Exam 1 Flashcards
(132 cards)
1
Q
What type of murmur is mitral stenosis and where do you listen?
A
Diastolic, loud S1 murmur, low pitched, apical crescendo rumble.
2
Q
What kind of murmur do you hear with mitral regurgitation and where do you hear it?
A
Systolic, S3 with a systolic murmur at 5th ICS MCL.
Heard with MVP
3
Q
What kind of murmur do you hear with aortic stenosis in where do you listen?
A
Systolic, “blowing“rough harsh murmur at second RIGHT ICS
4
Q
What kind of memory do you here with aortic regurgitation and where do you hear it?
A
Diastolic, “blowing“ murmur at second LEFT ICS
5
Q
Where to insert a chest tube
A
4th or 5th ICS, midaxillary line
6
Q
Indications for a chest tube
A
– >20% collapse (or 2 cm)
– Unstable patient
– Underlying etiology persists, likely progression (example: mechanical ventilation)
7
Q
Needle decompression
A
2nd ICS anterior at MCL
8
Q
Influenza Types
A
A, B, and C
2 surface glycoproteins: H & N
B &C- primarily human
A- primarily avian, but can be in humans
Further classified by H and N subtypes.
9
Q
Groups at high risk for influenza
A
- <24 mo
- 6 mo-5yrs
- older age (>50)
- long-term care
- pulmonary dz
- cardiac dz (not HTN)
- chronic dz
- immunosuppressive
- pregnant, post-partum
- BMI>35
10
Q
Influenza testing
A
Rapid test <15 minutes
Low sensitivity
May not distinguish btwn subtypes
NAAT testing (a few hrs)
Higher sensitivity
Rapid test of choice in hospitalized pts
Viral cx (2-3 days) Nasal, sputum, or secretions Higher sensitivity, longer wait
11
Q
Influenza: additional testing
A
CXR
eval for PNA if indicated
Lobular infiltrates are rare
CBC (if indicated)
Leukopenia
12
Q
Influenza: older adults
A
(Atypical presentation)
AMS
Cough
Fever
Fewer resp sx’s, but more pulmonary complications
Less common: muscle aches, sore throat
More GI sx’s when compares to other real viruses
13
Q
Influenza: acute management
A
ASAP antiviral therapy
Hospitalize if high risk
Xanamivir (inh) or oseltamivir (oral) covers A&B and have both therapeutic and prophylactic dosing regimens
Longer course for highest risk groups
14
Q
Pleural effusion: risk factors
A
Malignancy:
Infiltration of pleural space
Lymphatic system obstruction
Non-malignant HF CKD Liver dz Infection Hypothyroidism Trauma/iatrogenic
15
Q
Pleural effusion: transudative
A
Transudative
•Without pleural disease
•Example: heart failure (90%), renal failure
•↑ hydrostatic or ↓ oncotic pressure
16
Q
Pleural effusion: x-ray
A
CXR confirms presence of effusion
•PA & lateral preferred
•Lateral decub in select cases- bad side down
•Helps refine assessment
Minimum volumes needed for visualization
•75 mL lateral
•175 mL frontal (PA)
17
Q
Pleural effusion: ultrasound
A
- Provides target for thoracentesis
- Locates smaller effusions
- Locates loculated effusions
18
Q
Pleural effusion: CT chest
A
- Non-contrast unless contrast needed for differential
* Detailed assessment of lungs / effusion
19
Q
Indications for diagnostic thoracentesis
A
- New pleural effusion
- Underlying diagnosis is uncertain
- Confirmatory diagnosis needed (example: malignancy)
20
Q
Indications for therapeutic thoracentesis
A
- Larger volume
- Dyspnea, discomfort
- Hypoxemia
- Respiratory failure
Chest tube may be considered.
21
Q
Thoracentesis fluid testing
A
Chemistry
•Protein
•LDH
•Glucose
Hematology
•WBC – total and differential
•Hct if bloody
Microbiology
•Gram stain and culture
Cytology
•Assessing for malignant cells
•Can be non-diagnostic
22
Q
Thoracentesis: additional testing
A
For pleural fluid comparison
•Protein, LDH, glucose
Assessment of underlying disease
•Renal, liver disease, HF
CBC
•Platelets (procedure anticipation)
•WBC (infectious / inflammatory process)
Coags
•Anticipating procedure
23
Q
Pleural effusion: older adults
A
Toleration of pleural effusion may be less compared to younger adults
Antibiotic dosing needs to consider renal function and co-morbid conditions
Higher risk of malignancy, particularly lung cancer
Higher risk of chronic, co-morbid disease
24
Q
Exudative effusion
A
One or more of the following (Light’s criteria)
•Protein pleural fluid : serum ratio > 0.5
•LDH pleural fluid : serum ratio > 0.6
•LDH pleural fluid < 2/3 upper limit of normal for serum LDH (>200 IU)
Clinical pearl: exudes protein
25
Transudative effusion
* Pleural glucose = serum glucose
* pH 7.40 – 7.55
* WBC < 1,000
•Clinical pearl: think few cells, transparent
```
CHARM
(Common causes of transudative effusions)
•Cardiac failure / carditis
•Hypothyroidism
•Albuminemia (hypo)
•Renal failure
•Malabsorption
```
26
Pleural fluid analysis
Low pH
•Empyema (ex TB, anaerobes)
•RA
Hct pleural: serum ratio > 0.5
•Hemothorax
Purulent
•Empyema
White
•Empyema vs. chylothorax
•High trig / chylomicron presence: chylothorax
Microbes
•Pleural vs. parapneumonic infection
27
Thoracentesis: complications
Monitor for complications after large volume drainage (> 1,500 – 2,000 mL)
•Hypotension
•Pulmonary edema
•Inflammatory response (alveolar re-expansion)
Pneumothorax, hemothorax
28
Pneumothorax: risk factors
```
Trauma
Iatrogenic
•Central line
•Bronchoscopy (with needle biopsy)
•Needle insertion (biopsy of lung or liver, thoracentesis)
•Surgery: chest, neck, abdominal
•Mechanical ventilation
```
Intrinsic lung disease
•Examples: COPD (blebs), pneumonia, tumor
* Young, thin males
* Smoking
* HIV with pneumocystis jiroveci pneumonia
29
Tension pneumothorax
Air is unable to exit
Pressure rises
•Lung collapses
•Mediastinal shift away from injury
•Impairs venous return to right heart
30
Pneumothorax: physical exam
* Splinting, reduced respiratory expansion of involved side
