Cardio Test #1 Flashcards
Coronary arteries
Left main LCA -> Circumflex and LAD
Right Main (RCA) -> RPA and Marginal
Left Coronary Arteries supply:
LDA: Supplies front and bottom of left ventricle and the front of the septum
Circumflex: Supplies left atrium and back and sides of left ventricle
Right Coronary Arteries supply:
Right atrium
Right ventricle
Bottom portion of both ventricles and back of the septum
Coronary artery lost, worry about?
LCA: immediate bypass - worse
RCA: worry about SA Node, may need a pacemaker
Common cardiac problems
Plumbing = ischemic heart dx, MI, acute coronary syndrome
Mechanical = CHF, restrictive and constrictive cardiomyopathies
Electrical = arrhythmias
Structural = Congenital or acquired abnormalities
PMI location
5-6th rib along mid-clavicular line
Pericarditis
Mostly viral
occurs in the pericardial cavity between 2 serous layers
Can also be idiopathic, autoimmune, or cancer
Think AI/CA w/ multiple incidents of pericarditis
Heart and Pericardial layers
Superficial to deep
Superficial fibrous pericardium
Deep 2-layer serous pericardium
-parietal and visceral
Epicardium (continuous w/ visceral serous pericardium
Myocardium
Endocardium (continuous w/ inside of heart and vessels)
Angina perctoris
Heart reporting a lack of oxygen
Cells are weakened
Myocardial infarction
Prolonged coronary blockage causes more cells to die the longer it stays there
Dead cells are replaced w/ noncontractile tissue
Cardiac muscle cells
1% have automaticity
intercalated disks/gap junctions allow contraction as a unit
fibrous insulator keeps electrical signls orderly
Longer refractory period to prevent tetany
Bulk of heart muscle is contractile muscle fibers
Autorhythmic cells
Unstable resting potential (-55 to -60)
Slow Na+ channels bring potential up to threshold (-40)
Once at threshold, Ca2+ channels burst open and initiate depolarization
Repolarization occurs once Ca2+ channels close and K+ channels open
Pacemaker potential
Slow opening of the Na2+ channels that makes cardiac muscle resting potenial so unstable
SA Node
In RA, just below SVC
60-100 bpm, PNS keeps it around 75
SNS and PNS innervated
If this is firing, will have a P wave (sinus rhythm)
AV Node
50 bpm
Less gap junctions = slower rate
Junctional rhythm (no P wave but normal QRS)
Delays the electrical impulse for 0.1 seconds to allow complete atrial contracion
Purkinje fibers
30 bpm
Escape, ventricular only rhythm
Widened QRS
Defective SA Node
ectopic focus or AV nodal pacing -> junctional rhythm
Defective AV Node
Partial/total block -> ventricular pacing
Extrinsic heart innervation
Medulla oblongata has cardioacceleratory (SNS) and cardioinhibitory (PNS) centers
SNS innervates SA, AV nodes, heart muscle, and coronary arteries
PNS innervates SA and AV nodes via vagus nerve
P wave and PR Interval durations
P wave: <0.12
PR Interval: 0.12-0.20
Gets long PR w/ heart blocks
QRS and QT Interval duration
QRS: <0.12
QT Interval: 0.34-0.43
Valve auscultation points
SL valves @ 2nd intercostal margin
AV valves @ 5th intercostal margin
Ventricular filling phase
Mid/late diastole
AVs open, SLs closed
80% blood passively flows into vent, 20% w/ atrial kick
EDV
Ventricular systole
Atria relax and ventricles contract
AV valves close, SL valves open when intravent>aorta pressure
Isovolumetric contraction until SL open
ESV
Isovolumetric relaxation
Early in diastole
Ventricals relax => T wave
Blood backflow closes SL valves -> diacrotic notch
Stroke Volume
EDV-ESV
Regulated by preload, contractibility, and afterload
Cardiac output
SV x HR
= volume of blood pumped by each ventricle in 1 minute
Max = 4-5X normal, or up to 35L/min (athletes)
Cardiac reserve
CR = COmax - COresting
Vasodilating systems
PNS
Prostaglandins
ANP
Nitric Oxide
Vasoconstricting systems
SNS
Ca+
RAAS
Endothelin
Vasopressin
Ejection fraction (EF/LVEF)
measurement of ventricular systolic function
60% is normal
Measure via an echo or a cardiac cath
Preload
Cardiac muscle cell degree of stretch before contraction
Increased venous return stretches cells to optimal length in order to increase contraction force
Increased venous return via slow HR, exercise = more time to fill
Way to adjust EDV
Contractility
Contractile strength of a muscle cell
