CCP Final Exam Prep Flashcards

1
Q

Killip Classification for Heart Failure

A

Quantifies severity of heart failure in ACS and predicts 30-day mortality.

Class I: No signs of congestion/CHF
Class II: S3 and basal rales on auscultation and/or JVD
Class III: Acute pulmonary edema
Class IV: Cardiogenic shock

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2
Q

clinic features of right heart STRAIN on echo

A
  1. dilatation of the RV (ideally measured in the RV focused apical 4 chamber view)
  2. interventricular septal flattening (commonly referred to as “D sign”. look for the presence of septal flattening in LV via parasternal short axis)
  3. paradoxical septal motion
  4. right atrial enlargement
  5. right ventricular hypertrophy
  6. right ventricular systolic dysfunction (RV free wall hypokinesis with apical sparing “McConnell’s sign”)
  7. RV hypokinesia
  8. fat IVC (diameter >2.1cm with loss of phasic variation throughout the respiratory cycle)
  9. tricuspid regurgitation
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3
Q

define right heart STRAIN (or more precisely right ventricular strain)

A
  1. ventricular dysfunction where the RV is deformed
  2. used to denote the presence of RV dysfunction usually in the absence of an underlying cardiomyopathy
  3. can be caused by PHTN, PE, RV infarction, chronic lung disease (pulmonary fibrosis or COPD), pulmonic stenosis, bronchospasm, and pneumothorax
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4
Q

ECG signs of right heart strain

A
  1. Tachycardia
  2. Right axis deviation
  3. RBBB
  4. S1Q3T3 (insensitive and non-specific)
  5. T-wave inversion anterior leads
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5
Q

these conditions pre-dispose geriatrics to cervical spine injury

A
  1. osteoarthritis (OA)

2. cervical stenosis

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6
Q

what percent of geriatric patients develop life threatening ICH following minor head trauma

A

Fifteen percent (15%)

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7
Q

what percent of the north american geriatric population is on anticoagulants

A

Ten percent (10%)

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8
Q

discuss age-related Anatomic/physiologic/pharmacologic changes that affect the pathophysiology of head trauma in the elderly

A
  1. compared to young people, subdural hematomas (along with intraparenchymal bleeds) are the most common types of geriatric intracranial bleeds
  2. This is d/t ↑ adherence of the dura to the skull in elderly patients → the underlying bridging veins in the elderly being more likely to be damaged in head trauma
  3. As the bridging veins bleed, intracranial subdural hematomas form (as opposed to epidural hematomas, which are more common in young patients)
  4. advancing age → to progressive brain atrophy → more room for ↑ bleeding for the subdural hematoma within the cranial cavity
  5. This situation → delayed onset of symptoms → elderly patients to seek care later → Delay in presentation and delays in initiation of treatment
  6. higher incidence of chronic dementia in the elderly also → delays in presentation and treatment
  7. ~10% of geriatric population is on anticoagulation → increased risk of intracranial bleeding
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9
Q

pulmonary changes in geriatric patients

A
  1. ↓ in elastic fibers, ↓ intercostal muscle mass, ↓ rib articulation, changes in thoracic vertebral body height, osteoporosis, ↓ in alveolar surface area, ↓ gas exchange, ↓ mucociliary clearance and cough reflexes, and underlying pulmonary disease
  2. These changes lead to ↓ pulmonary reserve, with ↓ FEV, ↓ FRC, ↓ VC.
  3. Additionally, the elderly may mount only half of the compensations for hypoxia or hypercarbia compared to their younger counterparts, potentially leading to rapid decompensation
  4. The frail chest wall in the elderly patient ↑ their susceptibility to trauma, as low-impact forces may result in sternal + rib fractures w/ pulmonary contusions, leading to ↑ morbidity and mortality
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10
Q

