Cardio SMLE review

Abdulrahman A. Alahmadi
TW: @Abdulrahman95AA
Ischemic heart disease
Reperfusion therapy

• PRIMARY PCI PREFERRED

• First medical contact to PCI time of 120 minutes
• Those with absolute contraindications to fibrinolysis.
• FIBRINOLYSIS PREFERRED
• patients in whom there is a long-anticipated delay (greater than
120 minutes) to primary PCI.
IHD mortality reduction:

1-Aspirin

2-Beta blocker

3-ACE inhibitors

4-Statin
Rapid overview: Management of ST-elevation myocardial infarction (STEMI) or non-
ST-elevation acute coronary syndrome (NSTEACS)

Initial assessment: Ischemic heart disease mainly diagnosis clinically

Consider the diagnosis in patients with chest discomfort, shortness of breath, or other suggestive symptoms. Women, older
adults, and patients with diabetes may have "atypical" presentations.

Obtain 12-lead ECG within 10 minutes of arrival; repeat every 10 to 15 minutes if initial ECG is nondiagnostic but clinical
suspicion remains high (initial ECG often not diagnostic).

1. STEMI: ST-segment elevations ≥1 mm (0.1 mV) in 2 anatomically contiguous leads or ≥2 mm (0.2 mV) in leads V2
and V3 or new left bundle branch block and presentation consistent with ACS. If ECG suspicious but not diagnostic,
consult cardiologist early. This diagnostic of acute coronary syndrome you have to start perfusion therapy no need for wait cardiac enzyme

2. Non-STEMI or unstable angina: ST-segment depressions or deep T-wave inversions without Q waves or possibly no ECG
changes.

Obtain emergency cardiology consultation for ACS patients with cardiogenic shock, left heart failure, or sustained
ventricular tachyarrhythmia.

Initial interventions:

Assess and stabilize airway, breathing, and circulation.

Attach cardiac and oxygen saturation monitors; provide supplemental oxygen as needed to maintain O 2 saturation >90%.
Establish IV access.

Treat sustained ventricular arrhythmia rapidly according to ACLS protocols.

Give aspirin 325 mg (nonenteric coated) to be chewed and swallowed (unless aortic dissection is being considered). If oral
administration is not feasible, give as rectal suppository.

Perform focused history and examination: Look for signs of hemodynamic compromise and left heart failure; determine
baseline neurologic function, particularly if "brinolytic therapy is to be given.

Obtain blood for cardiac biomarkers (troponin preferred), electrolytes, hematocrit/hemoglobin. Perform coagulation studies
for patients taking anticoagulants or as otherwise indicated (eg, known coagulopathy).

Give 3 sublingual nitroglycerin tablets (0.4 mg) 1 at a time, spaced 5 minutes apart, or 1 aerosol spray under tongue every 5
minutes for 3 doses if patient has persistent chest discomfort, hypertension, or signs of heart failure and there is no sign of
hemodynamic compromise (eg, right ventricular infarction) and no use of phosphodiesterase inhibitors (eg, for erectile
dysfunction); add IV nitroglycerin for persistent symptoms.

Treat left heart failure if present: Give afterload-reducing agent (eg, nitroglycerin sublingual tablet and/or IV drip at 40
mcg/minute provided no hypotension and no phosphodiesterase inhibitors [eg, for erectile dysfunction]; titrate drip up
quickly based on response); give loop diuretic (eg, intravenous furosemide); administer noninvasive positive pressure
ventilation (eg, BLPAP) to appropriate patients.

Give beta blocker (eg, metoprolol tartrate 25 mg orally) if no signs of heart failure and not at high risk for heart failure and
no signs of hemodynamic compromise, bradycardia, or severe reactive airway disease. If hypertensive, may initiate beta
blocker IV instead (eg, metoprolol tartrate 5 mg intravenous every 5 minutes for 3 doses as tolerated).

Morphine sulfate is indicated for chest discomfort refractory to nitrates and other antiischemic therapies. Give 2 to 4 mg
slow IV push every 5 to 15 minutes.

Start 80 mg of atorvastatin as early as possible and preferably before PCI in patients not on statin. If patient is taking a low-
to moderate-intensity statin, switch to atorvastatin 80 mg.

Acute management STEMI:

Select reperfusion strategy: Primary PCI strongly preferred, especially for patients with cardiogenic shock, heart failure, late
presentation, or contraindications to "brinolysis. Activate cardiac catheterization team as indicated. For patients with
symptoms of >12 hours, "brinolytic therapy is not indicated, but emergent PCI may be considered, particularly for patients
with evidence of ongoing ischemia or those at high risk of death.

