Chest pain Flashcards
What RF can increase atherosclerosis
- cocaine
- HIV
classic presentation of CP
- Retrosternal in L anterior chest
- Crushing, tightness, squeezing, or pressure
- Worsened w/ exertion
- Alleviated w/ rest
- Dyspnea, diaphoresis, nausea
- Radiation to L shoulder, jaw, arm, or hand
onsets of classic chest pain presentations
Sudden or gradual:
* Angina: 2-10 min
* Unstable angina: 10-30 min
* AMI pain: >30 min
Two categories of ”chest pain” based on nerve fiber:
- Visceral:
- Located in heart, blood vessels, esophagus, and visceral pleura
- Pain difficult to describe and localize
- Discomfort, heaviness, pressure, tightness, aching
- Pain can radiate - Somatic:
- Innervates chest wall, from dermis to parietal pleura
- Easily described and precisely located
- Sharp, stabbing, scratchy, without radiation
atypical CP presentation can be seen in who?
- Pre & early menopausal women
- Racial minorities
- DM
- Elderly
- Pts w/ psychiatric disease or AMS
If any of these sx are present, it is unlikely an AMI:
- pleuritic in nature
- Positional
- sharp
- reproducible with palpation/positioning
Possible PE findings for cardiac CP
- Tachycardia - ↑ sympathetic tone, ↓ LV stroke volume
- Bradycardia - ischemia to conduction system
- Acute ischemia -
- 3rd/4th HS from changes in ventricular compliance
- new murmur from ruptured cordae tendineae
- aortic root dissection, or crackles on lung auscultation from CHF. - Chest wall tenderness in 15% of pts, unlikely to be useful by itself to exclude ACS
perform an EKG within ___ min if concern for myocardial ischemia
10
ECG findings of acute MI
tx?
new ST elevations ≥1 mm in two contiguous leads
rapid reperfusion interventions
ECG findings of ____ indicate ischemia → further eval
New ST elevations, Q waves, LBBB, T-wave inversions or normalizations in sx pts
CXR of classic CP presentation
nml MC
r/o thoracic aortic aneurysm, aortic dissection, pneumonia, pneumothorax, PE
next imaging choice after CXR?
r/o for what dx?
Non-contrast CT
PNA, pneumothorax
imaging modility for aortic aneurysm/dissection or PE
Chest CTA
ECHO Emergent may be useful with what severe dx?
- aortic dissection, cardiac tamponade, new regurg murmur
- This will vary on the hospital and staff/providers available
Other tests based on suspected DDx for chest pain
- CBC
- BMP or CMP
- PT/PTT
- ABG
- Type and Crossmatch
- Hcg in women of childbearing age
Best serum marker for myocardial injury
Troponin
AMI troponin measurements (onset, peak, elevated)
- Onset: 4 hours after onset of acute MI
- More reliable 6 hr after sx. - Peak: 24-48 h
- Elevated: 10 d
which serum marker
- useful if timing of infarction remains unclear
- used only if troponin isn’t available or if pt has had an MI in the last 2-3 days
- levels normalize in 48-72 hrs
CK-MB
Red flags during initial triage for chest pain
- Abnormal vital signs
- Concerning EKG findings (if already performed)
- Hx prior CAD
- Multiple ASCVD risk factors
- Advanced age, HTN, tobacco use, HLD, DM, obesity, family hx, ASCVD, sedentary lifestyle - Abrupt onset, new or severe chest pain or dyspnea
Hx for initial chest pain triage
- Should be FOCUSED!
- Include sx and the 7 attributes
- Focused PMH
- Assess for risk factors
- ROS - focused on DDx
sudden, pleuritic CP, focal chest w/ dyspnea, tachypnea, tachycardia, or hypoxemia.
what ddx
Pulmonary Embolism
RF for Pulmonary Embolism
prolonged immobilization, active cancer, recent surgery/trauma, procoagulant syndromes, exogenous estrogen, or previous thromboembolic disease.
