The document provides a comprehensive overview of hypertensive crises and peripheral arterial diseases, detailing definitions, causes, diagnostics, and management strategies. It describes various conditions associated with elevated blood pressure, such as hypertensive emergencies and severe asymptomatic hypertension, as well as risk factors and symptoms of peripheral artery disease. The management section emphasizes the importance of individualized treatment plans and monitoring, along with specific considerations for acute conditions.

1. HYPERTENSIVE CRISES AND
PERIPHERAL ARTERIAL
DISEASES
MUTYABA MICHAEL SEBITOSI

2. Outline
• Definitions
• Hypertensive emergency
• Severe asymptomatic Hypertension
• Causes of hypertensive crisis
• Diagnostics
• Management
• Special Considerations
• Differential diagnosis
• Complications

3. Definitions
• Hypertensive Crisis: sudden severe elevation of blood
pressure above 180/120mmHg.
• Severe Hypertension: Term used broadly to define a very high
blood pressure (>180/120 mmHg)
• Hypertensive Emergency: Severe elevation in blood pressure
above 180/120 mmHg accompanied by acute life-threatening
end-organ damage.
• Severe Assymptomatic Hypertension: Severe elevation in
blood pressure above 180/120mmHg in absence of symptoms
or evidence of Acute end-organ damage.

4. • Malignant Hypertension: A subtype of hypertensive
emergency characterized by severely elevated blood pressure
accompanied by end-organ damage. Commonly papilledema.
• Accelerated Hypertension: Refers to subtype of hypertensive
emergency characterized by a recent significant increase over
baseline blood pressure with end-organ damage.
• Hypertensive Urgency: Other name for severe asymptomatic
hypertension

5. • Note: There is potential for end-organ damage even when the
BP is below the 180/110-120mmHg.

6. Severe asymptomatic HTN
• BP ≥180/120 without evidence of end-organ damage (may have
mild headache)
• Assess adherence to prior treatment before aggressively up-
titrating regimen to avoid overcorrection of BPs & hypotension
• Assess cause before treatment; commonly due to pain, anxiety,
urine retention, meds (e.g. steroids), OSA, nausea, withdrawal,
etc.

7. Hypertensive emergency
• Refers to a BP ≥180/120 mmHg with evidence of acute end-
organ damage.
• Rate of rise is more often more important than the actual BP.
This explains why patients with a prior diagnosis of
hypertension tolerate higher levels of BP without symptoms
compared to those presenting with hypertension for the first
time.
• There is a characteristic fibrinoid necrosis of the arterioles and
small arteries leading to the end organ damage.

8. End-organ damage
• Neurological: HTN encephalopathy (severe HA, seizure, AMS),
PRES, TIA, CVA (SAH, ICH)
• Occular: Retinopathy, Papilledema, Hemorrhage
• Respiratory: Pulmonary edema
• Cardiovascular: MI, Angina, Aortic dissection
• Hematological: Microangiopathic Hemolytic Anemia
• Renal: Acute Renal Failure, Hematuria, Proteinuria

9. •The most common clinical presentation of
hypertensive emergency are:
• Cerebral infarction (24.5%)
• Pulmonary Edema (22.5)
• Hypertensive Encephalopathy (16.3%)
• Congestive Heart Failure (12%)
• Less common presentations include intracranial hemorrhage,
Aortic Dissection and Ecclampsia

10. Causes of Hypertensive crisis
• Idiopathic
• Non-adherence to drugs
• Secondary hypertension causes including:
• Pregnancy
• Hyperthyroidism
• Pheochromocytoma
• Renal artery stenosis
• Use of cocaine or MAOIs
• Withdrawal of alcohol, beta-blockers, alpha stimulants

11. Diagnostics
• Physical examination
• Vitals: Elevated BP and Tachycardia
• General examination: Edema
• CVS: tachycardia, added sounds(S4) displaced apex beat due
to dilated Cardiomyopathy, Jugular venous distention
• Respiratory exam: Rales
• Opthalmologic exam: Nicking of blood vessels, Retinal
hemorrhages, Soft exudates and papilledema

12. Diagnostics (Labs)
• Complete Blood Count
• Electrolytes
• BUN
• LFTs
• RFTs
• Urinalysis
• TSH
• 24h Vanillylmadellic acid

13. Diagnostics: Imaging
• Chest radiograph: Cardial enlargement, pulmonary edema other
structures
• Transesophageal electrocardiography
• Renal angiography
• Electrocardiogram

