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CardioResp > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Name three alpha antagonists.

A

Phentolamine

Phenoxybenzamine

Prazosin

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2
Q

For Phentolamine:

  • IV or oral? Fast or slow?
  • What is the receptor specificity?
  • What is its MOA?
  • What is it used for?
  • What is a big side effect of the drug?
A
  • IV and short acting (QUICK)
  • alpha1 = alpha2 ANTAGONIST
  • MOA: Competitive inhibitor
  • Hypertensive crisis
  • Reflex tachycardia due to resulting decreasing BP
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3
Q

For Phenoxybenzamine:

  • IV or oral? Fast or slow?
  • What is the receptor specificity?
  • What is its MOA?
  • What is it used for?
  • What is a big side effect of the drug?
A
  • Irreversible non-competitive inhibitor
    • Oral - slow
    • alpha 1 = alpha 2 ANTAGONIST
    • MOA: irreversible noncompetitive inhibitor
    • Use: Hypertensive crisis
    • Reflex tachycardia due to resulting decreased BP.
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4
Q

For Prazosin** and any other **-osin drugs:

  • What is the receptor specificity?
  • What is the use?
  • What is a possible side effect
A
  • Alpha1 Antagonist
  • Used for prostatic hypertrophy
  • Reflex tachycardia
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5
Q

Name 4 beta antagonists.

A

Propanolol

Metoprolol

Labetolol

Carvedilol

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6
Q

For propanolol:

  • What is the receptor specificity?
  • What are some possible physiological effects (2)?
  • What are some side effects?
A
  • Beta 1 = beta 2 antagonist
  • Effects
    • Negative inotropic (contractility) and chronotropic (HR) actions
    • Blocks renin release
  • Side Effects
    • Slows AV node firing
    • Crosses blood brain barrier - CNS effects (vivid dreams, depression, decreased libido)
    • Inhibits glycogenolysis
    • Vasoconstriction
    • Bronchoconstriction
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7
Q
  • What receptor blockage is specific for slowing of AV conduction?
  • What receptor blockage is specific for inhbiting glycogenolysis?
  • Bronchoconstriction?
  • Vasoconstriction?
A
  • slowing of AV conduction: Beta1
  • inhibition of glycogenolysis: Beta2
  • Bronchoconstriction: Beta2
  • Vasoconstriction: Beta2
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8
Q

For metoprolol:

  • What is the receptor specificity?
  • What is it used for?
  • What is a physiological effect?
A
  • Beta1 selective Antagonist (little beta2 activity)
  • Slows HR and therefore cardiac output is decreased
  • Bradycardia
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9
Q

For Labetolol and Carvedilol:

  • What is the receptor specificity?
  • What is it used in?
  • Is there a reflex tachycardia present? Why or why not?
A
  • Beta1 = beta2 > alpha1 = alpha2 antagonist
  • used in hypertensive crises and in heart failure
  • Does NOT have reflex tachycardia because beta1 is blocked
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10
Q

How are most beta blockers excreted and why is this important?

A

Most beta blockers are excreted via the liver, making it likely that they have drug interactions due to biotransformation by P450 enzymes.

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11
Q

Outline the process from the baroreceptors to renin to aldosterone release.

A
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12
Q

What 5 things causes renin release?

A
  • Renin release is stimulated by:
    • Sympathetic activation
    • Low pressure in renal vasculature
    • Sodium diuresis
    • Decreased blood volume
    • Decreased renal blood flow
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13
Q

With aldosterone release or inhibition, how can you get hyperkalemia?

  • Outline what occurs to Na+, H2O, K+ with Aldosterone.
  • Without aldosterone?
A
  • Normal: with aldosterone → increased expression of Na+ and Na+/K+ ATPase channels
  • Abnormal: without aldosterone → decreased expression of Na+ and Na+/K+ ATPase channels → excretion of Na+ and retention of K+ and H+ → hyperkalemia and metabolic acidosis
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14
Q

In the renin-angiotensin-aldosterone system, what are the 4 classes of drugs used to reduce BP?

