im Flashcards
emergent tx for hyperkalemia
hyperkalemia is treated emergently when ECG changes (peaked t waves, widened QRS, bradycardia, disappearance of p waves, sinus node dysfunction and av node block) or when K+ is really high (like >6.5) or rises really fast. Calcium is used to stabilize cardiac membrane. Since it’s faster to shift K+ intracellular than get it out of the body, insulin is given. Glucose is also given to prevent hypoglycemia.
acute epididymitis usually due to bladder obstruction and the organism ______ in men >35 and due to ________ in men <35
men >35: e coli men < 35 N gonorrhea, Chlamydia
dermatomyositis antibodies
anti RNP, anti JO 1, anti Mi2 bonus: highly elevated creatinine kinase
in patients wither dermatomyositis, you need to screen for…
internal malignancy! they are at much higher risk for cancer also interstitial lung disease, myocarditis, dysphagia
seen with heliotrope rash, proximal muscle weakness, rash on shoulders
dermatomyositis
anti RNP, anti Jo 1, anti Mi2
give high dose glucocorticoid steroid plus glucocorticoid steroid sparing agent and screen for malignancy
how do you tell the difference between IgA nephropathy and acute post infectious glomerulonephritis?
both are nephritic syndrome (blood in urine, htn). Ig A nephropathy will affect Adults (20s-30s usually men) while postinfectious GN usually affects kids ages 6-10. IgA nephropathy shows up 5ish days after an infection while postinfectious GN takes weeks after an infection and it’s usally strep throat or impetigo so check their antistretolysin O titers. Also in IgA nephropathy complement levels are normal while in postinfectious GN complement levels are low. both tend to have benign course but IgA nephropathy can cause rapidly progressive glomerulonephritis and postinfectious GN can possibly lead to CKD in adulthood
triad of paroxysmal nocturnal hemoglobinuria
- hemolytic anemia
- pancytopenia
- thrombosis (especially in weird places like in abdomen, hepatic, cerebral)
usually in middle age b/c acquired mutation, lack CD55, CD 59 on RBCs, tx: prednisone and eculizumab
describe cardinal symptoms of ACA, MCA, posterior, opthalmic, lacunar stroke syndromes
high fever, severe polyartheritis, lymphopenia & thrombopenia, macular rash 3-7 days after travel to tropical/subtropical regions of central/south america, asia, africa
chikungunya fever
transmitted by mosquito (Aedes)
supportive care
often causes chronic arthritis, may have to give methotrexate
opening snap with mid diastolic rumble heard best at the apex
mitral stenosis,
most commonly due to rheumatic fever (usually in immigrants)
-can cause right sided, heart failure, dyspnea, left atrium dilation –> bronchus elevation and afib
Think of new onset afib with RVR as a different disease than chronic afib. What do you do for someone with new onset afib with RVR?
- Are the symptomatic? Presumably yes or you wouldnt get called
- Are they unstable? Like will they die in seconds? If yes, you shock – synchronous cardioconversion. They will need anticoag for a month afterwards
- Much more likely scenario: symptomatic and stable: You need to RATE CONTROL. Goal: below 110. Here’s the all important question: are they in heart failure exacerbation or not?
Acute decomp HF: Give Digoxin or Amiodirone
No HF: CCB like diltiazam or beta blocker like metopropolol
Think of new onset afib with RVR as a different disease than chronic afib. What do you do for someone with chronic afib
per AFFIRM trial, you can either do rate or rhythm control. Really the only time you’ll do rhythm control is for somebody who has “no good reason”to be in afib and won’t hop right back into if you convert them out and you’ll for sure anticoag those peeps.
For rate control: diltiazem or metroprolol.
Anticoag? CHA2DS2VAS score >2
for score of 1, maybe, maybe aspirin, maybe nothing
Anticoag:
Warfarin: No bridge needed for afib. Reversible. Inconvenient. Have to worry about diet. INR 2-3.
