Hypotension-Hypertension Veterinary Review PDF

Hypotension/hypertension Spring 2025 Britt Thevelein, DVM, DACVECC Objectives Explain Explain the physiological mechanisms involved in blood pressure regulation Identify Identify common causes of hypotension and hypertension in veterinary patients Recognize Recognize...

Hypotension/hypertension Spring 2025 Britt Thevelein, DVM, DACVECC Objectives Explain Explain the physiological mechanisms involved in blood pressure regulation Identify Identify common causes of hypotension and hypertension in veterinary patients Recognize Recognize the clinical consequences of abnormal blood pressure Develop Develop a basic treatment approach for managing hypotension and hypertension Definitions – Arterial blood pressure Normal systolic pressure: 120mmHg Normal diastolic pressure: 80mmHg MAP = DBP + ⅓ (SBP – DBP) Normal mean arterial pressure (MAP): 90mmHg  Determinants of blood pressure Local: PG’s, histamine, NO MAP = CO x SVR Systemic: vasopressin, angiotensin II, symp tone SV HR Symp vs parasympathetic tone Preload Afterload Contractility Kidneys regulate amount of fluid in the system Nervous Regulation of the Circulation and Rapid Control of Arterial Pressure Sympathetic nervous system Basal tone → can increase or decrease Norepinephrine is most important neurotransmitter Binds to α1 receptors on vessels → Vasoconstriction Binds to ß1 receptors on heart → Tachycardia + Inotropy (increase in heart rate and contractility) Parasympathetic Minimal effects on blood pressure Stimulation of vagus nerve → bradycardia Kidneys and RAAS Kidneys: pressure diuresis Blood volume increases → kidneys excrete more water Blood volume decreases → kidneys excrete less water (ADH/vasopressin mediated) Kidneys produce renin when blood flow to kidney decreases →Angiotensin II → Renal retention of salt and water → Vasoconstriction →Stimulates Aldosterone production → Increase in sodium reabsorption by the kidney tubules Control of blood pressure Arterial Pressure Control Mechanisms That Act Within Seconds or Minutes Sympathetic nervous system (1) the baroreceptor feedback mechanism; (2) the central nervous system ischemic mechanism; and (3) the chemoreceptor mechanism → Vasoconstriction + increased heart rate and contractility of the heart to provide greater pumping capability → When the pressure suddenly rises too high the same control mechanisms operate in the reverse direction, again returning the pressure back toward normal. Arterial Pressure Control Mechanisms That Act After Many Minutes Renin-angiotensin vasoconstrictor mechanism Stress relaxation of the vasculature: When the pressure in the blood vessels becomes too high, they become stretched more and more for minutes or hours; as a result, the pressure in the vessels falls toward normal. This continuing stretch of the vessels, called stress relaxation, can serve as an intermediate-term pressure “buffer.” Shift of fluid through the tissue capillary walls in and out of the circulation to readjust the blood volume as needed. Long-Term Mechanisms for Arterial Pressure Regulation Kidneys control blood volume Aldosterone Renin - angiotensin How to measure blood pressure Direct Arterial catheterization = Gold standard Indirect Doppler (measures systolic bp) Oscillometric  Systemic arterial hypertension = Sustained, pathological increase in systemic arterial blood pressure Systolic BP >160 mmHg MAP > 130 mmHg Definitions Hypotension Decreased arterial blood pressure Systolic BP < 90 mmHg MAP < 80 → impaired tissue perfusion at MAP 160 mmHg Results should be confirmed by repeated measurements on multiple occasions Exception: evidence of TOD Acierno, M. J., Brown, S., Coleman, A. E., Jepson, R. E., Papich, M., Stepien, R. L., & Syme, H. M. (2020). ACVIM consensus statement: guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats. Journal of Japanese association of veterinary nephrology and urology, 12(1), 30-49. Causes of hypertension Situational = An artificial elevation in blood pressure created by the stress of being in the hospital setting, patient handling, and the very act of obtaining blood pressure Secondary = The presence high blood pressure in the context of a known predisposing disease process: Chronic kidney disease Acute kidney disease Diabetes mellitus (dogs>cats) Hyperadrenocorticism (dogs) Hyperthyroidism (cats) Pheochromocytoma (dogs) Hyperaldosteronism (cats) Idiopathic = Systemic hypertension without a discernable underlying cause. Consequences of hypertension - TOD Kidney Eye Progression of CKD Acute blindness Increase in create, SDMA, BUN Retinal detachment Proteinuria Retinal hemorrhage Brain Heart and blood vessels Encephalopathy Left ventricular hypertrophy Stroke 12 yo FS DSH is presenting for inability to walk TPR and general physical exam normal Neurological exam reveals a head tilt to the left, horizontal nystagmus, ataxia with proprioceptive deficits on the left Doppler blood pressure: 220 mmHg What do you do? A. Refer to a neurologist B. Figure out the cause for neuro signs and recheck blood pressure in 4-8 weeks C. There is obvious evidence of TOD so start IV medications to lower blood pressure D. I am concerned this could be TOD, I will run some initial diagnostics to look for other causes of the neuro signs and recheck the blood pressure within the hour. If it is still elevated, I should highly consider treatment 12 yo FS DSH is presenting for inability to walk Differentials left central vestibular dz Hypertensive