Independant of muscle stretch and EDV
Method of modifying EDV
Inotrope
Agent that alters the force/energy of muscular contractions
Chronotrophs
Agents that modify the heart rate
Afterload
Pressure to be overcome for ventricle ejection
HTN increases this = increases ESV = increases SV
Method of modifying ESV
Chronotrophic hormones
SNS -> norepinephrine which causes SA node to fire more rapidly and increases contractility
PNS -> acetylcholine which slows heart rate w/ no effect on contractility
Atrial reflex
Bainbridge reflex
SNS reflex w/ increased venous return
Atrial and carotid baroreceptors stretch and stimulate SA Node = increase in HR
Tachycardia decreases C.O. => heart doesnt have enough time to fill
Stroke volume modifiers
Increased preload = Increased SV
Increased afterload = Decreased SV
Increased contractibility = Decreased ESV = Increased SV
Chemical regulation of heart rate
- Hormones => Thyroxine increases HR, enhances NE and epi effects = increase in HR and contractility
- Intra/extracellular ion concentration must be maintained for normal heart function = arrhythmias from electrolyte imbalances
Drugs contraindicated w/ CHF
CCB = decreased heart contractility strength
BB = decreased heart rate and contractility
Perfusion assessment at bedside
Feel feet, check the urine output, and check BP
Primary HTN
Idiopathic, inherited, or genetic
Usually asymptomatic until end organ damage apparent
Secondary HTN
Caused by some other dx
-sleep apnea, thyroid, meds, illicit drugs
BP is dependent on:
- Cardiac output
- Peripheral vascular resistance
JNC 8
All age CKD w/ or w/o DM
BP goal < 140/90
All races:
First line: ACEI/ARB
JNC 8
All ages w/ DM w/o CKD
Age < 60yr
BP goal <140/90
Black: First line - Diuretic +/- CCB
Non-black: First line - Diuretic +/- ACEI/ARB/CCB
JNC 8
Age > 60yr
BP goal < 150/90
Pre-HTN
130-139/80-89
Symptoms of end organ damage
CHF
Cardiovascular disease
Cerebrovascular disease
Uremia
Microalbuminemia
Aortic dissection
Drugs that cause/worsen HTN
Oral contraceptives
Anabolic steroids
NSAIDS
Valves closed during ventricular diastole
Semi-lunar valves
Valves closed during ventricular systole
A-V valves
“Lubb” sound
S1
Created by mitral valve moving into LA w/ ventricular contraction and chordea tensing
“Dupp” sound
S2
When blood in the arteries flow back and depress the SL valves
S2 split
Occurs upon inspiration
A2 is usually louder and longer than P2 (higher pressure)
w/ inspiration, RA pressure increases -> increases RV ejection time -> P2 lasts longer
High frequency heart sounds and stethescope use
S1
S2 (plus split)
aortic regurgitation - hardest to hear
Low frequency heart sounds and stethescope use
S3
S4
Mitral diastolic murmur
Best to hear S3 and S4 @ the apex in left lateral position
S3
Normal in kids
Rapid filling of the ventricles - compliant in kids, dilated in elderly w/ AV valve distention - valve distention makes the sound
1,3,2
S4
Abnormal in all
Atrial contraction in the presence of a non-compliant ventricle
4,1,2
Acyanotic CHD
“pink babies”
Left to right cardiac shunt
Atrial septal defect (ASD)
Ventricular septal defect (VSD)
Patent Ductus Arteriosus (PDA)
Cyanotic CHD
“blue babies”
Right to left cardiac shunts
Tetralogy of Fallot
Transposition of the Great Arteries
Obstructive CHD
Narrowing structures
Right side: Pulmonic valve stenosis (PVS)
Left side: Coarctation of the Aorta
-Congenital aortic stenosis (AS)
Umbilical cord makeup
2 arteries (away from heart)
1 vein (towards heart)
Here, the arteries carry unoxygenated blood to mom while vein takes oxygenated blood to baby
Prostaglandin inhibitors
Ibuprofen
NSAIDS
If taken during pregnancy, may interfere w/ fetal circulation (ibuprofen is Class D in 3rd trimester)
Atrial septal defect
Ostium primum @ bottom atrias most common
Widely split and fixed S2 over P w/ a systolic ejection murmur and RV heave felt @ lower left sternal border
Dx: TTE
Tx: surgical percutaneous repair @ 1-3 yrs
Can be earlier in kids w/ CHF
Ventricular septal defect
Most common CHD, usually membranous
If small, the child may lack sx and require no intervention - may have a harsh holosystolic murmur
If large, child will present w/ CHF in 1-6 mo, failure to thrive (cant breathe to eat)
Dx: CXR, EKG, TTE
