cardiac 2024 pt 2 Flashcards
CAD usually due to what?
describe pathophysiology
r/f
ages gender
atherosclerosis.
inadequate tissue perfusion due to imbalance between increased demand and decreased coronary artery blood suppy.
DM is worse then smoking.
men >45 or women>55 with FH of CAD= male before 55 or female before 65.
virchow’s triad
think DVT risk factors:
intimal damage, stasis, hypercoagulability(protein S or C def, factor V leiden mutation, antithrombin III def, oral contraceptive, malignancy, PG, smoking
DVT
1. most specific sign
2. first line imaging
3. gold standard
- edema LE >3cm
- venous doppler ultrasound
- contrast venography, invasive
IVC filter for DVT when?
recurrent DVT/PE despite adequate anticoagulation OR stable pts in whom anticoagulation is contraindicated OR right ventricular dysfunction w/ an enlarged RV on echo
DVT tx in …
1. PG
2. malignancy
- LMWH as initial and long term therapy.
- same plus Warfarin or direct oral anticoagulants are alternatives to LMWH in these pts.
Common causes of right and left heart failure
left: CAD and HTN. Others include valvular disease and cardiomyopathyies.
right: left sided heart failure. Pulm disease(COPD and pulm HTN), mitral stenosis.
Rt sided heart failure pneumonic
S W E L L I N G
swelling in legs, feet, abdomen
wt gain (early sign, retaining fluid)
edema(pitting)
large neck veins
lethargic (low cardiac output)
irregular heart beat (careful to get afib)
nausea
girth of abdomen increased(hepatomegaly)
systolic heart failure.
describe EF,
___ ventricular systolic dysfunction,
___ ventricle cannot eject blood properly
reduced EF.
left, left
diastolic heart failure.
describe EF,
___ ventricular systolic dysfunction,
ventricle issue
preserved EF
left, ventricle too stiff to allow for filling of blood
left sided heart failure 5 S/S
SOB, crackles, orthopnea, difficulty breathing at night, pulm edema
gallop and LV chamber in systolic and diastolic heart failure
Systolic: S3, LV small with thick walls
Diastolic: S4, LV dilated with thin walls
left sided heart failure pneumonic for s/s
D R O W N I N G
difficulty breathing
rales/crackles
orthopnea
weakness
nocturnal paroxysmal dyspnea
increased hrt rate(fluid overload)
nagging cough(watch for frothy foam)
gaining wt
pathophysiology of heart failure: afterload, preload, contractility
initial insult leads to increased afterload, increased preload, and decreased contractility.
cheyne stokes breathing
deeper, faster breathing with gradual decrease and periods of apnea and cyanosis. think left sided heart failure.
3 ways to manage diastolic heart failure
- heart rate control
- BP control
- Relief of ischemia(BB, ACE, CCB, diuretics for volume overload).
No CCB in systolic heart failure.
4 ACE inh precautions
A A C E
avoid in PG
ANGIOEDEMA
Cough
Elevated potassium (watch for hyperkalemia)
high potassium on ecg
ST elevation (high pumps)
peaked T waves and ST elevations
No CCB in what d/s
SYSTOLIC heart failure
BB and CCB 3__ tropics
neg chronotropic(lower rate)
neg inotropic(less force)
neg dromotropic(less beats)
BB decreases what 3 things(not including HR and BP)
resistance, workload, cardiac output
avoid BB in what 2 conditions
COPD and asthma
avoid BB in 4 kinds of treatments (pneumonic)
B B B B
. bradycardia
2. breathing problems (wheezing, …)
3. bad for heart failure pts
4. blood sugar masking (70 or less)
Before giving CCB, count what
count HR and BP.
avoid in systolic below 100 and HR below 60
what is digoxin toxicity
Over 2.0
vision changes, anorexia, nausea, dizzy
creatinine levels
nml 0.6-1.2;
over 1.3 “no pee pee”
check what pulse and what lab in digoxin toxicity
apical pulse under 60
potassium below 3.5
digoxin, careful with what 2 pts
on diuretics or has renal problems
vasodilators do what 3 things.
