Common types of emboli: An embolus is material that travels through the bloodstream and becomes lodged in a blood vessel, blocking blood flow. Common emboli include a dislodged thrombus, air, cholesterol crystals, fat droplets, and components of amniotic fluid.
| Type of embolization | Characteristic features |
| Air embolism | Seen in central venous catheterization; cardiac bypass; childbirth; trauma; head and neck surgery; acute cardiac failure; hypoxia, hypercapnia; right ventricular strain; dyspnea, chest pain, headache, confusion, arrhythmias, collapse |
| Amniotic fluid embolism | Amniotic fluid, fetal cells or hair embolize to pulmonary vessels; occur in labour, C sections; amnio-infusions etc; vasoactive and procoagulant products including platelet-activating factor, cytokines, bradykinin, thromboxane, leukotrienes, and arachidonic acid in amniotic fluid lead to an anaphylactoid reaction; DIC; acute dyspnea, tachypnea, circulatory collapse, cardiac arrest. |
| Fat embolism | Fat embolizes to capillaries, blocking microcirculation most commonly in the lungs, brain, skin, eyes, and heart; seen in long bone fractures, pancreatitis, liposuction, bone marrow transplant; elevated free fatty acids cause systemic inflammation, and fat globules released from bone marrow cause mechanical obstruction; respiratory distress, altered mental status, DIC, fever, petechial rash, ARDS; prevented by early operative fixation of long bone fracture |
| Cholesterol embolism or atheroembolism | Cholesterol embolizes from an atherosclerotic plaque in a large proximal artery to smaller distal arteries; symptoms result from ischemia due to occlusion and an inflammatory response; may be spontaneous or follow cardiac catheterization or surgery in or around the aorta; typically multiple small embolizations occur over time; blue toes, fever, malaise, fatigue, weight loss, livedo reticularis, end organ damage like renal failure, amaurosis fugax, hypereosinophilia, and Hollenhorst plaques on ophthalmoscopy are seen. |
Hypertension:
Hypertension is a sustained elevation of systolic and/or diastolic blood pressure. It is classified as follows:
Classification: Normal blood pressure
Classification: Elevated blood pressure
Classification: Stage 1 HT
Classification: Stage 2 HT
Risk of developing HT is increased in:
Blood pressure can be falsely elevated due to:
“White coat hypertension” refers to high blood pressure seen only in a medical setting or in the presence of medical staff.
If a non-hypertensive person has high BP readings during an office visit, BP should be measured outside the medical office using:
If BP is very high, if there are signs of end-organ damage, or if there are underlying conditions known to cause HT (such as chronic renal disease), then home and ambulatory monitoring is not essential, and diagnosis and treatment of HT can be started early.
Screening recommendations (in the absence of signs/symptoms or conditions predisposing to HT; screen more frequently if these risks are present):
HT may be primary or secondary.
Primary (essential) HT is the most common type and is idiopathic. Hemodynamic and vascular factors correlate with the BP components:
Mechanisms that may increase vascular tone include:
An increase in cardiac output and/or total peripheral resistance increases blood pressure.
Other contributors include:
Secondary HT can result from:
Drugs that can cause HT include corticosteroids, excess alcohol, OCPs, cocaine, licorice, etc.
Renovascular hypertension: Renovascular hypertension is hypertension caused by occlusive lesions in the renal arteries (renal artery stenosis). Reduced renal blood supply activates the renin-angiotensin-aldosterone system, leading to HT. Typically, more than 70-75% luminal narrowing of the renal artery is needed before renovascular HT develops.
Most common causes include:
Clinical situations that should raise suspicion of renal HT include:
Fibromuscular dysplasia of the renal arteries is typically seen in young females, sometimes during pregnancy. Smoking is a risk factor.
Presentation is with resistant HT. Findings include:
A “beaded” appearance of the renal artery is seen on angiography in fibromuscular dysplasia.
ACE inhibitors are contraindicated in bilateral renal artery stenosis.
Complications of HT: Long-standing, uncontrolled HT can cause LVH, heart failure, chronic renal disease, peripheral artery disease, stroke, IHD, retinopathy, aneurysms, and vascular dementia.
HT emergency and urgency: Hypertensive crisis (also called accelerated HT or malignant HT) is defined as an acute and critical increase of blood pressure > 180/110 mmHg. These terms have now been replaced by HT emergency and HT urgency, depending on the presence or absence of acute end-organ damage, respectively.
Examples of end-organ damage include heart failure, AMI, HT encephalopathy, aortic dissection, ICH, SAH, acute renal failure, unstable angina, etc.
Antidepressants, when taken along with MAOIs, can precipitate a HT crisis. Because MAOIs inhibit the breakdown of tyramine, patients taking them should avoid tyramine-containing foods and herbal supplements like St. John’s wort, ginseng, and yohimbine.
Hypertensive retinopathy: HT causes endothelial damage in retinal blood vessels, leading to sclerosis and vasoconstriction, which then causes retinopathy. It is aggravated by DM and smoking.
Key retinal findings and what they represent:
| Grade | Changes seen |
| Grade 1 | Arteriolar constriction only, AV nicking |
| Grade 2 | Constriction and sclerosis of arterioles, more severe AV nicking, copper wiring |
| Grade 3 | Hemorrhages and exudates seen, soft and hard exudates, silver wiring |
| Grade 4 | Papilledema, plus grade 3 findings |
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