Firecracker 10/27 Flashcards
STEMI - EKG
hyperacute T waves
T wave inversions
ST segement elevation
Q waves
ST segment elevation =
transmural ischemia
Leads II, III, aVF
inferior
posterior descending artery or marginal branch.
Leads I, aVL, V4-V6
Lateral infarct of the left anterior descending artery or circumflex.
Leads V1, V2, V3
septal infarct of LAD
Leads V4, V5, V6
anterior infarct of LAD
serum cardiac enzymes for STEMI
cardiac-specific troponin T (cTnT),
cardiac-specific troponin I (cTnI),
creatine kinase MB-isoenzyme (CKMB)
troponins for STEMI
more specific and sensitive
elevated for 7-10 days after
CKMB for STEMI
rises within 8 hours
returns to normal after 72
AV block
impaired conduction between the sinoatrial (SA) pacemaker and the ventricles.
First Degree AV Block
PR > 0.2
normal 1:1 P:QRS ratio
First Degree AV Block Cause
increased vagal tone
AV nodal dz
electrolyte disturbance
med side effect
Second Degree AV Block - Mobitz Type I
progressive PR lengething until QRS is dropped
Group Beating
Group Beating
lumping of P-QRS-T elements leading up to the dropped QRS complex.
Second Degree AV Block - Mobitz Type II
random dropped QRS
discernible ratio of P:QRS
Mobitz Type I Causes
intranodal or HIS bundle conduction defects that result from medications (e.g., beta blockers, digoxin, calcium channel blockers),
increased vagal tone, or
right coronary artery mediated ischemia.
Mobitz Type II Causes
infranodal conduction abnormality in either the bundle of His or Purkinje fibers.
Mobitz Type I Treatment
adjusting medications or pacing if associated with symptomatic bradycardia
Mobitz Type II Treatment
always treated with a pacemaker due to the increased risk of progressing to high grade or third degree AV block.
Third Degree AV BLock
P waves separate from QRS
supra-ventricular impulses completely fail to conduct impulses to the ventricles, and ventricular depolarization is initiated by pacemaker cells distal to the block
Third Degree AV Block causes
coronary ischemia
also congenital AV block, lupus, or Lyme disease
Third Degree AV Block symptoms
hypotension, dizziness, syncope
Third Degree AV Block treatment
pacemaker
VF most commonly associated with
coronary artery dz
VF risk factors
MI, decreased left EF, electrolyte disturbance
long QT syndrome, A fib
most common cause of mortality following MI
V fib
Patients with VF
sudden LOC or comatose
symptoms of MI prior to collapse
VF results in
insufficient forward cardiac output –>
CNS ischemic injury, MI, sudden cardiac death
initial therapy for VF
defibrillation followed by 2 minutes of CPR
VF - after 2 rounds of defibrillation
epinephrine (1mg bolus, then every 3-5 minutes) should be administered followed by another shock.
medicines to consider with VF refractory to defibrillation
magnesium and amiodarone
asystole or pulseless electrical activity
immediate high-quality chest compressions.
not shockable arrhythmias
mildly elevated LFTs
chronic hepatitis
alcohol induced hepatitis
NAFLD
LFTs 100s or 1000s
acute viral hepatitis
LFTs 10,000
toxin-related hepatitis
liver ischemia
location of AST
liver, cardiac muscle, skeletal muscle
hepatic pattern of liver disease
markedly elevated AST and ALt
minimal to no elevation in alk phos
half life of albumin
20 days
albumin in patients with advanced liver cirrhosis
low
severe liver damage labs
increased PT/INR
PHT value
greater/equal to 12
increased resistance to portal blood flow
Prehepatic PHT
portal vein thrombosis
schistosomiasis
Intrahepatic PHT
cirrhosis
hep B/c
PBC
posthepatic PHT
right sided heart failure
Budd-Chiari syndrome
severe TR
hepatic venous pressure gradient
balloon catheter to monitor gradient pressure btwn portal vein and IVC
PHT complications
variceal bleedings
SBP
ascites
pleural effusion
PHT management
screening for GE varices, beta blockers, diuretics, sodium restriction
transjugular intrahepatic portosystemic shunt
shunt between portal and hepatic vein (allowing portal vein to drain properly)
metabolic acidosis
ph <7.37
decrease in HCO3- levels
metabolic acidosis lab values
low pH, high H+
very low HCO3-
low pCO2
compensation - hyperventilation
normal anion gap values
10-15
causes of anion gap metabolic acidosis
methanol, uremia, DKA, paraldehyde, INH, lactic acidosis, ethylene glycol, salicylates
increased osmolol gap
suggesitive of toxic alcohol ingestion
OG =
Osm - (2Na + glucose/18 + BUN/2.6)
normal OG
<10
normal anion gap metabolic acidosis (hyperchloremic metabolic acidosis)
GI HCO3- loss
renal acidosis
drug induced hyperkalemia with renal insuff
other
metabolic acidosis/ GI HCO3 loss
diarrhea
external pancratic or small bowel drainage
jejunal and ileal loops
Normal anion gap hypokalemic renal acidosis
Type 1 and 2 RTA
acetazolamide, topiramate, amph b
normal anion gap hyperkalemic renal acidosis
