CV Diseases Flashcards
s/s of LHF
orthopnea
paroxysmal nocturnal dyspnea
pulmonary edema
s/s of RHF
hepatomegaly
JV distension
peripheral edema
MCC of CHF?
ischemia and MI
Pump dysfunction primary etiology of what?
CHF
name 4 elements of CHF etiology:
- pump dysfunction
- decreased contractility
- increased afterload
- increased preload
pump dysfunction leads to
congestion and low perfusion
causes of decreased contractility:
- ischemia/MI
- cardomyopathy
- valvular heart disease
Valvular stenosis causes
pressure overload
valvular regurgitation causes
volume overload
systemic hyptertension causes
increased afterload
increased preload leads to symptoms of
pulmonary vascular congestion
s/s of increased preload include:
dyspnea
orthopnea
paroxysmal nocturnal dyspnea
pulmonary edema
MCC of Right sided HF
left sided HF
the RV may fail secondary to pulmonary disease (COPD) which causes increase in pulmonary vascular resistance, resulting in right sided pressure overload
• Backward congestion symptoms
o Dyspnea , orthopnea, PND
o JV distension ( venous pressure)
o Peripheral pitting edema
signs and symptoms of CHF
• Signs o Tachycardia o S3 (ventricular gallop), S4 (atrial gallop) o Rales o Cardiomegaly o Ascites o Hepatic congestion ( increased CVP) o Systolic dysfunction o Diastolic dysfunction
o Diastolic dysfunction (to ef, edv, etc)
heart unable to dilate/relax; becomes stiff
Preserved EF, normal EDV, ↓ compliance (↑EDP) often secondary to myocardial hypertrophy
o Systolic dysfunction (to EF, EDV, etc.)
Reduced EF, ↑ EDV, ↓ contractility often secondary to ischemia/MI or dilated cardiomyopathy
heart sounds associated with HF
o S3 (ventricular gallop), S4 (atrial gallop)
Diagnostics for HF
- BNP 100-300 (normal ~ 100)
- EKG - evidence of ischemia, chamber enlargement
- CXR - cardiomegaly, pleural effusion/edema
- Echo - systolic and diastolic dysfunction
Treatment for HF (broad goals):
- treat diminished contractility
- treat high preload
- treat high afterload
specific treatment for HF contractility
Amrinone (PDE inhibitor)
Beta agonist - Dopamine
Digoxin
Specific treatment of HF for high afterload
ACE inhibitors or ATR blockers
-reduce afterload and improve survival
Role of digoxin in HF treatment
o Inhibit Na/K ATPase
o BEWARE digoxin toxicity with hypokalemia (with diuretics) , elderly and renal insufficiency
o EKG finding in toxicity
—- PVC’s
—–ST depression ‘ dig effect’
—–Paroxysmal atrial tachycardia with varying block
ABCDE tx of HF
ABCDE
-ACE Inhibitors- reduce afterload -Beta-blockers -Calcium Channel Blockers -Diuretics - Endothelin Receptor Blockers --> decrease pulmonary vascular resistance
Anesthesia concerns for HF
- elevated head posture
- fluid status sensitive
- risk of OD due to slow circulation
- monitor I/O
- sensitive to gases
- avoid N2O in severe HF
- watch for arrhythmia - poorly tolerated
• Mean Arterial Pressure =
Cardiac output x SVR
Stroke volume x Heart Rate
Cardiac Output =
• Stroke volume is determined by three factors:
1.) preload, 2.) afterload 3.) contractility
• Preload is determined by two factors:
1.) intravascular volume 2.) venous tone
o Venous constriction –> high preload
what is the major determinant of intravascular volume?
NA in the body
** most important hormone for controlling vascular volume?
aldosterone
Normal EF =
60-80%
Ejection Fraction is …
the fraction of the end diastolic volume ejected in EACH stroke volume
Is an index of ventricular contractility- “systolic function”
formula for EF
EF = SV / EDV
** formula for SVR =
SVR = [ (MAP-CVP) / CO ] x 80
major determinant of SVR ?
arterioles
normal SVR?
1200-1500 dynes/sec/cm^-5
Afterload is
Afterload is the pressure against which the heart must work to eject blood during systole (systolic pressure).
The lower the afterload, the more blood the heart will eject with each contraction. Like contractility, changes in afterload will raise or lower the Starling curve relating stroke volume index to LAP.
