NURS2750 Quiz 1

Blood pressure formula

cardiac output x peripheral resistance

Hormones regulating blood pressure

-ADH (increases BP)
-RAAS: renin, angiotensin, aldosterone (causes vasoconstriction, increases blood volume & BP)

Control of blood pressure

-blood pressure falls
-blood flow to kidneys decreases, causing release of renin
-renin produces angiotensin 1, which is converted to angiotensin 2 (potent vasoconstrictor)
-angiotensin 2 stimulates aldosterone secretion
-aldosterone causes Na&H2O retention, increasing blood volume
-increased blood volume raises BP

Preload

the volume of blood returned by veins to the heart

Afterload

peripheral resistance that the heart must overcome to send blood to the circulatory system

How does vasoconstriction affect blood pressure?

increases blood pressure

How does vasodilation affect blood pressure?

decreases blood pressure

Cardiac output formula

heart rate x stroke volume

Stroke volume formula

EDV-ESV

Hypertension

-when the pressure of the blood being pumped through your arteries is higher than it should be
-140/90

Hypertension symptoms

-asymptomatic in early stages
-initial signs: fatigue, malaise, morning headache, nosebleeds
-organs eventually become damaged

Hypertension predisposing factors

-age
-gender (men)
-genetic factors
-sodium and alcohol intake
-obesity, smoking, stress
-race

Hypertension complications

-heart attack
-heart enlargement
-heart failure
-stroke

Primary (essential) hypertension

-idiopathic
-increase in arteriolar vasoconstriction over time, causing damage to arterial walls
-causes ischemia and necrosis of tissues

Secondary hypertension

-results from renal disease, endocrine disease, or benign tumor of the adrenal medulla
-underlying problem must be treated to reduce blood pressure.

Balance water and electrolytes

-thirst
-ADH (sodium and water retention)
-aldosterone (sodium and water retention)
-ANP and T-type natriuretic peptide (fluid, sodium, and potassium)

Causes of edema

-increased capillary hydrostatic pressure (high BP and blood volume)
-loss of plasma proteins (decreased plasma osmotic pressure)
-obstruction of lymphatic circulation
-increased capillary permeability

Causes of dehydration

-vomiting and diarrhea
-excessive sweating
-diabetic ketoacidosis
-insufficient water intake
-use of concentrated formula in infants

Dehydration symptoms

-dry mucous membranes
-decreased skin turgor
-low BP, weak pulse, fatigue
-increased hematocrit
-decreased mental function

Dehydration compensation

-increased thirst
-increased HR
-constriction of cutaneous blood vessels
-decreased urine production

Causes of hyperkalemia

-medications
-acidosis
-cellular destruction
-HYPOaldosetronism
-renal impairment

Hyperkalemia symptoms

-hypotension and bradycardia
-arrhythmias
-respiratory failure
-diarrhea
-muscle weakness
-tingling of hands, feet, and mouth
-paralysis

Hyperkalemia management

-monitor EKG
-kayexalate
-IV sodium bicarbonate
-diuretics (potassium wasting)
-dialysis

Causes of hypokalemia

-vomiting, diarrhea
-frequent urination
-potassium wasting diuretics
-alkalosis
-HYPERaldosteronism
-medications

Hypokalemia symptoms

-tachycardia (early), bradycardia (late)
-orthostatic hypotension
-arrhythmias
-decreased RR
-constipation
-muscle cramping
-paralysis

Hypokalemia management

-oral potassium
-IV potassium chloride
-diet: fruits, green leafy vegetables

Causes of hypernatremia

-fluid loss greater than sodium loss
-ADH insufficiency (diabetes insipidus)
-increased sodium intake
-increased aldosterone (Cushing's syndrome)
-deprivation of fluids

Hypernatremia symptoms

-hypertension, tachycardia
-cardiac dysrhythmias
-shortness of breath
-fluid overload
-nausea, vomiting
-decreased urine output
-thick salty CSF
-confusion, irritability
-seizures and coma
-muscle twitching and cramps
-edema
-dry mouth and mucous membrane

Causes of hyponatremia

-excessive sweating, vomiting, diarrhea
-insufficient aldosterone, excess ADH
-excessive water intake