A
  • Angiotensin Converting Enzyme (ACE) Inhibitors
  • Angiotensin Receptor Blockers (ARBs)
  • Direct Renin Inhibitors
  • Aldosterone Receptor Antagonists
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15
Q

For Angiotensin Converting Enzyme (ACE) Inhbitors:

  • What are three important drugs to know?
  • What is the MOA?
    • What is a secondary MOA that occurs with ACEI’s?
  • What are three side effects?
  • What are 5 main advantages?
A
  • Lisinopril**, Enala_pril, Captopril_**
  • MOA: Prevents conversion of ATI to ATII, reducing peripheral resistance (ATII causes vasoconstriction)
    • Bradykinin (vasodilator) is inactivated via ACE
    • ACEI: by blocking ATII synthesis and bradykinin inactivation, you get a double whammy of decreasing BP
  • Side Effects:
    • Cough/angioedema
    • Decreases renal function
    • Hyperkalemia
      *
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16
Q

For Angiotensin Converting Enzyme (ACE) Inhbitors:

  • What are three side effects?
  • What are 5 main advantages?
A

Lisinopril, Enalapril, Captopril

  • Side effects
    • Cough/angioedema
    • Decreases renal function
    • Hyperkalemia
  • Advantages
    • No effects on HR
    • No reflex actions of the sympathetic nervous systme
    • Prevents stroke
    • Beneficial in HF
    • Slow progression of kidney disease
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17
Q

For Angiotensin Receptor Blockers:

  • What are three drug names?
  • MOA?
  • What are two side effects?
  • What is the main advantage?
A
  • Losartan, Valsartan, Olmesartan
  • MOA
    • angiotensin I receptor inhibitors
    • antagonizes angiotensin II through actions at angiotensin I receptor
  • Side Effects
    • decreased renal funtion
    • hyperkalemia
  • Advantage
    • Better tolerated than ACE inhbitors
      • Less likely to cause cough/angioedema
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18
Q

For direct renin inhbitor:

  • What is a drug?
  • What is the MOA?
  • What are three side effects?
  • What is a minor advantage?
A
  • Drug: Aliskiren
  • MOA: inhibits renin
  • Side effects: diarrhea, cough, angioedema
  • Advantage: Can be tolerated better
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19
Q

For aldosterone receptor antagonists:

  • Name two drugs.
  • What is the MOA?
  • What are three side effects?
  • What is an advantage of one of the drugs compared to the other?
A
  • Spironolactone, eplerenone
  • MOA: Inhibits aldosterone receptor → increases Na+ excretion (and H2O) and conserves K+
  • Side Effects:
    • For Spironolactone: Hyperkalemia, Metabolic acidosis, sexual dysfunction
    • Advantage of Eplerenone: ONLY hyperkalemia
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20
Q

All renin, angiotensin, aldosterone system drugs are contraindicated in what two situations and why?

A

All drugs are contraindicated in:

  • Renal artery stenosis (because it blocks ATII from causing vasoconstriction → decreases perfusion pressure through glomeruli)
  • Pregnancy
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21
Q

In the renin, angiotensin, aldosterone system drugs: What are the two main prodrugs to know and what class of drug are they?

  • What is different about prodrugs?
A
  • Enalapril: ACE Inhibitor
  • Olmesartan: ARB (Angiotensin receptor blocker)

Must be metabolized before and therefore has a shorter half-life

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22
Q
A
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23
Q

What are (5) common heart related symptoms that patient can present with?

A
  • Angina – substernal pressure or tightness that lasts minutes to hours
    • Precipitated by physical or emotional stress and relieved by rest
  • Paroxysmal nocturnal dyspnea – waking up at high short of breath
  • Edema
  • Bendopnea – shortness of breath from bending over
  • Syncope – fainting
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24
Q

Explain the 4 Korotkroff sounds?