Preload is:
preload is a measure of the degree of the ventricular stretch when the heart is at the end of diastole
LVEDP (supplied by: DBP)
** 5% of cardiac output. 250 ml/min @ rest
coronary circulation
**Coronary perfusion pressure =
arterial diastolic pressure - LVEDP (preload)
maximum flow of coronary circuclation occurs during
diastole
– this is why diastolic dysfunctions interrupt blood supply
hypoxia and adenosine cause:
vasodilation
name two factors that reduce coronary blood flow:
- tachycardia (shorter diastolic time)
2. aortic stenosis
Autoregulation MAP =
50-120mmHG
how does the autonomic system influence coronary circulation?
minimally
the myocardium utilizes all the O2 from arterial blood. what does this result in?
“extraction ratio”
if demand increases, it must be met
so, coronary blood flow increases
*parallel
What are the major determinants of coronary blood flow?
LVEDP & HR
resulf of stenosis on Coronary blood flow?
stenosis –> angina
at rest, coronary circulation accounts for what % of CO?
5%
250ml/min
increased pressure (vol) at the end of diastole causes
coronary compression
(coronaries lie under the heart)
-coronaries perfuse with diastolic relaxation
most volatiles are ideal for MI because they
are coronary vasodilators
the RV is perfused throughout
systole and diastole
the LV is perfused largely during
diastole
name three things that can decrease coronary perfusion:
- decreased aortic pressure
- increased HR (d/t decreased diastolic time)
- Increased LVEDP (preload)
main coronary artery? what percent?
80% Left CA
name two forms of myocardial hypertrophy
- concentric hypertrophy
2. eccentric hypertorphy
form of hypertrophy d/t chronically elevated afterload (pressure overload) is:
concentric hypertrophy
**Increased systolic pressure
form of hypertrophy d/t chronically elevated preload (vol overload) is:
eccentric hypertrophy
**increased diastolic pressure
concentric hypertrophy results in:
o Increased Thickness of ventricular walls, (due to Increased ejection of blood)
o Chamber size remains normal
o Conditions causing LV concentric hypertrophy
Chronic untreated hypertension
Chronic aortic stenosis
Coarctation of aorta (“a kink”)
o Conditions causing RV concentric hypertrophy
Pulmonary artery HTN
Pulmonary valve stenosis
Eccentric hypertrophy is due to?
what happens to heart?
• Due to chronically elevated preload (volume overload)
• Chamber size increases to accommodate larger volume
a
• Causes of eccentric hypertrophy:
o Excessive intravascular volume
o Chronic mitral or aortic regurgitation (“leaking of volume”)
o Morbid obesity
x axis on PV loop =
preload (LV volume)
y axis on PV loop=
afterload (LV pressure)
MV opens at what point on PV loop?
A
Point A on PV loop =
MV opens
ESV
S3
Point B on PV loop =
MV Closes = S1
EDV
S4
** ATRIAL KICK!!
Point C on PV loop =
aortic valve opens
Point D on PV loop =
aortic valve closes = S2
b/w point A and B on PV loop=
filling period
Stroke volume
b/w point B and C on PV loop=
isovolumetric contraction
b/w point C and D on PV loop=
period of ejection
b/w point D and A on PV loop=
isovolumetric relaxation
the beginning of contraction and indication of compliance is at what point on the PV loop?
point B
o Beginning of contraction o Heart is biggest as it gets o Shows EDP/EDV relationship o Shows LVEDV. Pressure is fairly low o Indicates compliance; how easily ventricle takes in blood without significant rise in pressure
Ca ++ is releasing from troponin and going back into the SR at what point on the PV loop?
Point D
o Ventricle start relaxing
o Ca++ is releasing from troponin and going back to sarcoplasmic reticulum
o Shows ESP/ESV relationship
o ( or ) shows regurgitation
insert image assessment of ventricular function
A =
B=
C=
D=
- ‘A’ is normal single ventricular contraction
- ‘B’ shows increasing preload with constant contractility and afterload
- ‘C’ shows increasing afterload with constant preload and contractility
- ‘D’ shows increasing contractility with constant preload and afterload
ESP= End systolic point; EDP= End diastolic point
In Systolic failure, there is increase in LVEDV and reduction of SV. LVEDP is increased b/c LV vol is increased. Diastolic portion of PV loop has shifts
to the RIGHT
In Diastolic failure, diastolic portion of PV loop shifts
UP
o Heart is unable to pump to meet the need
o Low CO–> fatigue, oxygen debt and acidosis
o Damming –> pulmonary or systemic congestion
o Causes: CAD, valvular dysfunction or arrhythmia
What form of HF is this?