Tx: ACEI, Diuretic, trans-catheter close
Patent Ductus Arteriousus
Common in preterm - give Inodmethacin to close
Overloads lungs, causes pulmonary HTN and L side failure
Usually asx w/ continuous rough machinery murmur @ L sternal border
Dx: TTE
Tx: Indomethacin, cardiac catheter, or surgical ligation to close
Teratology of Fallot components
- VSD ( ventricular septal defect)
- Pulmonary artery obstruction/stenosis
- Overriding aorta
- RVH (right ventricular hypertrophy)
Teratology of Fallot presentation
May not come out blue, happens when PDA closes
Cyanotic, fatigue/dyspnea on exertion, harsh systolic ejection murmur
Tet spell - crying/pooping => increased systolic pressure => no blood flow => turn blue/limp, pass out
Teratology of Fallot diagnosis and treatment
Boot-shaped heart on CXR, TTE and Echo to confirm
Tx: prostaglandins to open PDA, Temporary Blalock-Taussig shunt between L subclavian and pulm-artery
Total surgical repair
Transposition of the Great Arteries
Babies COME OUT BLUE unless w/ other CHD defects
-issues once the foramen ovale closes
Dx: Egg on a string CXR, TTE for confirmation
Tx: prostaglandins/Rashkind balloon to open foramen ovale
Arterial switch surgery @ 4-7 days post-birth
Pulmonic valve stenosis
Prevent blood flow to lungs
Asx to cyanotic @ birth, rough ejection systolic murmur and click
Can get RV failure
Dx: echo, cath
Tx: balloon valvuloplasty or surgical repair
Coarctation of the Aorta
Narrowing @ juxtaductal aorta, associated w/ Turner’s syndrome
presents @ 4-10 days old, bounding upper limb pulses w/ absent femoral pulse and blowing systolic murmur
Dx: CXR (rib notches), echo
Tx: Prostaglandins, balloon angioplasty, surgical repair
Congenital aortic stenosis
asx until severe, can make it to 3rd-5th decade before heart failure
Dx: CXR, EKG, echo
Tx: cardiac cath, Ross procedure
Cardiac biomarkers
AKA cardiac enzymes
Troponin
CK-MB
Myoglobin
Lab tests for CV risk assessment
hs-CRP
homocystine
What makes a cardiac biomarker unnescessary?
Pt w/ ischemic chest pain and ST elevation => MI
Troponin
Highly specific, fairly reliable - used for Dx of MI
Rises in 2-6 hours, peask @ 12-16 hours, remains elevated for 10 days - 2 wks
Measure @ presentation, repeat @ 3-6 hours, may repeat after 6 hrs if initially normal, EKG changes, or high-risk pt
Creatine Kinase (CK)
CK-MB may help support Troponin - MI Dx
Rises @ 4-6 hrs, peaks @ 24 hrs, normalized in 48-72 hrs
Less reliable than troponin
Myoglobin
Found in skeletal and cardiac muscle, not cardioselective
rises @ 2-4 hrs, peaks @ 6-12 hrs, normalizes in 24-36 hrs
hs-CRP
Stronger predictor of heart disease and stroke than LDL
Use for primary/secondary prevention, not acutely
May help motivate pt to lower risk factors
Homocystine
Byproduct of meat protein
Does not change treatment
May be linked to CVD if B supplements don’t improve outcomes
Brain naturetic peptide (BNP)
Produced by heart in response to myocardial stretch
Triggers Na+/water excretion
May help differentiate CHF from lung disease
Suspected arrhythmias workup
Holter monitor
Event monitor
Electrophysiology Studies (EPS)
Good for syncope, A-fib, palpitations, dizziness, bradycardia
Interventions for arrhythmias/systolic heart failure
Pacemaker
Defibrillator
Advanced heart failure therapy:
- Bi-ventricular pacing
- LVAD
Pacemaker
Only treatment for bradyarrhythmias
provide electrical stimuli to cause cardiace contraction when intrinsic activity is slow/absent
Types of pacemakers
External/Transcutaneous
Permenent
Biventricular
ICD
External pacemaker
Used in emergencies - short term until permenant therapy applied
Pacing pads on front and back of pts chest
Recommended for stabilization of heodynamically significant bradycardia
Single lead or Dual chamber pacemaker indications
Single lead paces in ventricle
-for a BBB, or backup pacemaker
Dual chamber can pace in atrium or ventricle
-typical type, AV node must be intact
Pacemaker indications
Sick sinus syndrome
3rd degree block
Prolonged QT syndrome
A-fib w/ slow ventricular response
Pacemaker rate
Pacemaker checks seconds between beats, not bpm
May have recording of HR slower than 60, but unless pt is having sx, they are fine
Single chamber pacemaker EKG
No P wave
Wide QRS that is really just a QS
