Perfusion-Disorders of blood pressure

Exam 3

Systole

Heart contracts to push blood into circulation.

Diastole

Heart relaxes and allows chambers to fill.

Preload

Amount of blood is sitting in ventricles before it gets pushed into circulation.

Stroke volume

Amount pushed out of ventricle when they contract. SV.

Cardiac output

Amount pumped out in a whole minute. CO.

Contractility

Force of contraction of heart muscle, how hard is heart contracting.

Hypertension

Consistent elevation of blood pressure above 140 mmHg systolic or above 90 mmHg diastolic. Systemic arterial pressure and brachial artery, local HTN occurs in specific organs, pulmonary HTN. Causes: hypertension creates excess pressure on arterial walls, arteriosclerosis thickens arterial walls, categories of blood pressure. Contributing factors: endothelial dysfunction, sympathetic, nervous system, alcohol, lifestyle factors – increased stress, high salt intake, lack of physical activity, obesity, genetics. Clinical manifestations: long-term consequences – stroke, TIA, heart failure, MI, angina, dysrhythmia, chronic kidney disease, vision, loss, erectile dysfunction. Hypertensive, emergency, hypertensive, urgency, and chest pain and dyspnea. Non-pharmacologic treatment: restrict, sodium consumption, limit alcohol consumption, stop, smoking, maintain optimal, weight, reduce saturated, fat, cholesterol; increased fruits and vegetables, increase physical activity, reduce stress levels. Pharmacologic treatment: first line antihypertensives: thiazide diuretics, angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBS), calcium chain blockers (CCB). Second line antihypertensives: adrenergic blockers, centrally acting drugs, direct acting vasodilators, direct renin inhibitors.

Normal BP

Less than 120 systolic and less than 80 diastolic.

Elevated BP

120 to 129 systolic in less than 80 diastolic.

Hypertension stage 1

130 to 139 systolic and 80 to 89 diastolic.

Hypertension stage 2

140 or higher systolic and 90 or higher diastolic.

Hypertensive crisis

Higher than 180 systolic and higher than 120 diastolic. Acute heart failure, pulmonary edema, myocardial infarction, renal failure, thrombotic or hemorrhagic stroke, encephalopathy, retinal hemorrhage. Chest pain, dyspnea, oliguria, hematuria, proteinuria, headache, paralysis, seizures, coma, safely reduced blood pressure quickly – too fast, serious hypoperfusion of cerebral, coronary, and renal vasculature. Recommendations: 25% reduction over 30 to 60 minutes, additional reduction over 12 to 48 hours. Parental route preferred.

Primary hypertension

No known cause, accounts for 90% of cases. Factors: genetics, age, race, diet, smoking and alcohol consumption, sedentary lifestyle. Can exist for years with no symptoms. Mild hypertension may be treated with lifestyle modifications.

Secondary hypertension

Identifiable cause. Factors affect affecting blood pressure: hormones – Renin angiotensin aldosterone system (RAAS), nervous (sympathetic, and parasympathetic).

Diuretics

Reduction of blood volume – urinary excretion of water and electrolytes. Dehydration and electrolyte depletion possible. Classes: thiazide, potassium sparing, loop.

Thiazide diuretics

First line treatment, safe and cheap, oral. Mechanism of action: act on early distal tubule. Hypokalemia is a concern – lab monitoring and supplementation. Hydrochlorothiazide and chlorothiazide. Peak 2 to 4 hours after taking and last 6 to 12 hours. Education: take at same time each day and report weight loss, orthostatic hypotension changes.

Potassium sparing

Modest dieresis, act on late distal tubule. No hypokalemia – hyperkalemia possible. Spironolactone, amiloride, eplerenone. Only medication that does not make you pee out potassium.

Loop

Large diarrhea, act on loop of hence. Hypokalemia and dehydration are a concern. Ototoxic. Furosemide, bumetanide, torsemide.

Alpha-2 adrenergic agonist

Mechanism of action: stimulates, alpha, adrenergic, receptors – vasodilation and decreased BP, decreased PVR, increased blood flow to the kidneys. Not often used, used for BP and ADHD – sedation, dizziness, orthostatic hypotension, used for resistant HTN, rebound HTN if stopped abruptly. Example: clonidine.

Beta adrenergic blockers

Selective or non-selective. Block beta, one receptors in the heart – decreased heart rate, decrease myocardial contractility, slow conduction velocity. Inhibit the secretion of Renn from kidney. Non-selective block beta two receptors in lungs- bronchoconstriction and caution with asthma. Adverse effects: usually well tolerated at low doses, hypotension, bradycardia. Fatigue and activity and intolerance. Bronchospasm, dyspnea. Hypoglycemia – also masks effects of hypoglycemia. Decreased libido, impotence.

Selective beta blockers

Atenolol, esmolol, metoprolol, nebivolol.

Non-Selective beta blockers

Carvedilol, labetalol, nadolol, propranolol.

RAAS

Body's ability to fix BP if it is going low, raise his blood pressure.

1. Angiotensin produced in liver

2. Kidney sense drop in blood pressure and secrete renin

3. Renin changes angiotensinogen to angiotensin I

4. Angiotensin, I turned to angiotensin II by angiotensin converting enzyme (ACE) mainly from lung.

5. Angiotensin II is a potent vasoconstrictor

6. Stimulates release of aldosterone and ADH

7. It also promotes fluid retention.

ACE inhibitors

Mechanism of action: blocks the conversion of angiotensin I to angiotensin II leads to vasodilation, sodium and H2O excretion by blocking aldosterone. Use: reduce blood pressure, slow progression of heart failure, and reduce mortality, help reduce diabetic neuropathy. Lower risk for stroke and MI in high risk patients. En in -pril. Cautions: dry cough in 5 to 20% of patients. Buildup of bradykinin. Angioedema is 0.7%. Orthostatic hypotension, headache. Hyperkalemia – caution with potassium sparing diuretics, potassium supplements. Pregnancy category, D, black box warning.