Systolic
Causes: HTN, CAD, hypertrophic cardiomyopathy and pericardial diseases
What form of HF?
diastolic
normal atrial pressure =
8
according to the Heart Association classification of heart disease, class 1 is:
asymptomatic
according to the Heart Association classification of heart disease, class IV (4) is:
symptomatic at rest
in mitral stenosis; atrial pressure is=
high!!! 25/14 (normal is 8)
LA has to squeeze hard through a tight hole ==> less LV filling
what effects does Mitral stenosis have on the PV loop?
ABCD..
all decrease. loop shift DOWN and LEFT
preload LVEDV LVEDP SV EF
features of Mitral stenosis include:
• Delayed complication of RHD (antibodies), may occur 15-20 years after RF
• Normal left ventricle
• Narrowing of the mitral valve (Normal 4-6 cm2) rise in left atrial pressure which limits the pulmonary venous drainage –> increased PA pressure –> pulmonary hypertension –> RVH
o Ascites, peripheral edema, high risk of a.fib
PE of Mitral Stenosis
o Loud S1 o Opening snap o Loud P2 o Low pitched late diastolic murmur (mid diastolic murmur), best heard at apex o LA >> LV pressure during diastole o Right ventricular lift
symptoms of mitral stenosis
o Dyspnea, orthopnea , PND (due to pulm. congestion) “backup”
o Hemoptysis
o A fib –> embolization
dx of mitral stenosis
o ECG signs of left atrial enlargement, RVH (normal LV)
o A.fib
o CxR: straightening of the left heart border
o Dilation of pulmonary veins
o Echo : Narrowed, “fish mouth” – shaped orifice
medical tx for mitral stenosis includes:
MS = “ADDS”
- Anticoagulant
- diuretics (pulm congestion)
- Digoxin/ Diltiazem (afib)
- Surgical replacement
Anesthetic goals for patient with Mitral Stenosis would be:
*in regards to Heart Rate and rhythm, preload, afterload, contractility.
- Slow/Low HR (for LV filling)
- NSR
- Not too full, tight, or strong (maintain preload, afterload/SVR, and contractility
“remember: slow, regular, not too full/tight/strong”
causes of mitral valve regurgitation:
o Chronic: due to rheumatic heart disease, incompetent valve or destruction of mitral valve annulus
o Acute: due to ischemia, MI (papillary muscle dysfunction (D3 post MI), infective endocarditis (Bacterial Staph) or chest trauma
o Mitral valve prolapse
what effects does Mitral regurgitation have on the PV loop?
ABCD..
Afterload decreases SV decreases SVR decreases CO decreases -Acute: atrial compliance is normal or decreased (pulm congestion)
Left Atrial Pressure increases contractility increases LVEDV Increases LVEDP Increases -Chronic: atrial compliance is increased (low CO)
what form of hypertrophy develops as a result of mitral regurgitation?
eccentric
LV hypertrophy due to regurg vol > SV
symptoms of mitral regurgitation may include:
o Due to backward regurgitant flow: dyspnea, orthopnea, PND
o Regurgitation symptoms
<30 % mild symptoms
30-60 % moderate
> 60% severe symptoms
PE for mitral regurgitation:
o Diffuse and hyperdynamic ventricular impulse
o Holosystolic murmur best heard at apex, radiating to axilla
o Wide splitting S2
o S3 due to volume overload in left atrium
wide splitting S2 and holosytolic murmur are associated with what valvular heart disease?
MR
dx of MR includes:
o EKG: left atrial enlargement and left ventricular hypertrophy o Cx: enlarge left atrium o Echo: may show ruptured chordae o Cath: large v wave o TEE and doppler
a large V wave is associated with what valvular heart dx?
MR
- Present in chronic phase
- Shows decreased atrial and pulmonary compliance and
- increased pulmonary blood flow and regurgitant volume
Loud S1, opening snap, and a low pitched late diastolic murmur are associated with what valvular heart dx?
Mitral stenosis
Medical tx for Mitral regurg are:
MR = “VADDS”
- Vasodilator (ACE inhibitors) - reduce afterload; move fwd
- Anticoagulant
- diuretics (pulm congestion)
- Digoxin/ Diuretics (afib)
- Surgical replacement
Anesthetic goals for patient with Mitral Regurgitation would be:
*in regards to Heart Rate and rhythm, preload, afterload, contractility.
- Increase HR (avoid brady b/c regurg worsens)
- NSR
- Maintain Preload (increase PL = Increased regurg; decreased= decreased CO)
- Decrease Afterload - move flow fwd.
- Maintain Contractility (dig)
**remember: Fast, FWD, Regular and not too strong”
the most frequent valvular lesion commonly found in young women is
MV prolapse
clinical features of MV prolapse include:
-most asymptomatic; atypical chest pain or tachyarrhythmia
- pregnancy
- murmurs when supine to rising; infective endocarditis
Management of MV Prolapse:
minimal. most don’t require tx. complications are rare.