what about preload and afterload
D- decrease BP
D- dilates vessels
D-decrease vascular resistance
decrease preload and afterload
top 5 vasodilators
nitro, nitroprusside, hydralazine, isosorbide, minoxidil
when to stop a vasodilator
on viagra, systolic below 100 or drops by 30 mmhg, lack of coordination, irritability, sweating, pallor
3 normal SE of vasodilator
HA, hypoTN, hot flushing(facial redness)
2 K++ wasting diuretics
caution in who
furosemide and HCTZ.
isosorbide not one.
caution in hypokalemia 3.5 or less
top 3 loops to give for worsening heart failure
furosemide, torsemide, bumnetanide
loops MOA
blocks reabsorption of Na into kidneys
what 3 drugs spare K++
lisinopril, losartan, spirolactone
what 3 things to check before giving a diuretic. pneumonic
B B P
BP, hold for systolic under 100
BUN & Cr
K++ imbalances
what is dilated CM
common cause
chamber
hallmarks
most common CM.
systolic dysfunction, leading to dilated, weak heart
idiopathic cause or viral(enterovirus, coxsackievirus B, echovirus)
usually left ventricle.
S3 gallop(due to filling of a dilated ventricle); displaced apical impulse
postviral myocarditis, HIV, lyme, parovirus B19, chagas d/s
poss etio for dilated CM
ETOH abuse, radiation, PG, autoimmune, thyroid d/o, vit B1 def(thiamine)
poss etio for dilated CM
Dilated CM demographics
2:1 male to female
african amer more then whites
dilated CM, remodeling of what? affects what valves, EF
left ventricle, thin wall, reduced EF, increased end systolic and diastolic volume leads to dilation. mitral insuff, tricuspid insuff
how to calculate cardiac output
HR x stroke volume
what is preload
end diastolic volume
describe frank starling law in dilated CM
increased stretch=increased contractility
relationship breaks down causing stroke volume to decrease and so does cardiac output
dilated CM tx
systolic heart failure: ACE, BB.
symptom control with diuretics
3 etio of hypercholesterolemia
hypothyroidism, PG, kidney failure
4 etio of hypertriglyceridemia,
may cause what organ issue
DM, ETOH, obesity, steroids, estrogen
pancreatitis
goals of lipid lowering agents
plaque stabilization
reversal of endothelial dysfunction
thrombogenicity reduction
atherosclerosis regression
FH guidelines to screen for hyperlipidemia
first degree male relative with CHD before age 55,
first degree female relative with CHD before age 65
plaque stabilization
reversal of endothelial dysfunction
thrombogenicity reduction
atherosclerosis regression
goals of lipid lowering agents
AHA, describe screening in adults for hyperlipidemia
ages 20-39 who are free of CVD is reasonable to assess risk factors every 4-6 years to calculate their 10 year risk
optimal age to screen for hyperlipidemia
higher risk: >1 risk factor(HTN, smoking, FH) or 1 severe risk factor. initiate screening at age 20-25 for males and age 30-35 for females
lower risk: initiate screening for age 35 for males, 45 for females
lipid guidelines for initiation of statin therapy.
6 risk factors to look at
gender, age, smoking, BP, blood cholesterol level, DM, race
lipid guidelines for initiation of statin therapy.
- DM between ages what?
- pts without CV disease ages what and ___% risk of having a MI or stroke within __ years
*people age ____ 21 years of age with LDL > ____
*anyone with clinical atherosclerotic CV disease
Pts < ___ years old with familial hypercholesterolemia
DM ages 40-75 years old
CV ages 40-75 years old and 7.5% within 10 years
21 years old LDL >190
19 years old
what are the best meds to lower elevated LDL
statins and then bile acid sequestrants
what are the best meds to lower triglylcerides
fibrates then niacin
what are the best meds to increase HDL
niacin then fibrates
what are the best meds for DM for hyperlipidemia
statins and fibrates
statins MOA
affect on LDL…
inhibit rate limiting step in hepatic chol synthesis via inhibition of enzyme HMG-COA reductase.
increase LDL receptors, promoting LDL clearance, reduce Tg
niacin MOD
increase HDL(delays clearance), decreases hepatic prod of LDL and its precursor VLDL. Decreases Tg.
best drug for
1. decrease LDL
2. increase HDL
- statin
- niacin
contraindications: active hepatic d/s, persistant elevated LFTs, PG, breastfeeding
statin
active PUD, active liver d/s, arterial bleeding
niacin
fibrates MOA
inhibit triglyceride synthesis, increase activity of lipoprotein lipase(stim catabolism of Tg rich lipoproteins), increase HDL synthesis and decrease LDL synthesis
only fibrate approved to use in combination with statin
fenofibric acid
contraindications: active hepatobiliary ds, severe renal ds, breastfeeding, gemfibrozil+repaglinide
fibrates
chol med..