NOACs: Dabigatran, Apixiban, Rivaroxaban: easier, no reversal, insurance?
most common site of ectopic electrical foci causing afib
pulmonary veins
most common anatomic origin of atrial flutter
tricuspid annulus
status of pt with + Anti-HepB surface antibody and +Anti HepB core antibody and -HebBeAg
AntiHepB core antibody is present in acute or chronic infection but NOT after immunization; Anti-HepB surface antibody is present after immunization or succesfully clearing an infection so this person succesfully cleared an infection.
HepB e Ag indicates active infection and viral replication, infectivity
You have a patient with atypical community acquired pneumonia, GI symptoms and confusion – what tests would be really helpful besides the usual labs?
likely Legionnaire’s disease, especially if history of travel
Sputum culture Gram stain: lots of neutrophils, no organisms
Urinary legionella antigen
also low Na+ on BMP
acute symmetric arthritis in a school teacher/day care worker, maybe fever, fatigue, diarrhea
Parvovirus B19
describe areas of referred abdominal pain
test for suspected urolithiasis
abdominal US or noncontrast spiral CT
why is colonoscopy usually not performed in pts with acute abdominal pain
risk of perforation
what are 3 most common causes of esophogitis in patients with HIV?
- Herpes simplex virus
- candida
- CMV
How do you tell the difference? In Candida albicans, they will usually have oral thrush as well so that one is easy. For VIRAL esophogitis, the primary complaint is PAIN with swallowing but they can still swallow.
HSV: usually ulcers around mouth, round volcano-like ulcers in esophagus
CMV: linear ulcerations in esophagus
symptoms of hemorrhagic stroke in cerebellum
ipsilateral ataxia
nystagmus
occiputal headache, maybe neck stiffness
NO hemiparesis
facial weakness
symptoms of hemorrhagic stroke in Thalamus
contralateral hemiparesis and hemisensory loss
eyes deviate Toward hemiparesis
upgaze palsy
nonreactive miotic pupils
Pons coma symptoms
deep coma, total paralysis happens in minutes, pinpoint reactive pupils
symptoms of occipital lobe stroke
contralateral homonymous hemianopsia
euthyroid sick syndrome
happens in acutely ill patients, problems converting T4–> T3 in periphery
usually normal TSH and T4 but low T3 but everything can be low in extreme cases
pulmonary capillary wedge pressure is a measure of
left ventricle end diastolic pressure
elevated in left ventricle dysfunction
Name 3 complications of cirrhosis with portal hypertension
ascites
spontaneous bacterial peritonitis
variceal bleeding
cor pulmonale = impaired right heart function due to chronic lung disease
Name cor pulmonale signs and diagnostic tests
Elevated JVP
hepatomegaly, pulsatile liver
tricuspid regurgitation
right ventricular 3rd heart sound
edema in lower limbs
ascites
pleural effusions
Increased right heart pressures on ECHO, raised pulmonary artery systolic pressure on heart catheterization
back pain that gets better with sitting/walking uphill and worse with standing/walking downhill
spinal stenosis (better with flexion and worse with extenion)
MRI
asymmetric arthritis (even with warm swollen joints with leukocytes ), mouth ulcers, urethritis, conjunctivitis, low back pain
reactive arthritis
treat with NSAIDS
name 6 complications of ulcerative colitis
- spondyloartheritis
- colorectal cancer
- toxic megacolon
- erythema nodosum, pyoderma gangranosum
- uveitis
- primary sclerosing cholangitis
which type of IBD has skip lesions
chrons disease
age of presentation of ibd
bimodal
15-40 and 50-80
pt with large mediastinal mass
eosinophila
chest pain when drinking EtOH
elevated lactate dehydrogenase
Hodgkin lymphoma
elevated LDH associated with high tumor burden
remember to look for Reed Sternberg cells
what can happen when someone with myasthenia gravis has an infection?
myasthenic crisis
infection, surgery, preg/childbirth, tapering immunosuppressive drugs, certain meds lik beta blockers or aminoglycosides leads to extra muscle weakness. Watch out, they might be in serious respiratory distress but you don’t notice because they arent strong enough to struggle for air. Features might include dysphagia and choking sensation because they can’t clear secretions. Respiratory acidosis. They might be on death’s door before you realize it. Intubate. Plasmapharesis or IVIG. Corticosteroids.
transplanted kidney with recent increase in creatinine, proteinuria. On biopsy, lymphocyte infiltration of the intima, inflammatory tubular disruption, intimal arteritis. Transplant less than 6 months ago and pt is asymptomatic. What is it and what do you do?
