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CardioResp > Week 7 > Flashcards

Week 7 Flashcards

1
Q

For dilated cardiomyopathy:

  • Discuss ventricular morphology.
  • Ejection Fraction (increased or decreased)?
  • Etiologies of the cardiomyopathy
  • General pathophysiology associated with the myopathy.
A
  • Discuss ventricular morphology.
    • Ventricular: Dilated LV with little concentric hypertrophy
  • Ejection Fraction (increased or decreased)?
    • decreased
  • Etiologies of the cardiomyopathy
    • Genetic, infectious, alcohol, peripartum
  • General pathophysiology associated with the myopathy
    • Impaired systolic contraction
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2
Q

For dilated cardiomyopathy:

  • Symptoms?
  • Physical Exam?
  • Heart size?
A
  • Symptoms?
    • Fatigue, weakness, dyspnea, orthopnea, PND
  • Physical Exam?
    • Pulmonary rales, S3, if RV failure present; JVD, hepatomegaly, peripheral edema, mitral regurgitation
  • Heart size?
    • Enlarged
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3
Q

For hypertrophic cardiomyopathy:

  • Discuss ventricular morphology.
  • Ejection Fraction (increased or decreased)?
  • Etiologies of the cardiomyopathy
  • General pathophysiology associated with the myopathy.
A
  • Discuss ventricular morphology.
    • Ventricular: Marked hypertrophy, often asymmetric ​
  • Ejection Fraction (increased or decreased)?
    • Normal
  • Etiologies of the cardiomyopathy
    • Genetic
  • General pathophysiology associated with the myopathy.
    • Impaired diastolic relaxation
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4
Q

For hypertrophic cardiomyopathy:

  • Symptoms?
  • Physical Exam?
  • Heart size?
A
  • Symptoms?
    • Dyspnea, angina, syncope
  • Physical Exam?
    • S4, if outflow obstruction present, systolic murmur, mitral regurgitation
  • ​ Heart size
    • Normal/enlarged
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5
Q

For restrictive cardiomyopathy:

  • Discuss ventricular and atrial morphology.
  • Ejection Fraction (increased or decreased)?
  • Etiologies of the cardiomyopathy
  • General pathophysiology associated with the myopathy.
A
  • Discuss ventricular and atrial morphology.
    • Ventricular: Fibrotic or infiltrated myocardium
    • Atrial: prominent enlargement
  • Ejection Fraction (increased or decreased)?
    • Decreased
  • Etiologies of the cardiomyopathy
    • Amyloidosis, hemochromatosis, scleroderma, radiation therapy
  • General pathophysiology associated with the myopathy.
    • Stiff LV – impaired diastolic relaxation
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6
Q

For restrictive cardiomyopathy:

  • Symptoms?
  • Physical Exam?
  • Heart size?
A
  • Symptoms?
    • Dyspnea, fatigue
  • Physical Exam?
    • JVD, hepatomegaly, peripheral edema
  • Heart size?
    • Normal
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7
Q

For Arrhythmogenic cardiomyopathy:

  • Discuss ventricular morphology.
  • Etiologies of the cardiomyopathy
  • General pathophysiology associated with the myopathy.
  • Symptoms?
  • Cardiac size?
A
  • Discuss ventricular morphology.
    • Ventricular: Right prominence
  • Etiologies of the cardiomyopathy
    • Genetic
  • General pathophysiology associated with the myopathy.
    • Diffuse fatty replacement of ventricle
  • Symptoms?
    • Arrhythmias, death
  • Cardiac size?
    • Enlarged
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8
Q

For ventricular noncompaction:

  • Discuss ventricular morphology.
  • Etiologies of the cardiomyopathy
  • Cardiac size?
A
  • Discuss ventricular morphology.
    • Ventricular: Spongy left ventricular myocardium and increased trabecula carnae. No papillary muscles
  • Etiologies of the cardiomyopathy
    • Genetic
  • Cardiac size?
    • Normal
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9
Q

What cardiomyopathy?

A

Dilated

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10
Q

What cariomyopathy?

A

Ventricular non-compaction

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11
Q

What cardiomyopathy is seen here?

A

Hypertrophic

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12
Q

What type of cardiomyopathy?

A

Arrhythmogenic

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13
Q

What myopathy? Describe what is seen.

A

Dilated

Fibrosis - the blue

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14
Q

What myopathy? Describe what is seen.