* Tracheal / mediastinal shift
* Subcutaneous emphysema
* Decreased breath sounds affected side
* Hemodynamic instability with impaired venous return
31
Pneumothorax: CXR
* First line diagnostic test
* PA and lateral, UPRIGHT POSITION preferred, if possible. LATERAL DECUBITUS also helps detect pneumothorax
* Increased translucency to affected area
* Visible lung collapse demarcation
* Mediastinal shift
* Small pneumothorax may require expiratory CXR instead of standard inspiratory films
* CT (non-contrast acceptable if contrast contraindicated) may be required if diagnosis difficult to establish with underlying lung disease or other complicating factors
32
Pneumothorax: additional testing
ABG
•With indications of hypoxemia
•When diagnosis uncertain (evaluate differential diagnosis)
ECG
•Not required for diagnosis
•T wave changes may be noted with pneumothorax
33
Pneumothorax: diagnostic criteria
Clinical diagnosis sufficient for tension pneumothorax: significant history + exam findings
Radiographic diagnosis preferred if non-critical
•CXR, first line
•CT, if CXR non-diagnostic
34
Pneumothorax: goals of care
Decompression of intrathoracic pressure
•Depending on % of lung compression
Promote resolution of underlying etiology
•Normal healing (example: trauma)
Reduce recurrence
•Procedures to prevent recurrence
•Lifestyle modifications
35
Tension pneumothorax: acute management
* Clinical diagnosis often sufficient; time is critical
* Requires emergent intervention
* Needle decompression (scalpel acceptable in true emergencies)
* 14 to 16 g needed 2nd ICS anterior at MCL
* Subsequent chest tube placement
36
Open pneumothorax: acute management
Three-sided occlusive dressing placement until definitive treatment can be performed (surgery / permanent chest tube)
37
Acute management of pneumothorax (without severe decompensation)
* Determine underlying etiology
* Evaluate extent of pneumothorax
Conservative management (< 15 - 20% collapse)
•Supplemental oxygen (may increase rate of resolution)
•Monitoring
•Frequent vitals
•CXR
•Assessment of symptom worsening
•Small bore chest tube may be an option in select cases
38
Chest tube placement
* > 20% collapse (or 2 cm in size)
* Unstable patient
* Underlying etiology persists, likelihood of progression (example: mechanical ventilation)
* 4th or 5th ICS and mid-axillary line , over the rib
* Closed chest drainage (water seal)
* Add negative pressure
* If water seal insufficient after 24 – 28 hours
* Clinically unstable persists (hypoxemia / hypercapnia)
39
Pneumothorax: surgical considerations
Spontaneous pneumothorax
Failure to respond to chest tube
•Does not re-expand
•Persistent air leak
Bilateral pneumothorax
Surgery may play a role in reducing recurrence
40
Pneumothorax: causes (mneumonic)
```
Causes:
SIT, 3A’s, 3C’s
•Spontaneous (particularly tall, thin men)
•Iatrogenic
•Trauma
•Asthma
•Alveolitis
•AIDS
•COPD
•Carcinoma
•Cystic fibrosis
```
41
Pulmonary TB: HPI
Asymptomatic finding on CXR (subclinical)
Productive cough / sputum
•Purulent
•Blood streaked (frankly bloody less common)
•Cough > 3 weeks
Night sweats
Anorexia
Weight loss
Fever in approximately half of cases
Pleuritic CP uncommon unless significant inflammation
Dyspnea uncommon unless extensive disease
42
Pulmonary TB: risk factors
•HIV
•Immunosuppressive therapy (example: solid organ transplant)
•Young / elderly
•Country of origin with endemic TB
•Exposure to infected individual in close proximity
-Household contact
-Close living quarters: correctional facilities, shelters
-Occupational: healthcare, corrections
-Certain chronic diseases / malignancies
43
Pulmonary TB: physical exam
* Latent TB has no disease symptoms
* Active TB often “looks ill”
* May not be most helpful in diagnosis
* Dullness to lung percussion
* Hollow-sounding breath sounds
* Crepitations (occasional)
* Evidence of extra-pulmonary disease
44
TB skin test
•PPD (purified protein derivative) intradermal injection
•Non-specific reaction to mycobacterium
•Assesses 48 – 72 hours after administration
•Assessing INDURATION – if no induration then it is not a positive finding
•Negative findings can be found in recent TB exposure (< 8 – 10 weeks), overwhelming TB disease, immunocompromised / certain illnesses
•Cut-point varies based on population
-15 mm those without risk factors
-10 mm “healthy” with risk factors (such as healthcare workers, foreign-born persons)
-5 mm household contact, CXR suspicious of prior infection, and immunocompromised (example: HIV)
-If negative finding with CD4 count < 200 / uL, repeat once above 200
45
IGRAs
Interferon-gamma release assays
•Blood test
•Rapid results (24 hours)
•1 visit (compared to follow-up visit for PPD)
•Limited knowledge of role for testing in immunocompromised patients
•May be expensive testing
46
Sputum microscopy for TB
AFB sputum staining
•Detects any acid fast mycobacterium
Expert MTB/RIF Assay
•Rapid diagnosis test for Mtb complex and resistance to rifampin
Cultures take weeks to months to complete
•Cultures performed on all specimens (including negative AFB)
•Drug sensitivities in positive cultures take additional weeks
47
Pulmonary TB: CXR
Locations more typical
•Apical & posterior segments upper lobes
•Superior segment of lower lobe
```
Findings
•Hilar adenopathy
•Patchy opacities
•Consolidation
•Cavitation
•Pleural effusions in some cases
```
Findings vary from primary to reactivation disease
•Atypical findings possible in immunocompromised patient (example: not upper lobe predominant) or primary TB
CXR is rarely normal in active pulmonary disease (but possible in patient with + sputum and + symptoms).