14. Management: Severe Asymptomatic Hypertension
• Floor vs outpatient Management (with close follow up)
• ↓BP no more than 25-30% over hrs-days; then to goal as
outpatient.
• There is no evidence to support rapid lowering of BP in this case.
• If hospitalized for non-cardiac reason, worse outcomes with
intensifying anti-HTN immediately on admission
• Oral medication is preferred. IV or high-dose meds are avoided
due to increased risk for AKI, stroke and MI due to
hypoperfusion

15. • PO: start captopril, labetalol >> hydralazine (unpredict., reflex
tachy) & convert to long-acting before discharge OR start long-
acting agents

16. Management: Hypertensive Emergency
• Floor vs ICU
• Manage in the ICU if patient needs arterial line, anti hypertensive gtt
or if severe end organ damage.
• Continuous cardiac monitoring
• Frequent assessment of neurological status
• Monitoring fluid intake and output
• Excessive BP reduction will cause hypoperfusion. Thus:
• Reduce by max 25% within 1st hour and no lower than
160/100mmHg within 2-6 hours. Reduce to baseline over 24-48
hours.

17. Management: Hypertensive Emergency
• Start with short acting titratable IV agents, then transition to oral
agents on the floor or discharge.
• No single drug is recommeded, though IV: labetalol >>
hydralazine
• Rapid acting sublingual or oral medications (nitroglycerin and
captopril) may be used if there is no IV access.

20. Disease-process specific considerations
• Acute LV Failure with Pulmonary Edema
• Nitroglycerin OR Sodium Nitroprusside.
• Furosemide.
• Avoid hydralazine (increased cardiac work) and beta-blockers (decreased cardiac
contractility).
• Acute Coronary Syndromes
• Nitroglycerin OR Labetalol OR Esmolol.
• Avoid hydralazine (increased cardiac work).

21. Disease-process specific considerations
• Aortic Dissection
• Rapid HR reduction in first 10 minutes to <60.
• BP reduction to <120-140 mmHg in first 60 min
• ICU management due need for arterial line.
• Labetalol OR Esmolol OR Metoprolol OR Nitroglycerin OR Sodium Nitroprusside.
• Surgery consult
• Eclampsia/Pre-eclampsia
• Magnesium sulfate in eclampsia.
• Nifedipine OR Labetalol OR Hydralazine OR Methyldopa in pre-eclampsia.

22. Disease-process specific considerations
• Hypertensive Encephalopathy
• Diagnosis of exclusion after ruling out intracranial pathology.
• Labetalol OR Hydralazine.
• Avoid sodium nitroprusside if suspected ICP due to intracerebral shunting.
• Acute Ischemic Stroke
• Higher MAP essential to perfusion. BP should not be lowered acutely except at
extremes (some clinicians use >220/120). Gradual BP reduction should occur.
• Thrombolysis contraindicated with extreme hypertension due to risk of
bleeding. Lower BP to <185/110 pre-treatment and maintain <185/105
throughout treatment.
• Labetalol OR Hydralazine OR Enalapril often used.

23. Disease-process specific considerations
• Acute Intracranial Hemorrhage
• Systolic BP >220 mmHg can be harmful.
• Debate exists over target BP, <140 mmHg or <180 mmHg systolic often
used.
• Labetalol OR Esmolol OR Enalapril OR Phentolamine.

24. Management
• Ambulatory vital monitoring. IV monitoring may be neccesary
• Diet and Lifestyle modification
• Follow-up
• Patient education on warning signs

25. Differential Diagnosis
• Acute kidney injury
• Aortic coarctation
• Aortic dissection
• Chronic kidney disease
• Ecclampsia
• Hyperthyroidism
• Pheochromocytoma
• Renal artery stenosis
• Subarchnoid hemorrhage

26. Complications
• Renal Failure
• Vision loss
• Myocardial Infarction
• Stroke

27. Questions....?

28. Peripheral Arterial
Disease

29. Outline
• Definition
• Etiology
• Risk factors
• Presentation
• Diagnosis
• Management
• Acute Limb Ischemia

30. Definition
• PAD refers to tissue damage in the arms and legs arising from
a mismatch between blood supply relative to tissue metabolism
due to narrowing of the arteries.
• Peripheral artery disease is usually a sign of extensive
arteriosclerosis.
• The signature feature of PAD is claudication. Which refers to a
pain in the limb, normally the calves during walking. The papin
is normally relieved by rest.