Criterias used for PE
Wells, Revised Geneva Scores, PERC
diagnostics for PE
D-dimer
CT pulm angiography
- sudden, severe, tearing pain radiating to scapula; midline, substernal
- Secondary sx - ischemic stroke, AMI, limb ischemia; unilateral pulse deficits or focal neuro deficits
aortic dissection
RF aortic dissection
male, >50y, uncontrolled HTN, CTD, cocaine, bicuspid valve or AV replacement, pregnancy
dx aortic dissection?
CT aortogram / TEE
Nml CXR and (-) D-dimer does NOT r/o dissection
nonspecific ST or T-wave changes on ECG possible
- sudden, sharp substernal CP after episode of forceful vomiting; ill appearing w/ tachycardia, F, dyspnea, and diaphoresis
- Crepitus in neck/chest from SQ emphysema
Esophageal Rupture (Boerhaave’s Syndrome)
what is Hamman’s crunch
crepitus on cardiac auscultation
diagnostic for Esophageal Rupture (Boerhaave’s Syndrome)
- CT of chest w/ oral water-soluble contrast
- Nml or pleural effusion (left MC), pneumothorax, pneumomediastinum, pneumoperitoneum, or subcutaneous air.
esophageal rupture most often in the _____ of the esophagus, resulting in a _____
distal ⅓ of the esophagus resulting in a pneumomediastinum
tx esophageal rupture
- Stabilize air way
- NPO, IV fluids
- Broad spectrum IV antibiotics
- 1st line: ampicillin/sulbactam or pip/taz
- BL allergy: clindamycin + ciprofloxacin - NG or OG tube placement - prevent further saliva and gastric content contamination
- Consult surgery
sudden, sharp, pleuritic CP w/ dyspnea; ↓ breath sounds on affected side
MC tall, slender male pts
Spontaneous Pneumothorax
RF: smoking, COPD, and asthma
Dx: CXR
sharp, severe, constant, and retrosternal that radiates to back, neck, or jaw; worsened supine, relieved sitting forward; pericardial friction rub
Acute Pericarditis
ECG shows PR depressions, diffuse ST-segment elevations, or T-wave inversions; diffused
what dx?
Acute Pericarditis
CP worsened w/ movement of chest and palpation; CP d/t irritation/inflammation
MSK Causes
- Causes: costochondritis, xiphodynia, precordial catch syndrome, intercostal strain d/t coughing, pectoralis muscle strain w/ recent physical exertion.
- Clear MSK etiology + completely reproducible pain w/o other sx or RF
s/s of GI causes of CP
- Gastritis: gnawing / burning pain in lower chest
- PUD: postprandial dull, boring pain in epigastric region
- Esophageal spasm: reflux disease; sudden onset of dull or tight substernal chest pain; precipitated by drinking cold liquids and can be relieved by NTG
initial management for chest pain
- Placed in a treatment bed quickly
- Cardiac monitoring and IV access (2 large bore)
- EKG (within 10 minutes)
- Measure vital signs, then resuscitate as needed, following the ABCs
- supplemental O2 if O2 saturation at rest is < 95%*
for chest pain presentation; admit if they meet this criteria:
- Positive cardiac enzymes
- New concerning EKG changes
- Persistent pain
- Concerning physical exam findings
Heart Scoring
0-3 = DC
4-6 = Admit to observe
7-10 = early invasive strategies
MC sx of ACS
-
MC Chest pain
- substernal or left-sided CP,
- radiation to one or both arms, accompanied with N/V, diaphoresis.
- “Pressure”
- Exertional - Pallor, diaphoresis, AMS, elevated JVD, peripheral edema, or rales
atypical sx for ACS
SOB, N, diaphoresis, back pain, abd pain, dizziness, palpitations
RF for CAD
older, male, FHx, smoking, HTN, hypercholesterolemia, DM, cocaine
presentation of unstable angina
CP (or atypical ACS sx) + obstructive CAD and has one of the following:
- began within past 2 months
- has increasing frequency, intensity, or duration of existing angina sx
- existing angina begins to occur at rest
Dx ACS
cTn, CBC, lytes, PT/PTT, CXR
goals for care in ACS
- reperfusion by reducing thrombus
- limiting thrombus extension
- relieving obstructive CAD
tx options for STEMI
systemic thrombolytic 30 min of arrival / PCI 90 min
PCI preferred - greater benefits and fewer risks if no CI to thrombolysis who can achieve PCI within 120 min.