ARBS

Angiotensin II receptor blockers: mechanism of action – do not prevent formation of angiotensin II, but block it from activating target receptors. Can be used to treat heart failure, MI, and prevent stroke; prevent diabetic neuropathy. Do not cause cough – do not promote accumulation of bradykinin, angioedema lessened. End in -sartan. Cautions: orthostatic hypotension, headache. Hyperkalemia – Caution with potassium sparing diuretics, potassium supplements. Pregnancy category D, black box warning.

Direct acting vasodilator

Mechanism of action: act directly on vascular smooth muscle to cause relaxation. Adverse effects: reflex tachycardia from baroreceptor activation, sodium and water retention from aldosterone secretion, facial rash. Rarely a lupus like syndrome. Most often given an IV for hypertensive emergency. Example: hydralazine.

Calcium channels

Calcium channel blockers don't physically block the channel, change the shape. Channels in cardiac and vascular smooth muscle – different medication's block different channels. Dihydropyridine work on vascular smooth muscle. Non-dihydropyridine work on cardiac and vascular smooth muscle.

Dihydropyridine

Amlodipine, felodipine, nicardipine, nefedipine. Highly selective for calcium channels on vascular, smooth muscle – relax the smooth muscle of blood vessels, and cause vasodilation, at high doses they lose selectivity. Some can also be used for angina. Usually well tolerated – hypotension, headache, flushed skin, peripheral edema. Reflex tachycardia – use carefully with myocardial ischemia and dysrhythmia. Cautions: metabolized by CYP pathway. With beta blockers, increased risk of heart failure due to negative inotropic effects. Avoid alcohol. Immediate release formula should be avoided with history of myocardial ischemia and dysrhythmia.

Nondihydropyridine

Diltiazem, verapamil. Work on vascular, smooth, muscles and myocardium. Reduce blood pressure and angina, negative inotropic effect, slow heart rate. Can be used for a fib and a flutter. Usually while tolerated – hypotension, headache, flushed skin, peripheral edema. Cautions: worsening of heart failure, Brady cardia, reflex tachycardia, heart block.

Shock

Acute circulatory failure with inadequate or inappropriately distributed tissue perfusion. Inadequate tissue perfusion to meet metabolic needs of cells. Cellular hypoxia and end-organ dysfunction. Imbalance between oxygen supplied and oxygen demands of cells- anaerobic metabolism and lactic acid generation. Inflammation and clotting cascades. Types: obstructive, cardiogenic, distributive, hypovolemic, septic or anaphylactic. System failures: heart failure, low blood volume in circulation, redistribution of extracellular fluid to extravascular sites, obstruction of blood flow, blood pressure = cardiac output x systemic vascular resistance. Manifestations: systemic arterial hypotension – systolic arterial pressure less than 90 mmHg or mean arterial pressure less than 70 mmHg, tachycardia. Clinical signs – cold, clammy skin, renal output decreases, altered mental state, obtundation, disorientation, confusion, hyperlactemia. Factors influencing circulation: blood volume, systemic vascular tone, heart rate, force of contraction, blood pressure and vascular resistance affect blood flow. Multiple organ dysfunction syndrome (MODS)- resulting hypoxia and decreased oxygen delivery to cells shifts metabolism to an aerobic metabolism.

Hemodynamics

The force is the heart has to respond to in order to maintain blood flow through the cardiovascular system and supply oxygen to all tissues.

Stage 1 of shock

Early, reversible, or compensated shock. Increased heart rate and construction of blood vessels. Activation of renin-angiotensin-aldosterone system – due to response of kidney to poor perfusion. Strong chance of recovery with proper treatment.

Stage 2 of shock

Immediate or progressive shock. Failure of compensatory mechanisms, decrease in perfusion; lead to cellular hypoxia. Neurologic changes: confusion, disorientation. Angina, from decreased oxygen delivery to myocardium, muscular pain, reversible with prompt treatment.

Stage 3 of shock

Refractory or irreversible shock. Declining heart function, shutdown of kidneys, injury to cells in organs and tissues throughout body, death due to multiple organ dysfunction.

Hypovolemic shock

Also called hemorrhagic shock. Blossom more than 15% of bodies, fluids. Etiology and pathogenesis: rapid excessive loss of significant amount of whole blood, hemodynamic instability – decrease in tissue perfusion and oxygen delivery, compensatory mechanisms – address fall, perfusion, maintain cardiac output. Clinical manifestations: hypotension SBP less than 90 mmHg, orthostatic or postural hypertension – SBP decrease of 20 mmHg or DBP decrease of 10 mmHg or increase in heart rate of 15 bpm within three minutes of standing up. Science and symptoms: rapid breathing, severe shortness of breath, sudden, rapid heartbeat, a loss of consciousness, weak pulse, sweating, skin, cold, hands, or feet, urinating less than normal or not at all. Diagnosis: CBC, serum electrolyte concentrations, blood glucose level, arterial blood gas, prothrombin time and partial prothromboplastin time, hemoglobin and hematocrit, serum lactate concentration, and arterial pH. Treatment: primary objectives – maximize oxygen via mass, high flow, nasal, nasal cannula, prevent further fluid loss, replaced lost fluids. Basic life support – airway maintenance, high flow, supplemental, oxygen assistance, cardio, pulmonary resuscitation, intravenous access, fluid resuscitation. Cardiac monitoring, central venous line, control of bleeding, blood products: plasma expanders, pharmacotherapy – calcium, sodium bicarbonate, vasopressor, drugs.