Revision sheet: Veterinary Hypertension Management

📋 Course Outline

1. Systemic hypertension and causes
2. Target organ damage and clinical signs
3. When to start treatment
4. Dog antihypertensive therapy
5. Cat antihypertensive therapy
6. Adverse effects and RAAS activation

📖 1. Systemic hypertension and causes

🔑 Key Concepts & Definitions

• Systemic hypertension : Systemic hypertension is persistently elevated pressure in systemic arteries that raises the risk of target organ damage.
• Primary hypertension : Primary (essential) hypertension is idiopathic hypertension that is common in humans but extremely rare in dogs and cats.
• Secondary hypertension : Secondary hypertension results from a specific underlying disease that drives the elevated blood pressure.
• Target organ damage risk systems : The ocular, renal, cardiac, and neurologic systems are among the most vulnerable targets for organ damage.

📝 Essential Points

• Chronic renal disease is the most common associated disease with systemic hypertension.
• The treatment goal is to reduce blood pressure below 160 mm Hg to prevent lesions.
• Diabetes mellitus is linked to systemic hypertension in 46% to 55% of dogs and in less than 2% of cats.

💡 Memory Hook

Think 160 as the “treat-under” number that prevents lesions.

📖 2. Target organ damage and clinical signs

🔑 Key Concepts & Definitions

• Target organ damage (TOD) : Target organ damage is injury to body systems caused by sustained high systemic arterial pressure.
• Hypertensive retinopathy : Hypertensive retinopathy is a vision-related manifestation of high blood pressure affecting the retina.
• Azotemia and proteinuria : Azotemia and proteinuria are kidney-related signs that can accompany hypertensive target organ damage.
• Chromaffin cell tumor : A pheochromocytoma is a rare adrenal medulla tumor originating from chromaffin cells.

📝 Essential Points

• Common causes associated with TOD include kidney failure, primary hyperaldosteronism, hyperthyroidism, hyperadrenocorticism, diabetes mellitus, and pheochromocytoma.
• Typical signs include hypertensive retinopathy, a new cardiac murmur, azotemia, proteinuria, behavioral or consciousness changes, and seizures in severe cases.

💡 Memory Hook

Kidney + eye + brain: think retinopathy, azotemia/proteinuria, behavior/seizures.

📖 3. When to start treatment

🔑 Key Concepts & Definitions

• Life-long antihypertensive treatment : When systemic hypertension is associated with chronic renal disease, antihypertensive therapy is needed long term with periodic dose adjustments.
• Active TOD : Active target organ damage refers to current signs of injury from high blood pressure.

📝 Essential Points

• Treatment is initiated when SBP is >160 mm Hg with active TOD.
• Treatment is also initiated when persistent hypertension is confirmed several times with SBP >160 mm Hg.
• Recheck timing depends on presence of overt or new TOD: 1-3 days if ongoing TOD, otherwise 7-10 days.

💡 Memory Hook

Start if SBP >160 AND either TOD is active or it’s confirmed repeatedly.

📖 4. Dog antihypertensive therapy

🔑 Key Concepts & Definitions

• ACE inhibitor monotherapy : In dogs, ACE inhibitors can be used as the initial therapy and may be given alone when appropriate.
• Enalapril : Enalapril is an ACE inhibitor used in dogs for systemic hypertension treatment.
• Benazepril : Benazepril is an ACE inhibitor used in dogs for systemic hypertension treatment.
• Telmisartan : Telmisartan is an angiotensin II receptor blocker used in dogs to lower blood pressure and, in some situations, proteinuria.

📝 Essential Points

• ACE inhibitors used in dogs include enalapril or benazepril at 0.5–2 mg/kg given orally twice daily.
• If there is concurrent protein-losing nephropathy, combining an ACE inhibitor with telmisartan reduces blood pressure more than an ACE inhibitor alone.
• If SBP is >160 mm Hg persistently, increase ACE inhibitor dose and add a second-line option such as telmisartan, amlodipine, or (less commonly) a beta-blocker, alpha-blocker, or aldosterone antagonist.
• If SBP ≤120 mm Hg with clinical hypotension (pale mucous membranes, weak peripheral pulses, syncope, collapse, vomiting, or lethargy), decrease the antihypertensive dose.
• If SBP ≤160 mm Hg with no hypotension signs, continue current dosing and recheck every 3 months.

💡 Memory Hook

Dog step-up: ACE dose ↑ then add (telmisartan/amlodipine/others) if SBP stays >160.

📖 5. Cat antihypertensive therapy

🔑 Key Concepts & Definitions

• Amlodipine besylate : Amlodipine besylate is a calcium-channel blocker that dilates peripheral arteries and is used as first-line therapy for feline systemic hypertension.
• Telmisartan (ARB) : Telmisartan is an angiotensin II receptor blocker used in cats for systemic hypertension and can reduce proteinuria.
• FDA-approved indication : Telmisartan is approved by the FDA for the treatment of hypertension.
• Peak effect timing : Amlodipine reaches steady effect within days, while telmisartan reaches peak effect later after initiation.