Treat with "brinolysis if PCI unavailable within 120 minutes of !rst medical contact, symptoms <12 hours, and no
contraindications.*

Give oral antiplatelet therapy (in addition to aspirin) to all patients:

 1. Patients treated with !brinolytic therapy: Give clopidogrel loading dose 300 mg if age 75 years or less; if age over
75 years, give loading dose of 75 mg.

2. Patients treated with no reperfusion therapy: Give ticagrelor loading dose 180 mg.

3. Patients treated with primary PCI: Give ticagrelor loading dose of 180 mg or prasugrel loading dose of 60 mg (if no
contraindications: prior stroke or TIA, or relative contraindications for prasugrel such as those age 75 years or older,
weight less than 60 kg). For patients at high risk of bleeding or those for whom prasugrel or ticagrelor cannot be used,
we give clopidogrel 600 mg.

Give anticoagulant therapy to all patients:

1. For patients treated with primary PCI, we prefer UFH to bivalirudin. This recommendation assumes that patients will
receive a potent oral antiplatelet agent (ticagrelor or prasugrel), which we prefer to clopidogrel. For those patients who
receive clopidogrel, we prefer bivalirudin.

Dosing of UFH: An initial IV bolus of 50 to 70 units/kg up to a maximum of 5000 units. Additional heparin may
be given in the catheterization laboratory based on the results of ACT monitoring.
Dosing of bivalirudin: Initial bolus of 0.75 mg/kg IV followed by IV infusion of 1.75 mg/kg per hour; can be
discontinued after PCI.

2. For patients treated with !brinolysis, we prefer enoxaparin for patients not at high bleeding risk or fondaparinux for
those at high bleeding risk. For those patients in whom PCI is possible or likely after "brinolytic therapy, UFH is
reasonable.

Dosing of enoxaparin
Patients <75 years: Loading dose of 30 mg IV bolus followed by 1 mg/kg subcutaneously every 12 hours;
maximum of 100 mg for the "rst 2 subcutaneous doses. The "rst subcutaneous dose should be administered
with the IV bolus.
Dose adjustment for renal impairment (CrCl <30 mL/minute)*: Loading dose of 30 mg IV followed by 1
mg/kg subcutaneously every 24 hours. The "rst subcutaneous dose should be administered with the IV
bolus.
Patients ≥75 years: No IV loading dose. Administer 0.75 mg/kg subcutaneously every 12 hours; maximum of
75 mg for the "rst 2 doses.
Dose adjustment for renal impairment (CrCl <30 mL/minute)*: No IV loading dose. Administer 1 mg/kg
subcutaneously every 24 hours.
Supplemental IV bolus dose for patients who will receive PCI after >1 dose of therapeutic enoxaparin: 0.3
mg/kg if last enoxaparin dose was given 8 to 12 hours earlier; no supplemental IV dose if last enoxaparin dose
was within 8 hours; use UFH if last enoxaparin dose was more than 12 hours ago.
Dosing of UFH: IV bolus of 60 to 100 units/kg to a maximum of 4000 units, followed by an IV infusion of 12
units/kg per hour (maximum 1000 units per hour) adjusted to achieve a goal aPTT of approximately 50 to 70
seconds (1.5 to 2 times control).
Dosing of fondaparinux: 2.5 mg intravenously, followed by 2.5 mg subcutaneously every 24 hours. This drug
should be avoided in CrCl <30 mL/minute.

3. For patients not receiving reperfusion therapy, we use enoxaparin or UFH.

Dosing of enoxaparin: Dose same as for patients treated with "brinolysis (refer to section 2 above).
Dosing of UFH: IV bolus of 50 to 70 units/kg to a maximum of 5000 units, followed by an IV infusion of 12
units/kg per hour adjusted to achieve a goal aPTT of approximately 50 to 70 seconds (1.5 to 2 times control).

Acute management of unstable angina or non-STEMI:

Give antiplatelet therapy (in addition to aspirin) to all patients:

1. Patients not treated with an invasive approach: Give ticagrelor loading dose 180 mg. For these patients who are at
very high risk (eg, recurrent ischemic discomfort, dynamic ECG changes, or hemodynamic instability), consider adding a
GP IIb/IIIa inhibitor (either epti"batide or tiro"ban).