If no PCI is available, what do you use
fibrinolytics IF:
- < 6-12 hrs of sx onset
- ECG 1 mm ST elevation in 2 contiguous leads
- Full dose anticoag for 48 hrs
- Avoid: arterial puncture, venipuncture, central lines in areas which are not readily compressible
tx for suspected ACS
- cardiac monitoring, IV line, O2 if < 95%.
- ASA 160-325 mg PO chewed; Alt: Clopidogrel
- NTG PO, transdermal, or IV to treat any ongoing angina.
- Morphine if pain continues despite NTG.
- Metoprolol in first 24h
- +/- antiplatelet
- Dual therapy: clopidogrel w/ ASA
- Antithrombin: heparin/enoxaparin
which med recommended for use along with aspirin in pts w/ mod-high risk NSTEMI and STEMI, and in all pts in whom PCI is planned?
Clopidogrel
Hold 5 d before CABG - ↑ risk of bleeding
which anticoag options for use in unstable angina or NSTEMI pts?
- LMWH - Can be used in PCI revascularization
- Unfractionated heparin - CABG
- Factor Xa inhibitor - fondaparinux - Similar efficacy to unfractionated; Good for renal impaired
- Direct thrombin inhibitor - Bivalirudin - Less bleeding and no dosage adjustment in renal impairment ; Alt in STEMI to unfractionated and GP IIb/IIIa inhibitor
tx STEMI
immediate cath
tx for CP treated Thrombolytics but still hemodynamic instability and pain / have not reperfused
rescue angioplasty
Emergent CABG may also be indicated for some patients.
tx for Refractory cardiogenic shock
emergent angioplasty
Other: Intraaortic balloon pump or other LVADs
Admitted to critical care unit
tx NSTEMI or unstable angina w/ ongoing CP, ECG changes, dysrhythmias, or hemodynamic compromise
admitted in cardiac ICU
tx for Unstable angina but no/resolved s/s
admitted to monitored inpatient bed
thrombolytic options
- tPA
- Reteplase (rPA) - Pro: double bolus rather than continuous infusion
- Tenecteplase (TNK) - alt for tPA
-
Streptokinase (SK)
- Can cause allergic reaction
- CI: HoTN, prior SK within 6 mo, strep within year
- Start heparin within 4 hrs of starting SK
complications for thrombolytics?
tx?
bleeding/intracranial hemorrhage
- DC thrombolytics, heparin, ASA
- Crystalloid and RBC infusion possible
- Cryoprecipitate + FFP
-
10 U cryoprecipitate and get fibrinogen levels
- < 1 g/L - +10 U
- Still Bleeding but >1 g/L or < 1 g/L after 20 U → 2 U FFP
- Bleed continues → platelets / antifibrinolytic (aminocaproic acid or tranexamic acid)
what med is given the first 24 hrs of admission if significant tachycardia or HTN for ACS/MI/unstable angina?
BB PO
Upon completion of the primary evaluation, classify patients into one of
the following categories of the prognosis-based classification system: (4)
- Acute myocardial infarction (AMI)
- Probable acute ischemia - Additional TIMI & HEART
- Possible acute ischemia - Additional TIMI & HEART
- Definitely not ischemia
secondary assessment for CP pt with No ST elevation
serial cTn to r/o MI
- Low-risk - 2 cTn measurements 2 hrs apart; one measurement at least 6 hrs after onset of pain
- Does not r/o unstable angina
secondary assessments for continued suspicion for ACS w/ negative biomarkers
cardiac testing
- exercise/pharm ECG stress test
- Stress Test: echo, nuclear imaging, MRI
- CTCA
- Cath
MC cardiomyopathy
Dilated cardiomyopathy
idiopathic (MC), familial, secondary
what is Peripartum CM
dilated cardiomyopathy affecting pregnant women from 20 wks into postpartum period
what type of cardiomyopathy condition is the primary indication for cardiac transplant?