A normal CXR can help rule out TB in person with + TST and absence of symptoms
48
Pulmonary TB: diagnostic findings
•Assess findings in context of the patient (such as, immune compromised vs. non), often a diagnosis of exclusion
•Clinical findings
Symptoms of active infection
* Signs of active infection / transmission risk Those at highest risk of rapid progression warrant earlier treatment without culture confirmation (such as, HIV patients)
* Assessing exposure
- Indicates exposure only, does not distinguish latent vs. active disease, limited role in recent exposure
- Positive tuberculin skin test (PPD)
- Difficult interpretation in immunocompromised and active TB
- IGRA (blood test)
•Assessing active infection
- Sputum findings
- AFB on sputum (about half are negative)
- Bronchoscopy lavage / tissue biopsy
- MIT/RIF Assay (rapid results)
- Culture and sensitivity (delayed results)
- CXR findings
- Active lesions vs. scarring of past infection
- Not diagnostic by itself, supports diagnosis
- Symptoms and PE findings consistent with TB
49
Pulmonary TB: older adults
•Incidence 2 – 3 x higher
•Risk of death higher
•Risk factors
Long-term care
•Underlying comorbidities
Associated with TB diagnosis: DM, malignancy, CV disease
May delay diagnosis (example: COPD)
•Symptom presentations overall similar to those < 60
More likely: non-specific symptoms
Less likely: fever, sweats, hemoptysis, cavitation, + TST
50
Assessment of TB
•Latent vs. active TB
Latent: assess risk of developing active TB and prioritize therapy for high risk
Based on TST or IGRA results, clinical findings, risk factors
•Medical / social history
Immunocompromised, liver disease, routine alcohol use
•Baseline labs, when indicated
Liver function tests (if risk factors)
CBC, if indicated
Renal function, if indicated
51
Active TB: goals of care
•Minimize transmission
-Example: healthcare settings
•Manage treatment issues
- Multi drug-resistance (multi-drug regimens)
- Patient non-adherence (DOT)
- Medication side effects (symptoms, labs)
* Phased therapy
* ~2 month: intensive phase
* 4 – 6 month or more: continuation phase
* Overall, therapy ranges from 6 – 9 months
* Cure the patient
* Basic principles for HIV patients
- Consult specialist
- Longer treatment
- Assess drug-drug interactions
52
Management of the new diagnosis of TB
•Admission considered for
- Risk of non-adherence to medications
- Serious disease manifestations
* Isolate patient
* Labs, if indicated
- Example: liver function, CBC, renal function
- HIV screening, if not already diagnosed
•Consult specialist for
- Drug-resistance
- HIV (treatment indications, drug interactions)
•Verify health department notification
53
Management of known TB
•Isolate patient?
-Need three negative sputum specimen for Mtb
•Assess
- Medication adherence
- Current response to disease (example: AFB smear)
- Treatment side effects (liver function, symptoms)
•Consult specialist for
- Drug-resistance
- HIV
54
Intensive phase of TB treatment
•Typically first two months (eight weeks)
•Four-drug therapy (daily)
-INH (isoniazid)
-RIF (rifampin)
-EMB (ethambutol)
-PZA (pyrazinamide)
•Alternative regimens may use different dosing schedules (such as, not daily or not eight weeks)
•Check sputum at completion of intensive phase
•Assess response to therapy, if non-responsive, consider drug resistance
•Some approaches require DOT (directly observed therapy)
55
Continuation phase of TB treatment
•Typically four months after initiation phase but can be longer
•Two-drug therapy
-INH
-RIF
56
Latent TB
```
•Easier treatment regimen than active TB
•Active TB MUST be ruled out
•Regimens (four common options)
-INH (Isoniazid) x 9 months: daily or twice weekly
-INH x 6 months: daily or twice weekly
-INH + Rifapentine x 3 months once weekly
-Rifampin x 4 months daily
•Some approaches should include directly observed therapy
•Consult specialist
-With drug-resistance risk
-HIV
-Immunocompromised
-Occupational settings (?)
```
57
TB treatment mnemonic
```
If you do not treat TB, you may die and need a PRIEST
•Pyrazinamide
•Rifampin
•Isoniazid
•Ethambutol
•STreptomycin
```
•Note: streptomycin is utilized less for empiric therapy due to drug resistance development.
58
Hypertensive emergency
•Characterized by severe hypertension (>180/120 mm Hg) A
•Associated with target organ dysfunction
-Hypertensive encephalopathy, intracerebral hemorrhage, acute myocardial infarction, acute left ventricular failure with pulmonary edema, unstable angina, dissecting aortic aneurysm, acute renal failure, microangiopathic hemolytic anemia or eclampsia.