2. For patients managed with an invasive approach: Give ticagrelor loading dose of 180 mg at presentation. Prasugrel
loading dose of 60 mg may be used as an alternative if given after diagnostic coronary angiography.

For patients age 75 years or older, who weigh less than 60 kg, or with past stroke or TIA, ticagrelor or clopidogrel are
preferred to prasugrel. Clopidogrel may be given in a dose of 300 to 600 mg, but we prefer 600 mg. For patients
otherwise at high risk for bleeding due to prior hemorrhagic stroke, ongoing bleeding, bleeding diathesis, or clinically
relevant anemia or thrombocytopenia, clopidogrel 300 to 600 mg is an option.

For patients treated with an invasive approach and who receive bivalirudin, we do not recommend routinely giving a
GP IIb/IIIa inhibitor; for those patients treated with heparin and who are troponin-positive, we suggest adding a GP
IIb/IIIa inhibitor (either abciximab or epti"batide) given after diagnostic angiography. For those undergoing an
 invasive approach who are at very high risk (eg, recurrent ischemic discomfort, dynamic ECG changes, or
hemodynamic instability), we consider adding a GP IIb/IIIa inhibitor prior to diagnostic angiography (either
epti"batide or tiro"ban) or after diagnostic angiography (abciximab or epti"batide). Refer to text for dosing.

Give anticoagulant therapy in all patients:

1. For patients undergoing urgent catheterization (within 4 hours) or those managed with an early invasive
strategy (angiography within 4 to 48 hours), we use either heparin or bivalirudin. We prefer initiation of heparin in
the emergency department and a switch to bivalirudin in the catheterization laboratory.

Dosing of UFH: IV bolus of 60 to 70 units/kg to a maximum of 5000 units, followed by an IV infusion of 12

units/kg per hour adjusted to achieve a goal aPTT of approximately 50 to 70 seconds (1.5 to 2 times control).
Dose of bivalirudin: If bivalirudin is given in the emergency department, IV bolus of 0.1 mg/kg and an infusion
of 0.25 mg/kg per hour before angiography. If PCI is performed, an additional 0.5 mg/kg bolus is given and the
infusion rate is increased to 1.75 mg/kg per hour.

2. For patients receiving a noninvasive approach, we recommend either fondaparinux or enoxaparin.

Enoxaparin is an alternative to UFH for patients not undergoing an early invasive approach. No loading dose is
necessary. Dosing is 1 mg/kg subcutaneously every 12 hours. Dose adjustment for renal impairment (CrCl <30
mL/minute)*: 1 mg/kg subcutaneously every 24 hours.
Fondaparinux: 2.5 mg subcutaneously every 24 hours. This drug should be avoided in patients with a CrCl <30
mL/minute.

Other important considerations:

Cocaine-related ACS: Give benzodiazepines (eg, lorazepam 2 to 4 mg IV every 15 minutes or so) as needed to alleviate
symptoms; Give standard therapies (eg, aspirin, nitroglycerin) but do not give beta blockers.

Stop NSAID therapy if possible.

Correct any electrolyte abnormalities, especially hypokalemia and hypomagnesemia, which often occur together.

ECG: electrocardiogram; STEMI: ST-elevation myocardial infarction; ACS: acute coronary syndrome; IV: intravenous; ACLS: advanced
cardiac life support; BLPAP: bilevel positive airway pressure; PCI: percutaneous coronary intervention; TIA: transient ischemic attack;
UFH: unfractionated heparin; ACT: activated clotting time; CrCl: creatinine clearance estimated using Cockcroft-Gault equation (a
calculator is available in UpToDate); aPTT: activated partial thromboplastin time; GP: glycoprotein; NSAID: nonsteroidal
antiin#ammatory drug.

* Repeated doses of low molecular weight heparin in patients with renal insu$ciency may lead to accumulation and increased risk of bleeding to
varying degrees. By contrast, UFH is not dependent primarily upon renal function for clearance and may be a preferred option for patients with CrCl
<20 mL/minute, kidney failure, or receiving dialysis.

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Selecting a reperfusion strategy in patients with acute STEMI

STEMI: ST-elevation myocardial infarction; PCI: percutaneous coronary intervention; ED: emergency department; AMI: acute myocardial
infarction.

* This time includes all time required for transfer and other aspects of care until balloon dilation, thrombectomy, or other de!nitive percutaneous
intervention is performed.

