3 methods for diagnosing a MI?

A
  1. Plasma markers
  2. Hx of prolonged chest pain
  3. ECG abnormalities
159
Q

Which cardiac enzyme is the best indicator of an MI in an emergency?

A

CK-MB

160
Q

What are the limitations of CK-MB?

A

False positive for significant skeletal injury and cardiac injury other than MI
(Defibrillation, chest trauma, cocaine abuse)

161
Q

What is the onset/peak/RTB of CK-MB?

A

Onset: 4-6 hrs
Peak: 18-24hrs
Return to baseline: 36-48 hrs

162
Q

What is the onset/peak/RTB of Tropinin 1?

A

Onset: 2-4 hrs
Peak: 10-24 hrs
Return to baseline: 10 days

163
Q

What is the onset/peak/RTB of Troponin T?

A

Onset: 2-4 hrs
Peak: 10-24 hrs
Return to baseline: 14 days

164
Q

What is the onset/peak/RTB of Myoglobin?

A

Onset: 1-3 hrs
Peak: 6-12 hrs
Return to baseline: 24 hrs

165
Q

What does S-T segment of an ECG represent?

A

The end of ventricular depolarization and the beginning of ventricular repolarization

166
Q

What are typical ECG changes after an MI?

A
  1. Prolonged Q wave
  2. ST elevation
  3. T wave inversion
167
Q

What are 4 determinants of cardiac oxygen demand?

A
  1. Heart rate
  2. Contractility
  3. Preload
  4. Afterload

Nursing - Bloomberg (52 decks)

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