Acute transplant rejection (predominantly T cell mediated)
mostly reversible
give high dose glucocorticoids and increase immunosuppressive doses
pt with kidney transplant. Pt is asymptomatic but has recent increase in creatinine. Biopsy shows intranuclear inclusions and mixed neutrophils and lymphocyte infiltration
BK virus reactivation due to immunosuppression
severe headache that came on within a few minutes with photophobia and vomiting and neck stiffness. Noncontrast CT is negative.
Get lumbar puncture to rule out subarachnoid hemorrhage.
Signs of SAH on LP: high opening pressure, xanthochromia (yellow-pink color), lots of RBCs
CT is sensitive for bleeds but might not pick up smaller or older bleed
rash
fever
AKI
eosinophilouria + WBC casts
interstitial nephritis
usually due to drugs
According to AHA, who gets a statin? (name 4)
If you are 40-75 and have diabetes
pts with known ascvd, stroke/tia, pad, other coronary revascularization procedure…
LDL >190
40-75 with ascvd 10 year risk >7.5%
symptoms/signs of the most common side effect of statins
myopathy
elevated CK
tender muscles
(you can also get elevated liver enzymes!)
which antilipid drug is best at raising HDL
niacin
remember can cause flushing and tachycardia so best to take aspirin first
fenofibrate and gemfibrozil are fibric acid derivatives used to lower triglycerides. What are their side effects?
gallstones! raised LFTs! and other gi effects
acute coronary syndrome pathophysiology
usually in situ thombosis at the site of ruptured athrosclerotic plaque
can also be due to thromboembolism causing occlusion, vasospasm, vasculitis, aortic root or coronary artery dissection, or cocaine use (cause both vasospasm and thrombobosis)
unstable angina happens when the thrombosis doesnt cause complete occlusion or there is spontaneous lysis; in chronic stable angina there is usually stenosis from an athrosclerotic plaque that’s only a problem when demand is increased due to exercise
in setting of MI, S4 suggests….
S3 suggests….
*persistent* ST elevation suggests….
S4 suggests noncompliance of the ventricles due to ischemia
s3 gallop is severe systolic dysfunction
*persistent* ST elevation is left ventricular aneurysm
what’s the difference in pathophysiology of STEMI vs NSTEMI
in STEMI we’re talking transmural ischemia whereas in NSTEMI it’s usually subendocardium
ST elevation in leads II, III, aVF suggests a problem where….
inferior surface of heart
supplied by right coronary artery
ST elevation in V2 V3 and V4 suggests a problem where?
anterior aspect of heart supplied by left anterior descending artery
ST elevation in I, aVL, V5, V6 suggests a problem where?
lateral aspect
supplied by lateral circumflex coronary artery
physical exam findings of aortic dissection
unequal pulses and BPs in each arm
widened mediastinum
murmur of aortic insufficiency
pericarditis ECG finding
diffuse ST elevation (not by vascular distribution like we see in MI)
MI Tx
- anticoagulation: aspirin, heparin
- beta blockers to lower demand
- nitrates to increase coronary blood flow
all of the above reduce mortality
patients may also be given morphine for the pain and tachycardia as well as oxygen
If pt with acute STEMI presents within 2-3 hours of symptom onset and receive ___ ideally within 90 minutes, then ____is the recommended reprofusion therapy
PCI, percutaneous reprofusion intervention
also appropriate if contraindication for thrombolytics, hypotensive or in cardiogenic shock
what are two most common causes of death in setting of an MI
ventricular arrythmia
cardiogenic shock (pump failure)
unilateral headache, ipsilateral Horner syndrome (ptosis and constricted pupil)
carotid dissection
headache, lethargy, photophobia, vomiting, CN palsy
subarachnoid hemorrhage
saccular aneurysms can compress CNs, for example compression of CNIII can cause one pupil to be dilated (think rupture of posterior communicating artery), compression of CNII can cause vision loss (internal carotid or anterior communicating artery), or compression of CN IV (trochuler) by superior cerebellar artery
or CNVI abducens by inferior cerebellar artery
blowing highpitched holosystolic murmur heard at apex plus S3
severe mitral regurgitation
Due to backflow of blood from LV to LA during systole (because mitral valve is jacked), the total amount of blood entering LV during systole each time goes way up. To compensate, the LV undergoes eccentric hypertrophy. The apical impulse will probably be displace to the left on palpation. The S3 happens when all that increased volume rushes into the dilated floppy LV and slams against the wall during systole. S3 is highly suggestive of severe mitral regurg and its absence helps rule out severe mitral regurg. Pts with bad mitral regurge will start to develop dyspnea because the floppy dilated LV has decreased output. They will also get pulmonary hypertension eventually.