31. Etiology
• Atherosclerosis.
• Swelling or irritation of blood vessels
• Injury/Trauma to the limbs
• Changes in muscles or ligaments
• Radiation exposure

32. Risk factors for PAD
Modifiable
• Smoking
• High blood pressure
• High cholesterol
• Diabetes
• Obesity
• Physical inactivity
Non-Modifiable
• Age
• Family history

33. Common symptoms of PAD
• Leg pain or cramping especially when walking:
• Classic claudication: reproducible exertional pain distal to occlusion,
relieved by rest.
• Numbness
• Coldness
• Sores
• Changes in skin color or teture
• Reduced or absent pulses in the limbs

34. Rutherford Classification

35. Diagnosis of PAD
• History
• Physical examination
• Checking local pulse
• Local examination of skin texture, temperature, hair or ulcers
• Labs
• Doppler Ultrasound
• MRA
• CTA
• Exercise testing: if high suspicion for PAD & normal resting ABIs

36. Doppler US findings

37. Management
• Optimize CV risk factors (e.g., HTN, DM, HLD, weight loss),
formal exercise program, high-intensity statin, smoking
cessation
• CLEVER-RCT: supervised exercise therapy is at least as
effective as stenting
• ERASE-RCT: supervised exercise therapy + revascularization
>exercise alone

38. Management
Ischemic ulcers
• Proper wound care (proper fitting breathable shoes,
Moisturising creams, Hygiene)
• Revascularization for appropriate healing depending on ABI

39. Management: Pharmacologic
Treatment is not as effective as CAD. Especially the use of
vasodilators.
Anti-platelets
• If symptomatic, low dose aspirin <300mg or clopidogrel 75mg
qd to decrease risk of MI, CVA and vascular death
• If asymptomatic, consider low dose aspirin.

40. Management
• Avoid Dual antiplatelet therapy (DAPT) unless clinically
indicated, usually post-revascularization.
• Anti-coagulation: rivaroxaban 2.5mg BID + Aspirin:decreases
adverse cardiac & limb events vs ASA alone . Use with caution
as this increases major bleeding, but no fatal bleeding in pts w/
stable PAD in study
• Thrombolysis: Streptokinase and Ralteplse are effective in
acute cases.

41. Management
• Cilostazol: Start 100mg BID. PDE3 inhibitor with vasodilatory
and anti-platelet effects. Adjunct for symptom relief refractory
to exercise therapy/smoking cessation. Use in combination with
ASA or anti platelet
• Only AHA/ACC recommended drug to increase exercise
capacity Contraindicated in HF. Ie helps relieve symptoms of
claudication.
• Angiogenic growth factors like VEGF and bFGF are being
studied. They are also been shown in reduce claudication.

42. Management
• Revascularisation:
• Endovascular repair (Percutaneous Transluminal Angioplasty
(PTA) vs stent vs Athrectomy) if threatened limb and/or severe
symptoms refractory to medical management. Assess benefit of
revascularization vs amputation.

43. Complications of PAD
• Tissue damage:
• Ulcers
• Gangrene
• Amputation secondary to critical limb ischemia
• Myocardial infarction
• Stroke

44. Acute Limb Ischemia
• Sudden decrease in limb perfusion threatening viability. It is the
most severe pattern of PAD. It develops over hours to days.
• It is a surgical emergency that requires immediate consultation
with vascular surgery
• Viable: no immediate threat of tissue loss; audible arterial
Doppler signal, intact motor/sensory
• Threatened: salvage requires prompt intervention; no audible
arterial Doppler signal, motor or sensory deficits

45. Etiologies
• Embolic (e.g., AF, endocarditis, proximal lesion)
• Thrombosis (e.g., atherosclerosis, APS, HITT)
• Trauma

46. Precipitating factors
• Dehydration
• Hypotension
• Abnormal posture (i.e. kneeling)
• Malignancy
• Hyperviscosity
• Hypercoagulability

47. Presentation
(6Ps)
• Pain
• Poikilothermia
• Pallor
• Pulselessness
• Paresthesia (unable to sense light touch)
• Paralysis

48. Diagnosis
• Pulse with Doppler ultrasonography
• Angiography

49. Treatment
• Urgent Vascular Surgery consult
• Anti-coagulation ± thrombolytic therapy
• Endovascular repair

50. Complications
• After treatment, monitor for:
• Reperfusion acidosis
• Hyperkalemia
• Myoglobinemia (AKI)
• Compartment syndrome
• Monitor for other complications like Stroke, MI etc

51. • Harrison’s Principles of Internal Medicine
• Up-to date
• Medscape

52. The end
• Questions???