A

Hypertrophic cardiomyopathy

Dissaray of myofibrils

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15
Q

What myopathy? Describe what is seen.

A

ventricular non-compaction

non-compacted layer is seen

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16
Q

What myopathy? Describe what is seen.

A

Arrhythmogenic

Fat - adipose tissue

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17
Q

What cardiomyopathy is seen here? Describe what is seen.

A

Restrictive cardiomyopathy

Amyloidosis is the red stuff

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18
Q

What cardiomyopathy is seen here?

A

Dilated cardiomyopathy.

The ventricles are large

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19
Q

What cardiomyopathy is seen here?

A

S indicates hypertrophic septum.

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20
Q

What cardiomyopathy is seen here?

A

Ventricular non-compaction

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21
Q

What cardiomyopathy is seen here?

A

Arrhythmogenic

RV IS HUGE

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22
Q

What cardiomyopathy is seen here?

A

Restrictive

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23
Q

For stress/takotsubo cardiomyopathy:

  • What is the etiology?
  • What can it often be confused with and why?
  • Where is it diagnosed?
A

Stress or Takotsubo Cardiomyopathy

  • Stress induced morphological changes of the heart
    • Looks like a takotsubo – a clay pot on its side
  • Can be confused with MI (+troponin, acute EKG ST changes)
  • Diagnosed in the cath lab
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24
Q

Define heart failure in precise terms.

A
  • Heart failure is when the heart is unable to pump blood forward at a sufficient rate to meet the metabolic demands of the body or is able to do so only if cardiac filling pressures are abnormally high
  • It is the final and most severe manifestation of most cardiac diseases
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25
Q

What are the two types of heart failures and what kind of dysfunction are they each associated with?

A
  • Reduced Ejection Fraction Heart Failure - associated with systolic dysfunction
  • Preserved Ejection Fraction Heart Failure - associated with diastolic dysfunction
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26
Q

For Reduced EF HF, what are the two main reasons for HF?

A

Impaired contractility and increased afterload

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27
Q

What are the three ways that contractility is impaired in HF REF?

A
  • Coronary artery disease – lack of perfusion does not get blood to myocardial cells → myocardial cells cannot contract fully
    • Myocardial infarction, transient myocardial ischemia
  • Chronic volume overload – chronic dilation of the ventricles causes remodeling of the ventricle walls to be more fibrotic
    • Mitral/aortic regurgitation
  • Dilated cardiomyopathies – fibrosis and myocyte atrophy cause impaired contraction (myocytes grow in series instead of in parallel – decreased ability to cross-link)
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28
Q

What are the three ways that increased afterload occurs in HF REF?

A
  • Increased Afterload
    • Hypertension – Ventricle contracting against increased pressure → less volume leaves ventricle
    • Aortic stenosis – Ventricle contracting against increased pressure → less volume leaves ventricle
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29
Q

What are the two main conditions in which HF PEF occurs?

A

Impaired early diastolic relaxation and Increased stiffness of the ventricular wall

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30
Q

What main situation causes impaired early diastolic relaxation in HF PEF?

A
  • Impaired early diastolic relaxation – external force limits ventricular filling
    • Cardiac tamponade
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31
Q

What 3 situations causes increased stiffness of the ventricular wall in HF PEF?

A
  • LVH, fibrosis, restrictive cardiomyopathy
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32
Q

What are the compensatory mechanisms that occur with the Frank-Starling curve acutely and chronically?

A
  • Frank-Starling Mechanism
    • Acute: increase in preload causes an increase in stretching (cross-linking) of cardiac muscle
    • Chronic: increase in preload causes dilation (remodeling of myocardium)
33
Q

What are the compensatory mechanisms that occur with the adrenergic system (a neurohormonal system) acutely and chronically?

A
  • Adrenergic system
    • Acute: drop in CO → drop in BP (BP = CO x TPR) → decrease in baroreceptor firing → increase in sympathetic activity
    • Chronic: down regulation of beta receptors, increased catecholamine releases causes increase intracellular Ca2+ → activation of apoptosis pathway
34
Q

What are the compensatory mechanisms that occur with the RAAS (a neurohormonal system) acutely and chronically?

A
  • Acute: decreased CO → decreased GFR → renin, angiotensin II, aldosterone release → increase in vasoconstriction and volume retention → increases preload
  • Chronic: excessive stimulation of RAAS receptors causes hypertrophy and fibrosis
35
Q

What are the compensatory mechanisms that occur with the antidiuretic hormone (a neurohormonal system) acutely and chronically?

