Symptom To Diagnosis - Dyspnea Flashcards
MCCs of dyspnea:
- Heart.
- Lung.
- Anemia.
3 tests that are mandatory in the initial evaluation of dyspnea:
- Chest radiograph.
- ECG.
- Ht.
Diagnostic approach of dyspnea - Cardiac etiologies - History:
Valvular heart disease –> Rheumatic heart disease.
Arrhythmia –> Palpitations.
HF –> CAD or risk factors, HTN, alcohol abuse, PND.
Acute coronary syndrome –> Chest pain, CAD risk factors.
Diagnostic approach of dyspnea - Cardiac etiologies - Physical findings:
Valvular heart disease –> Significant murmur.
Arrhythmia –> Irregular pulse.
HF –> S3, JVD, crackles on exam.
Acute coronary syndrome –> S3, JVD, crackles on exam.
Diagnostic approach to dyspnea - Cardiac etiologies - Tests:
Valvular heart disease –> Echo.
Arrhythmia –> ECG, holter, event monitor.
HF –> Chest radiography, BNP, echocardiography.
Acute coronary syndrome –> ECG, troponin, stress test, angiography.
Diagnostic approach of dyspnea - Pulmonary etiologies:
- COPD.
- Asthma.
- PE.
- Pneumonia (CAP, TB, PCP).
- ILD.
Pulmonary etiologies - History:
COPD –> >20pack years tobacco.
Asthma –> Cold +/- exercise –> Symptoms; + family history.
PE –> Sudden onset, pleuritic pain, cancer, surgery, immobilization, estrogen.
Pneumonia –> Fever, productive cough, high-risk sexual exposures, injection drug use.
ILD –> Known connective tissue disease, Raynaud, vocational, occupational exposure.
Pulmonary etiologies - Physical findings:
COPD --> Decr. breath sounds, wheezing. Asthma --> Wheezing. PE --> Unilateral leg swelling. Pneumonia --> Crackles, fever, thrush, Kaposi sarcoma, skin pop marks. ILD --> Diffuse lung crackles.
Pulmonary etiologies - Tests:
COPD –> CXR, PFTs.
Asthma –> PFTs, bronchodilator response, methacholine induced.
PE –> D-dimer, CTA, V/Q scan, Leg duplex.
Pneumonia –> CXR, HIV, CD4 (when appropriate).
ILD –> PFTs, High res chest CT.
Anemia as a cause of dyspnea - History, physical findings, and tests:
History –> Menorrhagia, melena, rectal bleeding.
Physical findings –> Pale conjunctiva.
Echo –> Ht.
Mortality in patients with SHF and DHF?
Similar.
Progression of HF:
- Heart failure often triggers maladaptive neurohormonal changes including increased activation of the SNS and the RAA.
- These neurohormonal changes promote Na retention –> Incr. afterload –> Progressive HF.
- Therapies that interrupt these responses reduce mortality.
NYHA:
I –> Asymptomatic.
II –> Symptoms on ordinary exertion (climbing stairs).
III –> Symptoms with less than ordinary exertion (walking on flat surface).
IV –> Symptoms at rest.
4 STAGES OF HF - ACC/AHA:
A –> At risk for HF.
B –> Structural changes (LV hypertrophy or decr. EF) but no symptoms.
C –> Structural changes and symptoms.
D –> Structural changes and refractory symptoms despite therapy.
HF complication - Stroke and thromboembolism:
2-4% annual incidence.
Death in HF:
Symptomatic mild to moderate HF –> 20-30%/y.
Symptomatic severe HF –> Up to 50%/y.
HF - Mechanism of death:
Sudden in 50% - Secondary to V-tach or asystole.
Progressive in 50%.
Evidence-based diagnosis - History in HF:
Should assess risk factors:
- HTN.
- CAD.
- Alcohol.
- Illicit drug use.
- Adiamycin.
EBD - Physical exam - Clinical signs and symptoms may be affected by:
- Patient’s CURRENT volume status.
2. Chronicity –> CHRONIC HF is frequently asymptomatic.
EBD - S3 gallop:
Occurs when large volume of blood rushes from the LA into the LV at the start of diastole (just after S2).