- Beta Blocker for palpitation
- abx prophylaxis with MR
major anesthesia concerns for MV prolapse
avoid increasing HR
avoid histamine release
valvular disease associated with pregnancy?
MV prolapse
-ideal to allow for tolerance in the increased blood volume associated with pregnancy.
in mitral stenosis; what are the considerations for spinal/epidural use?
avoid
don’t want to decrease preload
Aortic Stenosis - when you see this dx, what should we automatically associate it with?
coronary perfusion!!!
what effects does Aortic Stenosis have on the PV loop?
ABCD..
-SV Decreases
-Due to the stenosis; almost everything INCREASES: LVESP = 200mmhg LVESV LVEDV/ Preload Contraction
This moves the loop to the RIGHT and UP - isovolumetric sides.
aortic stenosis is what form of hypertrophy?
Concentric LV hypertrophy
Clinical symptoms of Aortic Stenosis:
AS = “SAD”
- Syncope (fall in SV and BP)
- Angina (decreased O2 supply)
- Dyspnea
PE for Aortic Stenosis:
o Paradoxical splitting of S2
o P2 comes before A2 in expiration
o Very narrow pulse pressure due to low systolic BP
o S4
o Systolic ejection murmur, with LV pressure»_space; aortic pressure during systole
splitting of S2
S4 (‘atrial kick’)
and systolic ejection murmur
associated with what valvular disease?
aortic stenosis
low pulse pressure d/t low SBP is associated with:
aortic stenosis
does age matter in regards to AV replacement?
no
if you need it, you need it.
Anesthetic goals for patient with Aortic Stenosis would be:
*in regards to Heart Rate and rhythm, preload, afterload, contractility.
MAINTAIN!!
Maintain HR / NSR (avoid brady ) Maintain/increase Preload & Afterload Maintain Contractility (not too strong)
MAINTAIN coronary perfusion
“remember: slow, full, tight, regular, and not too strong”
coronaries feed during
diastole
**Normal aortic valve distance =
[ N=2.5-3.5 cm2]
narrowed aortic valve: 0.7-0.9 cm2
in aortic stenosis; what are the considerations for spinal/epidural use?
contraindicated in severe stenosis
-can lead to decrease in SVR
what effects does Aortic Regurgiation have on the PV loop?
ABCD..
NO isovolumetric relaxation or contraction as blood is still coming in during systole.
INCREASED:
LVEDV
SV
LVESP
Moves the loop to the RIGHT and UP (major volume increase)
causes associated with aortic regurgitation:
o Rheumatic heart disease or congenital o Infective endocarditis o 3 Syphilis o Aortic dissection o Marfan’s syndrome o Collagen vascular disease e.g. SLE
in AR the Regurgitant flow from aorta during diastole results in
left ventricular dilatation and volume overload
a widened pulse pressure is often associated with what valvular disease?
AR
Reduction in systemic diastolic blood pressure leading to increased pulse pressure – Widened pulse pressure (160/50)
clinical features of AR
“AR = SAL”
o Syncope, weakness due to reduction in the diastolic arterial pressure
o Angina- because reduce coronary blood flow (coronary arteries are perfused during diastole)
o Left ventricular failure (PND) due to volume overload
o High pitch “blowing” diastolic murmur is associated with
AR
rapid rise followed by a rapid fall of carotid pulse is known as:
Corrigan pulse
A Pistol-shot –
femoral pulse “bounding”
a diastolic bruit over the femoral artery
Duroziez sign –
De Musset’s sign
– bobbing motion of head
systolic blushing and then diastolic blanching of the fingernail bed
Quincke’s pulse –
Anesthetic goals for patient with Aortic Regurgitation would be:
*in regards to Heart Rate and rhythm, preload, afterload, contractility.
“remember: Fast, Full, and forward”
- Maintain HR/NSR and maybe slightly tachy
- Increase Preload
- decrease Afterload (TPR)
avoid vasoconstrictors in what valvular disease?
AR
in AR, what’s the rule for spinal and epidural management?
they’re generally well tolerated
insert pic PV loops
A=normal, B= mitral stenosis, C= aortic stenosis, D= mitral regurgitation (chronic), E= aortic regurgitation (chronic)
insert pic abnormal pressure pulse
know
this decreases compliance of arterial tree, thus leading to increase in pulse pressure.
Arteriosclerosis
this is associated with low diastolic pressure and high systolic pressure, net result is very high pulse pressure.