Hypovolemic hyponatremia

loss of fluid and sodium

Hypervolemic hyponatremia

increase in body water greater than sodium

Hyponatremia symptoms

-cardiac dysrhythmias
-shortness of breath
-nausea, vomiting, abdominal cramping
-seizures and coma
-muscle weakness

Hyponatremia management

\-isotonic IV solution for hypovolemic hyponatremia -loop diuretics or hypertonic sodium for hypervolemic hyponatremia (and limit water) -high salt diet

Hyperthyroidism symptoms

-nervousness
-weight loss
-increased appetite
-excessive sweating and heat intolerance
-muscle weakness

Hypothyroidism symptoms

-weight gain
-fatigue
-puffy face
-muscle pain

Arteriosclerosis

a general term for thickening and hardening of the arteries
-leads to increased blood pressure, ischemia, and necrosis

Atherosclerosis

-specific type of arteriosclerosis
-presence of atheroma
-rigidity and narrowing of large and medium sized vessels due to plaque buildup
-may occlude a vessel or form a thrombus

Atheroma

plaques consisting of lipids, calcium, and possible blood clots

Coronary circulation: Deoxygenated blood

-superior and inferior vena cava
-right atria
-tricuspid valve
-right ventricle
-pulmonary valve
-pulmonary artery
-lungs

Coronary circulation: Oxygenated blood

-pulmonary veins
-left atria
-mitral valve
-left ventricle
-aortic valve
-aorta
-body

Coronary artery disease

-narrowing of the coronary artery due to atherosclerosis
-results in ischemia of heart muscle
-types: stable angina and acute coronary syndrome (unstable angina and MI)

Stable angina

-caused by a degree of atherosclerosis
-partially blocked coronary artery
-at rest, blood flow meets the demand of the heart, so no pain
-with exercise, demand increases and not enough blood is available, causing pain
-pain is relieved with nitroglycerin

Unstable angina

-a progress of stable angina
-plaque ruptures and collects blood clots due to its thrombogenic material
-ruptured plaque flaps in the artery, causing complete occlusion at times (pain)
-may progress to MI

Myocardial infarction

-occurs when the atherosclerotic artery becomes completely blocked
-plaque rupture and clot formation causes thrombosis or embolization

Thrombosis

a clot (thrombus) gets big enough to completely block the vessel

Embolization

part of the clot breaks off (embolus), flowing downstream until it blocks a smaller blood vessel

STEMI

-ST elevated MI
-full thickness (transmural) infarct
-occurs with occlusion of a major artery

Non-STEMI

-non ST elevated MI
-partial thickness (subendocardial) infarct
-occurs with occlusion of smaller artery

Myocardial infarction symptoms

-abrupt chest pain
-indigestion, nausea, vomiting
-tachycardia, anxiety, sense of doom
-dysrhythmias and ECG changes

Myocardial infarction complications

-arrhythmia
-heart failure
-cardiogenic shock
-pericarditis
-sudden death
-cardiac tamponade (heart is compressed and can't pump)
-stroke

Inferior myocardial infarction

-right coronary artery
-elevations in 2,3 and AVF

Anterior myocardial infarction

-left anterior descending artery
-elevations in V3 and V4

Septal/apical myocardial infarction

proximal/distal left anterior descending artery or circumflex artery
-elevations in V1-V6

Lateral myocardial infarction

-left circumflex artery
-elevations in 1, AVL, V5, and V6

Troponin

-appears after 2-4 hours
-peaks at 14-28 hours
-stays for 7-14 days

Myocardial infarction blood work markers

-troponin
-myoglobin
-creatine kinase

Myoglobin

-appears after 2 hours
-peaks at 3+ hours

CK-II MB

-appears after 3-6 hours
-peaks at 18-24 hours
-stays for 3 days

Percutaneous coronary intervention (PCI)

-reopens a blocked artery
-catheter with attached balloon is passed through the femoral artery to the blockage
-balloon is inflated to open the artery
-a stent can be placed to keep the artery open permanently

Coronary artery bypass graft (CABG)

-creates new route for blood flow around the site of blockage
-healthy blood vessel is taken from patient's chest or leg to form a graft
-graft is connected just below the blocked artery

