Module 5 - Cardiovascular and Urinary System 2

Hypertension

Chronic elevation of systemic blood pressure at rest.

Benefits of intermittent high BP:

• ↑ blood flow = ↑ oxygen and glucose delivered to muscle.

• Useful to run faster, hit harder, yell louder, etc.

• Will ↑ with emotions like anger, worry, or excitement.

Drug Therapy for Hypertension

A - ACE-Inhibitor or ARB

B - Beta Blocker

C - Calcium Channel Blocker

D - Diuretic

Common adverse effects:

• Dizziness, or lightheaded.

• Orthostatic hypotension.

Diuretic

Kidneys can play a role in hypertension if it fails to eliminate enough fluid.

Commonly used diuretics inhibit sodium reabsorption in the kidneys.

More sodium in the urine = more fluid excreted.

Common adverse effects:

• Dehydration

• Electrolyte abnormalities

• Nocturia

Calcium Channel Blockers (CCB)

Blocks calcium from entering the cell = no muscle contraction = vasodilation of arterioles.

Common adverse effects:

• Peripheral edema

• Constipation

• Headache

RAAS Inhibitors

ACE-Inhibitors - blocks ACE enzyme, stopping Angiotensin I to II conversion

ARBs - block angiotensin from binding to AT1 receptors.

Common adverse effects:

• Dry cough - more common in ACE-I

• Hyperkalemia

• Risk to kidneys

Beta Blockers

Blocks beta-1 and sometimes beta-2 receptors

Common adverse effects:

• Bradycardia

• Reduce recognition of hypoglycemia

Receptors to Remember

Beta-1 - ­­­­↑ heart rate and contractility

Beta-2 - vasodilation

Alpha-1 - vasoconstriction

Alpha-2 - ↓ heart rate and BP

Heart Failure

Inability of ventricles to pump enough blood for body’s needs.

Common causes: heart attack (70%), hypertension.

Left-sided failure - blood backs up into pulmonary circulation; pulmonary edema; more common.

Right-sided failure - blood backs up into systemic circulation; peripheral edema; less common.

Can be classified based on the ejection fraction:

• Reduced - decreased contractility - leads to decreased ejection fraction.

• Preserved - decreased filling - normal ejection fraction but less blood available to be pumped.

Symptoms:

• Dyspnea

• Fatigue

• Exercise intolerance

Hemostasis

1. Vessel injury

2. Vessel spasm

3. Platelets adhere to injury site and aggregate to form a plug

4. Formulation of insoluble fibrin strands and coagulation

Fibrinolysis

1. Clot in vessel containing inactive plasminogen

2. Plasminogen converted to plasminogen, which digests the clot

Activation enhanced by thrombolytics and inhibited y hemostatics

Thromboembolic Disorders

Venous Thromboembolism (VTE)

• Pulmonary Embolism (PE)

• Deep Vein Thrombosis (DVT)

• Anticoagulant - warfarin, apixaban, heparin

Arterial Thromboembolism

• Stroke

• Myocardial Infarction (MI)

• Antiplatelet - aspirin, clopidogrel

Anticoagulants

Used to prolong bleeding time to prevent clots from forming.

Parental:

• Heparin - faster acting

• low-molecular-weigh-heparins (LMWH)

Oral Anticoagulants:

• Warfarin - delayed onset

• DOAC (e.g., apixaban) - faster onset

Dietary Vitamin K can affect the amount of Warfarin needed.

• Vitamin K intake too high = Warfarin less effective.

Antiplatelets

Interfere with platelet function.

Aspirin/ASA, clopidogrel, prasugrel, ticagrelor.

Risk of bleeding.

Combining with drugs that increase bleed risk:

• Caution with NSAIDs, SSRI/SNRI, ginger, garlic.

Thrombolytics

Break down existing clots; will dissolve all clots in the body, bleeding can be fatal.

Alteplase, Tenectelplase (IV).