📝 Essential Points

• First-line options in cats include amlodipine besylate 0.625 mg PO q24h or telmisartan 1.5 mg/kg PO q12-24h.
• Amlodipine steady state is reached within 3 to 5 days, while telmisartan peak effect is reached after around 14 days.
• Recheck timing in cats is 1-3 days after starting amlodipine and 7-10 days after starting telmisartan.
• If SBP ≤120 mm Hg with hypotension, decrease the antihypertensive dose.
• If SBP persistently >160 mm Hg: increase amlodipine by 0.625 mg each intake without exceeding 2.5 mg/day, or increase telmisartan by 0.5 mg/kg without exceeding 2 mg/kg.
• If SBP persistently >160 mm Hg, another second-line approach can be adding telmisartan or benazepril, or (less commonly) atenolol or spironolactone.

💡 Memory Hook

Cats: telmisartan is slower (≈14 days peak) but amlodipine is faster (3–5 days steady state).

📖 6. Adverse effects and RAAS activation

🔑 Key Concepts & Definitions

• Hypotension from therapy : Antihypertensive drugs can cause severe hypotension, especially in patients with low baseline blood pressure.
• RAAS activation : RAAS activation is the hormonal response that regulates blood pressure via its renin-angiotensin-aldosterone pathway.

📝 Essential Points

• In dogs, ACE inhibitors may cause hypotension, weakness, loss of appetite, vomiting, and diarrhea.
• Enalapril may induce fever and coughing, while benazepril may cause changes in thirst and urination.
• Amlodipine and telmisartan share similar adverse effects, and amlodipine may cause collapse and severe weakness in cats and dogs as described.
• Telmisartan can lead to possible anemia in cats.
• In hypertensive cats treated with amlodipine, RAAS was found to be activated, and long-term RAAS activation can allow cardiac fibrosis risk plus salt and water retention, so RAAS-suppressing meds may be needed in some…

💡 Memory Hook

Treat BP down → RAAS may rise; long-term RAAS activation can harm heart and fluids.

⚠️ Common Pitfalls & Confusions

1. Mixing the “start treatment” trigger: therapy begins with SBP >160 mm Hg plus active TOD or repeated confirmation, not just any elevated reading.
2. Confusing dog vs cat dosing schedules for ACE inhibitors versus first-line drugs (dogs use enalapril/benazepril BID; cats use amlodipine q24h or telmisartan q12-24h).
3. Forgetting hypotension management: when SBP ≤120 mm Hg with clinical hypotension signs, the dose should be decreased to avoid worsening low blood pressure.
4. Using the wrong recheck interval after starting therapy: 1-3 days when there’s ongoing/new TOD, and 7-10 days when there’s no overt/new TOD (and for cats telmisartan is rechecked later than amlodipine).
5. Assuming telmisartan works as quickly as amlodipine in cats; telmisartan peak effect occurs after ~14 days.
6. Overlooking that amlodipine can be associated with RAAS activation in cats and that long-term activation may contribute to cardiac fibrosis and salt/water retention.
7. Underestimating second-line options escalation in persistent SBP >160 mm Hg; the regimen must be adjusted rather than kept unchanged.

✅ Exam Checklist

1. Define systemic hypertension and distinguish primary (idiopathic) from secondary hypertension in dogs and cats.
2. State the BP target for treatment (goal below 160 mm Hg) and what this target is meant to prevent.
3. List the systems most at risk for target organ damage (ocular, renal, cardiac, neurologic).
4. Match common TOD-associated diseases to systemic hypertension (kidney failure, hyperaldosteronism, hyperthyroidism, hyperadrenocorticism, diabetes mellitus, pheochromocytoma).
5. Recognize core clinical signs of TOD (hypertensive retinopathy, new cardiac murmur, azotemia, proteinuria, behavior/consciousness changes, seizures).
6. State when treatment is initiated (SBP >160 mm Hg with active TOD or repeated confirmation of SBP >160 mm Hg).
7. Explain the need for life-long antihypertensive treatment when hypertension is associated with chronic renal disease and the role of periodic BP-based dose changes.
8. For dogs, give first-line ACE inhibitor choices and dosing (enalapril or benazepril at 0.5–2 mg/kg PO BID).
9. For dogs with protein-losing nephropathy, state that ACE inhibitor + telmisartan outperforms ACE inhibitor alone for BP reduction.
10. For dogs, apply the adjustment rules for hypotension (SBP ≤120 with hypotensive signs → decrease dose) and for persistent SBP >160 (ACE dose ↑ and add a second-line drug).
11. For dogs, apply monitoring rules for stable non-hypotensive cases (SBP ≤160 with no hypotension signs → recheck every 3 months).
12. For cats, state first-line dosing options (amlodipine besylate 0.625 mg PO q24h; telmisartan 1.5 mg/kg PO q12-24h).
13. For cats, compare onset/peak timing (amlodipine steady state in 3-5 days; telmisartan peak around 14 days) and match recheck timing accordingly.
14. For cats, state escalation limits when SBP remains >160 (maximum amlodipine 2.5 mg/day; maximum telmisartan 2 mg/kg) and the dose-step increments.