-Other hypertensive emergencies include pheochromocytoma crisis, food or drug interactions with monoamine-oxidase inhibitors, sympathomimetic drug use (cocaine) and rebound hypertension after abrupt cessation of some antihypertensive drugs such as clonidine.
59
Hypertensive urgency
Characterized by severe hypertension
| Without target organ dysfunction
60
Hypertension: physical exam
```
Take BP in both arms
•Fundoscopic exam for hemorrhages, exudates, papilledema
•Assess jugular venous pressure
•Lung exam for signs of pulmonary edema
•Heart exam for S3, S4
•Check for edema
•Neurologic exam
```
61
Symptoms of SVCS
* consists of various symptoms due to compression of the SVC
* Early signs and symptoms include cough, dyspnea, hoarseness, chest pain, jugular vein distention, and edema of the hands, face, and/or neck
* Family members may note these signs to be more prevalent in the early morning
* More advanced signs and symptoms can be life threatening, such as respiratory distress, stridor, mental status changes, syncope, and cyanosis of the face and upper body
62
Superior vena cava syndrome
* Superior vena cava syndrome is a rare oncologic
* Superior vena cava syndrome has a distinct clinical presentation and can be life threatening.
* It is found in 3.8% of lung cancer patients at the time of diagnosis and more frequently associated with superior vena cava obstruction
* Superior vena cava syndrome is caused by cancer 95% of the time
* The other 5% of cases could be related to thrombosis from insertion of venous catheters or pacemaker wires (National Cancer Institute, 2011).
* Characteristically, the onset of symptoms in SVCS occurs gradually over
63
SVCS: acute treatment
- airway protection
- elevated HOB
- consult oncology
64
HTN guidelines- pearls
* All medications are “relatively” identical in efficacy
* The higher the starting BP the more efficacious
* Remember special considerations – CKD, DM, Coronary artery disease, Heart failure, Stroke
* If a patient does not respond appropriately to therapy – think!!!!
65
Lack of appropriate response to HTN treatment
* Non compliance with therapy
* Drug interactions, medications (estrogens, CNI, etc)
* OTC (NSAID, decongestants), herbal medications, illicit medications
* Office BP not reflecting home BP or incorrect BP cuff size
* Cuff inflation hypertension
* Extracellular fluid volume expansion – dietary sodium excess
* Obstructive sleep apnea
* Secondary hypertension – Chronic kidney disease
66
Pneumothorax: CXR
* First line diagnostic test
* PA and lateral, UPRIGHT POSITION preferred, if possible. LATERAL DECUBITUS also helps detect pneumothorax
* Increased translucency to affected area
* Visible lung collapse demarcation
* Mediastinal shift
* Small pneumothorax may require expiratory CXR instead of standard inspiratory films
* CT (non-contrast acceptable if contrast contraindicated) may be required if diagnosis difficult to establish with underlying lung disease or other complicating factors
67
Pleural effusion: exudative
* Pulmonary disease, infection
* Malignancy (~ 50%)
* ↑ fluid accumulation: abnormal capillary permeability or ↓ lymphatic clearance
68
Pleural effusion: physical exam
• Diminished lung sounds at lung base when upright
• Dullness to percussion, decreased tactile fremitus
• Appears anxious
• Increased work of breathing – Tachypnea
– Accessory muscle use
• Hypoxemia
• Fever (with infection)
• Severe
– Tracheal shift (when severe) – Confusion
69
Multi focal atrial tachycardia
* Multiple p wave morphologies
* Often have co-morbid severe COPD
* May not cause symptoms or hemodynamic compromise
* Focus on identifying underlying cause
* Check electrolytes K and Mg and replace as needed
* Intervene only if significant symptoms of worsening myocardial ischemia, HF, perfusion, oxygenation
70
Atrial flutter
• The treatment approaches for afib and aflutter are very similar
– Ex: cardioversion, rate control and anticoagulation
• Aflutter is very responsive to cardioversion • Aflutter may progress to afib
71
Atrial fibrillation
* Can produce ventricular rates 100 – 160 bpm
* Irregularly irregular rhythm
* Increases risk of embolic stroke due to impaired emptying of atria (left)
* Reduces CO by 20 – 30% through loss of “atrial kick”
* May be proceeded by PAC’s, SVT
* Can be chronic or paroxysmal
* More common in males
72
Atrial fibrillation: causes
* Age: ↑ age
* CV: HTN, CAD, valve ds, ACS, HF, left atrial enlargement, myocardial irritation / inflammation, cardiac surgery
* Resp: PE, pneumonia, COPD, carcinoma, thoracic surgery
* Endocrine: hyperthyroid, thyrotoxicosis, pheochromocytoma
* Metabolic:electrolyteimbalance
* Neuro: ↑ SNS or PNS tone
* Other:EtOH,illicits,OSA,obesity(includingacute EtOH excess or withdrawl)
73
Atrial fibrillation symptoms
```
• May be asymptomatic
• Generalized complaints (chronic AF)
• Symptoms of reduced cardiac output
– Tachycardia, hypotension, palpitations, CP, chest pressure
– Lightheadedness, dizziness, syncope
– Dyspnea
– Fatigue
– Diaphoresis
```
74
Atrial fibrillation testing
• Echo to assess underlying causes and predict cardioversion success
• Testing to work-up underlying etiology – TSH and free T4