1. risk of increased gallstone
2. taken in evening
3. can interact with drugs that inhibit CP450 systems
4. avoid with warfarin
- fibrates
- most statins (atorvastatin and rosuvastatin can be taking anytime)
- statins (erythromycin, diltiazem, -azoles)
- BAS
name fibrates
fenofibrate and gemfibrozil
name bile acid sequestrants
cholestyramine, colestipol, colesevelam
cholestyramine, colestipol, colesevelam
bile acid sequestrants
bile acid sequestrants affect what lipids
increase LDL receptors and decrease LDL levels
lipid drug safe in PG
bile acid sequestrants
bile acid sequestrants…
1. used in combo with what
2. adverse affect on tg
3. long term use
4. may impair absorption of what
- statin to reduce LDL, mild to mod increase in HDL
- increase Tg
- osteoporosis
- antibiotics, digoxin, warfarin, fat soluable vitamins… so take these meds 1 hour before BAS
contraindications to BAS
severe hypertriglyceridemia, complete biliary obstruction
cholestyramine used to treat what else
pruritus assoc with biliary obstruction
ezetimibe MOA, indication, SE
inhibit intestinal chol absorption
often used in combo with statin to reduce LDL level
SE: HA, diarrhea, increased LFTs
main effect on BP: ACE inh and ARBs
decrease SV and SVR
main effect on BP: alpha blockers, BB, CCB
alpha: decrease SVR
BB: decrease HR and SVR
CCB: decrease SVR
alpha receptors
think sympathetic system(fight or flight) and vasoconstriction of blood vessels
beta receptors on heart
increase HR and SV, both leading to increase CO and increase BP
BP equation
CO x SVR
CCB work on what cells
vascular and muscle cells, block vasoconstriction
diuretic MOA for HTN
decrease Na and H2O reabsorption therefor decrease BP
HTN med for gout pt
CCB, losartan is the only ARB that doesn’t cause hyperuricemia
HTN emergency
SBP > 180 and/or DBP >120 with evidence of end organ damage
HTN emergency managment
IV BP agents. Mean arterial pressure should be reduced gradually by about 10-20% in 1st hour and additional 5-15% over the next 23 hours
meds to treat HTN emergency
IV labetalol or Na nitroprusside infusion
hypotension reading
affected by 3 things
90/60
CO
blood viscosity
total peripheral resistance
4 kinds of shock
hypovolemic, cardiogenic, obstructive, distributive/impaired vasoconstriction
pancreatitis, vomiting, bowel obstruction, DKA, renal loss, resp loss, severe burns
non haemorrhagic causes of hypovolemic shock
S/S of hypovolemic shock
pale cool extremities/dry skin, slow capillary refill, decreased skin turgor, AMS, dry mucous membrane
no profound resp distress
hallmark of hypovolemic shock
vasoconstriction, increased SVR, hypotension, decreased CO and decreased pulm capillary pressure
class 1 and 2 of hypovolemic shock
- <15% blood loss: nml pulse, SBP nml
- 15-30% blood loss: pulse >100 (tachycardic), SBP >100
class 3 and 4 of hypovolemic shock
- 30-40% loss: SBP <100, tachycardic, confusion, decreased urine output
- > 40%: lethargy, no urine output, …
CBC in hypovolemic shock
increased hgb/hct due to dehydration(hemoconcentration.
decreased hgb/hct in late hemorrhagic shock
Hallmark of distributive shock
decreased ALL
CO, SVR, PCWP
most common form of distributive shock
septic shock.
early septic shock has increased CO and SVR due so warm extremities in these pts.
pathophys of septic shock:
infective organism activate _____ system, then host produces ___ ___ ___ then ____ cause prompt peripheral ____then ___ in SVR. ____ capillary permeability (initiating ____), and end organ thrombosis.