Can’t assess ST abnormalities w/ a pacemaker or BBB
Pacemaker syndrome
Pt feels worse or CHF symptoms worse
Loss of atrioventricular synchrony causes this
Biventricular pacing
Adds a 3rd lead to Left ventricle
Reserved for advanced heart failure
Get synchronized ventricular pumping to increase EF
ICD Therapy
Pacing, cardioversion, and defibrillation abilities
Used w/ previous MI, cardiomyopathy
Used to prevent sudden cardiac death
LVAD
Left ventricular assist device
For severe systolic heart failure, bridge/pallative alternative to transplant
Balloon Angioplasty
Balloon infalted to compress plaque
Very high restenosis rate
Angioplasty/Stent placement Post OP
ASA for life
P2Y12 inhibitor w/ stent placement for at least 12 months
CABG
Coronary artery bypass graft
Reserved for multicoronary vessel disease
Arteries have the highest success rate
Post-op A-fib is common - myocardium is irritated and inflamed
Contraindications to stress testing
Acute MI
Unstable angina
Acute pericarditis
Acute systemic illness
Severe aortic stenosis
CHF exacerbation
Severe HTN
Uncontrolled arrhythmias
Exercise EKG positive test criteria
Can only rule in/out ischemia
Horizontal/downsloping 1 mm ST depression 0.08 s after J point in 3 continuous leads
Exercise EKG immediately admit if:
BP drops as exercise increase
>2mm ST depression
Downsloping ST depression
ST depression or sx < 6min into test or HR <70% predicted
ST depression doesnt not resolve quickly in recovery
Stress imaging indications
Abnormal Resting EKG
Confirm exercise EKG results
Localize region of ischemia
Distinguish ischemia from MI
Assess revascularization post-stent
Evaluate prognosis
Myocardial perfusion scintigraphy w/ SPECT
AKA radionuclide imaging/nuclear stress test
Measure myocardial uptake of radionuclide tracer to determine dead spots
Take nuclear images before and after stress (exercise or pharmacologic)
Look for wall motion abnormalities
Stress Echocardiography
Evaluate Left ventricle for wall abnormalities
Only gives information about presence/absence of ishcemia
Good for CAD, not good for LBBB or previous wall motion abnormalities
MUGA scan
Most precise way to measure ejection fraction
Multi-gated axquisition scan
Radionuclide tracers to image left ventrical wall motion and calculate ejection fraction
Use for cancer pts on cardiotoxic drugs
Cardiac CT
Imaging blood flow through coronaries
Trying to avoid heart cath in no risk pts w/ abnormal stress test
-Have to cath if you find a lesion
EBCT - electron beam
correlates w/ stenosis likelihood - cannot determine degree
What test if the pt has a LBB, pacemaker, or afib?
Nuclear scan, w/ either exercise or pharmacologic stress
Test for pt w/ known LV wall abnormalities?
Stress echo w/ exercise/pharmacologic stress
Stable angina
Predictable, pt knows their limitations
Fixed atherosclerotic plaque which can cause symptoms if pt increases workload and oxygen supply is reduced
Relieved by rest/nitrates
Long-standing >1-2 months
Unstable angina
Plaque rupture w/ thrombus
Arterial dissection also occurs at site of rupture
MI is impending if it hasn’t already occurred
Chest pain @ rest
New onset/worsening angina w/ a change in pattern
History of Angina must contain
- Precipitating and alleviating factors
- Characteristics of discomfort
- Location and radiation
- Duration - of this episode and all incidences
- Effects of nitro (if the pt has it prescribed)
Typical angina criteria
Substernal pain
Provoked by stress or exertion
Relieved by rest or nitro
Class 1 angina
Asymptomatic
Class 2 angina
Mild exercise limitations
Symptoms w/ ordinary exertion
Class 3
Moderate exercise limitations
Symptoms w/ minimal exertion
Class 4
Severe activity limitation
Symptoms at rest
Angina physical exam
Look for Levine’s sign
Diaphoresis
S4(decreased LV compliance)/S3 (decreased systolic function)
Mitral regurge systolic murmur
Paradoxically split S2 (LV is not working, occurs w/ expiration)
Stable angina labs
Look for precipitating cause
- CBC (check for anemia)
- TSH
- Check lipids and A1C
- Update BMP
Unstable angina labs
Troponin
CBC
TSH
Lipids/A1C
CMP
Ischemia on EKG
New bundle branch block
T wave inversion/depression/flattening
ST depression/elevation
(new) Q waves
Changes from previous EKG?