Patent ductus arteriosus
this condition associated with backward flow of blood through the aortic valve. Low diastolic and high systolic pressure leads to high pulse pressure.
aortic regurgitation
criteria for systemic htn
≥ 140/90 mmHg
Risk Factors of Primary/Essential HTN:
• Risk factors ↑Age Obesity High-sodium diet DM Smoking Genetics Black>White>Asian
what is the racial order of primary htn predominance
Black>White > Asians
Primary HTN may present with these features:
o Retinal changes (copper wires, AV nicking)
o Systolic click
o Loud S2
o S4; may
retinal changes (nicking, etc) is often associated with what CV disease?
Primary HTN
The cause of Secondary HTN? TX?
- Renal Vascular Disease
- Renal Artery Stenosis
- PO BC
- Pheochromocytoma
- Cushing’s syndrome
- Primary Hyperaldosteronism (Conn’s Syndrome) - hypokalemia/ elevated aldo
- Hyperthyroidism
- Drugs, steroids, cocaine
Tx: ACE inhibitors, CCB’s, Diuretics, Alpha/beta blockers; lifestyle modification
HTN can predispose one to what disease/processes?
o Atherosclerosis o LVH --> subendocardial ischemia o Loss of cerebral and coronary blood flow autoregulation o Stroke o CHF o RF o Retinopathy o Aortic dissection
extremely high blood pressure is known as:
malignant HTN
malignant HTN can lead to what if not treated?
o Progressive renal failure and/or encephalopathy plus papilledema
tx for malignant htn
IV nitroprusside and diuretics
to decrease HR during intubation anesthesia provider would give:
Beta blocker (esmolol)
volatile agents lower what?
BP
to control HTN during general anesthesia, what do you do?
- deepen anesthesia
- Phentolamine (alpha 1 antagonist)
- Nitroprusside
antihypertensive choice for African American Men:
Diuretics
Beta blockers not effective
antihypertensive choice in diabetics with renal insufficiency/CHF:
ACE inhibitors
antihypertensive choice in exertional angina:
beta blocker
beta blockers are ineffective in:
“beta blockers bad in black men”
antihypertensive drugs to avoid in elderly are:
clonidine (alpha 2 agonist)
prazosin (alpha 1 antagonist)
cause orthostatics = falls
antihypertensive drugs to avoid in smokers, COPD:
beta blockers
antihypertensive drugs to avoid in renal insufficiency:
beta blockers and diuretics
antihypertensive drugs to avoid in diabetes, gout
thiazide diuretics
isolated right heart failure due to pulmonary disease (pulmonary HTN). It is characterized by RVH and eventually RVF. this defines
cor pulmonale
MCC of chronic cor pulmonale is
COPD
acute cor pulmonale is due to
extensive PE
alveolar hypoxia results from vasoconstriction of pulmonary vasculature.
clinical features of cor pulmonale include:
- Peripheral edema, liver enlargement and distended neck veins
- Loud P2 (normally A2 is louder) suggest pulmonary hypertension
- Low Sat.
- EKG shows right axis deviation
- High mean pulmonary artery pressure
tx for cor pulmonale
O2 to keep > 90%
diuretics
heart-lung transplant
right axis deviation on ekg is associated with
cor pulmonale
Primary pulmonary HTN is associated with a mean PA pressure of
> 25mmHg in absence of cardiac/lung dx
- poor prognosis
- unknown cause
Normal mean PA pressures are
12-16mmHg
Secondary Pulmonary HTN is more common. It’s frequently associated with:
- COPD (d/t SMOKING!)
- congenital Right to left shunt of pulm BF
- Increased resistance w/in pulm circulation d/t PE or hypoxic vasoconstriction
- polycythemia (increased blood viscosity)
- collagen diseases (SLE, Scleroderma)
secondary pulmonary HTN often leads to
right ventricular hypertorphy
secondary pulmonary HTN is associated with what phenomenon? what %?
10% with Raynaud’s Phenomenon
Acute pericarditis has many associated causes; however there is one cause secondary to MI. What is it and what happens?