A
  • S1 – AV valves closing
  • S2 – SL valves closing and can have normal inspiratory splitting of A2 and P2
  • S3 – “ventricular gallop”
    • Rapid filling into very compliant (dilated) left ventricle during early diastole
  • S4 – “atrial gallop”
    • Generated by an atrium ejecting blood into a stiffened ventricle (hypertrophied)
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25
Q

What is the Internal jugular venous pulse?

A
  • Parallel and medial to sternocleidomastoid muscle and inferior to ear lobe
  • Visualization of pulsation reflects RA pressure
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26
Q

What is the common carotid arterial pulse?

A
  • Use the bell and ask patient to hold breath
  • Listen for turbulent flow (bruits)
  • Reflects rate of LV ejection
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27
Q

What are three factors that effect the PMI?

A
  • Size
  • Duration
  • Placement
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28
Q

What is the RV lift?

A
  • Parasternal impulse felt by heel of the hand; more than slight impulse indicates RVH
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29
Q

Abdominal aortic pulse

A

non-tender pulsating mass in the abdomen

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30
Q

Facial features that mark heart disease

A

Malar flush, central cyanosis

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31
Q

Endocarditis

A
  • inflammation of the endocardium that causes marks, sores, or pain in peripheral extremities + eye
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32
Q

Clubbing is casued by what?

A
  • Hypoxia – clubbing of fingernails; unable to make diamond between distal fingers
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33
Q

Pitting edema

A
  • Increased hydrostatic pressure, decreased oncotic pressure, increased capillary leakiness
  • Grade 0 to 4+
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34
Q

non-pitting edeme

A
  • Lymphedema – obstruction of lymph system
  • Woody, “tree-bark” look
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35
Q

What 2 things are caused by renal insufficency?

A
  • Varicose veins – convoluted veins with chronic venous insufficiency (deformed valves that allow backflow of blood)
  • Brawny discoloration – extravasation of RBCs into interstitial fluid
    • Chronic venous insufficiency or elevated right atrial pressure
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36
Q

4 symptoms of left heart failure

A
  • Dyspnea – exertional and resting
  • Orthopnea – shortness of breath when lying flat
  • Paroxysmal Nocturnal Dyspnea
  • Fatigue
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37
Q

4 symptoms of right heart failure

A
  • Jugular venous distension
  • Hepatic congestion (symptom: early satiety)
  • Ascites
  • Pedal edema
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38
Q

Recognize the signs and symptoms of clinical hypoperfusion.

A
  • Very dangerous, act quickly!
  • Signs/symptoms:
    • Cool extremities
    • Weakness and fatigue
    • Poor urine output
    • Confusion
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39
Q

Hydrachlorothiazide/chlorthialidone

MOA?

A

MOA

  • Inhibit Na+/K+/Cl-/H+ reabsorption in the distal tubule by inhibiting Na+/Cl- symporter → increased excretion of water → lowers BP
  • Stimulates Ca++ reabsorption
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40
Q

Hydrachlorothiazide/chlorthialidone

Side Effects?

A
  • Hypokalemia
  • Glucose intolerance (lower K+ → less depolarization → less insulin release)
  • Gout
  • Metabolic alkalosis
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41
Q

Triamterene

MOA?

Side Effects?

A

MOA

  • Inhibits sodium reabsorption through ion channels

Side Effects

  • Hyperkalemia
  • Acidosis
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42
Q

Dihydropyridines

Nifedipine**, amlo_dipine_**

MOA?

Side Effects?

A

MOA

  • Calcium channel blocker
  • Causes relaxation of vessels (used for angina, Raynaud’s phenomenon)

Side Effects

  • Peripheral edema
  • Gingival hyperplasia
43
Q

Non-dihydropyridines:

Verapamil, diltiazem

MOA?

Side Effects?