– Electrolytes, renal function
– CBC
– Cardiac biomarkers – BNP, if indicated
– CXR
• TEE to assess clot when sx began > 48 hours prior (or unknown time frame) prior to cardioversion when indicated
75
Atrial fibrillation
* 12 lead EKG diagnosis
* Irregularly irregular rhythm
* Often non-discernable p waves or PR interval
* Narrow QRS complex (< 0.12 seconds)
* Ventricular rate 100 – 160 without meds for rate control
76
HAS-BLED
• Hypertension (uncontrolled, SBP > 160)
• Abnormal renal / liver function (either = 1 with
2 possible points )
• Stroke hx
• Bleeding hx or tendency (major bleeding)
• Labile INR on warfarin (therapeutic < 60%)
• Elderly (age > 65)
• Drug / alcohol use or Drugs/medications that predispose to bleeding (antiplatelet) (either = 1, 2 possible points
77
VT and VF causes
• Cardiac
– CAD, MI, CM, VHD, myocarditis
• Metabolic
– Hypoglycemia, metabolic acidosis, hypoxemia, electrolyte abnormality (K, Mg)
• Proarrhythmic agents
– Caffeine, cocaine
– Digoxin, theophylline, antipsychotics, tricyclic antidepressants
– Proarrhythmic medications (class I & III) • VT may precipitate VF
78
VT diagnostic criteria
• ≥ 3 ventricular contiguous beats
– Sustained: lasts > 30 seconds – Non-sustained < 30 seconds
• EKG features:
– Wide QRS (≥ 0.12 seconds)
– Rate 160 – 240 bpm
– Regular rate
– monomorphic (polymorphic = torsades de pointes)
• Additionally may be described as pulseless VT in the patient who cannot generate an effective pulse during VT
79
VF diagnostic criteria
* Absent p waves
| * Absent QRS complex (unlike VT) • “Wavy” baseline – course or fine
80
AV valves
– Stenosis (insufficient opening)
| – Regurgitation / insufficiency (insufficient closure) – Mixed lesions
81
Valve stenosis
```
• AV valves
– Open to allow blood to move from atrial to ventricles
– Tricuspid
– Mitral
• Semilunar valves
– Open to allow blood to exist ventricles
– Aortic
– Pulmonic
```
82
Valve regurgitation
– Insufficient closure, valve “leaks” rather than blocking backflow during chamber contraction
– “Leaking” results in volume overload by the receiving chamber, chamber dilates in response
– Damage by infection, inflammation or structural changes to heart (ex: HF)
83
Mitral stenosis
• Causes / Epi
– Rheumatic heart disease (RHD) primarily – Women > men
• Manifestations:
– ↑ LA pressure → LA/LV dilation → LHF
– 5th ICS LMCL (apex) in left lateral position, low pitch, diastolic (if murmur heard)
– Mild – asymptomatic or exertional symptoms (ex: fatigue), hemoptysis, dyspnea, orthopnea
– Late (less common) – pulm congestion, RVF, pulmonary hypertension
– Afib (1/3 of symptomatic MS)
• CXR: LAE, prominent PA, RVH
• EKG: LAE, RVH
84
Mitral regurgitation
• Causes / epi
– RHD, congenital, muscle rupture / dysfunction
• Manifestations:
– Backflow into LA → ↑ LA pressure → LA / LV dilation → LVF
– 5th ICS, LMCL (apex), holosystolic, high pitch, blowing
– Symptoms: exertional dyspnea/fatigue, orthopnea, LE edema, anxiety, chest pain, palpitations, LVF, afib
• CXR: LVH, LAE (CM)
85
MVP
• Causes / Epi
– Varied causes including congenital and Marfan syndrome
– Often benign, but can progress
– Women age 20 – 40
– 5-10% of population
• Manifestations
– Enlarged valvular leaflets
– Often asymptomatic
– 5th ICS, LMCL, late systolic or pansystolic murmur
– Exercise intolerance, dysrhythmias, syncope, dizziness, palpitations
- management: BB’s. Repair preferred over replacement.
86
Aortic stenosis
• Causes / Epi
– Congenital, atherosclerosis, RHD
– 80% male
– 50% occur age 30 – 70, increases with age
– Two common types: congenital unicuspid/bicuspid valve, degenerative / calcified
– Degenerative AS risk factors same as atherosclerosis • Manifestations
– Congenital may not be symptomatic until middle / older age
– ↑ resistance to LV contraction → LV hypertrophy / dilation and ↓ CO → RVF
– 2nd ICS, RSB midsystolic murmur, medium pitch, “harsh”, palpable heave/thrill (severe AS)
– Symptoms:
• Triad: exertional angina + lightheadedness or syncope + dyspnea or orthopnea
• DOE, angina, syncope with exertion (late marked fatigue, cyanosis, debilitation, LVF)
• Asymptomatic phase longer, symptomatic phase shorter
87
Aortic regurgitation
• Causes / Epi
– HTN (most common non-valve cause), congenital, Marfan syndrome, calcified valve
– 75% men
• Manifestations
– LV backflow → LVH, LAE → LVF / pulm congestion → RVF
– 2nd & 3rd ICS RSB, high pitch, blowing
– Symptoms: DOE, PND, orthopnea, palpitations, nocturnal angina/diaphoresis, fatigue, late sign – RHF
• CXR: LAE, LV dilation, pulm edema
88
AS intervention
• Interventionconsideredfor:
– Symptomatic severe AS
– Asymptomatic severe AS (valve area < 1.0 cm2) if • Undergoing other card surgery or
• Reduced LVEF < 50%
• Mean gradient > 55 mmHg
• BP non-responsive to exercise (< 20mmHg rise) • Severe calcium on the valve
• Rapid peak aortic gradient rise
• ? BNP elevations over time
• Interventions tailored to individual patient
– Valvuloplasty, surgical replacement
– Mechanical valves require anticoagulation with goal INR 2.0 – 3.0 (some may have different strategies
89
Aortic insufficiency management
• SevereAI:
– Surgical evaluation
• Regardless of LV systolic function • For LFEF < 50%