EBD - S3 - Is it an important finding?
Virtually PATHOGNOMONIC of volume overload and occurs most commonly in patients with decompensated HF.
EBD - S4 gallop:
Occurs when the LA contracts and sends blood into the LV (just before S1).
EBD - S4 importance:
An S4 gallop may be heard in some normal patients and in many patients with HTN and LV hypertrophy.
–> NOT SPECIFIC FOR HF.
EBD - JVD:
> 3cm of elevation above the sternal angle.
EBD - JVD importance:
Highly specific for HF (>95%) –> May occur in RV or LV failure.
Importance of classic signs/symptoms (orthopnea, PND, crackles, gallops, and edema) in the diagnosis of HF:
NOT SENSITIVE - Their absence does NOT RULE OUT HF.
Even in severe CHRONIC HF –> 42% of patients did NOT have crackles, increased JVP, or edema.
Most sensitive CXR finding in HF?
Cardiomegaly in CXR –> 74%. Its absence decreases the likelihood of HF (LR- 0.33).
Most specific CXR findings for HF:
Pulm. venous congestion and interstitial+alveolar edema –> 96-97%. When present, strongly suggest HF (LR+12).
Pleural effusions are seen in …% of patients with HF.
26%.
When is BNP secreted?
FROM LV/RV –> In response to increased volume or pressure or both.
BNP
Sens: 87-93%.
Spec: 66-72%.
LR+ 2.7-3.1.
LR- 0.11-0.12.
BNP
Sens: 35%.
Spec: 90%.
LR+2.6.
LR-0.05.
BNP in COPD patients:
May not rule out HF in patients with coexistent COPD: Sens: 35%. Spec: 90%. LR+ 3.5. LR- 0.72.
BNP>250:
Sens: 89%.
Spec: 81%.
LR+ 4.6.
LR- 0.14.
BNP and PE?
BNP is elevated due to RV dilatation:
34% –> BNP=88-487.
33% –> BNP=527-1300.
Some authorities use the following criteria to interpret BNP levels:
HF unlikely.
100-500 –> Indeterminate.
>500 –> LR+ 6 –> HF most likely diagnosis.
Test of choice to diagnose HF:
2D echo.
HF is frequently present but UNSUSPECTED in patients in whom COPD is diagnosed:
Studies report unsuspected HF in 25% of patients with COPD.
–> Fewer years of tobacco use than patients without HF (9.6 vs 22.7).
MR - Textbook presentation:
Patients with MR may be identified due to an asymptomatic holosystolic murmur at the apex or during an evaluation of:
1. Shortness of breath.
2. Dyspnea on exertion.
3. Orthopnea.
4. Fatigue.
Alternatively –> During evaluation of patients with AF.
MR diagnosis - Average delay from diagnosis to symptoms is …?
16y.
In patients with severe MR, annual mortality is?
5%.
EBD of MR - Physical exam - Grade 3 or louder systolic murmur:
Sens: 85%.
Spec: 81%.
LR+ 4.5.
LR- 0.19.
EBD - S3 gallop in MR?
May be heard due to increased flow across the mitral valve.
EBD of MR - Role of ECG and chest radiograph:
May demonstrate LA or LV enlargement –> NEITHER is sensitive/specific for the diagnosis.
EBD of MR - Test of choice?
Echo –> Diagnosis + Quantification of MR.
Transesophageal echo –> More details.
Chronic AR - Textbook presentation:
Typically complain of progressive dyspnea on exertion or the sensation of a pounding heart.
Alternatively, may be asymptomatic, and the diagnosis may be suspected when an EARLY DIASTOLIC murmur is detected by a careful examiner.
Chronic AR - Progression to symptoms or LV dysfunction in patients with normal LV function develops in …% of patients per year.
4%.
EBD of chronic AR - Why is the pulse pressure wide?
2 processes:
- Large SV increases the SBP.
- Regurgitation of blood back into the LV rapidly lowers the DBP.
EBD - Are wide pulse pressures specific for chronic AR?
NOT SPECIFIC.
- Anemia.
- Fever.
- Pregnancy.
- Large AV fistulas.
- Cirrhosis.
- Thyrotoxicosis.
