MI patients are classified based on their hemodynamic status:

1. Hemodynamically stable (mild). Treated with anti-ischemic drugs.
2. Hypotension without pulmonary edema. Treated with anti-ischemic + normal saline.
3. Pulmonary edema without hypotension. Treated with anti-ischemic + diuretics.
4. Pulmonary edema & hypotension (cardiogenic shock, severe). Treated with anti-ischemic + positive inotropic agents + ACEi + diuretics (even if the patient is severely hypotensive, we should give them diuretics).

An ischemic heart wall is hypokinetic. If it goes through MI, the infarcted segment of the heart becomes akinetic, then dyskinetic (moves in the opposite direction of the normal heart wall; if the normal wall contracts, the infarcted wall bulges out), leading finally to the formation of an aneurysm.

Aneurysm complications:
• Thrombus/embolus formation.
• Arrhythmia.
• Persistent ST-elevation.
• Cardiac wall rupture.

Heart failure (HF) can be a complication of MI because of cardiac remodelling.

The artery most commonly occluded in MI is the LAD (Left Anterior Descending). It leads to anterior MI.

Occlusion of the RCA (Right Coronary Artery) leads to inferior MI.

Occlusion of the PDA (Posterior Descending Artery) leads to posterior MI.

Occlusion of the circumflex artery leads to lateral MI.

Lifestyle factors are common contributors to resistant hypertension:

• Elderly patients, black patients, and those with CKD tend to be particularly salt sensitive.
• In an estimated 10% of adults with hypertension in the United States, the hypertension is due primarily to alcohol consump-tion.
• For every 10% increase in body weight, systolic BP increases by 6.5 mm Hg.

What's your dx?
@contactzero_bot

ها صدك

The patient is an old, thin woman with abdominal pain

أول ما شفت الأشعة ضربتلي صفنة داحاول أفتهم شديصير. من جهة هي تبدو كأنها gallstones ومكانها هو نفسه مكان المرارة بس من جهة ثانية شكلها عبالك حبوب كهوة وما يرهم يكون gallstones... مع ذلك سألت المُرافقة إذا الحجية عدها ألم ببطنها أو حصوة بالمرارة... المُرافقة افتهمت السالفة (على ما يبدو هالأشعة محيرة كم شخص قبلي وسائليها نفس الاسئلة) ف كالتلي أنّ الحجية عايفة السبحة بجيبها وما تقبل تعوفها ولهذا طالعة هيج.

الظاهر الردهة كلها طلعت تعرف بالسالفة، بحيث لما انداريت لكيت المريضة اللي كبالنا هم دتضحك وتكلي "والله الحجية عدها سوالف"

As for the abdominal pain, I forgot to even ask about it or take a proper hx tbh... I have seen enough medicine for the day

They are used to rule out stable angina. Theyshouldn't be used in low-risk patients because they have a high false-positive probability.
They induce ischemia by various ways and then detect it by ECG, echocardiography, or radionuclide imaging.

Stress tests can be divided into:

• Exercise stress test, most commonly using a treadmill.

• Pharmacological stress tests. They are used in patients who are unable to exercise or the exercise stress test is contraindicated (like in LBBB). They are further divided based on the drug being used into:

A. Positive inotropic/chronotropic drugs like dobutamine which is a B1-receptor agonist and simulates the heart physiology during exercise (in terms of increasing the heart contractility & rhythm).

B. Vasodilators like adenosine & regadenoson (adenosine analogue). They make heart ischemia manifest via a mechanism called coronary steal.

The idea is fairly simple: Adenosie and the likes of it specifically activate the A2A adenosine receptor in the coronary vessels which causes coronary vasodilation. In terms of blood flow, normal coronary vessels are up to 400% more responsive to the vasodilatory effect of adenosine than stenotic vessels. Therefore, they dilate & the blood flow increases in them. Meanwhile, atherosclerotic coronary vessels cannot dilate properly (because they are already maximally dilated) and blood flow is stolen from these narrowed coronary vessels to normal coronary vessels. This induces symptoms of ischemia, and perfusion defects appear in cardiac nuclear imaging or as ST-segment changes on the ECG.