• Chronic vasodilators
– Symptomatic or LV dysfunction, non-surgical – HTN (including asymptomatic) goal < 150 / 90 – B blocker use controversial
90
Cardiomyopathy
• Heart muscle structural or functional disorder NOT caused by significant CAD, HTN, valve disease, congenital heart disease
• Multiple types
– Major types: dilated, hypertrophic, restrictive
– Others: tako-tsubo and arrhythmogenic right ventricular CM (ARVC)
• “Ischemic CM” is not considered an actual form of CM using formal criteria, however term is still used in association with impaired LV function associated with CAD specifically
91
Dilated CM
Dilated LV or LV/RV with impaired systolic function without compensatory hypertrophy (without CAD, valve ds, pericardial ds)
• Often idiopathic (~50%)
– Associated with neuromuscular disorders, certain congenital disorders, familial patterns and acquired etiologies (next slide)
• May be detected incidentally in early disease
• Progressionvariable,canbemorestableinsome, but development of heart failure worsens prognosis
• 10% of age > 80 have dilated CM
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Acquired dilated CM
– Infectious myocarditis (ex: viral infections, HIV)
– Chemotherapy (ex: anthracycline agents) – Radiation therapy
– Chronic alcohol use
– Cocaine
– Nutritional deficiencies
– Iron overload
– Inflammatory disorders (ex: SLE)
– Endocrine disorders (ex: DM, hypothyroid)
– Pregnancy (late pregnancy or post-partum up to 5 mo) – Tachyarrhythmia (ex: afib)
– Obesity
93
Dilated CM symptoms
• DOE, reduced exercise tolerance
– Worsened may include dyspnea at rest, orthopnea, PND, LE edema, ascites
• Arrhythmia symptoms
– Ex: palpitations, presyncope, syncope
• Symptoms depend on age / severity
• Generally present with symptoms consistent with high pulm venous pressure or low CO
• Acute presentation may be acute worsening of underlying chronic progression
94
Dilated CM physical exam
• In earlier disease, PE may be less helpful
• Signs of heart failure (left or bilventricular)
– LE edema
– Ascites, hepatomegaly
– Basilar crackles
– Elevated JVP
– Displaced PMI
– Possible pansystolic (MR) murmur @ apex, possible TR
– S3, S4
– Cardiomegaly
– Hypotension, weak pulses, sinus tachycardia, pallor, cyanosis
– Possible Cheyne-Stokes respirations (crescendo- decresendo pattern)
95
Dilated CM testing
* Echo initial diagnostic test
* Enlargedventricularend-diastolic dimension
* Reduced EF (worsened disease)
* MR, TR
* Diastolic LV dysfunction
* Usedformonitoringdiseaseprogression
* Evaluates other exclusions (ex: valve ds
ECG
• May be normal
• Sinustachycardiacommon
• Non-specificabnormalities: tachyarrhythmia, LVH associated ST and T changes, atrial enlargement, ventricular enlargement
• Arrhythmias:ventricular,supraventricular, atrial (ex: afib, PACs, PVCs, vtach)
```
CXR
– Left / right heart failure
– Pulmonary edema
– Cardiomegaly
– ↑ cardiothoracic ratio (LV & LA dilation) – Pleural effusions R>L
```
96
Dilated CM management
```
• Tailor to underlying cause, if known – Behavioral counseling (ex: EtOH)
– Thyroid disease treatment
– Peripartum support
– Arrhythmia
• Supportive care
– Heart failure (see heart failure)
• Diuretics,betablockers,aceinhibitors
– Arrhythmia
• Cardiology referral
– Management
– Assess for role of transplant, AICD
```
97
Hypertrophic CM
LV hypertrophy that is unexplained by identifiable etiologies (ex: HTN, valve ds)
• Slow disease progression with age (decades) is most common (can present early age or acutely)
• Less common (prevalence 0.2 – 0.5%)
• Usually familial
• May have co-existing right ventricular hypertrophy (up to 40% of cases)
• Increased risk sudden death, can initially present as sudden cardiac death
• May progress to dilated CM
• Can be obstructive or non obstructive
98
Hypertrophic CM symptoms
* Palpitations (frequent)
* DOE
* CP(~1/3)withpostprandialmildexertion features
* Syncope
* Paroxysmal nocturnal dyspnea
* Tachyarrythmias
* Symptoms associated with diastolic dysfunction
* Family history a very important assessment for this population, 50% will have first degree relative with disease (premature cardiac death, known CM) but also assess extended generations
* May have associated HTN
99
Hypertrophic CM physical exam
Loud S4
| • Maximized apical pulse
100
Hypertrophic CM testing
Echo
• Echo initial diagnostic test
• Asymmetricalhypertrophy
• Increased LV wall thickness (w/o dilation) • LAenlargementcommon
• Usedformonitoringdiseaseprogression
– Increased LV wall thickness (based on age, gender and height but generally ≥ 1.5 cm men, ≥ 1.3 cm women) helps diagnosis in conjunction with clinical history
• EKG
– 95% have abnormal findings
– Symptomatic patients often have LVH
– Nothing specific to CM
• Examples: LVH QRS voltage changes or left axis deviation, Q wave, ST segment and T wave changes
– Used for asymptomatic screening of any conduction abnormalities or assessment / monitoring in diagnosed CM
101
Hypertrophic CM management
* Beta blockers
* Possible Ca channel blockers
* Diuretics, when indicated
* Aggressive management of afib
* EP interventions – ablation, PPM, AICD
* Close monitoring in pregnancy for patients with known HOCM (obstructive)