Dressler’s Syndrome
-immune reaction against necrotic myocardium
Clinical and diagnostic findings with pericarditis:
o Pleuritic chest pain o Pericardial friction rub that occurs in systole and diastole o Pain often positional o Tachycardia o Diffuse ST segment elevation
the hallmark finding of pericarditis:
diffuse ST-segment elevation
tx for pericarditis includes:
o NSAID
o Ketorolac
o Codeine
o Steroid for non-responders
exudative pericardial effusion is always the result of
infection
the fluid of a pericardial effusion in cancer and TB will be
bloody
“bag of fluid” is a description of distant heart sounds heard in this disease
pericardial effusion
is there friction rub in pericardial effusions?
no - two pericardial layers are no longer opposed
CXR of pericardial effusion will show
globular shaped heart
Water Bottle Heart on CXR is diagnostic of
cardiac tamponade
pathophysiology of cardiac tamponade:
Cardiac ____ d/t increased pressure from _____ ___.
o Cardiac compression due to Increased pressure from pericardial fluid
o Impaired left ventricular filling (preload) and decrease in SV and CO
o Equalization of pressures (Swan) because all four chambers are subjected to the external pressure
Kussmaul’s sign and pulsus paradoxus are PE’s of this cardiac disease process
cardiac tamponade
- as well as diminished heart sounds
- hypotension
- JVP
- tachycardia
- hepatomegaly
- edema
Anesthetic considerations for surgical mgmt of cardiac tamponade:
Ketamine induction
increased IVF’s
avoid vasodilation and cardiac depression
“Heart in Shell” is the nickname for what cardiac condition?
constrictive pericarditis
-the heart becomes encased in a rigid, chronically inflamed, calcified pericardium
Kussmal’s sign =
is a paradoxical rise in jugular venous pressure (JVP) on inspiration, or a failure in the appropriate fall of the JVP with inspiration. It can be seen in some forms of heart disease and is usually indicative of limited right ventricular filling due to right heart dysfunction.
pericardial knock manifests with constrictive pericarditis. describe the cause of pericardial knock:
o As the ventricles fill, the distending ventricles “knocks” against the pericardium
treatment of constrictive pericarditis is
surgical stripping of pericardial shell
Type A aneurysms involve:
ascending aorta
Type B aneurysms do not.
MCC associated with AAA is
atherosclerosis
Other causes: genetics, HTN, injury, inflammation, Marfan’s, Ehlers-Danlos
Pulsatile abdominal mass, bruits, and sometimes hypotension are physical exam findings for
Abdominalaortic Aneurysm (AAA)
AAA rupture is associated with what s/s:
Grey turner’s sign
Cullen’s sign
CV Collapse –> emergent laparotomy
general repair measurement guidelines for AAA
repair if diameter > 5cm
b/c rupture risk 30% in 3 yrs
dissecting thoracicaortic aneurysms start from a tear in the
intima
-blood then seeps in between layers of vessels leading to medial layer destruction and the Double Barrel Aorta
Atherosclerosis is a disease of elastic arteries and
large and medium sized muscular arteries
name 4 risk factors of atherosclerosis:
- smoking
- DM
- HTN
- Hyperlipidemia
tell me the progression of atherosclerosis
“FPC”
Fatty streak (young age) –> proliferative plaque –> Complex Atheroma (middle age to elderly)
tell me location of atherosclerosis:
AA.CPCa
Abdominal Aorta> coronary artery > popliteal artery > carotid artery
Takayasu Arteritis
- vessels affected
- is
- highest at risk
- symptoms
- LARGE Vessel vasculitis
- Inflammation of aorta and major vessels; causes weak pulse
- Young, Asian women at highest risk
Symptoms:
pain in arm (carrying bags), angina/CHF, absent pulses, arterial bruits, BP different in each arm
Temporal Arteritits
- vessels affected
- is
- highest at risk
- symptoms
- LARGE vessel vasculitis
- Pathologically identical to Takayasu Arteritis; occurs in Temporal artery
- Over age of 50
Symptoms:
unilateral H/A, visual disturbance, jaw claudication (“sore”); may have tenderness over temporal artery and elevated ESR (>50mm//hr)
tx for temporal arteritis is
steroids
to prevent blindness
increased ESR (>50mm/hr) is associated with what systemic vasculitis?
temporal arterititis
this vasculitis is known as “smokers disease”
Buerger’s disease / “thromboangititis Obliterans”
Buerger’s disease (also known as thromboangiitis obliterans) affects blood vessels in the body, most commonly in the arms and legs. Blood vessels swell, which can prevent blood flow, causing clots to form. This can lead to pain, tissue damage, and even gangrene (the death or decay of body tissues).
This vasculitis effects what size arteries?
medium and small
Known as a triad of upper and lower airway and renal disease - glumerulonephritis.
what is this form of vasculitis? what size vessels are affected?