¶ Refer to UpToDate content on selecting a reperfusion strategy in STEMI for more information on patients with late presentation.

Δ For patients who do not undergo either PCI or !brinolysis, refer to UpToDate content for a discussion of optimal medical management.

◊ The selection and use of a speci!c !brinolytic agent and the associated anticoagulant and antiplatelet therapies are discussed in UpToDate
content on !brinolysis in AMI.

§ Patients at high risk of reocclusion should undergo PCI sooner, while low-risk patients can undergo PCI later. More information on the use of
angiography and PCI after !brionlysis for the treatment of STEMI can be found in UpToDate.

¥ Refer to UpToDate content for the details on the absolute and relative contraindications to !brinolysis in patients with acute STEMI.

Graphic 138821 Version 1.0

© 2023 UpToDate, Inc. All rights reserved.

• 60 YO male patient k/c of DM and HTN presented to ER with neck
pain and sweating for one hour. He has a previous history of
recurrent chest pain which resolve spontaneously after resting.
ECG done and showed non-specific ST segment and T wave
changes. Troponin is normal. What is your next step?
A. Repeat troponin after 6 hours
B. Discharge the patient
C. Do stress ECG test
D. Give aspirin and nitroglycerin
 Hx subjection

nitroglycerincuenioritations
pisixon
BB
ace
If there bradycardia causing hemodynamic instability (hypotensive, or syncope or any changes in conscious) here first line : Iv
atropine sulphate before anything , we repeat 3 times if no improvement
minteriorm

hypotensionseconoorstosmonroia
sintervationsuonoon.io
Correction of bradycardia may improve and correct BP

If give alone, still heart rate dec maybe pt have heart blook bec MI affect conduction system AV
node second or third heart blook

Pt recent did surgery so this contraindication

Even if no contraindication i will choose PCI

ACEI not intinal

Antiplatelet

No role in ST depression Unexplaine palpation with Nomal ecg is holter ecg monitor to know causes bec maybe have
arrhythmia but not appear in normal ecg may be paroxysmal SVT or paroxysmal AF

ACEI dec mortality but not indicators in all ischemic heart except if have hypertension or heart failure or start after intinal
management after pt hospitalize and finish PCI or reprefusion therapy then well be intinally and optimally medical management

Once suspect pt have acute coronary syndrome but no suspicion of aortic dissection give aspirin
Pt not in active chest pain so = Well not have depressed St = not have any ECG change

Pt now not have chest pain

Here pt ongoing chest pain

ongoing ischemia= Ecg change
= acute coronary syndrome
Or if there PCI ‫اختاره‬

aowatrmusonotonstabnansinanaee.esonaraicani Any pt do stent or PCI

Any pt acuteshould
coronary
notsyndrome
stoped special after PCI stating
should be give aspirin and clopidogrel
antiplatelet (asprin and
criptropril
AF never stop anticoagulant

Pt have inferior MI

Less than 135 systolic, or 130/90

Most important , and HbA1c should be less than7%

No evidence to have to increasing by intervantion

Massimino.mg nssutsin
Execration pain not MI bec, MI Pain
ongoing chest pain, pt when come
still have pain and last 30min
Not significant

Presentation equivalent angina but pt present by SOB not chest pain and this common with DM

Bec any pt have previous hx of ACS should start lipid lowering (first line atorvstatin)

Second line of lowering lipid medication

Presention may be ACI maybe not, here case intermittent

May be second Troponin well be high

Contraindications with pt have chest pain

ARRYTHMIA
 Approach
A-fib/A-flutter
Stable Unstable

BB (CCB if contraindicated,
Electrical cardioversion
digoxin if in DHF)
 0= no anticoagulation needed
1= consider anticoagulation
2 or more = DOACs or warfarin
DOACs are preferred over warfarin in all cases
Sever mitral stenosis

except in valvular AFib or in patients with

prosthetic valve
 Approach
SVT
Stable Unstable

Vagal maneuver (carotid

Electrical cardioversion
massage, Valsalva)

failed

IV adenosine
 Hyperthyroidism

For rate control and symptomatic control of hyoerthyrodisum and Thyrotoxicosis

If CHA2 score :
Desading, SOB, crackles, • In male 1 or more : anticoagulants for
life
• If female 2 or more : anticoagulants
for life
If pt is in acute heart failure: desading, requires O2, SOB, orthopnea, PND = acute Decompensated heart failure Even if no no AF now and rhythm
control no change bec may be in
anytime sudden paradoxical AF

is contraindication to give in acute Decompensated heart failure

Bradycadia + chest pain

If heart rate 40 or 37 + no symptom + pt stable = conservative

Any pt come with tachycardia more than 200 it’s SVT narrow
complex (come from atrial) if until proven otherwise

sut stablecnoangianohypotensionnosyncope

Used in Heart failure Decompensated Only.