Type 4 RTA (hypoaldosteronism)
Drug-induced hyperkalemia with renal insufficiency leading to normal anion gap metabolic acidosis is seen in
potassium sparing diuretics
trimethoprim
ACEI/ARB
NSAIDs, cyclosporine
other causes of normal anion gap metbaolic acidosis
acid loads (ammonium chloride) expansion acidosis from rapid saline adminstration hippurate
urine anion gap
Na(urine) + K - Cl
negative UAG
high levels of NH4 excretion
suggests normal renal function
positive UAG
low NH4 excretion
suggests renal tubular dysfunction
Compensation for metabolic acidosis
hyperventilation
cause reduction in pco2
expected PCO2 range with metabolic acidosis
Winter’s formula
1.5 (measured HCO3) + 8 +/- 2
acute and severe metabolic acidosis treatment
administration of NaHCo3
absolute iron def
decreased iron levels in body stores
- poor nutriion
- impaired absorption
- blood loss
Functional iron def
insuff availability of iron to incorporate into precursors
- anemia of chronic dz
- treatment with erythropoiesis-stimulating agents
anemia of chornic dz
hepcidin-induced block on iron release from stores
etiology of iron def anemia
menorrhagia
gi bleed (colon polyp or cancer)
meckel’s diverticulum in child
breast milk contains low
iron
iron absorbed in
duodenum
stages of iron def
loss of iron stores -> decreased ferritin –> decreased serum iron –> increased TIBC –> decreased iron sat –> normocytic anemia – > microcytic anemia
symptoms of iron def anemia
pallor, fatigue
exertional dyspnea, orthostatic hypotension
tachycardia
koilonychia (spoon nails)
plummer-vinson syndrome
anemia + glossitis + esophageal webs
ferritin
intracellular protein that stores iron
transferrin
decreased in total iron –> upregulation of transferritin synthesis
iron def anemia gold standard
bone marrow biopsy - hardly ever performed
treatment of iron def anemia
trial or oral iron to menstruating women
work up
oral iron, don’t take with
tea, coffee, calcium (decreased absorption)
acidity (increase absorption)
oral iron side effects
n/v, constipation, black stool
dextran
parenteral iron
can cause life-threatening anaphylaxis
blood transfusion for iron anemia
unstable patients (hypotensive, hypoxic) hemoglobin of 7 for healthy patients, 10 for patients with CAD
acute mesenteric ischemia causes
arterial thrombus (atherosclerosis)
venous thrombus (hypercoaguable)
arterial occlusion from emboli
hypoperfusion - blood loss, CHF
CMI cause
ischemia due to long standing atherosclerotic dz or 2 or more mesenteric vessels
also, vasculitidies
CMI - age
over 60
females > males
CMI - vessels
celiac trunk
superior mesenteric artery
inferior mesenteric artery
AMI symptoms
diffuse non localized pain
N/v
bloody diarrhea
CMI symptoms
postprandial pain
weight loss
n,v,diarrhea
AMI pe findings
hyperactive/absent bowel sounds
positive occult blood
tachycardia
CMI PE findings
malnutrition
abdominal bruit
signs of peripheral vascular dz
diagnosis of mesenteric ischemia
CT angiography
mesenteric ischemia - plan films
can be used to exclude perforated viscus and free air under diaphragm
AMI complications
bowel necrosis, perforation, peritonitis, sepsis, death
CMI complications
acute thrombosis/embolism
prolonged hospitalization due to chronic malnutrition
AMI treatment
fluid resuscitation, ng tube, IV antibodies
embolectomy + thrombolytic influsion via angiography catheter
CMI treatment
open or endovascular revasc
warfarin
CMI with bowel necrosis
laparotmy to remove tissue
systolic dysfunction due to
decreased ventricular contraction
diastolic dysfunction due to
noncompliant ventricle
causes of systolic dysfuncton
ischemia/CAD
anemia, myocarditis, dilated CM, fluid overload
causes of diastolic dysfunction
HTN increased afterload (Aortic stenosis) restrictive processes
LSHF symptoms
pulmonary congestion - DOE, orthopnea, paroxysmal noctural dyspnea
LSHF - DOE
caused by interstitial fluid in lung stimulating juxtacapillary receptors
LSHF - orthopnea
because of increased venous return to right side of heart, worsen pulmonary congestion
paroxysmal nocturnal dyspnea
gradual reabsorption of fluid from interstitium into vascular compartment that leads to increase in venous return, worses PCongestion
LSHF - fluid overload
decreased CO
activates RAAS
retention of salt, water
hemoptysis in LSHF
rupture of engored bronchial veins
brick red sputum in LSHF
increased pressure in alevolar capillareis –> alevolar macrophages inget RBC –> hemosiderin laden macrophages
systolic HF ausculation
S3 gallop - kentucky
diastolic HF ausculation
S4 gallop - tennessee
BNP cutoff
400
Chest x ray findings HF
Kerley B lines – thin pulmonary opacities caused by fluid in the interstitium of the lung
Enlarged cardiac silhouette
Peribronchial cuffing – excess fluid in the small airway passages of the lung causes localized patches of atelectasis.