dilated CM
s/s Dilated CM
-
Acute HF from systolic pump dysfunction
- DOE, orthopnea, paroxysmal nocturnal dyspnea
- Rales, dependent edema, hepatomegaly, holosystolic murmur
- CP possible
diagnostic findings of dilated CM
- ECG → LVH, LAE, Q/QS waves, poor R wave progression across precordium
- CXR → enlarged cardiac silhouette, biventricular enlargement, pulm vascular congestion
- Dx: ECHO → ↓ EF, ventricular enlargement, ↑ systolic & diastolic volumes
management for new and old dilated CM?
- New - admit; monitored or ICU
- Known CM → identify cause - MI, anemia, infection, afib, bradyarrhythmia, valvular insufficiency, renal dysfunction, PE, thyroid dysfunction
complex ventricular ectopy in dilated cardiomyopathy may be treated with ?
amiodarone
chronic therapy for dilated CM
- diuretics, digoxin - improves sx, no effect on survival
- ACE, BB (carvedilol) - better for survival
management for advanced dilated CM
LVADs while awaiting transplant
a common cause of dilated CM
Inflammation of myocardium - Systemic disorder or infectious agent
Pericarditis MC accompanies
Myocarditis
s/s Myocarditis
- Nonspecific - Myalgias, HA, rigors, F, tachycardia
- CP, pericardial friction rub
- Severe - HF: DOE, Rales, Pedal edema, Cardiogenic shock
w/u for myocarditis
-
ECG - nml; nonspecific
- AV block , prolonged QRS, ST elevation, PR depression - CXR - nml; pulm congestion (severe)
- Biomarkers - elevated
management for myocarditis
- Admit, supp care = mainstay
- Abx with suspected bacterial myocarditis
- Progressive HF - ICU
what is a LVAD
Implanted pump transferring blood from apex of LV to proximal aorta
PE of LVAD
- Pump creates continuous blood flow to maintain nml MAP - May not have nml palpable pulse
- BP obtained by doppler or mechanical cuff
- “Whirr” heart sound from LVAD pump
- ECG - discernible QRS
- CXR - LVAD components
NEVER perform what intervention on an LVAD pt with hemodynamic instability?
why?
- CPR → displaces LVAD
- LVAD causing LV rupture with intractable hemorrhage
process of listening to the heart with LVAD pt
- “Whirr” heard → get BP, place on monitor, IV access, nml saline bolus
- No “whirr” → enlist the pt and family to help find cause of mechanical failure and change battery and controller; do not disconnect any equipment
common complications and tx of LVAD
- Infection at abdominal wall outlet → abx
- Anemia secondary to red cell destruction from pump/hemorrhage from anticoag → blood transfusion
- Thromboembolic event - heparin once bleeding r/o
LVAD: HoTN persists or RV failure, what tx?
pressors
what is hypertrophic CM
Asymmetric LVH and/or RVH involving interventricular septum = ↓ compliance of LV → impaired diastolic relaxation and diastolic filling
s/s hypertrophic CM
- More severe when older
- DOE MC
- CP, palpitations, syncope; may be aware of forceful ventricular contractions
-
S4 HS, systolic ejection murmur heard at lower left sternal boarder or apex = does not radiate to neck
- Enhanced by valsalva or stand
- ↓ by squatting and passive leg elevation - ↑ LV filling
EKG findings of HCM
nonspecifc; LVH, LAE, deep S waves with large septal Q waves and upright T waves possible
Inverted T waves = ischemia
dx HCM?
echo = disproportionate septal hypertrophy
CXR nml
management for HCM
- Mainly supp
- Suspected hypertrophic CM → echo
- Suspected hypertrophic CM + syncope → admit for cardiac monitoring and eval - sudden cardiac death!!
