CBL: Hypertension PDF - August 2024

CBL: HYPERTENSION Block: Foundations Block Director: James Proffitt, PhD Session Date: Thursday, August 08, 2024 Time: 10:00 - 12:00 pm Instructor: Zoe Cohen, PhD Department: Physiology Email: [email protected] Instructor: Wi...

CBL: HYPERTENSION Block: Foundations Block Director: James Proffitt, PhD Session Date: Thursday, August 08, 2024 Time: 10:00 - 12:00 pm Instructor: Zoe Cohen, PhD Department: Physiology Email: [email protected] Instructor: William Adamas-Rappaport, MD Department: General Surgery Email: [email protected] INSTRUCTIONAL METHODS Primary Method: IM01:Case-Based Instruction/Learning ✓ Flipped Session ✓ Clinical Correlation Resource Types: RE18: Written or Visual Media (or Digital Equivalent) INSTRUCTIONS Review learning objectives below and notes below in preparation. READINGS Review Dr. Cohen’s Cardiovascular Physiology Lecture Material & the Notes below LEARNING OBJECTIVES 1. Define Hypertension. 2. Explain lifestyle changes that should be instituted in patients with hypertension. 3. Describe the mechanism of action of Lisinopril and HCTZ in the treatment of hypertension. 4. Define shock. 5. Describe the first sympathetic nervous system response to hypovolemic shock and the effect produced on the arteriole and the heart. CURRICULAR CONNECTIONS Below are the competencies, educational program objectives (EPOs), course objectives, session learning objectives, disciplines and threads that most accurately describe the connection of this session to the curriculum. Related Related Competency\EPO Disciplines Threads COs LOs CO-02 LO-01 MK-01: Core of basic sciences Physiology N/A Pathology Block: Foundations | RAPPAPORT / COHEN [1 of 6] CBL: HYPERTENSION Related Related Competency\EPO Disciplines Threads COs LOs CO-01 LO-02 MK-02: The normal structure and Embryology H & I: Chronic function of the body as a whole Gross Anatomy Care and of each of the major organ systems CO-01 LO-03 MK-02: The normal structure and Embryology H & I: Acute Care function of the body as a whole and of each of the major organ systems CO-02 LO-04 MK-05: The altered structure and Clinical skills N/A function (pathology & Gross Anatomy pathophysiology) of the Embryology body/organs in disease CO-02 LO-05 MK-06: The foundations of Clinical skills H & I : Acute Care therapeutic intervention, including Pharmacology concepts of outcomes, Physiology treatments, and prevention, and Pathology their relationships to specific Biochemistry disease processes NOTES: High blood pressure, or hypertension, is the most common disease seen in US medical practice and the most common cardiovascular disease worldwide. In practice we call it the “silent killer” because patients remain asymptomatic while the heart, kidney and brain suffer disease. Although hypertension can be caused by certain diseases, it’s more common that there isn’t an identifiable cause. This form is called Essential, or Primary Hypertension. Primary hypertension is diagnosed when blood pressure is >130-140 mm Hg systolic or >80-90 mm Hg diastolic on two or more office visits in the absence of another identifiable cause. These cutoffs are determined because chronic exposure to blood pressures above this level leads to deleterious effects on certain organs. *In 2019, the American Heart Association stated that a blood pressure of 120-129 mmHg systolic is considered “Elevated”. This is new, so some doctors believe this and others don’t. **It’s also important to know that blood pressure minimums often change with age. Block: Foundations | RAPPAPORT / COHEN [2 of 6] CBL: HYPERTENSION What Causes Hypertension? To gain a better understanding of the mechanisms, it is important to understand two factors that impact blood pressure: cardiac output and systemic vascular resistance (SVR), which is also called total peripheral resistance (TPR). Dr Cohen covered this so we will briefly review this. Cardiac Output (ml/min) = Stroke Volume (ml/beat) x Heart Rate (beat/minute) BP is proportional to Cardiac Output x Systemic Vascular Resistance of the peripheral arteriole system Patients with hypertension tend to have normal heart rate so this is not often a target in treating hypertension. Therefore, elevations in SVR are the most common driver of primary hypertension. Second would be an increase in intra-vascular volume often due to excess salt intake and/or excess reabsorption from the kidney (increased Stroke Volume). One of the factors that can affect blood pressure, both