here pt Heart failure + asymptomatic + stable pt

Management for pt Ventricular fibrillation or pt with pulsesless Ventricular tachycardia

Pt unstable (hypotension or syncope) having SVT management should be electric Cardioversion same atrial fluter and atrial fibrillation

in
symptombradycardia

If pt Bradycardia caused hemodynamic unstablity

Pt AF May be give no anticoagulation or give anticoagulant (warfarin or oral

anticoagulants (as apixaban or rivaroxban or dabigatran) only

no
role
norole
Congestive heart failure
 upwee.I.o.ee
walking
as amigos us
d
CHF mortality reduction:

1-ACE inhibitors

2-Beta blocker

3-Spironolactone
 If pt AF , Decompensated heart failure • Pt in ACEI and have dry cough? Change medication to ARBs (Sartan)
• Pt can’t tolerate ACEI or ARBs bec have hypokaemia or hypotension when he
taken this medication the alternative is Hydralazine/nitrate

Dec less ordinary activity

This pt is controlled heart failure

But this pt not Decompensated heart failure required diuretic

He has heart failure and take ACEI only next step should add BB

When stop ACEI in pt with AKI ? If come baseline creatinine and after 3
months and more than percentage 30% of increasing is …. ? Stop ACEI

Never change thiazides to furosemide bec pt already have hypertension and taken thiazides for indication

Dehydration pt , prerenal AKI

Bec pt heart failure

Pt overload
= acute pulmonary edema

Decompensated heart failure, may be right heart failure then become Decompensated heart failure

Pt not improved by oral diuretics so you have to give iv diuretics (iv lasix)

Second step if not improved after iv diuretic and still symptomic

We give first BB then spirainolactone, and here pt Decompensated heart failure

Here pt asymptomatic, not Decompensated, no problem only EF 40% we well start ACEI = heart failure with reduce EF
stage
Pt here not Decompensated heart failure ( no SOB, no ascites, no crackles)
Pt here hypotension shock cause prerenal AKI = tx iv fluid

Bec pt acute heart failure

Decompensated

No Decompensated No symptomatic

If EF become 40 and less symptomatic or not symptomatic start ACEI

then after 2 week start BB even no change in symptomatic after many
week start Spironolactone
Hypertension
HTN

• Choice of antihypertensive drug:

• Non-African American patients: calcium channel blocker (CCB) is preferred in old
patients )< 55 YO), while angiotensin-converting enzyme inhibitor (ACE-I) is
preferred in young patients )> 55 YO).
• African American patients: thiazide-type diuretic or CCB
• HTN + DM = ACEI
• HTN + CKD = ACEI
• HTN + CHF or CAD = ACEI
• Essential tremor or Hyperthyroidism or Migraine + HTN = Beta blocker
• Beta blockers should not be used as a 1st line except in case of CAD
HTN
Labetalol
Uncontrolled asthma

Methydopa
 If pt preeclampsia: first choice is magnesium sulfate

Pt DM should start ACEI

CKD

CKD not AKI

ACEI

CCB ARBs

Thiazides
Thiazides
Weak Anti-hypertension , we may be use as 4 line

ACEI stop bec cause hyperkalemia

We Stop ACEI in AKI:
• Should stop ACEI If increasing creatinine above 30% from baseline

s
In this case : 1.5 - 1.2 = 0.3/1.2 =0.25 *100= 25% this increasing not
significant to stop ACEI but here we stop bec Potassium high

Dry cough

Gold standard for diagnosis hypertension

We not start medication first thing we start lifestyle modification and even we need to confirm diagnosis

Not recommended

More available to measure in home, but need at least 12 measurement

‫ونحسب متوسطها‬
Infective endocarditis
 Most common causative organisms in infective endocarditis

IV drug abusers
Prosthetic valves Native valves
(right side valves)

Less more
than than
60 60
days days

staph aureus Strep. Viridans Strep. Viridans Staph aureus

Extracardiac manifestations of IE

• Peripheral embolic and immunologic phenomena seen in only 5–10% of patients.