- When definitive dx → atenolol
CM - Uncommon; idiopathic or secondary
Sarcoidosis, scleroderma, amyloidosis
Ventricular filling restricted → nml or diminished diastolic volume, systolic nml
Restrictive CM
s/s Restrictive CM
- Dyspnea, orthopnea, pedal edema W/O assoc CM or systolic dysfunction
- CP UNCOMMON
- PE - consistent with degree of disease
- S3/S4
- Cardiac gallop
- Rales
- JVD, inspiratory JVD (kussmaul sign)
- Hepatomegaly
- Pedal edema
- Ascites
diagnostic findings in restrictive CM
- ECG - nonspecific; conduction disturbances, low voltage (sarcoidosis/amyloidosis)
- CXR - HF w/o cardiomegaly
management for restrictive CM
- Admit
- Diuretics & ACEI → sx control
- Tx underlying
- Sarcoidosis → corticosteroid
- Hemochromatosis → chelation
what is Acute Pericarditis including causes
- Inflammation of layers covering heart
- Idiopathic or infection (virus, bacterial, fungus)
- Causes: malignancy, drugs, radiation, CTD, uremia, myxedema, postmyocardial infarction (Dressler’s syndrome)
MC - sharp/stabbing precordial or retrosternal CP - radiating to back, neck, shoulder, or arm
Worsens lying supine, movement, swallowing, inspiration
Alleviated by sitting up and leaning forward
Assoc sx - infection, low-grade F, dyspnea, dysphagia
PE - nml; friction rub at lower left sternal border or apex
what dx
acute pericarditis
ECG acute pericarditis
Stage 1 - diffused ST elevation - I, V5, V6; PR depression II, aVF, V4-6
Stage 2 - ST normalized; T-wave amplitudes ↓
Stage 3 - T-wave inversion - I, V5, V6
Stage 4 - Normalized ECG
if sequential EKGs are not avail, what EKG findings are suggestive of pericarditis?
ST-segment/T-wave amplitude ratio > 0.25 in leads I, V5, or V6
tx for Stable, idiopathic/presumed viral pericarditis
outpatient, ibuprofen
ED mgmt when to admit pericarditis pts?
- Colchicine - beneficial adjuvant, can prevent recurrence
- Pericarditis + myocarditis/enlarged cardiac silhouette/effusion via echo/uremic pericarditis/ hemodynamic compromise → admit
Fluid accumulation in pericardial space → exceeds pressure of RV → tamponade = restricted filling and ↓ CO
Nontraumatic cardiac tamponade
causes of Nontraumatic cardiac tamponade
- uremia
- malignant effusion/Metastatic Malignancy
- hemorrhage d/t anticoag
- bacterial or tubercular infection
- chronic pericarditis
- lupus, radiation, myxedema, idiopathic
- Penetrating or blunt chest wall trauma
Development of diastolic dysfunction results in relation to:
- rate of fluid accumulation
- pericardial compliance
- intravascular volume (hypovolemia lowers ventricular filling pressure)
s/s cardiac tamponade
- Mild to severe shock
- MCC - dyspnea
- Tachycardia, HoTN/low SBP, narrow pulse pressure
- Pulsus paradoxus - drop in SBP >10 during normal inspiration
- Neck vein distention, distant HS, RUQ pain (hepatic congestion)
- NO RALES
-
Beck’s Triad of Cardiac Tamponade
- Hypotension
- JVD
- muffled heart sounds
ECG of cardiac tampanode
- low-voltage/small QRS, ST elevations w/ PR depression as in pericarditis
- Electrical alternans
diagnostic for cardiac tampanode
TTE - Large pericardial effusion with RA/RV diastolic collapse
TTE - most sensitive and specific; US can be used too
cardiac tampanode can lead to HoTN and cardiac arrest with ____
pulseless electrical activity (PEA)
mgmt cardiac tampanode
- Peripheral IV, O2, continuous cardiac monitoring
- BP monitoring q5-15 min
- IV saline/Large bore IV fluids - helps with right heart filling, temp improves hemodynamics
-
Pericardiocentesis when hemodynamically stable
- Emergency pericardiocentesis
if signs of decompensation, performed at bedside with US and/or EKG guidance
- Urgent consult to cardiology and cardiothoracic surgery for pericardiocentesis
what is constrictive pericarditis
- Pericardial injury/inflammation → abnml diastolic filling → constrictive pericarditis
- Causes: fungal, TB pericarditis, uremic pericarditis, postcardiac trauma, post surgical changes after pericardiotomy
presentation constrictive pericarditis
- Gradual development of sx similar to HF and restrictive CM
- DOE, pedal edema, hepatomegaly, ascites
- Kussmaul’s sign frequent
w/u and findings for constrictive pericarditis
- ECG: Nonspecific; small QRS, inverted T waves
- CXR - nml; enlarged cardiac silhouette
- 2D Echo - not helpful!!