Chronic stable anigna cath indications
Worsening symptoms
Persistent limiting angina w/ maximal medication
Stress test indicates high risk
Hx aortic valve disease -> check to see if cause is valve disease or ischemia
Chronic stable angina meds and treatment goal
Nitrates
BB
CCB
Na-channel blocker
Antiplatelet agents
GOAL: prevent chest pain
Ranolazine
Specialist-only, last resort medication
Blocks sodium channel into myocyte during repolarization
->decreased ICF Na+ => decreased ventricular tension => decreased myocardial oxygen consumption
Lots of DI, Can cause QT prolongation
Chronic angina pt other medications
ASA/P2Y12I
Statin - decrease chances of plaque rupture
Coronary vasospasm/Prinzmetal’s angina/Variant angina
Chest pain that lacks usualy precipitating facors
ST elevation w/ episodes, cyclical pain pattern over months
Tx: CCB, long and short term nitrates to prevent
Avoid BB, they may provoke spasm (angiogram may as well)
CABG grafts and ACS
Worry about 10 year mark of CABG - think that lesion is in vein graft, not in new coronary vessel
Myocardial infarction definition
Elevated Troponin/CK-MB
+ (at least one)
- ischemic symptoms
- Ischemic EKG chances
- new Q waves
- Imaging shows new wall motion abnormality
if not an MI = unstable angina
EKG criteria for NSTEMI
New horizontal or downsloping ST depression
> 0.5 mm in 2 contiguous leads
+/- T wave inversions
EKG criteria for STEMI
ST elevation of > 1mm at J point in 2 contiguous leads
ST elevation >2mm (men) or > 1.5 mm (women) in V2, V3
Distingush Unstable angina from STEMI/NSTEMI
Cardiac enzymes will be normal w/ UA
Medical therapy for unstable angina and NSTEMI
To relieve pain and decrease myocardial O2 consumption:
- Oxygen - only if they’re hypoxic (worse outcomes if not)
- Nitro
- Morphine
- BB - CI if HOTN, bradycardia, or CHF exacerbation
Also add on antiplatelet and anticoagulation therapy
NSTEMI antiplatet therapy
ASA 325 mg chewed
+ P2Y12 blocker*
*Check w/ cardiologist first*
Unstable angina anticoagulation
Enoxaparin (Lovenox) - 1 mg/kg SQ q12hrs
NSTEMI anticoagulation
Put them on Heparin (UFH)
Lovenox cause too much bleeding when combined w/ plavix
May also want to add GPIIB/IIIA inhibitor for high-risk
Cocaine-associated MI
Managed similar to all other ACS except:
Give benzodiazepines early
Do no use BB - can cause further vasospasm
STEMI Medical therapy
O2, nitro, morphine, BB
Antiplatelet therapy, anticoagulation
+ go straight for PCI or get fibrinolytic therapy
STEMI Reperfusion therapy
1st line: PCI w/in 90-120 mins
2nd line: fibrinolytics IF
- PCI not available w/in 90-120 mins
- Symptoms have occured for <12 hrs
- No contraindications
STEMI anticoagulation therapy
A. Unfractionated heparin - undergoing PCI who got fibrinolysis
B. Bivalrudin + GPIIB/IIIA inhibitor
C. LMWH (lovenox) - small loading dose then SQ
-no antidote to lovenox, can’t take it back
Absolute fibrinolytic contraindications
Any intracranial hemorrhage
Ischemic stroke w/in 3 months
Cerebral vascular malformation
Bleeding disorder/acting bleeding
Closed head injury/facial trauma in last 3 months
Relative fibrinolytic contraindications
Severe uncontrolled HTN
Ischemic stroke > 3months ago
Dementia/any known intracranial dx
Traumatic/prolonged CPR
Pregnancy
Major surgery w/in 3 weeks
Internal bleeding/active peptic ulcer
Systolic blood pressure
Force the blood exerts on the artery walls as the heart contracts to pump out blood
Diastolic blood pressure
Force as the heart relaxes to allow blood frlow into the heart
Mean arterial pressure
Determined by cardiac output, systemic resistance, and central venous pressure
MAP = (COxSVR) - CRP
Arterial pulse pressure
Difference between systolic and diastolic readings during ejection