infective organism activate immune system, then host produces systemic inflammatory response then cytokines cause prompt peripheral vasodilation then decrease in SVR. Increased capillary permeability (initiating shock), and end organ thrombosis.
what is the only shock associated with increased CO (fast capillary refill time: warm, flushed extremities)
septic shock
S/S of septic shock
hypotension with WIDE pulse pressure
bounding arterial peripheral pulses
hypotension with WIDE pulse pressure
bounding arterial peripheral pulses
S/S of septic shock
tx of septic shock
pan culture before initiating: zosyn + ceftriaxone or imipenem. gentamycin for pseudomonas. vanco for mrsa. clinda or flagyl for intra-abdominal infections, ceftriaxone in asplenic pts to cover N. Menigitidis & H. Influez
IV fluid resus with isotonic crystalloids (Normal saline , LR)
vasopressors: if no response to 2-3L of IV fluids with goal of MAP >60 +/- IV hydrocortisone.
Septic shock organism tx
pseudomonas
mrsa
intra-abd infections
asplenic pts with cover what 2 organisms
gentamycin for pseudomonas. vanco for mrsa. clinda or flagyl for intra-abdominal infections, ceftriaxone in asplenic pts to cover N. Menigitidis & H. Influez
anaphylactic shock
Ig _______________
tx med
cardio issue?
airway
observe pt for how long
IgEEEEEEEEEEEEEEEEEEEEEEEEEEEEE
epi 1st line (0.3 mg IM of 1:1,000 repeat q 5-10 min as needed).
if cardiovascular collapse, give epi 1mg 1:10,000
airway mgmt with benadryl 25-50mg IV blocks H1, ranitidine blocks H2
observe pt for 4-6 hours b/c 20% pts have a biphasic phenomenon (return of symptoms 3-4 hours before initial reaction)
neuropathic shock
d/t what
pathophys
HR, SVR, pulse pressure
tx
due to acute spinal cord injury, regional anesthesia
pathophys: autonomic sympathetic blockade then unopposed increased vagal tone then BRADYCARDIA and HYPOTN. loss of sympathetic tone then warm, dry skin
decreased HR and SVR, hypovolemia, and WIDE pulse pressure
tx: fluids, pressors, +/- corticosteroids
decreased HR and SVR, hypovolemia, and WIDE pulse pressure
neuropathic shock
endocrine shock
for example: adrenal insuff (addisons)
tx hydrocortisone 100mg IV (often unresponsive to fluids and pressors)
CO decreased, PCWP decreased, SVR increased
hypovolemic shock
CO decreased, PCWP increased, SVR increased
cardiogenic and obstructive shock
CO increased, PCWP could be up of down, SVR decreased
septic shock
shocks with severe and no resp distress
hypovolemic has none. skin pale, mottled
cardiogenic and obstructive has severe. plus cool clammy skin
HOCM definition
autosomal dominant d/o. diastolic dysfunction.
subaortic outflow obstruction due to asymmetrical septal hypertrophy and systolic anterior motion of the mitral valve
obstruction in HOCM worsens with what 2 things
increased contractility and/or decreased LV volume
HOCM murmur
- harsh systolic murmur best heard at LSB
- increased murmur intensity with decreased venous return(valsalva, standing) or decreased afterload
- decreased murmur intensity with increased venous return(squatting, leg raise) or increased afterload(handgrip). increased LV volume preserves outflow.
*possible loud S4, MR, pulsus bisferens
harsh systolic murmur best heard at LSB
HOCM
most common symptom in HOCM
diastolic dysfunction leading to increased left atrial pressure and left pulmonary vein pressure and therefore exertional dyspnea.
other symptoms in HOCM
arrhythmia, angina, syncope
HOCM tx
BB first line. CCB the alternative.
caution with digoxin(increased contractility), nitrates, diuretics(both decrease LV volume)
AS vs HOCM
squatting and leg raise (increase LV volume)
this will decreased HOCM and increase AS
dizziness, lightheadedness, palpitations, blurred vision, darkening of visual fields and/or syncope
cerebral hypoperfusion
orthostatic hypotension
criteria for orthostatic hypotension
at least 20 drop in systolic or at least 10 drop in diastolic
med tx for orthostatic hypotension
fludrocortisone