wide fixed splitting of S2 occurs with…
atrial septal defect
what type of hypersensitivity reaction is this and what causes it?
this is erythema multiforme and it is type IV hypersensitivity (delayed Tcell mediated)
Herpes simplex virus, Mycoplasma pneumonia
medications like Phenytoin, beta lactams (e.g penicillins), sulfonamides
a lot of people with cirrhosis wind up with esophogeal varices and 1/3 of ppl with esophogeal varices wind up with hemorrhage. So most ppl with cirrhosis should get diagnostic upper endoscopy to look for varieces. If nonbleeding varices are found, what is 1st line prophylaxis to prevent progression?
beta blockers
eg propranolol, nadolol
(endoscopic variceal ligation is alternative if beta blockers contra indicated)
patient with few symptoms over months to years, palpable spleen, huge leukocytosis and low leukocyte alkaline phosphatase
low leukocyte alkaline phosphatase should make you think CML, chronic myeloid leukemia. Low leukocyte alkaline phosphatase distinguishes CML from leukomoid rxn and all other leukemia!
most commonly caused by t(9;22) translocation (Philadelphia) –> BCR-ABL fusion protein that is constitutively active protein kinase
if you suspect lymphoma what do you always do?
cut it out! excisional biopsy is a must
older patient with increased hematocrit, leukocyte count, and platelet count. +pruritis, dizziness, headaches, blurred vision.
what’s going on? what are potential complications? how do you treat?
Polycythemia vera caused by JAK2 mutation
complications: usually goes on for a long time without problem and then you get hypercoagulable –> thrombosis–> stroke
Treatment: repeated phlebotomy until you get hematocrit below 45% + aspirin
if you think your patient has CML, what should you do next?
get cytogenetic studies so you can see if they have t(9;22) BCR-ABL which has targeted therapy
imatinib
dasatinib
nilotinib
imatinib
targeted against BCR ABL in CML
dasatinib
targeted against BCR ABL in CML
nilotinib
targeted against BCR ABL in CML
Leukomoid reaction
what causes it?
lab findings?
Leukomoid reaction: extreme leukocytosis with increase in all of the cell lines and increase in leukocyte alkaline phophatase (LAP) score. (Decreased in CML)
Often secondary to solid tumor like lung or kidney, infections, drugs like steroids
older patient with lymphocytosis
smudge cells on smear
B cells with CD19, CD20, CD23 on flow cytometry
CLL, chronic lymphocytic leukemia
usually just watch!! patients are usually asymptomatic when diagnosed and chemo is just for symptoms not for increased survival. very slow moving malignancy
if you do tx: fludarabine, cyclophosphamide, rituximab
A_L is most common leukemia of childhood
A_L is most common acute leukemia of adulthood
ALL kids
AML adults
Auer rods
acute myeloid leukemia (myeloperoxidase positive)
t(15;17) common
pathophysiology of myasthenia gravis
autoantibodies against acetylcholine receptors at neuromuscular junction
treatment is cholineasterase inhibitor: pyridostigmine
2nd line: glucocorticoids
ptosis improved with ice pack over eyes bc it slows down breakdown of acetylcholine
first line tx for myasthenia gravis
pyridostigmine (cholinesterase inhibitor)
2nd line is glucocorticoid
IVIG/plasmapharesis in crisis
thymectomy in some cases
Name symptoms and treatment of hypercalcemia
Bones, abdominal groans, moans, neuropsychiatric overtones: Bone pain, GI distress, weakness, confusion, lethargy, stupor
For severe, **symptomatic** hypercalcemia: IV Saline hydration!!! you want to dilute that calcium. also CALCITONIN (tone down the calcium). (only if they are crazy volume overloaded will you give furosemide)
Long term: Bisphosphonates.