A

MOA

  • Calcium channel blocker
  • Blocks main depolarizing ion in SA and AV nodes to decrease contractions

Side Effects

  • Inhibit P450s
  • Contraindicated in patients with HF and conduction defects/SA node arrest
44
Q

Non-dihydropyridines:

Verapamil, diltiazem

MOA?

Side Effects?

A

MOA

  • Blocks main depolarizing ion in SA and AV nodes to decrease contractions

Side Effects

    • Contraindicated in patients with HF and conduction defects/SA node arrest

Inhibit P450s

45
Q

Hydralazine

MOA? Side Effects?

A

MOA

  • Relaxes smooth muscle in vasculature to decrease total peripheral resistance
  • Used in resistant hypertension

Side Effects

  • Lupus-like syndrome
46
Q

Nitroprusside (IV)

MOA? Side Effects?

A

MOA

    • Relaxes smooth muscle in vasculature to decrease total peripheral resistance
      • Prodrug = NO and cyanide
        Used in hypertensive crises because fast-acting

Side Effects

  • Cyanide toxicity
47
Q

Drug interactions with diuretics

A

NSAIDs and Steroids cause Na+ retention

48
Q

Why aren’t loop diuretics a first-line choice for hypertension?

A

Because they must be give 2x daily due to short duration of activity and activation of RAAS

49
Q

Etiologies of cell injury (4)

A

ATP Depletion, Increased cytosolic Ca2+, increased mitochondrial permeability, free radical mediated

50
Q
  • ATP depletion MOA
A
  • Decrease in ATP → decrease in Na+/K+ ATPase activity → less Na+ is excreted from cell → more water is absorbed by cell → cellular swelling
51
Q

Increase cytosolic Ca++ MOA

A
  • Activation of PLC → cleavage of phospholipids into DAG and IP3 → IP3 stimulates SR to release Ca++ → increase in cytosolic Ca++
52
Q

Increased mitochondrial permeability MOA

A
  • Releases cytochrome c into cytoplasm → activates caspases (pro-apoptotic enzymes)
53
Q

Free radical mediated injury MOA

A
  • Donation of electron from reducible ions (i.e. Fe3+) can generate highly reactive substance that can cause damage
54
Q

Outline mechanisms of cell damage and consequences (4)

A
  • The cellular response to injury depends on: the type of injury, its duration, and its severity
  • The consequence of cell injury depends on: the type and adaptability of the injured cell
  • Cellular function is lost far before morphologic changes of the cell
  • The “point of no return” at which cell death has irreversibly occurred is difficult to determine
55
Q

Reversible cell injuries

A
  • Cellular swelling
  • Fatty change
56
Q

Irreversible cell injuries

A
  • Plasma membrane alteration
  • Mitochondrial changes
  • Dilation of ER
  • Nuclear alteration
57
Q

Necrosis

A
  • Necrosis is initiated by exogenous stimuli leading to the denaturation of cellular components
    • Always pathological (aka secondary to a disease)
    • Initiates inflammation because cell spews components which are picked up by the host defense mechanism
58
Q

Morphology of Necrosis

A
  • Increased eosinophilia (lysozyme releases acidic contents causing cell to be more acidic)
    • Loss of RNA
    • Denatured cytoplasmic proteins
59
Q

Nuclear changes in necrosis

A
  • Nuclear changes (its a process)
    • Pyknosis – shrinkage
    • Karyorrhexis – break up
    • Karyolysis – DNA lysis
60
Q

Apoptosis

A
  • Apoptosis is initiated by intracellular signals and leads to phagocytosis
    • Does not have inflammation response because cell debris is still contained within membrane
    • Can be pathological or physiological
61
Q

Liquefactive necrosis

(gross and microscopic)

A
  • Gross: produces a gelatinous and purulent (aka pus)
  • Microscopic: infiltration of ghost cells without nuclei and debris by neutrophils
62
Q

Caseous necrosis

(gross and microscopic)

A
  • Gross: cottage cheese appearance
  • Microscopic: cell debris walled off by WBCs after infection (i.e. TB)
63
Q