• Petechiae, especially splinter hemorrhages (hemorrhages underneath fingernails)
• Janeway lesions :small, nontender, erythematous macules on palms and soles
• Osler nodes: painful nodules on pads of the fingers caused by immune complex
deposition
• Roth spots: round retinal hemorrhages with pale centers
• Emboli to intraabdominal organs
• Acute kidney injury
• Splenomegaly and possible LUQ pain
A • Neurological manifestations (e.g., seizures, paresis): due to septic embolic stroke,
hemorrhage, meningitis, encephalitis, and/or abscess
• Pulmonary manifestations: caused by septic emboli resulting from tricuspid valve
involvement
 Infective endocarditis prophylaxis

• Indications: • Procedures:

1. Previous Hx of IE. 1. Dental work.

2. Unrepaired cyanotic congenital 2. Respiratory procedure involving
heart disease. incision of respiratory mucosa
3. Prosthetic heart valves. (tonsillectomy, adenoidectomy).
3. Skin procedure (surgical procedure
involving infected skin or
musculoskeletal structure.

Drug of choice: Oral Amoxicillin

IE:
Pt have vagitaion
New onset murmur

vegetation is fibrin and platelets and bacteria come on surfaces of valve , vegetation may have
embolizatiom and clot have the organism and go to brain or pulmo

Prophylaxis for skin or respiratory or dental surgery + he prosthetic heart valve

stroke
s epsis

Risk factor of infective endocarditis in Congenital heart disease:

• VSD
• Aortic stenosis
• PDA
• Pulmonic stenosis
Valvular heart disease
 Aortic stenosis treatment
• Indications for Aortic valve replacement:
1. Symptomatic AS (syncope, angina, SOB).
2. Asymptomatic patients with left ventricular ejection fraction (LVEF) <50 percent.
3. Patient with severe aortic stenosis going for other cardiac surgery.
 Once pt symptoms SAD (Syncope,Angina, Dyspnea) = one of this symptoms should valve replacement

Ef

Any pt have valve disease + symptoms of heart failure or angina + syncope: should do surgery valves replacement
Pericardial diseases
• Cardiac tamponade • Constrictive pericarditis
1. Acute presentation. 1. Chronic presentation.
2. Hypotension. 2. No hypotension.
3. Muffled quiet heart sound. 3. Normal heart sound.
4. JVP waves: prominent X & absent Y. 4. JVP waves: prominent X & Y.
NexstepEcho

Cardiac tamponade diagnosis by ECHO then pericardiocentesis

If ask what is next step

Shock
Cardiac index high = septic shock

Backward pressure inc inside heart

PCWP low bec low pressure so no
then back to pulmonary circulation
volume in circulation and heart and
cause pulmonary edema
pulmonary circulation
So high PCWP

Bec vasoconstriction as response to hypotension

 If high COP

Pneumothorax, cardiac tamponade: shock obstruction outflows left ventricle.

No exposure for allergy

Cold extremities

Cold extremities

When use rifampicin stimulates enzymes increases metabolism in liver so need inc dose some drugs
Syncope
 Approach to syncope
• Typical vasovagal syncope (preceded by symptoms) + normal ECG>>>
Reassurance and education.
• Situational syncope (with coughing, micturition) + normal ECG >>> Reassurance
and education.
• Recurrent unexplained syncope>>> Tilt table testing + Holter monitoring.
• Syncope + murmur or abnormal ECG>>> ECHO.
 Situational syncope

vasovagal syncope

Should be cause of syncope is cardiac sources clear (pt have murmurs, ECG abnormalities, family hx of early cardiac death
PERIPHERAL ARTERY DISEASE
 Index :
• Less than 0.9 : confirm ischemia
• Less than 0.4 : critical ischemia need immediately start heparin

Confirm with ankle brachial

Absent pulse Start heparin
index

Angiography with
revascularization CT angiography
(definitive)
 = lower limb ischemia (present as intermittent claudication)

Risk factor control (asprin)

Whats is most important step In Peripheral artery disease ? smoking cessation
What is best way to prevent cardiovascular is aspirin

mostaccuratetest
Inject contrast and do CT: we see blood vessel and see if there occlusion, good way to visualize vascular anatomy

This diagnostic and therapeutic

Bilateral

After MI + Unilateral limb , sudden

This is arterial so immediately start anticoagulantion

Imagining just for confirme

Do prevent ant further thrombosis or occlusion, ‫عشان اتاكد ما في حالة حتصير اسوء‬

= angio
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