A
  • Antidiuretic Hormone (ADH – vasopressin)
    • Acute: released from posterior pituitary gland in response of low BP → increase in water retention → increase in preload
    • Chronic: excessive stimulation causes hypertrophy and fibrosis
36
Q

What are the compensatory mechanisms that occur with the Natriuretic peptides?

A
  • Natriuretic Peptides
    • Atrial natriuretic peptide (ANP) – released in response to atrial distension
    • B-type natriuretic peptide (BNP) – released when ventricular myocardium is subjected to hemodynamic stress
      • Correlated with severity of HF
    • Result in excretion of Na+ and water, vasodilation, inhibition of renin secretion, and antagonize effects of ATII and vasopressin
      • Not fully sufficient to counteract the other hormones
37
Q

What are the compensatory mechanisms that occur with the development of ventricular hypertrophy acutely and chronically?

A
  • Development of ventricular hypertrophy
    • Acute: increased mass of muscle fibers helps maintain contractile force and counteracts the elevated ventricular wall stress
    • Chronic: unfortunately, increased stiffness of the hypertrophied wall causes higher-than-normal diastolic ventricular pressures, which are transmitted to the LA and pulmonary vasculature
38
Q

Name 5 precipitating factors of heart failure and conditions that would cause these factors.

A

Precipitating Factors

  • Increased metabolic demands – supply does not meet demand
    • Fever, infection, anemia, tachycardia, hyperthyroidism, pregnancy
  • Increased preload – increases pulmonary capillary pressure à pulmonary edema/congestion → decreased gas exchange
    • Sodium diet, renal failure, excessive fluid
  • Increased afterload – decreased forward CO
    • Hypertension, PE
  • Impaired contractility – decreased forward CO
    • Negative inotropes, CAD, alcohol
  • Sudden inappropriate HR – decreased CO or decreased diastolic filling
    • Bradycardia, tachycardia
39
Q

What are the 4 classifications of heart failure?

A
  • I: No limitation of physical activity
  • II: Slight limitation of activity. Dyspnea and fatigue with moderate exertion (walking upstairs quickly)
  • III: Marked limitation of activity. Dyspnea with minimal exertion (walking upstairs slowly)
  • IV: Severe limitation of activity. Symptoms are present even at rest.
40
Q

What is the general prevalence of heart failure?

What is the age group?

Males or females more likely to die?

Which one has an increased mortality (HFrEFF or HFpEFF?)

A
  • Prevalence: 5.1 million with 500,000 new cases annually
    • Increase over the next few years as elderly population increases
  • “Old person’s disease” – ages 70-89
  • Males have a higher mortality rate
  • HFrEFF barely has an increased mortality
41
Q

Name the symptoms associated with right HF

A
  • Symptoms
    • Peripheral edema
    • RUQ discomfort (due to hepatic enlargement)
42
Q

Name the physical findings associated with right HF

A
  • Physical findings
    • Elevated JVP
    • RV Heave
    • Right sided S3
43
Q

Name the symptoms associated with left HF

A
  • Symptoms
    • Dyspnea
    • Orthopnea
    • PND
    • Fatigue
44
Q

Name the physical findings associated with left HF

A
  • Physical Findings
    • Diaphoresis
    • Tachycardia
    • Pulmonary rales, wheezes
    • Loud P2
    • S3 (in systolic dysfunction HF)
    • S4 (in diastolic dysfunction HF)
    • LV heave
45
Q

What are the 4 stages of HF?

A

AT RISK

  • Stage A: High risk for developing HF
  • Stage B: asymptomatic LV dysfunction

HF

  • Stage C: past or current symptoms of HF
  • Stage D: End-stage HF
46
Q

How do you treat Stage A HF?

A
  • Stage A: High risk for developing HF
    • Treatment:
      • Treat risk factors (i.e. HTN, smoking, cholesterol, alcohol)
47
Q

How do you treat Stage B HF?

A
  • Treatment used for A:
    • Treat risk factors (i.e. HTN, smoking, cholesterol, alcohol)

PLUS

  • Treatment for B:
    • ACEI (indicated in PMHx of MI or decreased EF)
    • Beta-blockers (indicated in recent MI)
    • ICD
    • Digoxin: reduces progression of HF
48
Q

How do you treat stage C HF?