Cardiovascular changes in geriatric patients

A
  1. after 40yo vasculature + myocardial connective tissue hardens d/t elastin and collagen changes
  2. ↑ sympathetic activity and norepinephrine baseline levels lead to ↑ SVR.
  3. These physiologic changes in aging lead to ↓ vascular compliance and an ↑ in systolic HTN.
  4. β-adrenergic responses to endogenous and exogenous stressors in the geriatric patient are also altered, resulting in an inappropriate ionotropic and chronotropic compensation for traumatic insults.
  5. Vital signs in the geriatric trauma patient may be unreliable and may appear normal, given that a baseline of HTN is common in this population.
  6. The blunted response may also be altered by medication use (eg, beta blockers).
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11
Q

neurologic changes in geriatric patients

A
  1. Underlying dementia, visual, auditory, and cognitive decline, slower reaction times, and concomitant medication use may influence mental status evaluation (eg, GCS)
  2. After the age of 40 y, brain volume ↓ 5% per decade of life
  3. An occult brain bleed, commonly d/t shearing of the bridging veins resulting in a SDH, is possible given the ↑ potential space d/t age-related brain atrophy that can be occupied by an intracranial bleed before clinical symptoms become apparent
  4. ↓ cerebral autoregulation with aging renders the geriatric trauma patient with head injury more sensitive to hypotension
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12
Q

Musculoskeletal changes in geriatric patients

A
  1. ↓ in bony and cartilaginous mass and volume
  2. OA is a risk factor for fractures
  3. geriatric trauma patient is prone to ↑ rates of fractures, even from low MOI
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13
Q

Renal/Hepatic changes in geriatric patients

A
  1. renal function decline is common in the geriatric population, GFR ↓ approx ~7.5 mL/min per decade in geriatrics
  2. renal changes contribute to disturbances in electrolyte hemostasis and worsened autoregulation of volume status
  3. hepatic mass ↓ up to 40% w/ advancing age, correlating with a ↓ in function
  4. pharmacokinetics in the geriatric patient are affected by ↓ renal + hepatic function, resulting in altered absorption, elimination, distribution, and metabolism of drugs
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14
Q

explain how drug METABOLISM is altered in the elderly (pharmacokinetics)

A
  1. Diminished phase one metabolism, resulting in accumulation of phase-1-dependent medications
  2. Diminished hepatic blood flow, resulting in altered metabolism
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15
Q

age-related changes to the Resp system in elderly

A
  1. Decreased VC

2. Decreased compliance

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16
Q

describe airway management changes in the geriatric patient

A
  1. ↓ Neck mobility d/t cervical spine degenerative changes
  2. poor pulmonary reserves + more susceptible to hypoxic insults
  3. difficult BMV d/t atrophy of the perioral musculature and edentulous
  4. lips are friable and prone to laceration, teeth susceptible to breaking
  5. Mouth opening may be affected by microstomia and TMJ arthritis
  6. ↑ aspiration risk d/t swallowing muscle atrophy, ↓ larynx sensitivity, ↓ esophageal motility, and comorbidities (eg, Parkinson’s disease)
  7. Vocal cord visualization may be obscured by bleeding (friable oral tissue trauma), masses, epiglottis floppiness, or pre-existing infections (Candida)
  8. Geriatrics are more sensitive to medications and doses used in RSI. more likely to develop peri-intubation hypotension and apnea and have an ↑ risk of cardiac arrest. Dose adjustments for induction medications are recommending up to a 50% reduction in dose
17
Q

What are the primary causes of massive pulmonary hemmorhage (actual legit pulmonary hemorrhage, not undifferentiated hemoptysis)

A
  1. Bronchiectasis
  2. Tumours/CA
  3. AVM’s
18
Q

treatment considerations for massive hemoptysis/ pulmonary hemorrhage

A
  1. Early intubation
  2. Consider unilateral lung isolation with selective intubation of the “good lung” and lung “isolation” of the bad lung
  3. Dependent positioning. Trendelenburg with “bad side” down (theoretical belief to minimize reflux of blood into normal lung)
  4. High PEEP to improve V/Q matching
  5. If major pulmonary haemorrhage target SBP <140 mmHg
  6. Consider IV TXA. If patient is not intubated and can tolerate it, consider nebulizer TXA
19
Q

criteria for “massive hemoptysis”

A
  1. ≥50cc blood in single cough or
  2. ≥600ml in 24 hours or
  3. Needs transfusion