* Cardiology evaluation & management
102
Restrictive CM
* Beta blockers
* Possible Ca channel blockers
* Diuretics, when indicated
* Aggressive management of afib
* EP interventions – ablation, PPM, AICD
* Close monitoring in pregnancy for patients with known HOCM (obstructive)
* Cardiology evaluation & management
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Restrictive CM symptoms
* Symptoms of heart failure (R > L)
* Arrhythmia
* DOE, fatigue, weakness
* Progressivedisease:DOE,orthopnea, PND, abd discomfort (hepatomegaly)
* CP
* Palpitations
* PossibleKussmaulrespirations
104
Restrictive CM physical exam
* Primarily assess signs of heart failure
* Elevated JVP
* Prominent S2
* Possible S3 or S4
* LE edema, ascites, hepatomegaly
* PE findings suggestive of amyloidosis (ex: thickened tongue, peri-orbital purpura, hepatomegaly) or hemochromatosis (ex: skin changes, hepatomegaly)
105
Restrictive CM management
• Management dictated by the underlying etiology (ex: therapeutic phlebotomy, steroids)
• Heart failure management – Diuretics
– Beta blockers and ace inhibitors have unclear role and may be contraindicated in some underlying etiologies (avoid Digoxin)
• Antiarrhythmics, when indicated
• Cardiology referral for comprehensive evaluation and consideration of role of transplant or other therapy in select patients
• Limited therapy options
106
Takotsubo
• Acute presentation of CM
– Associated with catecholamine surge
– Presentation after traumatic/stressful events (ex: natural disaster, emotional stress, surgery, alcohol withdrawal)
• Post-menopausal women predominate in presentation of this type of CM
• Aka “broken heart syndrome” or stress cardiomyopathy
• PresentssimilartoACS
– Anterior MI type presentation with normal coronaries
– ST segment elevation and T wave inversion
– Cardiac enzyme elevation, but rapid reduction
• Echo shows characteristic left ventricular ballooning at the apex resembling shape of takotsubo fishing pot
• Generally a CM that shows full recovery over time (weeks to months)
• May have beta blockers, aspirin and ace- inhibitors during recovery phase until LV function normalizes
107
Pericarditis
```
Types
– Acute pericarditis (< 2 weeks)
– Pericardial constriction (chronic)
– Cardiac effusion & tamponade (potentially life- threatening)
• Involves the pericardium
– Relatively avascular sac
– Surrounds the heart
– Contains 10 – 50 mL fluid normally
– Two layers, visceral and parietal
– Chronic stress can dilate pericardium, a constricted pericardium can limit heart filling and function
```
108
Pericarditis HPI
* RetrosternalCP
* Pain is sharp, severe
* Worse with inspiration & supine / recumbent position
* Relieved with sitting / leaning forward
* Referred pain to scapular ridge (phrenic nerve involvement)
* May be asymptomatic (ex: RA)
* Acute vs. chronic onset
109
Pericarditis physical exam
```
• Pericardialfrictionrub
– High-pitched, scratchy
– More localized compared to murmur
– May change with position change
– Assess with full expiration / not breathing
• Fever
– Low grade or high (> 38°C)
• Signs of cardiac decompensation
```
110
Acute pericarditis testing
• EKG
– Diffuse ST elevation (all but aVR) w/PR ↓
– MI related pericarditis may be more localized
– Resolve over days to T wave inversion, then normal
• Labs
– Acute inflammation (↑ leukocyte, ↑ ESR, ↑ CRP)
– ↑ troponin (modest elevations)
– Assess BMP, lytes, CBC, BNP, blood cultures (if indicated)
• Echo
– Key in diagnosing pericarditis but normal echo does not rule out
– Presence of effusion supports diagnosis
– Needed to evaluate for tamponade
• Cardiac cath
– Rules out CAD (clean coronaries)
• MRI
– Assessed pericardial inflammation
111
Pericarditis admission
```
• Admissionconsideredfor – Fever
– Effusion
– Tamponade
– Acute kidney injury
• Pericarditis without above findings may undergo outpatient evaluation and management in select cases
```
112
Pericarditis treatment
• Acute idiopathic / viral can be self-limited
• NSAIDS
– NSAIDorASAhigherdoseq6–8hourscheduleddosing – Minimum3-4weeks
– Add/increasePPI
– Cautionwithanticoagulation
• Colchicine x 3 months
– Checkrenal/liverfunction
• Pain management, if indicated
• Avoid systemic corticosteroids (if possible)
– Minimum1monthdosing,whenrequired
• Treat underlying cause
– Ex: antibiotics
• Surgical intervention for refractory disease
113
Cardiac effusion/ tamponade
• Majority of causes idiopathic or viral
– Can be caused by any pericarditis cause
• Tamponade more common in malignancy, TB, purulent pericarditis
• Fluid accumulation 100 – 200 mL
• Tamponade is caused when pericardial fluid impairs cardiac filling / function
– Acute development is not well tolerated – Can be fatal
• Can be caused by medications
114
Cardiac effusion/tamponade findings
• May be asymptomatic w/slower onset
• Underlying pericarditis presentation, cough, dyspnea
• Muffled / soft heart sounds
• Tamponade
– Early: anxious, ↑ HR, dyspnea, CP, orthopnea
– Pulsus paradoxus is the hallmark • ↓ BP > 10 mmHg with inspiration
– Cardiac decompensation – Possible JVD
– Right heart failure
115
Constructive pericarditis
• May be asymptomatic w/slower onset