A

Treatment used for A:

  • Treat risk factors (i.e. HTN, smoking, cholesterol, alcohol)

PLUS

Treatment for B:

  • ACEI (indicated in PMHx of MI or decreased EF)
  • Beta-blockers (indicated in recent MI)
  • ICD
  • Digoxin: reduces progression of HF

PLUS

  • Treatment for C
    • Hydralazine-Isosorbide Dinitrate Combo (balanced vasodilator)
    • Biventricular Pacing/Cardiac Revascularization Therapy (CRT): device placed that stimulates ventricular contraction at same time
      • Indicated in QRS ≥ 120ms and LVEF ≤ 35%
    • Neprilysin inhibitor
49
Q

How do you treat Stage D HF?

A

Treatment used for A:

  • Treat risk factors (i.e. HTN, smoking, cholesterol, alcohol)

PLUS

Treatment for B:

  • ACEI (indicated in PMHx of MI or decreased EF)
  • Beta-blockers (indicated in recent MI)
  • ICD
  • Digoxin: reduces progression of HF

PLUS

Treatment for C

  • Hydralazine-Isosorbide Dinitrate Combo (balanced vasodilator)
  • Biventricular Pacing/Cardiac Revascularization Therapy (CRT): device placed that stimulates ventricular contraction at same time
    • Indicated in QRS ≥ 120ms and LVEF ≤ 35%
  • Neprilysin inhibitor

PLUS

  • Treatment/Care for stage D:
    • Surgical therapy: cardiac transplantation, valve repair/replacement
    • Drugs
    • Palliative care
50
Q

For ACEi, ARB, Aldosterone Antagonists in HF:

  • What MOA/effect do they have?
  • What is the rationale of that effect?
  • What are side effects?
  • Can you combine ACEI and ARBs?
A
  • What effect do they have?
    • Balanced vasodilators (dilate arteries and veins both)
  • What is the rationale of that effect?
    • Reduces BP
    • Decreases preload and afterload → reduces myocardial oxygen demand
    • Limits remodeling (aldosterone)
  • What are side effects?
    • Monitor potassium, especially if combining!
  • CANNOT COMBINE ACEI AND ARBs
51
Q

For Hydralazine/Isosorbide (combo drug), in HF:

  • What MOA/effect do they have?
  • What is the rationale of that effect?
A

MOA:

  • Hydralazine: vasodilates arteries
  • Isosorbide: vasodilates veins

Rationale

  • Reduces BP
  • Decreases preload and afterload → reduces myocardial oxygen demand
  • Limits remodeling (aldosterone)
52
Q

For Nitroprusside, in HF:

  • What MOA/effect do they have?
  • What is the rationale of that effect?
A

MOA:

  • Balanced vasodilators (arteries and veins)

Rationale:

  • Reduces BP
  • Decreases preload and afterload → reduces myocardial oxygen demand
  • Limits remodeling (aldosterone)
53
Q

For beta blockers (Metoprolol succinate, Carvedilol, bisoprolol), in HF:

  • What MOA/effect do they have (Acutely and chronically)?
  • What is the rationale of that effect?
A

MOA

  • Acute: decreases contractility and HR
  • Chronic: increases contractility (due to up-regulation of beta receptors)

Rationale

  • In HF, beta receptors are down-regulated due to chronic compensatory sympathetic stimulation
  • Beta blockers can up-regulate beta receptors à resulting in increased contractility
54
Q

For loop diuretic like Furosemide, in HF:

  • What MOA/effect do they have?
  • What is the rationale of that effect?
  • What are the side effects of this drug?
A

_**PNEUMONIC ALERT BIATCHES: Furosemide (FURY has no wrath aka potent)**_

MOA:

  • Inhibits sodium reabsorption at the Loop of Henle blocking Na/K/Cl

Rationale

  • Reduces BP – works well in renal failure
  • More potent, helps with edema

Side Effect

  • Dehydrating
  • Hypokalemia
  • Hyperuricemia
  • Ototoxicity
55
Q

For digoxin, in HF:

  • What MOA/effect do they have? LONG
  • What is the rationale of that effect?
  • What are the side effects of this drug?
    • How do you treat digoxin toxicity? TWO WAYS
A

MOA:

  • Blocks Na/K ATPase → resulting in greater driving force for Na/Ca exchanger → increased intracellular Ca
  • Positive Inotrope
  • Hypokalemia – increases effectiveness (risk Digoxin toxicity)
  • Hyperkalemia decreases effectiveness

Rationale

  • Increase in contractility → Increase SV and CO → leads to increased reflex vagal tone → reduce O2 demand

Side Effects

  • Chromatopsia
  • Drug Interaction:
    • Diuretics
    • P-glycoprotein inhibitors
      • Quinidine, Verapamil
  • Tx toxicity: w/ potassium or Digibind
56
Q

For dobutamine, in HF:

  • What MOA/effect do they have?
  • What is the rationale of that effect?
  • What are the side effects of this drug?
A

MOA

  • Beta-1 agonist

Rationale

  • Increases SV by increasing contractility

Side Effects

  • Tachycardia, arrhythmias, angina, myocardial ischemia
57
Q

For dopamine, in HF:

  • What MOA/effect do they have?
    • Specifically for Low dose, intermediate dose, high dose!
  • What is the rationale of that effect?
  • What are the side effects of this drug?
A

Dobutamine and dopamine are similar in MOA, Rationale, and Side Effects

MOA

  • Low dose: stimulate dopamine receptors to vasodilate (Ehhh)
  • Intermediate dose: stimulate beta-1 receptors (GOOD)
  • High dose: stimulate alpha-1 receptors (BAD)

Rationale

  • Increases SV due to increased contractility

Side Effects

  • Tachycardia, arrhythmias, angina, myocardial ischemia
58
Q

For Milirinone, in HF:

  • What MOA/effect do they have?
  • What is the rationale of that effect?
  • What are the side effects of this drug?
A

MOA

  • Increase cAMP by phosphodiesterase-3 → activation of Ca channels → positive inotrope

Rationale:

  • Vasodilation → decrease BP, preload, afterload

Side Effects

  • Teratogenicity, hypotension, hyperkalemia
59
Q

What is hypertriglyceridemia defined as?

A
  • Hypertriglyceridemia
    • Elevated fasting TGs without a clear secondary cause >150
    • Average to below average LDLc
60
Q

What is the number one way to manage hypertriglyceridemia?

A
  • Diet – weight loss and caloric restriction
61
Q

What are some secondary causes of hypertriglyceridemia?

A
  • Eliminate secondary causes: hypothyroidism, DM, drugs, EtOH excess, renal disease, estrogens, obesity
62
Q

What medical therapy is used in hypertriglyceridemia and when is it indicated?

A
  • Medical therapy (indicated in TG levels > 500mg/dL)
    • Fibrates – PPAR alpha agonist (nuclear transcription factor)
    • Niacin
    • Fish Oil
63
Q

What is the effect of niacin in terms of treating hypertriglyceridemia?

A
  • Niacin
    • Increases HDL
64
Q

What is the effect of fish oil in terms of treating hypertriglyceridemia?

A

Fish oil

  • reduces TG
65
Q

For Fibrates:

  • What receptor do they attach at?
  • What is their effect?
  • What do you include with this usually?
  • What are two examples of a fibrate?
A
  • Fibrates – PPAR alpha agonist (nuclear transcription factor)
    • MOA: decreased TG and cholesterol synthesis and increases LPL activity (cleaves TGs from lipoproteins) leading to increased LDL
    • Must include statin therapy due to increased LDL levels
    • Examples: fenofibrate, gemfibrozil
66
Q

What is the alveolar gas equation?

When does the value of R in the equation increase?

A
  • PAO2 = PIO2 – (PACO2 / R) = FIO2 (Patm – 47) – (PACO2 / R)
    • R reflects the ratio of O2 consumption for every molecule of CO2 generated
      • The greater the value, the more CO2 is generated (i.e. fever, sepsis, more anaerobic respiration)
      • Typically 0.8
67
Q

What is the equation for the A-a gradient?

What is the normal pressure gradient across the alveolar space?

What does it mean if the A-a gradient is large?

A
  • A-a gradient = PAO2 – PaO2
    • The normal pressure gradient across the alveolar space is 5 mmHg
    • If the pressure gradient is large, that means the O2 in the alveolus is not able to get across the barrier to saturate the blood (aka a diffusion impairment)
68
Q

Define the following:

  • acidemia
  • alkalemia
  • acidosis
  • alkalosis
A
  • Acidemia – low blood pH (not used clinically)
  • Alkalemia – high blood pH (not used clinically)
  • Acidosis – increased acid content, but the pH may or may not be low due to buffering, compensation, or competing acid-base disorders
  • Alkalosis – decreased acid content, but the pH may or may not be high due to buffering, compensation, or competing acid-base disorders
69
Q

What is a buffer?