- Dx: CT/MRI/Doppler echo
mgmt constrictive pericarditis
- Eval ventricular function
- Surgical pericardiectomy if significant construction and impaired ventricular filling
AAA definition
- ≥3.0 cm in diameter
- Symptomatic aneurysms and ≥5.0 cm require prompt operative repair
- Emergent!!
classic presentation of aortic rupture
- Older male, smoker, atherosclerosis; Sudden severe back or abd pain; HoTN; Pulsatile abdominal mass
- Syncope, pain localized to flank, groin, hip or abdomen possible
- Severe and abrupt ripping/tearing pain = rupture
- Femoral pulsations nml
- Retroperitoneal hemorrhage rarely
Aortoenteric fistula presentation
- GI bleeding - small or life-threatening
- H/o aortic grating at higher risk
- Duodenum MC site for fistula
- Hematemesis, melena, hematochezia
- High output cardiac failure with ↓ arterial blood flow distal to fistula
presentation of Rupture into retroperitoneum
- Fibrosis → chronic contained rupture
- Appear nml, may have pain for long time before dx is made
MC incorrect initial dx of aortic rupture/AAA
Renal colic
Back pain, intraabdominal process, testicular torsion , GI bleeding
additional w/u when dx is unclear with AAA
- Bedside abd US - >90% sensitivity
- Aortic rupture/retroperitoneal bleed not reliably identified - CT - can delineate where aneurysm and any associated rupture
possible XR finding with AAA
calcified, bulging aortic contour (only in some)
general mgmt for AAA
- Consult vascular surgeon if rupturing AAA or aortoenteric fistula
- Fluids (for HoTN)
- Target SBP: 90mmHg
- Tranfuse PRBC if needed
- Pain control while avoiding HoTN
tx small asx AAA (3-5 cm)
- Incidental finding
- Refer to vascular surgeon
tx for Large AAA (>5cm)
Higher risk for spontaneous rupture; close f/u
dx & mgmt/tx for Nonaortic large-artery aneurysms
Dx: US/CT
1. Popliteal/femoral - thrombolysis, ligation, arterial bypass, endovascular repair
1. Hepatic - surgical ligation, embolization
1. subclavian/femoral pseudoaneurysm/ renal/splenic - surgical repair
- renal/splenic - +ectomy
for Aortic Dissection, the blood dissects between ___ and ___ layers of aorta
intimal
adventitial
RF aortic dissection
- MC male, >50y, h/o HTN
- Chronic cocaine use
- h/o cardiac surgery
- Younger pts - CTD, congenital heart disease, pregnancy - Marfan’s syndrome
presentation aortic dissection
Acute CP
- Most severe at onset
- Radiates to back
- Sharp, ripping, tearing pain
- Syncope possible
- Location dependent on area of aorta involved:
— Anterior CP - ascending aorta
— abd/back pain - descending aorta
— Diastolic murmur of aortic insufficiency possible
— HTN and tachycardia common; HoTN can be present
- ↓ pulsation in radial, femoral, or carotid arteries
- Neurologic sequelae
what is Stanford Classification ?
aortic dissection
Type A - Ascending Aorta
Type B - descending Aorta
what is DeBakery Classification
- Type I - ascending & descending
- Type II - ascending only
- Type III - descending only
presentation of progressed dissection
- AV insufficiency
- coronary artery occlusion - myocardial infarction
- carotid involvement - stroke sx
- occlusion of vertebral blood supply - paraplegia
- cardiac tamponade - shock and JVD
- compression of recurrent laryngeal nerve - hoarseness of the voice
- compression of superior cervical sympathetic ganglion - Horner’s syndrome.
w/u and findings with dissection? What is the diagnostic w/u?