Wegner’s granulomatosis
small/ micro vessels
Granulomatosis with polyangiitis is an uncommon disorder that causes inflammation of the blood vessels in your nose, sinuses, throat, lungs and kidneys. Formerly called Wegener’s granulomatosis, this condition is one of a group of blood vessel disorders called vasculitis. It slows blood flow to some of your organs
Methotrexate, cyclophosphamide, and/or steroids may be used to treat this vessel disorder
wegner’s granulomatosis
Polyarteritis nodosa involves arteries of the:
Medium sized arteries in the:
Kidneys
Gut
SKin
**Microaneurysms on angiogram
common s/s of polyarteritis nodosa include:
fever, weight loss, malaise, abdominal pain, melena, headache, myalgia, hypertension and cutaneous erruption
TX with cyclophosphamide, and/or steroids
Kawasaki Disease
signature s/s =
affects =
Tx =
acute, self-limiting necrotizing vasculitis
- ASAIN population; Infants/Children
- Fever, conjunctivitis, “strawberry tongue”, desqumative rash
TX ASA and Immunoglobulins
DVT facts
arise from lower limbs
may –> PE
tx - anticoagulants; thrombolytic therapy
Protein C & S deficiency may put someone at risk for
DVT
“natural anticoagulants”
CAD is also known as
Ischemic Heart Disease
o Ischemia is defined as the state of insufficient O2 supply
o Supply can’t meet demand inadequate perfusion of heart
stable vs unstable angina
unstable - pain at rest (or without provoking cause)
new dramatic onset
in diabetic patients, how does CAD manifest?
silent ischemia - w/o pain in diabetics
third heart sound in CAD
bad sign
shows global ischemia
Cannon “a’ wave” is evidence of
arrhythmia
Diagnostics of CAD/ ischemia.
What is the gold standard in the first 6hrs?
blood test of choice during/after ischemia?
- gold standard = EKG
- Cardiac Troponin-I first 4hour to 7-10 days; CK-MB is test of choice in first 24 hrs POST MI
-LDH is elevated 2-7days post MI
ST Elevation on EKG =
transmural ischemia
Q waves on EKG =
transmural infarct
indications for cardiac cath include:
Suspicion of severe or extensive CAD
Marked positive stress test
Failure to respond to medical management
differential diagnosis for angina - CV related:
- aortic stenosis
- pericarditis
- Aortic dissection
differential diagnosis for angina - NON- CV related:
Esophageal disease e.g. reflux
PUD
Biliary disease e.g. gall stones
Musculoskeletal disease e.g. costochondritis
Pleurisy
Pulmonary infarction
Pneumothorax–> diminished breath sounds
treatment for unstable angina:
Hospitalization “ ROMI”
IV Nitroglycerine
Aspirin and anti-platelet therapy to prevent thrombus
Patients who don’t stabilize with medical therapy should undergo cardiac cath for revascularization
angina at rest that is associated with ST Segment elevation (hallmark) secondary to coronary artery spasm is known as:
Prinzmetal’s angina
TX with nitrates and CCB’s to tx vasospasm
this form of angina is associated with raynauds disease?
prinzmental’s angina
both associated with vasospasm
silent ischemia usually seen in
diabetics
– nitrates and CCB’s
• Nitrates relieve angina by
venodilation which decreases cardiac wall tension
• Ca++ channel blockers relieve angina by
decreasing afterload, HR and contractility
the most potent CCB in lowering HR and decreasing contractility
o Verapamil is
o Verapamil > Diltiazem>Nifedipine
What medication for tx of CAD
↓ HR, ↓BP, ↓contractility resulting ↓ O2 consumption
• Beta blockers:
o Most effective, useful in exercise induced ischemia. Avoid in bronchial spasm, CHF or bradycardia
what two medications reduce myocardial O2 demand
• Diuretics and ACE inhibitors
what reduces the risk of MI?
Low dose ASA
• Coronary revascularization—CABG improves survival in patient with (3)
o Left main coronary disease –>Left main=OR
o Triple vessel disease
o EF < 50%
success rate of angioplasty is what %?
80-90%
Acute MI clinical presentation:
- severe, persistent anginal pain > 30 mins
- associated symptoms : jaw/arm pain, SOB, fatigue, adrenergic symptoms
hypotension d/t HF
increased JVP
arrhythmias
S3 - Volume Overload = significant LV dysfunction
Tachycardia in the presentation of AMI may be due to
anxiety
pericarditis
pump failure
Bradycardia in the presentation of AMI may be due to
Inferior wall ischemia (RCA)
or Increased Vagal Tone
acute management of AMI is
“BOOMAR”
Bed rest, Oxygen, Opiate, (morphine) Monitoring, Anticoagulation, (thrombolysis) Reduce clot size
therapy required for first degree HB
rarely required
therapy required for second degree HB - mobitz type 1
Mobitz type I associated with ischemia at or ABOVE AV node and occurs with INFERIOR wall MI, rarely progresses to complete block.
