Acute Coronary Syndrome & HTN

Question 1

Describe the Acute Coronary Syndrome Cascade

Answer 1

Unstable Angina worsens into NSTEMI which worsted into STEMI

Question 2

What causes decompensation from Unstable Angina to STEMI?

Answer 2

Increasing Ischemia starves the heart muscle of O2 and eventually there is an infarction, represented on the EKG as ST Elevation as electricity finds the longer route around necrotic tissue.

Question 3

Describe Non-Stentable Coronary Dz

Answer 3

Essentially this is STABLE ANGINA

Coronary Artery Occlusion doesn’t exceed 50%

The Risk/Benefit Ratio does not favor Stenting yet as Lifestyle Modifications, Weight Loss, Stopping Smokine, Nitroglycerine and Exercise can freeze the damage at this manageable level.

Question 4

What is Stentable Disease

Answer 4

All the Acute Coronary Syndromes are settable:

Unstable Angina
NSTEMI
STEMI

STEMI is URGENT, needs PCI asap, go directly from the scene to the cath lab

NSTEMI may have more time, try to stabilize and get to cath lab within 24 hrs

Unstable Angina can also be stabilized and cathed by appointment

Question 5

Describe Tropinin Levels and ST Elevations in the different phases of Acute Coronary Syndrome

Answer 5

Negative Troponins and no ST-Elevations in UnStable Angina

Positive Troponins (after 3 hrs) but no ST-Elevations in NSTEMI

Positive Troponins (after 3 hrs) AND ST-Elevations in STEMI. Elevations may precede Troponin rise here.

Question 6

Stable vs UnStable Angina

Answer 6

Stable Angina is caused by exertion and relieved by rest or sublingual Nitroglycerine

UnStable Angina is present even at rest, exertion may be altogether too painful, and it is NOT relieved by sublingual Nitroglycerine

Question 7

Troponins vs CKMB

Answer 7

Both rise within 3 hrs of damage to heart muscle but Troponin is 100% cardio specific whereas CKMB, while more cardiospecific than CK, may still rise on damage to skeletal muscle.

Troponins rise as early as 3 hrs after damage, they peak 18-24hrs after Damage BUT… the don’t return to baseline for 10 - 14 days after MI

CKMB rises 4 hours after damage, peaks 10-24 hrs BUT… CKMB returns to baseline in 48 - 72 hrs whereas Troponins take 10-14 days - so if there is another MI 3+ days after the first, which is common, CKMB may show that second rise better than Troponins, which may still be too elevated to show a second rise.

Question 8

What is the DEFINITIVE test for Acute Coronary Syndrome

Answer 8

Coronary Catheterization, aka:
Angiography
Angiogram
PCI, percutaneous coronary intervention
is a cath wherein a blockage is cleared
and usually stented.

This is the ONLY test that actually SHOWS a blockage.

Question 9

Describe grades of ischemia/infarction amongst the three levels of Acute Coronary Syndrome

Answer 9

50-60% occluded = Unstable Angina. Ischemia, No Infarction,

60-80% occluded = NSTEMI. This can be a complete occlusion of a minor coronary artery or a partial occlusion of a major coronary artery. NSTEMI can even be a partial wall infarction.

80-100% = STEMI Full occlusion of a major coronary artery. Usually a TRANSMURAL infarction.

Question 10

Why use ECHO in MI?

Answer 10

Echo can visualize the heart muscle and show you if part of the wall is not contracting (necrosis). You can measure ejection fraction with ECHO too. It is really a before or after sort of test, to determine risk of MI or the extent of damage.

During an attack you might use Trans Esophageal Echo to see if there were any blood clots developing. This is done in AFIB to clear the pt for cardioversion by scanning the little atrial extensions for clots.

Question 11

Name the 3 main responses to endothelial injury anywhere in the body :

Now describe which medications we give in Acute Coronary Syndrome to disrupt each response:

Answer 11

1) Vasoconstriction - shut down the leak
2) Platelets Adhere to the wound and then to each other
3) Sticky Platelets call out the Coagulation Cascade, activating factors that will eventually make the platelet plug a permanent seal of the leak.