- D-Dimer
- CXR
- MC - Abml aortic contour, widening mediastinum
- Deviated trachea, mainstem bronchi, esophagus, apical capping, pleural effusion, displacement of aortic intimal calcifications - Dx: CT w/ contrast; TEE
tx aortic dissection
- Consult vascular or thoracic surgeon
- Fluids
-
Esmolol/labetalol
- Goal HR: 60-70
- Goal SBP: 100-120 - SBP >120 → nitroprusside/nicardipine
HTN emergency definition
Defined as a SBP >180 and/or DBP >120
BP should be assessed in both arms multiple times
Two types of hypertensive crisis
- HTN urgency - no evidence of end-organ damage
-
HTN emergency - evidence of end-organ damage
- brain, heart, aorta, kidneys, eyes
s/s of HTN emergency
- Brain: HTN encephalopathy, SAH, ICH, Ischemic CVA
- Heart: Acute pulmonary edema, MI, ACS
- Aorta: Aortic dissection
- Kidney: Acute renal failure
- Eyes: Hypertensive retinopathy
- Multiorgan: Preeclampsia, Eclampsia, Acute perioperative HTN, Sympathetic crisis
for HTN emergencies how do you eval them?
Look for signs of end-organ damage
H&P
- Mental status changes, neurologic dysfunction, seizure, acute severe HA
- Visual changes, retinopathy, papilledema
- Sudden onset chest pain
- Dyspnea
- Peripheral edema
- Oliguria
labs that indicate end-organ damage
- BMP: acute elevation of serum creatinine
- UA: proteinuria, RBC, or red cell casts
imaging needed for HTN emergencies
- CXR - pulmonary edema or thoracic aortic dissection
- ECG - cardiac ischemia
-
CT head w/o contrast - neurologic changes/CVA
- Follow up with CTA head & neck if noncontrast CT is negative - CTA chest - chest pain/aortic dissection
tx HTN urgency
- BP control within 24–48 hours
- No hx of HTN: HCTZ
- Hx of HTN: reinstitution or intensification of oral antiHTN
- DC home with rapid follow-up with PCP
tx HTN emergency
- Rapid, controlled reduction in BP w/ IV antiHTN
- Reduce SBP by no more than 25% in the first hour
- If stable: reduce to 160/100 over next 2-6 hrs
- If stability remains reduce to normal over the following 24 to 48 hour
- Admit to a critical care floor (CCU, ICU)
3 conditions that are the exception in reducing SBP by no more than 25% in the first hour during HTN emergency
Aortic dissection, acute ischemic strokes, intracerebral hemorrhage
HTN emergency: Rapid reduction of BP can lead to ?
watershed cerebral infarction
which agent is preferred for SAH, ischemic stroke
Nicardipine (Cardene) - CCB
Nicardipene may precipitate myocardial ischemia, what other agents are alternatives
- Labetalol (Trandate)
- Enalaprilat (Vasotec)
which antiHTN agent is used in most patients, aortic dissection, stroke
Labetalol (Trandate)
which antiHTN agent is preferred for aortic dissections
Esmolol (Brevibloc)
which antiHTN agent is preferred for renal insufficiency or failure; May protect kidney function.
Fenoldopam (Corlopam)
which antiHTN agent is preferred for CHF, stroke
Enalaprilat (Vasotec)
which antiHTN agent is preferred in pregnancy
hydralazine (apresoline)
Avoid in CAD, dissection. Rarely used except in pregnancy.
which 2 antiHTN agents should be avoided in acute LV systolic dysfunction, asthma.
Labetalol (Trandate)
Esmolol (Brevibloc)
which antiHTN agent is no longer the first-line agent d/t wide variety of SE?
Nitroprusside (Nitropress)