Coagulative necrosis

(gross and microscopic)

A
  • Gross: occurs after an ischemic event and the architecture is preserved (wedge shape)
  • Microscopic: ghost cells without nuclei maintain cell outline
64
Q

Fibrinous necrosis

(microscopic)

A
  • Microscopic: autoimmune deposits of antigen-antibody onto blood vessel walls
    • Inflammation of blood vessels (vasculitis) causes pinkish tint
65
Q

Fatty necrosis

(microscopic)

A
  • Microscopic: occurs due to trauma; fatty acids and triglycerides precipitate as calcium salts
66
Q
A

ATP depletion

67
Q
A
  • Liquefactive necrosis
68
Q
A
  • Caseous necrosis
69
Q
A

Coagulative necrosis

70
Q
A

Fibrinous necrosis

71
Q
A

Fatty necrosis

72
Q

inflammation and its major functions (3)

A
  • Inflammation: reaction/response of a vascularized tissue to infection and damaged tissues
  • Major functions
    • Destroy and remove injurious agents
    • If destruction is not possible, limit the effects by confining the pathogen and its products
    • Repair and replace tissue damaged by pathogen and its products
73
Q

pathophysiology of inflammation

A
  • Vasoconstriction followed by vasodilation causes redness and warmth
  • Increase hydrostatic pressure – edema and pain
  • Permeability – more porous venules
74
Q

Steps of permeability

A
  • Permeability – more porous venules
    • RAT SIP
      • Rolling – Selectins
      • Adhesion – Integrins
      • Transmigration – PECAM-1
75
Q

acute inflammation features

A
  • Short
  • Includes neutrophils and macrophages
  • Utilizes complement, immunoglobulins
76
Q

chronic inflammation features

A
  • Long (weeks to months)
  • Includes lymphocytes, plasma cells, monocytes/macrophages
  • Tries to repair as it destroys
77
Q

Outline the major steps in tissue repair.

A
  • H – hemostasis
  • E – extravasation of GFs
  • A – angiogenesis
  • L – leukocyte activation
  • I – inflammation
  • N – new tissue formation
  • G – gradual strengthening
78
Q
  • For atherosclerosis:
    • What is the mortality rate when compared to other diseases?
    • What are some co-morbidities associated with it?
A
  • Mortality: leading cause of death in all ages
  • Morbidity: can lead to angina, myocardial infarction, HF, stroke, TIA, claudication, ruptured aneurysms
79
Q

What are the overall steps in atherosclerosis?

A
  1. Fatty Streak
  2. Endothelial Dysfunction
  3. Liporprotein Entry and Modification
  4. Leukocyte Recruitment
  5. Foam Cell Formation
  6. Plaque Progression
  7. Smooth Muscle Cell Migration
  8. Extracellular Matrix Metabolism
  9. Plaque Disruption
80
Q

What are some charactersistics of a fatty streak?

  • When does it occur?
  • Does it protrude blood flow?
  • Where does it usually occur?
A
  • Fatty streak
    • The earliest visible lesions of atherosclerosis
    • Do not protrude into arterial lumen nor impede blood flow
    • Exist in the aorta and coronary arteries of most people by age 20
81
Q

What occurs in endothelial dysfunction in terms of atherosclerosis? What is the the “physics” reason behind it?

A
  • Endothelial Dysfunction
    • Injury to the arterial endothelium represents a primary event in atherogenesis
      • Straight sections of arteries, the normal laminar flow’s shear forces favor the endothelial production of NO, a vasodilator, and other atheroprotective mechanisms
      • Compared to areas with bifurcations in arteries (i.e. LCA), where disturbed flow occurs, causing low shear stress, and impairs atheroprotective mechanisms
82
Q

What are some modifiable risk factors that can lead to endothelial dysfunction (5)? What is the process for each one?