Pacemaker is not indicated
therapy required for second degree HB - mobitz type 2
Mobitz type II due to ischemia BELOW the AV node; associated with ANTERIOR wall MI and often progresses to complete AV block.
Pacemaker is indicated.
Temporary pacemaker for
both RBBB & LBBB
Pacemaker for
Alternating bundle branch block
Bundle branch block with AV block / MOBITZ II
MCC of death (90%)
cardiac arrhythmia
Complications associated with AMI:
- cardiac arrhythmia
- post infarct ischemia (mc after non-Q wave MI)
- Pump Failure
- Cardiogenic shock (low BP; large infart - large risk of mortality)
- Rupture of ventricular free wall
- Papillary muscle rupture
- Fibrinous Pericarditis
- Dressler’s Syndrome
- LV mural thrombus
- RV infraction
rupture of ventricular free wall is a complication associated with MI. this results in:
interventricular septum rupture === Left to Right shunting
- occurs 4-10days post MI
- results in SHOCK and Cardiac Tamponade
*** Dressler’s Syndrome is an autoimmune phenomenon resulting in fibrinous pericarditis.
- what’s the timeframe of occurance?
- tx?
- 2-6weeks post MI
- low fever
- Tx: NSAIDS
RV Infarction occurs with ______ , due to occlusion of ___.
- should be suspected in patient with?
- TX?
Occurs w/ INFERIOR wall MI; due to occlusion of RCA.
-suspected in pt with INFERIOR wall MI that is HYPOtensive, increased JVP and CLEAR Lungs; ST elevation.
TX hypotension with FLUIDS to maintain right sided filling pressures
dilated cardiomyopathy associated with:
*MC form
- Low EF
- Ischemia (mcc)
- alcoholism / BeriBeri
- chemo agents
- LVH
- Nonspecific ST or T abn
- Sequellae (HIGH risk of PE, arrhythmias, MV or Tricuspid regurgitation)
“holiday heart syndrome”
alcohol acutely diminishes LV function
-5-10 yrs of heavy drinking
Peripartum cardiomypathy develops
- most cases are reversible
- just before and 3 mos after delivery
- is Autoimmune
diastolic dysfunction is the “hallmark” of
Restrictive Cardiomyopathy [MYOCARDIUM}
amyloidosis, hemochromoatosis “Iron Heart” are diseases that can cause what kind of cardiomyopathy?
restrictive cardiomyopathy
with restrictive cardiomyopathy; what happens to heart:
- stiff ventricle –> restrict ventricular filling = to hallmark of DIASTOLIC DYSFUNCTION
- cardiac size and fxn are normal
- atrial arrhythmias or AVB may occur
TX - CCB increase diastolic relaxaction and allow better filling
Hypertrophic Cardiomyopathy (aka: Idiopathic Hyptertrophic Subaortic Stenosis -IHSS)
Features:
- asymmetric Ventricular concentric hypertrophy with LV outflow Obstruction (b/w hypertorphied septum and MV leaflet)
- Diastolic dysfunctions d/t hypertrophied and stiff ventricles
- Increased LVEDP
IHSS effect on decreasing and increasing the obstruction
conditions enlarge the LV – increase in Preload and afterload seperate the septum and anterior leaflet of teh MV and DECREASE the obstruction
conditions that make the ventricle smaller; increases velocity of blood flow (dehydration; + ve inotrops) INCREASE obstruction
Factor increasing outflow obstruction (IHSS):
- increased contractility
- Increase HR
- DECREASE Preload (vol) or afterload
MCC of sudden death in young athletes is
IHSS / cardiomyopathy
preferred tx for IHSS
Beta blockers
CCB
Surgical excision of hypertrophied septum
spinal and epidural considerations for IHSS patients
o Spinal and epidural blocks are CONTRAINDICATED– will decrease preload and afterload
anesthesia considerations for IHSS:
- GIVE FLUID! avoid hypovolumia “FULL, FULL, FULL” increase PRELOAD
- Neo and alpha stimulants are ideal b/c they increase SVR w/out increasing contractility “UP, UP, UP” (increase afterload)
- reduce LV - aortic systolic pressure gradient
- Avoid decrease in LV afterload
- beta blockers to decrease contractility
- halothane is ideal gas - direct myocardial depressant but doesn’t decrease SVR
would you use fentanyl for pt with IHSS?
no use; does not depress myocardium or increase SVR
IHSS and Bernoulli’s theorem
-in regards to increased afterload (b/c a decrease in afterload worsens the obstruction)
Bernoulli’s principle: Within a horizontal flow of fluid, points of higher fluid speed will have less pressure than points of slower fluid speed.