directly and indirectly, is the sympathetic nervous system (SNS). In a direct manner, the SNS and adrenal medulla release catecholamines, including norepinephrine, which binds to alpha1-receptors in vascular smooth muscle. Alpha1-Receptor activation causes vasoconstriction, which subsequently increases SVR and BP. Although this is a normal mechanism to help control blood pressure, it is thought that some patients either release too much or are simply too sensitive to norepinephrine, ultimately resulting in hypertension. Block: Foundations | RAPPAPORT / COHEN [3 of 6] CBL: HYPERTENSION A second potent vasoconstrictor of the arteriole is Angiotensin 2 which binds the AT2 Receptor. You will learn more about this on the CPR block but it is a key target in treating hypertension. Medications that block AT2 production are front line drugs we use to treat hypertension. Systemic vascular resistance (SVR) is the opposing resistance created by the passage of blood through the systemic vessels. How do we treat hypertension ? In clinical practice we target SVR and SV. This is because heart rate doesn’t seem to play as large a role in the increase in blood pressure. The 2 most common drugs that are used are: 1- Lisinopril 2- -Hydrochlorothiazide. Lisinopril - inhibits conversion of Angiotensin 1 (AT 1) to Angiotensin 2 (AT 2). The enzyme that produces this conversion is Angiotensin Converting Enzyme (ACE) Angiotensin 2 is a potent vasoconstrictor binding AT2 receptors on the arteriole and increasing SVR. You will learn more about the Angiotensin Pathway in the CPR block but we are mentioning it here as it has a key role in producing hypertension. Our second go-to drug is Hydrochlorothiazide (HCTZ) which is a diuretic. It increases urine output thereby decreasing SV. Block: Foundations | RAPPAPORT / COHEN [4 of 6] CBL: HYPERTENSION It is so important that for every drug you learn you learn its contraindications and side effects. One side effect of Lisinopril is cough. Angiotensin Converting Enzyme breaks down bradykinin and substance P and other inflammatory agents in upper respiratory tract and lung, so some patients will develop a dry cough due to a build up of these inflammatory chemicals forcing you to stop the medication and try another. HCTZ is a diuretic and most diuretics can result in Hypokalemia -excess loss of potassium. That is one of the key complications of HCTZ Patients with hypertension tend to have normal cardiac output. Though some do have increase intra-vascular volume due to increased sodium reabsorption. Therefore, elevations in SVR are the most common driver of primary hypertension. This occurs for a variety of reasons, different in each patient. SHOCK The opposite of hypertension (high blood pressure) is hypotension (low blood pressure). This can be caused by shock. Shock is defined as the “inadequate delivery of O2 to the peripheral tissues” and is accompanied by hypotension. There are many forms of shock, including septic, but for this case, we will concentrate on hypovolemic (low blood volume) shock. Let’s look at the formula for Blood Pressure again: BP = CO (HR x SV) x SVR we can figure out how to treat hypovolemic shock. a- Hypovolemic shock – loss of intra-vascular fluid from hemorrhage (blood loss) or profound dehydration. The first response PHYSIOLOGIC RESPONSE TO BLOOD LOSS IS ACTIVATION OF THE SYMPATHETIC NERVOUS SYSTEM. With profound hemorrhage pressure receptors in some of the arteries stimulate release of Norepinephrine from the sympathetic nervous systems and profound arteriolar constriction as Norepinephrine binds alpha 1 receptors. This diverts blood to the vital organs (heart and brain) away from the skin and intestines. This produces a barely palpable arterial pulse in the ED due to profound vasoconstriction of the smaller arteries such as the radial and dorsalis pedis artery. Norepinephrine also is a B1 receptor agonist so it binds the B1 receptors of the cardiac muscle increasing contractility and binds B1 receptors in the AV node increasing heart rate in an attempt to increase Cardiac Output. b- What would be your next step to increase BP? c- IV fluid what is missing in the formula? BP = SV x HR (CO) x SVR. d- Which is low? Block: Foundations | RAPPAPORT / COHEN [5 of 6] CBL: HYPERTENSION BELOW IS A CXR OF A NORMAL 3 YEAR OLD THINK WHAT WOULD HAPPEN IF MORE BLOOD WENT FROM THE LEFT VENTRICLE TO THE RIGHT VENTRICLE WE WILL DISCUSS THIS IN CLASS Block: Foundations | RAPPAPORT / COHEN [6 of 6]