symtpoms of CO poisoning
lab signs
treatment
confusion, wheezes, dyspnea, nausea, headache
seizure, coma, cherry red lips
anion gap metabolic acidosis
**pulse oximeter usually normal bc can’t distinguish oxyhemoglobin from carboxyhemoglobin
can cause irreversible hypoxic brain damage
100% oxygen through nonrebreather face mask, hyperbaric O2 in extreme cases
How can you prevent renal calcium stones?
low sodium diet
pesticide (organophosphate) poisoning mechanism, symptoms, antidote
cholinergic stimulation (both muscarinic and nicotinic)
SLUDGE: Salivation (also secretion in lungs), Lacrimation, Urination, Diaphoresis/Diarrhea, GI distress/Gasping for air, Emesis
Atropine followed by Pralidoxime
what should you suspect if someone has blood on urine dipstick but no RBCs on urine microscopy
and elevated [K+] and [PO4]?
rhabdomyolysis
think crush injury, intense mm activity including seizures, drug toxicity including statins
lysed mm fibers release potassium and phosphorous
causes AKI, tubular necrosis
increased AST>ALT
dx made by hugely elevated CK
stroke that causes pure sensory loss and then weeks later may cause allodynia => severe burning pain at light touch to contralateral limbs
thalamus
symptoms of lateral medulla stroke
Wallenberg syndrome
temperature regulation probs
horner syndrome (ptosis, miosis, anhidrosis)
*crossed sensory deficit (ipsilateral face, contralateral body)
ataxia
criteria for starting long term O2 for ppl with COPD
-sat 88% on room air at rest
or
-sat 89% at rest with cor pulmonale or hematocrit >55%
(remember secondary polycythemia can result from chronic hypoxemia)
Name 2 tests to make MS diagnosis
T2 MRI - look for lesions disseminated in time and space
IgG oligoclonal bands on CSF analysis
describe 4 common types of MS symptoms/lesions
- “optic neuritis” mononuclear vision loss, afferent pupillary defect
- transverse myelitis – loss of function below of certain spinal level. first flacid paralysis (spinal shock) followed by spastic paralysis c hyperreflexia. often incontinence
- internuclear opthalmoplegia - demylelination of medial longitudinal fasiculus; the eye on the same side as the lesion cant adduct towards the nose and the eye on the contralateral side abducts with nystagmus
- cerebellar dysfunction: ataxia, intention tremor, nystagmus
what do you give elderly patients with dementia for delierium in the hospital?
low dose haldol
can also do quetiapine, risperadone
what to do for esophagitis symptoms in a pt with HIV and oral thrush?
empiric treatment for Candida esophagitis: oral fluconazole. If it doesn’t get better you can do endoscopy, culture/cytology and look for viral etiology. Remember that linear ulcers point to CMV and volcano like ulcers point to HSV. Treat CMV with ganciclovir and HSV with acyclovir
healthy kid with very low platelet count
isolated thrombocytopenia, usually due to autoimmune thrombocytopenia
a diagnosis of exclusion
usually healthy kids 2-5 or teens. Everything is normal but platelet count.
what is considered a narrow QRS (in ms)? what is considered a wide QRS?
narrow qrs is <.12 ms (three little boxes)
wide qrs is greater than 0.12 ms (three little boxes)
what rhythm is this? what do you do for it?
sinus bradycardia
if unstable, pace
if stable and symptomatic, adenosine
what is length of normal PR interval on ECG?
0.12-0.2 ms (3 to 5 little boxes)
what rhythm is this? what do you do for it?
1st AV block – the PR interval is prolonged and no beats are dropped. if the patient is unstable, you pace them (unstable signs: LOC, AMS, hypoperfusion, shock, pulmonary edema)
if stable, you can use adenosine
what rhythm is this? what do you do about it?