• Underlying pericarditis presentation, cough, dyspnea
• Muffled / soft heart sounds
• Tamponade
– Early: anxious, ↑ HR, dyspnea, CP, orthopnea
– Pulsus paradoxus is the hallmark • ↓ BP > 10 mmHg with inspiration
– Cardiac decompensation – Possible JVD
– Right heart failure
116
Constructive pericarditis findings
```
• Chronic development of congestion
• Dyspnea, fatigue, weakness
• Right sided congestion (> left) – JFD
– Hepatic congestion
– Ascites (with elevated liver enzymes) – LE edema
– (clear lungs)
• Pericardial knock
– High pitched, early diastole
```
117
Constructive pericarditis management
* Diuresis
* Treat underlying cause
* Consider role of surgical intervention in select patients
118
Infective Endocarditis
• Endocardial heart surface infection
• Often bacterial, can be viral / fungal
• Primarily impacts cardiac valves, hardware
• Men > women (when age > 35)
• Increases with age (valve degeneration)
• Commonorganisms:
– Viridans streptococci, S. aureus, enterococci, gram-neg, fungi
• Suspect in any fever of unknown origin with new murmur / worsened murmur
119
Infective endocarditis findings
```
• Wide variation in presentation
• Non-specific, chronic sx possible
• Joint pain / myalgias
• Pleuritic CP
• Pneumonia
• Obtain detailed social history – Travel, IVDA, sexual
• PMH/PSH
– Hospitalizations, vascular access, hardware, valves
```
120
Infective endocarditis physical exam
```
Fever
• Worseningmurmur
• New murmur
• Vascularembolicevent
• Splenomegaly
• Heart failure
• Other findings: petechiae, osler nodes, Janeway lesions, Roth spots (fundoscopic)
```
121
Infective endocarditis testing
```
• Labs
– CBC, chem panel, renal, UA (hematuria) – Elevated WBC common
– Immunologic testing, when indicated
• Blood cultures
– Isolating bacteria can be difficult
– 3 sets, 1 hour apart, 3 sites, ideally puncture sites vs. line draws
• Echo
– TEE often preferred over TTE
• CXR
– May show abnormalities
```
122
Infective endocarditis management
• Antibiotics / antimicrobials
– Empiric antibiotic likely started after cultures obtained if clinically indicated
• Cover s. aureus, s. viridans, HACEK gram negatives and MRSA (if indicated)
– Treat high risk patients (ex: valve replacements)
– Empiric therapy may be delayed / avoided if patient clinically stable until cultures confirm etiology
– Specific to cultures, once available
– ID often consulted
• Monitor response – Fever
– Labs
– Clinically
– Serial blood cultures
• Monitor for complications – Cardiac worsening
– Infectious worsening
– CNS emboli
• Anticoagulation ??: many factors involved in decision including CNS disease, mechanical valves
123
Myocarditis
```
Canbe
– Viral / infectious
– Drug / toxic substance induced
– Associated with certain chemo or XRT – Inflammatory
• Often associated with URI
• Types
– Primary: acute viral infection
– Secondary: inflammation, non-viral
• Mimics other diseases, limited testing option
```
124
Myocarditis findings
* Presentation may vary
* Acute respiratory / cardiac presentation • Heart failure
* Cardiomyopathy
* Pleural / pericardial CP
* Tachycardia
* Gallop
* Ventricular arrhythmia
* Possible ACS presentation
125
Myocarditis diagnostic procedure of choice
Endomyocardialbiopsy
| – Diagnostic procedure of choice
126
Myocarditis management
```
• Cardiologyconsult
• Supportivecare – Diuresis
– Afterload reduction
– Consider IABP or LVAD, consider ECMO
• Treat underlying pathogen, if identified
```
127
Pulmonary HTN: 5 categories for pathological mechanisms
Group 1: idiopathic, inherited PAH, HIV infection, drugs/toxins, portal hypertension, congenital heart disease.
Group 2: Left heart disease with LV dysfunction and valvular heart disease.
Group 3: lung disease
Group 4: chronic thromboembolism
Group 5: PAH due to systemic, hematologic, or metabolic causes
128
Diagnosis of pulmonary hypertension
right-sided heart catherization is considered the GOLD standard for the quantification and definitive diagnosis. The normal range of this pressure is 15-30 mm Hg while at rest, with a mean of 10-18 mm Hg
Echo with doppler- pulmonary artery systolic pressure (PASP) >50.
129
Pulmonary hypertension findings
initial finding typically is a change to the second heart sound. This includes increased intensity that may be PALPABLE and a narrow split.
jugular venous distention, an S3, hepatomegaly, peripheral edema, ascites, and pleural effusions.
130
TB treatment
Two Month Initiation Phase using 4 different drug concomitantly which include Pyrazinamide, Rifampicin, Ethambutol, and Isoniazid.
The Continuation Phase which continues a 4 month course of Rifampicin and Isoniazid only.
Fixed doses of each treatment phase are available which can help to reduce the patient cost and pill burden.
131
Well’s score
Calculates pretest probability for PE. Score out of 11 points.
Low (<2): apply PERC criteria. If does not fulfill all 8, perform D-dimer. If >500, get CTPA.
Moderate (2-6): get a D-dimer. If >500, get CTPA.
High (>6): skip the D-dimer and get a CTPA (anticoagulate if unstable)
132
TB First-line drug susceptibility testing
Liquid medium
1 to 2 weeks to result
**Gold standard** Perform on initial isolate