Nitroglycerine disrupts Vasoconstriction, keeping the coronary arteries as open as they can be. Nitroglycerin is standard Rx for all stages of ACS

Aspirin, Plavix and Abciximab are all “Anti-Platelet” drugs that interfere with Platelet adherence to endothelium and to one another.
Aspirin inhibits the COX bind site
Plavix inhibits the ADH bind site
Abciximab binds up the Glycoprotein
IIb/IIIa receptor on platelets.

Heparin is an “ANTICOAGULANT” it disrupts the Coagulation Cascade by binding up THROMBIN and preventing activation of Fibrinogen to Fibrin.

tPA, tissue plasminogen activator (Altaplase, Tenecteplase are recombinant tPA replacing streptokinase) is an enzyme that catalyzes plasminogen’s activation to plasmin. Plasmin breaks down fibrin strands and dismantles the CLOT

Question 12

ST Depressions and T-Wave Inversions on the EKG indicate:

Answer 12

Ischemia

Question 13

ST Elevations and Q-Waves on the EKG indicate:

Answer 13

Infartion

Question 14

Significance of the TP Segment?

Answer 14

It is the baseline by which you measure Elevations and/or Depressions

Question 15

TIMI SCORE evaluates what?

Answer 15

The RISK of Unstable Angina and/or NSTEMI becoming STEMI and/or causing death IN THE NEXT 14 DAYS.

On a scale of 1-6 with 1 being lowest mortality risk and 6 being over 40% risk IF NO ACTION IS TAKEN.

It helps evaluate the urgency with which to get the patient to the cath lab.

Question 16

TIMI PNEUMONIC?

Answer 16

AMERICA: 1 Point each

A- AGE over 65
M- MARKERS cardiac markers elevated
E- EKG, st elevations on EKG
R- Risk Factors 3 or more they get 1pt
I- Ischemia 2+ Anginic events in past 24 hrs
C- CAD: prior coronary stenosis of over 50%
A- Aspirin, pT has taken aspirin in last 7 days

Risk factors for “R” include:

 - Age over 45 male, over 55 female
- CAD in 1st Degree Relative
- HTN
- Hyperlipidemia
- Smoking
- Diabetes    - Obesity/Metabolic Syndrome

Question 17

Hypotension during MI, think:

Answer 17

Right Coronary Artery blockage

The Right Ventricle’s systole rather sets the volume for the entire heart, whatever it sends out comes back to the left ventricle and out to the body so if it is unable to completely fill or efficiently push, there will not be enough volume to fill the pipes.

Question 18

How to stop a seizure:

Answer 18

Lorazapam or Diazepam (IV or IM) or Nasal Midazolam spray or Rectal Diazepam suppository.

give O2 and assist respirations if possible, place in recovery position to prevent vomit aspiration

Question 19

Once you control the seizure, what is possibly the most important diagnostic test you can do to find the underlying cause?

Answer 19

EKG - Seizures occur during VTACH when the brain is not supplied with enough O2.

Hook your seizing/post-dictal patient up as soon as possible and get a 12-lead.

Next do a full medication check, if possible, if no family in ER, to a tox screen and a CBC, CMP

What the heck, get a wave form capnography nasal canula on this pt with 2-4 L of O2, just to ensure respiration is not compromised.

Question 20

If you determine your seizure patient IS indeed having an MI, which coronary artery do you think is blocked?

Answer 20

Right Coronary artery

In the ER, this might make you leery about given Morphine as it can really tank BP in a Right Sided MI/failure or in an inferior MI.

Regardless of suspected side, you’re going to follow ACLS protocols and treat the rhythm or, if its just an NSTEMI/STEMI, you’ll stabilize and get them to the cath lab for PCI, THEN it will matter where the blockage is.