This is 2nd degree AV block type 1 (Mobitz 1)
the PR interval gets longer and longer until a beat is dropped.
If unstable, pace; otherwise give adenosine or atropine (anticholinergic)
what are causes of AV block?
Ischemia! STEMIs, acute coronary syndromes
infectious diseases: Chagas, Lyme, endocarditis, acute rheumatic fever, diphteria, toxoplasmosis
inflammatory/infiltrative diseases: myocarditis, sarcoidosis, rhemautic diseases like SLE, sclerosis, rheumatic artheritis, reactive artheritis,
cardiac procedures
congential
metabolic/endocrine probs like thyroid
certain drugs like beta blockers, digoxin, calcium channel blockers…
and more!
what rhythm is this? what do you do?
This is AV block type II (Mobitz II)
Prolonged PR with random dropped beats
tx: try to identify and remove underlying cause, e.g. a medication
for acute management: usually atropine and pacing
what rhythm is this? what do you do?
This is 3rd degree AV block; there is no AV conduction
definitely permenant pacing
medical therapies include atropine, beta adrenergic agonists like dopamine, dobutamine, isoproterenol, epinephrine ; also IV aminophylline
what rhythm is this? what do you do?
idioventricular rhythm – ventricles running the show but it’s not vtach. So notice slow rate but complete absence of p waves
i think the answer is pacing? same meds as other serious av blocks?
what rhythm is this? what do you do?
supraventricular tachycardia
notice fast rhythm, ABSENCE OF P WAVES, narrow QRS
Pathophys: usually some reentry pathway around AV + exacerbating factor
If unstable: SHOCK -synchronized cardioversion
If stable: try Vagal maneuver, IV adenosine
diltiazem, verapamil, propranolol, metropolol
After defibrillation, an ecg of sinus rhythm shows prolonged QT interval (this tidbit important!)
what rhythm is this? what do you do?
torsades de pointes
Note that this polymorphic vtach is not proven torsades if you don’t know there is underlying QT prolongation
I gave away treatment: If unstable: shock. If “stable” – give IV magnesium but stay close and be ready to shock.
what is considered prolonged QT?
>450-470 ms
Name antidepressants that can prolong qt
citalopram, escitalopram, TCAs
what rhythm is this? what do you do?
ventricular tachycardia
causes: structural heart probs including old infarct scars; congenital stuff like congenital long QT or hypertrophic cardiomyopathy; reversible causes like electrolyte imbalance, drugs, acute ischemia, hypoxia
Unstable: SHOCK
Stable: IV procainamid, IV amiodarone, or IV sotalol to try to stop Vtach
urgent catheter ablation
MI patient with cold extremities, elevated JVP, crackles, hypotension (systolic <80), high left and right filling pressures (measured indirectly with pulmonary capillary wedge pressure >18mmHg)
Cardiogenic shock
oxygen, vasopressors like dobutamine and dopamine, might also need reduce afterload through intra aortic balloon counterpulsation and iv nitroglyverin or nitroprusside
might have to do urgent revascularzation with PCI
MI patient with markedly elevated JVP, hypotension, but clear lungs
right ventricular infarction, tends to be a complication of inferior STEMIs
The first step to spotting RV infarction is to suspect it… in all patients with inferior STEMI!
In patients presenting with inferior STEMI, right ventricular infarction is suggested by the presence of:
ST elevation in V1 – the only standard ECG lead that looks directly at the right ventricle.
ST elevation in lead III > lead II – because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle.
RV infarct is very preload sensitive DO NOT GIVE NITRATES
Name 3 MI complications that would cause systolic murmurs
- papillary muscle dysfunction –> mitral regurg
- papillary muscle rupture–> flail mitral leaflit and acute mitral regurg–> cardiogenic shock and heart failure
- new holosystolic murmur due to ventricular septal rupture
these usually happen in the first week
what should you suspect if ECG still shows ST elevation several weeks after an MI?
ventricular anuerysm
Dressler syndrome is a complication of MI that occurs several weeks later. What are symptoms?