encephalopathy Neoplasia Infectious (uncommon) Diagnostic work up CBC/Chem/T4 Kidney dz, hyperthyroidism are common causes for hypertension Ophthalmic exam → look for evidence of retinal hemorrhage Thoracic radiographs: evaluate for metastasis MRI 12 yo FS DSH is presenting for inability to walk TPR and general physical exam normal Neurological exam reveals a head tilt to the left, horizontal nystagmus, ataxia with proprioceptive deficits on the left Doppler blood pressure: 160 mmHg What do you do? A. Refer to a neurologist B. Figure out the cause for neuro signs and recheck blood pressure in 4-8 weeks C. There is obvious evidence of TOD so start IV medications to lower blood pressure D. I am concerned this could be TOD, I will run some initial diagnostics to look for other causes of the neuro signs and recheck the blood pressure within the hour. If it is still elevated, I should highly consider treatment Hypertensive emergency = Marked hypertension (SBP >180 mmHg) in combination with evidence of ongoing acute TOD (mostly ocular/neuro) GOAL: ↓SBP of 10% over the first hour →15% over the next several hours → normalization over the next couple of weeks Treatment usually in 24h care facility IV medications vs oral medications IV antihypertensive medications More potent → more effective but also more dangerous! Easier to titrate to effect Definitely requires 24h care facility Options: Fenoldopam: Dopamine 1 receptor agonist → renal arterial vasodilation, natriuresis, ↑GFR, diuresis Nitroglycerine: metabolized to nitric oxide (NO) → vasodilation Hydralazine: potent arterial vasodilator  Not as effective but also not as dangerous (less likely to cause hypotension) Options Calcium channel blocker – amlodipine → preferred oral medication for emergency Oral Long term management - especially in CKD: antihypertensive ACE inhibitors: enalapril, benazepril medications Angiotensin receptor blockers – telmisartan Others α1 blockers – prazosin, phenoxybenzamine specifically used for pheochromocytoma (tumor of the adrenal glands excreting excessive amounts of norepi and epi Hypotension Causes of hypotension Hypotension = reduction in systemic arterial blood pressure Reduction in preload Reduction in cardiac function Reduction in systemic vascular resistance  Consequences hypotension Decreased perfusion → decreased oxygen delivery → SHOCK →Sympathetic tone ↑ → tachycardia, inotropy ↑, vasoconstriction →Renin-Angiotensin system stimulated → vasoconstriction →Aldosterone: decreased Na excretion and increased water reabsorption in kidneys Organs most sensitive to hypoperfusion Kidneys → acute kidney injury Brain → altered mentation Heart → arrhythmias Reduction in Preload Preload = the amount of blood in the heart's ventricles just before they contract →Decreased venous return → decreased preload → decreased CO → hypotension →Decreases in preload caused by: Hypovolemia Hemorrhage GI/kidney fluid loss → severe dehydration Cavitary effusions Obstruction of blood flow GDV → obstructs caudal vena cava Pericardial effusion → obstructs right atrium (RA) → RA can’t fill Treatment of decreased preload Hypovolemia Obstruction of blood flow IV fluid bolus Start with IV fluid bolus to → 10-20 ml/kg balanced increase preload isotonic fluid Remove the obstruction Hemorrhage may require GDV → decompress transfusions Pericardial effusion → pericardiocenthesis Reduction in cardiac function →Decreased contractility of the heart (inotropy) → decreased pumping → decreased cardiac output → hypotension Primary heart disease Secondary Severe acidosis or alkalosis Dilated cardiomyopathy Toxin/drug exposure Systemic inflammatory response syndrome (SIRS)/sepsis Reduction in cardiac function Positive inotropes = drugs that Dobutamine = β1-adrenergic increase cardiac contractility agonist Effect: increased contractility Given IV as a CRI Adverse effects Increased myocardial O2 demand Can cause arrythmias May cause mild vasodilation Cats: can cause seizures Reduction in systemic vascular resistance Inappropriate vasodilation resulting in maldistribution of blood flow → maldistributive or vasodilatory shock Most common causes: Sepsis Excessive production of nitric oxide from upregulation of induced nitric oxide synthase by assorted cytokines (e.g., TNF-α, IL-1β, IL-6) and direct vasoactive properties of various other inflammatory mediators Anaphylaxis Immunoglobulin E (IgE) produced in response to allergen exposure binds to mast cells → release of histamines, leukotrines, and other substances that promote vasodilation and increased vascular permeability  Norepinephrine α-receptor agonist Dopamine Treatment of Endogenous precursor to norepinephrine → β- reduction in and α-agonist activity SVR Epinephrine Potent β1-, β2-, α1-, and α2-receptor agonist Vasopressin These are all IV medications run as V1 receptor agonist CRI’s → only in 24/7 hospitals Norepinephrine α-receptor agonist → First choice in vasoconstriction sepsis (VC) Dopamine Endogenous precursor to norepinephrine β-agonist → inotropy α-agonist → vasoconstriction Moderate VC and mild increase in cardia output Epinephrine Potent β1-, β2-, α1-, and α2-receptor agonist → positive inotrope and chronotrope, vasoconstrictor, and bronchodilator Drug of choice in anaphylaxis Used in CPR Vasopressin V1 receptor agonist Strong vasoconstrictor Second line vasoconstrictor Can also be used in CPR Case: Dolly 6 yo FS labrador Vomiting profusely for 3d, anorexia T 98.7, P 170 bpm, R 40 brpm, dull, pulses weak, mm pink, CRT