Question 21

Acute Coronary Syndrome ER Rx:

Answer 21

1) Aspirin 325 mg chewed
2) O2 high flow - get a wave form canula on under the mask and start monitoring CO2
3) 300mg Plavix as soon as IV access available.
4) Nitroglycerine IV 5mcg/min q3-5min up to 20mcg For pain if SBp is over 100. Have a second large bore IV ready to run in NS in case Bp tanks.
4) Morphine - If Nitro doesn’t relieve pain, you can give Morphine 2-4mg IV every 5-15 minutes, monitor Bp and be ready to resuscitate fluids
5) If Bp and/or rate are high (140/90 or well over 100) consider Diltiazem or Verapamil. Calcium Blockers instead of Beta Blockers.
6) Heparin: Anti-Thrombin 60mg/Kg bolus (max 4000 units) then a 12-15 mg/kg/hr drip. Goal is PTT of 50-70 seconds so ORDER serial PTTs
7) If pt has ST-Elevations and will be on the table in the cath lab within the hour, you can give Abciximab (ReOpro) a GP IIa/IIIb receptor inhibitor (super duper anti platelet with short half life)

Question 22

When might you not give Morphine in MI?

Answer 22

In a Right Sided MI (I, V1 & V2) or in an inferior MI (I, IIII, aVF)

Bp may seriously tank. You can still give it if needed, but be ready to run in enough fluid to fix Bp and make sure there wasn’t pulmonary edema to start as all that fluid can worsen it.

Question 23

Indications for CABG vs PCI

Answer 23

3 Vessel Occlusion

Question 24

MI vs Cardiac Arrest

Answer 24

MI: Pt HAS a PULSE
Pain, ST elevations or depressions
Not YET in VT, VF, PEA or Asystole
THIS IS VERY SALVAGABLE
MONA for MI

Arrest: Yikes! You are past MI and this is much less salvageable unless high quality CPR & care are immediately available. Pt is likely pulseless or close to it. SHOCK, Epi, Vasopressin & Amiodarone for Arrest.

Question 25

Hypertensive EMergency vs Hypertensive Urgency

Answer 25

This is a continuum. In Hypertensive Urgency we do NOT have end organ damage YET even though Bps may be in the 18- - 220 + range.

Hypertensive Emergency sees the same Bp range but WITH End organ damage:
-Papillodema (check that FIRST! It is Brain
Swelling!)
-Stroke
-Intracranial Hemorrhage/burst aneurysm
Blood in the eye? Severe HA, LOC
Alt Ment Status? Depressed Respir
ations? Coma?
-Aortic Dissection
-Pulmonary/Ankle Edema and Heart Failure
-Hematuria (if cathed, is urine pink? Foamy?)

Question 26

If you have pulmonary edema in the setting of Acute MI, use

Answer 26

Nitroglycerine. It decreases venous return and gives a tired heart a br

Question 27

In Aortic Dissection use:

Answer 27

IV Lobetalol to bring down Bp fast

also in HTN Emergency

Question 28

MAP =

Answer 28

(2*DP) + SP/ 3

(2D + S) / 3

Question 29

In Hypertensive Emergecy and Urgency reduce MAP by 25% in how much time?

Answer 29

HTN Emergency: In 1-2 Hrs, slowly thereafter
Use Lobetalol IV - Admit this patient

HTN Urgency: In 24 hrs, slowly thereafter
Use Metoprolol Oral, start it in office. Keep
Pt in office until Bp has responded to
the beta blocker

Question 30

How do you bring down Bp in Subarachnoid Hemorrhage?

Answer 30

Use Nifedapine

Beta Blockers, Diltiazem and Verapamil are too strong.

Question 31

Nifedapine vs Diltiazem vs Verapamil

Answer 31

All three suppress SA function but their hypotensive effects on the peripheral vasculature rather negate their rate reduction action at SA.

Diltiazem Verapamil prolong refractory periods in the AV Node, slowing conduction. This is great for Atrial Tachycardias in that fewer beats get through to the ventricles. Not good at all in heart block. Verapamil is the stronger.

Nifedipine doesn’t affect AV nodal conduction and its hypotensive/dilation effect exceeds that of both Diltiazem and Verapamil. Nifedipine can dilate coronary arteries without blocking the AV node so is the better choice for CAD with heart block

Also the choice for Prinzmetals Angina and Intracerebral bleeding - haven’t yet figured them out.