A
  • Modifiable risk factors that lead to endothelial dysfunction
    • Hyperlipidemia – more LDL means increased entry into tunica intima
    • Diabetes – increased glycosylation of LDL, making mLDL
    • Smoking – increased ROS, causing endothelial damage
    • Hypertension – promotes retention of lipoproteins in the tunica intima, exacerbating the production of proteoglycans by smooth muscle cells to bind the increased LDL molecules
    • Decreased physical activity – decrease in high shear stress
83
Q

What is a non-modifiable risk that can lead to endothelial dysfunction and how does it occur (1)?

A
  • Non-modifiable risk factors that lead to endothelial dysfunction
    • Reduced endothelial shear stress/blood flow velocity – creates an activated state: impairment of endothelium’s role as a permeability barrier, release of inflammatory cytokines, increased production of cell surface adhesion molecules, reduced release of NO
84
Q

What occurs in the lipoprotein entry and modification stage of atherosclerosis?

A
  • Activated endothelium no longer serves as an effective barrier to the passage of circulating lipoproteins
  • LDL can enter into the intima
  • Once within the intima, LDL accumulates in the subendothelial space by binding to proteoglycans in the ECM
  • Possible modifications of LDL in the tunica intima
    • Oxidation – a result from the local action of ROS
    • Glycation – a result of increased sugars in plasma
  • Modified LDL (mLDL) is pathogenic, stimulating release of cytokines and chemoattractants
85
Q

What occurs in the leukocyte recruitment stage of atherosclerosis?

A
  • Leukocyte Recruitment
    • Recruitment of leukocytes to the vessel wall dependent on leukocyte adhesion molecules
    • Selectins, integrins (ICAM) and vascular cell adhesion molecule (VCAM) direct leukocytes to the forming lesion
      • mLDL may also stimulate endothelial and smooth muscle cells to produce proinflammatory cytokines as well
86
Q

How are foam cells formed in atherosclerosis?

A
  • Macrophages are recruited and penetrate the intima
  • Macrophages take up LDL via scavenger receptors rather than classic LDL receptors because the classic receptors do not recognize mLDL
    • Negative feedback inhibition is inhibited because another pathway besides the controlled “classic LDL receptors” are not being used
87
Q

How does plaque progression in atherosclerosis occur?

A
  • Accumulation of the plaque occurs primarily because the rate of foam cell formation outpaces foam cell degradation
  • The clearance of dead foam cells becomes inefficient, promoting the accumulation of cellular debris and extracellular lipids → forming lipid-rich center of a plaque (aka necrotic core)
  • Early plaque growth grows outward, avoiding detection by angiography
  • Later plaque growth grows inwards, cutting off blood suppl
88
Q

What occurs in the smooth muscle cell migration phase of atherosclerosis?

A
  • Smooth Muscle Cell Migration
    • Move from tunica media to tunica intima and replication → pushes endothelial layer along with plaque into the lumen
89
Q

What occurs in the extracellular matrix metabolism phase of atherosclerosis?

A
  • Extracellular Matrix Metabolism
    • Smooth muscle cells produce collagen fibers to produce the fibrous cap around the necrotic core
    • Net matrix deposition depends on the balance of synthesis by SMCs and degradation by MMPs
    • Smooth muscle cells are inhibited by T-cells to produce collagen fibers, decreasing the formation of the fibrous cap
    • Foam cells are stimulated by T-cells to release Matrix Metalloproteinases (MMPs) to degrade the fibrous cap, predisposing the plaque to rupture
90
Q

What occurs in the plaque disruption phase of atherosclerosis?

A
  • Plaque Disruption
    • Rupture of atherosclerotic plaque does not inevitably cause major clinical events such as myocardial infarction or stroke
    • Post-rupture, small nonocclusive thrombia may incorporate into the plaque, stimulating further smoother muscle proliferation and ECM deposition
91
Q

What are the 5 types of plaque morphologies and describe each one?