-indicator of vessel wall stiffness and inflammation
Peripheral vascular resistance (PVR)
Defines the resistance to flow that must be overcome by the heart in order for blood to flow through the circulatory system
Systemic vascular resistance (SVR)
Resistance offered by the peripheral circulation
Arterial baroreceptors
Carotid sinus and aortic arch
-inhibit SNS w/ arterial wall stretching to regulate arterial pressure
Arterial chemoreceptors
In the carotid bodies and aortic arch
Sense the O2, CO2, and H+ concentrations in blood
Communicate w/ vasomotor center to induce widespread vasoconstriction
SNS neurotransmitter
Norepinephrine -> Adrenergic
Works on both alpha and beta adrenergic receptors
alpha = vasoconstriction
beta = vasodilation
PNS neurotransmitter
Acetylcholine -> Cholinergic receptors
Ischemic response
Cushings reflex
Ischemic = increased flow causes cerebral HTN
Cushings = peripheral vasocostriction w/ increased cardiac output causes cerebral edema
Increases in PVR
May be caused by an increase in intracerllular calcium which causes structural arteriol changes => increased in resistance
This may explain why CCB work so well
Aldosterone functions
Causes the kidney to retain salt and water and secrete potassium
Angiotensin II functions
Induces widespread vasoconstriction
Induces aldosterone release from the kidney
Enhances SNS function w/ NE reuptake inhibition
Released vasopressin from pituitary - antidiuretic
Stimulates brain thirst center
Renin
Released from Juxtaglomerular cells in afferent arteriole
Macula densa cells
In distal tubules
Sense sodium and chloride ions in tubular fluids
Control renin release
Natiuretic peptides
Also regulate RAAS
Peptides (ANP, BNP) released from heart in response to atrial distention
Vasodilate
Increase GFR for sodium and water excretion
POTASSIUM SPARING
Nitric oxide
Vasodilator - affects smooth muscle
Endothelin
Vasoconstrictor - activates renin, intracellular calcium release, to produce a sodium-sensitive rise in blood pressure
Bradykinin
Vasodilator - released by ACEI
ACE inhibits bradykinin release
This is what causes the ACEI dry cough
Isolated systolic hypertention
Elevated systolic pressure w/ normal diastolic
Pt is at danger for heart/stroke events
Often develop LVH
Due to elevated pulse pressure
Renovascular HTN
Renal artery stenosis
Fibromuscular dysplasia
Most common
Tx w/ stents
AVOID ACEI
Adrenal caused HTN
Hyperaldosteronism
Pheochromocytoma
Primary Hyperaldosteronism
Benign adrenal gland secretes aldosterone -> pressure issues
Can be unilateral or bilateral
Renin is low w/ high serum aldosterone
Tx: Resect tumor, Spironolactone and diuretics if hyperplasia
Spironolactone
Aldosterone antagonist
Treatment for Adrenal hyperplasia
Pheochromocytoma
Over abundance of NE and epi in a episodic release pattern
Resect tumor w/ alpha and beta blockage pre-op in case of “spills”
Or Phenoxybenzamine (alpha blocker) if unresectable
24 UA for Dx - check for cetecholamines and meninephrines (byproducts)
HTN labs
CMP - potassium, glucose, electrolyte levels
Fasting lipid
U/A
CBC - hematocrit
EKG
Echo
Long-term HTN treatment goals
Controll CV risk factors
Reduce HTN-induced mortality
Hypertensive crisis
Sudden increase in BP
Urgent and Emergency types
Usually occur in pts w/ existing/poorly controlled HTN
Also rebound HTN
Hypertensive crisis staging
Fundoscopic exam
CMP (kidney function)
CBC
U/A
Urgent Hypertensive crisis
No end-organ damage
Lower BP over 1-2 days w/:
Captopril/Amlodipene/Clonidine
Emergent Hypertensive crisis
Organ damage is apparent/impending
Admit, lower BP carefully but efficiently - 10mmHg/6 hrs
Nitroprusside - low and slow
Nitroglycerin/Fenoldopam/Lebetalol/Hydralazine also work
Fedoldopam is good w/ renal failure