- PDA.
EBD of chronic AR - Auscultation:
May demonstrate an EARLY decrescendo DIASTOLIC murmur following S2. Best heard at the left sternal border.
EBD in chronic AR - Auscultation sens/spec?
- More sensitive for moderate to severe AR.
- 0-64% sens among students and residents.
- 80-95% sens among experienced cardiologists.
EBD in chronic AR - Importance of diastolic murmur finding?
Highly specific –> 98%.
EBD in chronic AR - Systolic murmur?
A systolic murmur suggesting AS may be heard.
–> Regurgitation results in increasing end diastolic volumes –> Stroke volumes increase to maintain forward flow –> Incr. CO may exceed the capacity of even a normal AV to accommodate flow –> High flow systolic murmur across the aortic valve.
EBD in chronic AR - One study reported that …% of patients with mild to moderate AR had a SYSTOLIC murmur (…% in moderate AR and …% in mild AR).
51%.
86%, 50%.
Bottom line about murmurs in chronic AR:
Although a diastolic murmur strongly suggests AR, systolic murmurs are often the only murmur heard in patients with AR.
EBD in chronic AR - Austin Flint murmur:
- Aortic regurgitant streams may impact the MV leaflets during diastole resulting in functional mitral stenosis and a late diastolic murmur over the apex.
- Sensitivity varies from 0-100%.
EBD in chronic AR - Test of choice:
Doppler echo.
AF - Textbook presentation:
Classically –> Palpitations.
Abrupt onset often prompts patients to be seen emergently. Patients may also complain of shortness of breath and dyspnea on exertion.
Occasionally, AF is detected during a routine office visit when an irregularly irregular pulse is noted and evaluated.
MC clinical arrhythmia:
AF –> Incidence increases with AGE: 3.8% of patients >60yr to 9% in those >80yr.
AF - MC etiologies:
- HTN.
- CAD.
- HF.
Annual stroke rate in AF patients not receiving anticoagulation is …%.
4.3%.
AF accounts for … of all strokes at an annual cost of … billion.
1/6.
6.6.
Stroke is more common in patients with AF who have other clinical risk factors:
- Valvular heart disease.
- Prior transient ischemic attack or stroke.
- Increasing age.
- HTN
- DM.
- HF.
- Gender (women 1.5-3x more than men).
AF - Worsen HF?
AF –> Loss of atrial kick –> Especially important in patients with stiff LV (ie diastolic dysfunction).
EBD about AF:
- Easily recognized on ECG.
2. Episodic AF can be detected with Holter or event recorders.
…% of patients with PE have DVT.
80%.
…% of patients with DVT have PE (often asymptomatic).
48%.
PE - 3-month mortality is …%.
17.5%.
MC thrombophilia?
Factor V Leiden - 11% of patients with DVT.
EBD - Classic presentation of PE:
20-33% –> Chest pain with dyspnea or chest pain, dyspnea, and hemoptysis.
12-25% –> Isolated dyspnea.
80% –> Have risk factors.
EBD of PE - Tachypnea has been reported in …-…% of patients and an accentuated P2 in …-…%.
54-85%.
15-57%.
EBD of PE - One study reported that …% of patients with an unexplained exacerbation of COPD actually had a PE.
25%.
Bottom line about EBD of PE:
The classic presentation of PE is actually the exception. Patients may have very few symptoms.
A high index of suspicion must be maintained for the diagnosis of PE.
EBD of PE - CXR:
- Normal in 50% of patients with PE.
2. Focal oligemia (45%), wedge-shaped infiltrate (15%), or pleural effusions (45%).
EBD of PE - ABG:
May demonstrate hypoxemia and hypocarbia, but findings are neither sensitive nor specific for PE.
PaO2
EBD of PE - Bottom line about ABG:
Patients with PE may NOT be hypoxic.
Therefore normal arterial O2 does NOT rule out PE.
EBD of PE - Troponin?
Elevated in up to 57% of patients with documented PE.
Diagnostic approach of dyspnea - Cardiac etiologies - Diagnostic hypothesis:
- Valvular heart disease.
- Arrhythmia.
- HF.
- Acute coronary syndrome.