Cephalization of the pulmonary vasculature – antigravitational redistribution of the pulmonary blood flow due in part to increased pulmonary vascular resistance and pulmonary HTN.
LSHF acute treatment
Lasix (furosemide) morphine nitroglycerin oxygen positioning
LSHF morphine
decreases anxiety and preload through venodilation
Nitroglycern in LSHF
titrate IV SBP no less than 80
long term treatment of LSHF
beta blockers
spironolactone
ACE inhibitors
CCB and LSHF
not recommended
physical findings of atypical pneumonia
slower onset, insidious
no signs of consolidation
maintaining K balance
excreted in distal nephron
excretion enhanced with reabsorption of Na+
secretion increased by aldosterone
GI tract absorbs 90%
pleurisy
any condition that causes an irritation of the parietal pleura.
diastolic HF - echo
normal/high EF
decreased EDV
increased EDP
digoxin in HF
symptoms relief, reduce hospitalization
no effect on mortality
tetanus management
benzos
immune globulin
metronidzale or penicllin g
lifestyle modifications for CHF
exercise, sodium restriction
Mobitz Type I pathophysiology
intranodal or HIS bundle conduction defects that result from medications (e.g., beta blockers, digoxin, calcium channel blockers), increased vagal tone, or right coronary artery mediated ischemi
Mobitz Type II pathophysiology
infranodal conduction abnormality in either the bundle of His or Purkinje fibers.
LS CHF x ray findings
cardiomegaly
kerley b lines
peribronchial cuffing
cephalization of pulm vasculature
clinical features of pleurisy
sharp knife like pain worse on inspiration
after preceded by URI symptoms
emphysema
lung condition highlighted by pathological enlargement of distal airways due to airway destruction.
chronic bronchitis
productive cough of at least 3 months per year for 2 consecutive years.
COPD risk factors
smoking!!
pulmonary irritants, alpha-1 antitrypase, asthma
protease-antiprotease hypothesis
Nicotine and smoke derived free radicals cause accumulation of PMNs and macrophages in the alveoli.
Activated PMNs → release proteases which result in tissue damage.
Smoking also enhances macrophage elastase activity, which is not susceptible to cleavage by α1-antitrypsin.
functional alpha1-antritrypsin def
smoking derived free radicals can disrupt the balance between proteases and anti-proteases by inactivating α1-antitrypsin → “functional” α1-antitrypsin deficiency.
COPD patient presents with
combination of cough (productive or non-productive) and dyspnea of insidious onset and chronic duration.
COPD PE findings
Hyperinflation or “barrel chest” (increased AP diameter)
Diminished breath sounds
Hyperresonance to percussion
Prolonged expiration with “pursed lips” breathing → sudden expiration may cause atelectasis due to rapidly decreased alveolar pressure.
obstructive pattern COPD symtpoms
tachypnea, tachycardia, and cyanosis.
wheezes
expiratory, obstruction
crackles
inspiratory, opening of collapsed alveoli
COPD diagnosis
hyperinflation with an obstructive pattern, and systemic findings of hypoxemia and hypercapnia
COPD PFTS
Decreased FEV1 Decreased FEV1/FVC ratio Decreased VC Decreased DLCO Increased TLC, RV, FRC (from trapped air)
COPD ABGs
Chronic respiratory acidosis, leading to chronic metabolic alkalosis → elevated PCO2 and bicarbonate.
Polycythemia may occur in response to chronic hypoxemia.
COPD CXR
hyperlucent lung fields. Air trapping can lead to flattening of the diaphragm. In severe disease the heart can also become elongated and tubular shaped as a result of the increased air in the thorax.
COPD death
Respiratory acidosis and hypercapnic respiratory failure Cor pulmonale (rare) Massive spontaneous secondary pneumothorax
cor pulmonale occurs as result of
hypoxia
increased afterload can cause
RV failure
COPD treatment goals
reduce obstruction by dilating the airways and reducing mucus secretion, and prevention of disease progression.
COPD treatment
1) smoking cessation 2) antitussives/expectoants 3) inhaled b2 agonists 4) anticholinergics 5) inhaled corticosteroids
antitussives
dextromethophran
codeine-guaifenesin
inhaled b2 agonists
bronchodilators
salmeterol
inhaled anticholinergics
bronchodilator
ipratropium bromide
slower onset, longer duration
inhaled corticosteroids
budesonide, fluticasone