A
  • Plaque morphology
    • Non-atherosclerotic intimal lesions – intimal thickening, fatty streak
    • Progressive atherosclerotic lesions – fibrocalcific lesions, fibrous cap atheromas
    • Vulnerable plaques – thin fibrous cap atheromas
    • Unstable thrombosed plaques – ruptured plaque with thrombus, ulceration
    • Healed lesions – thickened fibrous cap overlaying necrotic core and small, non-occlusive thrombus
92
Q

The clinicial manifestations of a plaque are dependent on what two main things?

A
  • Clinical manifestations are dependent on the morphology and location of atherosclerotic lesions
93
Q

What are two risk factors for atherosclerosis?

A
  • Clinical data
    • High levels of Lp(a), CRP
    • Low levels of estrogen pre-menopause
94
Q

For cardiac catherization:

  • Provide the technical aspects on how it works.
  • What is it used for?
  • What are some strengths of the imaging?
  • What are some limitations?
A
  • Technical Aspects
    • Invasive
    • Continuous XR transmission
    • Intravenous dyes
    • Rotating C-arm
    • 2D images
  • Uses:
    • Coronary angiography (only see lumen)
    • Hemodynamic assessment (pressure across stenosis)
  • Strength
    • Gold standard for coronary stenosis assessment
    • Used for both diagnosis and treatment
  • Limitations
    • Contrast/radiation exposure
    • Invasive
    • Only lumen, not vessel, is visualized
95
Q

For echocardiography:

  • Provide the technical aspects on how it works.
  • What is it used for?
  • What are some strengths of the imaging?
  • What are some limitations?
A
  • Technical Aspects
    • Ultrasound with real time images
  • Uses:
    • Chamber size and function
    • Valve stenosis
    • Doppler – assesses flow across valve
  • Strength
    • Gold standard for chamber size and function
    • Portable
    • Low cost
    • No radiation
  • Limitations
    • User dependent images
    • Ribs limit image angles
96
Q

For cardiac CT:

  • Provide the technical aspects on how it works.
  • What is it used for?
  • What are some strengths of the imaging?
  • What are some limitations?
A

Technical Aspect

  • XR source
  • EKG gating used for function and coronaries

Uses:

  • Ca++ scoring
  • Coronary CT angiogram (see soft tissue)
  • Cardiac structural assessment

Strength

  • Gold standard for atherosclerotic burden
  • 3D reconstruction

Limitations

  • Radiation exposure
  • HR/arrhythmia affect EKG gating images
97
Q

For Cardiac MRI:

  • Provide the technical aspects on how it works.
  • What is it used for?
  • What are some strengths of the imaging?
  • What are some limitations?
A
  • Technical Aspects
    • Radiofrequency pulses manipulate H+ alignment
    • Electromagnetic pulse emitted as H+ atoms realign
  • Uses
    • Cardiomyopathies
    • Tumors
  • Strengths
    • Gold standard for chamber volume, mass, and ejection fraction
    • No radiation
    • 3D reconstruction
  • Weakness
    • $$$$
    • Non-portable
98
Q

For Nuclear Cardiac Imaging:

  • Provide the technical aspects on how it works.
  • What is it used for?
  • What are some strengths of the imaging?
  • What are some limitations?
A
  • Technical Aspects
    • SPECT and PET
    • Photon and Positron emission by nuclear dyes absorbed by cells picked up by detector
  • Uses:
    • Stress testing (evaluate for ischemia)
    • LV function
    • Myocardial viability
  • Strengths
    • Can measure glucose activity
  • Weaknesses
    • LOTS OF RADIATION
99
Q

What type of cardiac imaging?

A

Cardiac Catherization

100
Q

What kind of cardiac image?

A

Electrocardiography/Ultrasound

101
Q

What kind of cardiac imaging?

A

Cardiac CT

102
Q

What kind of cardiac imaging?

A

Cardiac MRI

103
Q

What kind of cardiac imaging?

A

Nuclear Cardiac Imaging

CardioResp (14 decks)

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