Pleuritis
Pericarditis
Fever
(immune mediated)
tx with nsaids, sometimes prednisone
drugs for someone having a heart attack
MONA BASH C
Morphine
O2
Nitrates (unless you think its RV)
Asprin
Beta blocker
ACE-i
Statin
Heparin
Clopidegrel
underlined = they should def go home on; they might also go home on nitrates if chest pain; they will go home on clopidagrel for 1 year if they have drug eluding stent and for 1 month if they have bare metal stent
ST elevation in leads II, III, and aVF suggest an infarct in which region of the heart
inferior (right coronary artery)
you’ll often see bradycardia
which biomarker should you use to look for a re-infarct of myocardium
CK-MB
(remember that troponin stays elevated for 7–10 days so it probably wont be helpful info that troponin is elevated…from previous infarct)
a 60 smoker patient has squeezing chest for 30minutes and EMTs give him oxygen and nitroglycerin. BP is 110/70, pulse =90, and ECG is normal. What’s the next step.
Give aspirin.
remember that initial ecg and biomarkers can be normal in MI
what ecg leads show the lateral aspect of the heart
V5, V6, AVL, I
in heart failure, the renin-angiotensin-aldosterone axis and sympathetic system are activated. These help initially but in the long run make for more cardiac decompensation and remodeling. Heart failure can look like forward failure or backward failure. Describe these.
Forward failure: heart isn’t pumping enough blood out so pt has fatigue and lethargy, perhaps even hypotension
Backward failure: increased filling pressures or diastolic dysfunction. Blood backs up–> dyspnea, elevated JVP, perpheral edema, ascites and hepatic congestion
New York Heart Association functional classification of heart failure:
I: no limitation of ordinary physical activity
II: slight limitation of physical activity; develops fatigue or dyspnea c moderate exertion
III: marked limitation, even light activity produces symptoms
IV:__________________
NYHA classification IV: symptoms at rest, any activity causes worsening
name major causes of heart failure
what drugs have been shown to decrease mortality in HFrEF?
ACE-inhibitors*
beta blockers (carvedilol, metropolol, bisoprolol)
*In black pt, use HYDRALAZINE + NITRATES
spironolactone (aldosterone antagonist) can also be used for NYHA class III, IV.
digoxin can be used for symptoms but doesnt affect mortality
why is digoxin used to help relieve symptoms of heart failure
digoxin increases heart contractility somewhat
(does not improve survival - for symptomatic relief)
how do nitrates and nitrites help CHF symptoms (note that these aren’t as commonly used although hydralazine + nitrates confere improved survival in black pts)
Nitrates reduce preload and clear pulmonary congestion
(remember that’s why we don’t use nitrates for RV infarcts bc the RV is really dependent on preload)
Pts with HFrEF and advanced symptoms may have widened QRS (>120ms), indicating dyssynchronous ventricular contraction. Placement of biventricular pacemaker called………………………………..to stimulate both ventricles simultaneously can reduce symtpoms and imrpvoe mortality
Cardiac resynchronization therapy (CRT)
Pts with higher class HFrEF are at increased risk of ventricular arrhythmia and sudden cardiac death. What therapy can be considered?
implantable cardiac defibrillator (ICD)
In acute decompensated heart failure, you would treat elevated LV filling pressures with_____________.
You would treat decreased cardiac output with______________ and hypotension with ________________.
In acute decompensated heart failure, you would treat elevated LV filling pressures with IV nitroglycerin to decrease preload.
You would treat decreased cardiac output with ionotropes like dobutamine and hypotension with vasoconstrictors like dopamine.
Aortic stenosis is most common symptomatic valvular abnormality in adults. If younger than 30, think congenital bicuspid valve. Pt 30-70, think congenital stenosis or acquired rheumatic heart disease. Older than 70 think calcification. What is the classic *progression* of symptoms of aortic stenosis
angina –> syncope –> heart failure
“harsh” systolic murmur
name the three layers of the aortic vessle wall. What predisposes somebody to aortic dissection?
intima, media, adventitia. In dissection, there is hematoma in the media that propogates distally. Hypertension is biggest factor in propogation of the hematoma.
cystic degeneration of the media in connective tissue diseases like Marfans and Ehlers-Danlos
hypertension
valve dysfunction like stenois, congenital bicuspid valve
aortic coarctation
pregnancy
athrosclerosis
What do you do for someone with aortic dissection
- intravenous vasodilator like sodium nitroprusside and introvenous beta blocker like metroprolol or esmolol. Or IV labetalol does both function. Hypertension, shearing forces are what will propogate the dissection so this is most important thing to do.