What is the most common buffer in the human body?

What are some other buffers in the human body?

A
  • Buffers
    • Weakly dissociated acid or bases that are capable of minimzing pH swings by mass effect on equilibrium
    • Most common buffer is the bicarbonate-carbonic acid buffer
      • H2CO3 ⇔ H+ + HCO3-
    • Other buffers used: albumin, intracellular blood proteins, hemoglobin, bone (holds large reservoir of HCO3-)
70
Q

What equation defines the compensation of the lungs and kidney in relation to acidosis or alkalosis?

What occurs in the lungs in response to metabolic acidosis?

What ocurs in the kidneys in response to respiratory acidosis or alkalosis?

A
  • CO2 + H2O ⇔ H2CO3 ⇔ H+ + HCO3-
    • CO2 is blown off by the lungs
    • HCO3- is excreted by the kidneys
  • Lungs: hyperventilate in response to metabolic acidosis
  • Kidneys: increase bicarb reabsorption or elimination in response to respiratory acidosis or alkalosis
71
Q

In the following, indicate if the pH, bicarb, pCO2 is high or low:

  • respiratory alkalosis
  • respiratory acidosis
  • metabolic acidosis
  • metabolic alkalosis

*IMPORTANT TO MEMORIZE THIS TABLE*

A
72
Q

What occurs in the lungs and kidneys in respiratory alkalosis?

What occurs in the lungs and kidneys in respiratory acidosis?

A
  • Respiratory alkalosis: lungs are hyperventilating → decrease in CO2 → increase in pH → kidneys respond by excreting bicarb to make blood more acidic
  • Respiratory acidosis: lungs are hypoventilating → increase in CO2 → decrease in pH → kidneys respond by reabsorbing bicarb to make blood more basic
73
Q

What occurs in the lungs and kidneys in metabolic acidosis?

What occurs in the lungs and kidneys in metabolic alkalosis?

A
  • Metabolic acidosis: kidneys are excreting too much bicarb → decrease in pH → lungs respond by blowing off CO2 to make blood more basic
  • Metabolic alkalosis: kidneys are reabsorbing too much bicarb → increase in pH → lungs respond by hypoventilating to keep CO2 to make blood more acidic
74
Q

How can the pH of the blood be approximated?

A
  • pH ~ [HCO3-] / PaCO2
75
Q

What occurs in a competing acid-base disorder?

A
  • If there are two competing acid-base disorders, the pH may remain within normal limits (i.e. respiratory acidosis and metabolic alkalosis)
76
Q

What occurs to the HCO3- for increase in pCO2 in respiratory acidosis?

What occurs to the HCO3- for increase in pCO2 in respiratory alkalosis?

A

Respiratory acidosis: HCO3- increases with an increase in pCO2

Respiratory alkalosis: HCO3- drops for an increase in pCO2

77
Q

What are the three steps to determine acid-base status?

A
  • Steps to approaching acid-base status
    • Identify the predominant acid-base abnormality
      • Using the table with the pH, bicarb, and pCO2 for all conditions (memorized)
    • Calculate the expected degree of compensation to see if a single acid-base abnormality exists (NB. compensation takes time!)
      • the changes in HCO3- for every pCO2 will be given on test
    • Make the diagnosis
      • Etiologies
78
Q

What are some things that can cause respiratory alkalosis (hypertventilation)?

A
  • Respiratory alkalosis (hyperventilation)
    • Anxiety or pain
    • CNS disease
    • Sepsis (increase in bacteria generating lactic acid from anaerobic respiration)
    • Hypoxia, V/Q mismatch, severe anemia (low O2 getting delivered to periphery so you breathe more)
79
Q

What are some things that can cause respiratory acidosis (hypoventilation)?

A
  • Respiratory acidosis (hypoventilation)
    • Disorders of gas exchange (inability to blow off CO2)
      • COPD, asthma, pneumonia, pulmonary edema, foreign body aspiration, laryngospasm, chest wall trauma, tension pneumothorax
    • Respiratory center abnormalities
      • CNS lesions, sedatives

CardioResp (14 decks)

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