- Noninvasive imaging: TTE (transesophogeal echo), CT or MRI depending on availability. You need to class the AA as Type A (involving ascending aorta) or Type B (not involving ascending aorta)
- Type A dissection requires urgent surgery. Type B only requires surgery for complications
Operative repair is indicated for abdominal aortic aneurysms > _____ cm
5.5cm or those expanding >0.5cm per year
for smaller aortic aneurysms, serial noninvasive imaging like ultrasound is indicated
A pt presents with severe chest pain radiating to his back, unequal brachial BPs and pulse strengths, and a widened mediastinum on CXR. What do you do next?
Get CT. Symptoms consistent with acute aortic dissection.
What defines first degree AV block?
prolonged PR interval - longer than 200ms (1 large box)
There is conduction delay in AV node. prognosis is good, usually dont need pacing
CCauses of secondary HTN
CHAPSS
Cushings
Hyperthyroidism, hyperaldosteronism
Aorta coarctation
Pheochromocytoma, Polycystic kidney disease
Sleep apnea
Stenosis of renal arteries
what are the initial labs you get for HTN?
UA - look for hematuria
urine albumin/creatine spot –check for proteinuria
BMP with calcium and creatinine to check kidney/GFR
Fasting glucose - diabetes
Lipid panel -cvd risk
*base line ECG*
+/- TSH, T4, ECHO, evaluation for 2* causes
Stage II hypertension (what is cut offs) need what kind of pharma therapy
Stage II >160/100
Usually need to go ahead and be on 2+ drugs
What antihypertensive drug do you use in pt with diabetic nephropathy or CKD + proteinuria?
ACE-i or Arb
SPRINT trial showed that pts 50+ with one or more cardiovascular risk factors had a 30% CVD event risk reduction if BP target was:
120 systolic
what are the two common causes of renal artery stenosis?
- Athrosclerosis
- Fibromuscular dysplasia
bilat flank masses and pain
HTN
hematuria
ask about family hx! These are symtpoms of polycystic kidney disease
carcinoid syndrome is caused by overproduction of….
serotonin , carcinoid tumors arise in GI tract and lungs
in hypertensive emergency/urgency, don’t lower BP too much…probably 160/100 range.
What are definitions of hypertensive emergency vs hypertensive urgency?
Hypternsive urgency: >180/110
Hypertensive emergency: acute elevation in BP with end organ damage
(encephalopathy, MI, aortic dissection, declining renal function, stroke, pulmonary edema from acute LV failure)
tx for hypertensive emergency vs hypertensive urgency
Hypertensive emergency: immediate lowering of BP with IV sodium nitroprusside. Lower to 25%/ or 160/110 ish.
*using nitroprusside for multiple days –> cyanide toxicity. May need to use nitroglycerin plus loop diuretics which both reduce preload,
If pt presents with cerebral infarct, don’t lower BP unless systolic >220
Hypertensive emergency: lower BP over few days with oral meds, outpt setting
Pheochromocytomas are usually in medulla of adrenal gland. Test with 24 hr urine VMA, metanephrine, catecholamine. Surgical resection AFTER alpha blockade with phenoxybenzamine.
What are symptoms of pheochromocytoma?
what medication must be given before surgical resection of pheochromocytoma?
phenoxybenzamine (alpha blocker)
beta blockers may also be given but beta blocker alone will make HTN much worse because alpha adrenergic activity will be unopposed
generally beta blockers are avoided when pt is volume overloaded bc beta blockers reduce cardiac contractility
generally beta blockers are avoided when pt is volume overloaded bc beta blockers reduce cardiac contractility
what are two most common causes of afib
htn
coronary atherosclerosis
most cases of mitral _____ are due to rheumatic fever worldwide
rheumatic fever –> mitral stenosis
opening snap after S2 followed by low pitched diastolic rumble heard best at the apex