PVD

-narrow veins
-warm legs, edema
-dull pain
-yellow/brown ankles
-elevate legs

PAD

-narrow arteries
-absent pulses
-hair loss
-cool legs, pale toes
-sharp calf pain
-hang legs off ledge

Cardiogenic shock

inability of the heart to maintain cardiac output due to issue with wirculation

Shock symptoms

-early: anxiety/restlessness
-compensation: tachycardia, pallor, sweating, low urine output
-progressive: lethargy, weakness, metabolic acidosis

Shock compensation mechanisms

-SNS and adrenal medulla stimulation
-renin secretion
-increased ADH
-increased glucocorticoids
-acidosis stimulates respirations

Congestive heart failure

heart is unable to pump its required amount of blood

Congestive heart failure forward effects

\-hypoxia (decreased blood supply)

\-fatigue and weakness

\-dyspnea

\-exercise and cold intolerance

\-dizziness

Congestive heart failure compensation

\-tachycardia
\-pallor
\-decreased urine output
\-secondary polycythemia

\-vasoconstriction

Systolic left-sided heart failure

\-contractions of the muscle wall of the left ventricle malfunction

\-decreased ejection fraction and ventricular enlargement

Diastolic left-sided heart failure

\-left ventricle muscle wall is unable to relax normally due to stiffness

\-the heart does not fill properly, reducing stroke volume

Left sided CHF symptoms

\-increased pressure in the heart

\-lung congestion

\-orthopnea

\-paroxysmal nocturnal dyspnea

\-cough

Right-sided heart failure

\-a result of left-sided heart failure

\-back up in the circulatory system supplying the rest of the body, causing fluid retention

Right-sided heart failure symptoms

\-edema of the limbs, liver, and abdomen

\-jugular vein distention

\-hepatomegaly and splenomegaly

\-ascites

\-flushed face

\-visual disturbances

Right sided CHF symptoms

-early manifestations are similar to left-sided CHF
-edema in feet
-hepatomegaly, splenomegaly
-ascites
-distended neck veins
-headache
-flushed face

Causes of congestive heart failure

-coronary artery disease
-hypertension
-high cholesterol
-smoking, drinking, drug use
-heart valve disease
-infection of heart or lung
-overactive thyroid
-anemia
-congenital heart disease

Types of antihypertensives

\-adrenergics

\-calcium channel blockers

\-drugs affecting RAAS system

\-diuretics

\-direct vasodilators

Centrally-acting adrenergic 2 agonists

\-stimulate alpha 2 adrenergic receptors in the brain

\-decrease sympathetic outflow from CNS

Clonidine

-alpha 2 agonist
-must be tapered
-sometimes used to treat hot flashes or lessen withdrawal symptoms

Methyldopa

-alpha 2 agonist
-safe in pregnancy

Peripherally-acting adrenergic 1 blockers

\-antagonize alpha 1 adrenergic receptors

\-dilates blood vessels and increases urinary flow rates

\-prevents smooth muscle contractions in the bladder/urethra

\-not used often for hypertension

Tamsulosin

-alpha 1 antagonist
-used for benign prostatic hyperplasia

Beta blockers

\-beta adrenergic antagonists

\-can be cardio-selective or non-specific

\-reduce MI and HF mortality

Beta blockers adverse effects

-hypotension
-bradycardia
-dyspnea
-propranolol can cause confusion by passing through BBB

ACE inhibitors

\-first line drugs

\-inhibits ACE, preventing the RAAS pathway

\-reduce MI and HF mortality

ACE inhibitors adverse effects

-benign dry cough
-angioedema
-orthostatic hypotension
-hypotension/dizziness
-hyperkalemia
-increase in creatinine

Angiotensin II receptor blockers (ARBs)

\-very similar to ACE inhibitors

\-useful to switch to when ACE inhibitors cause a dry cough

Calcium channel blockers adverse effects

-hypotension/dizziness
-reflex tachycardia
-peripheral edema
-constipation

Non-dihydropyridine CCBs

\-slow conduction in SA and AV nodes

\-relax smooth muscles in vasculature

Dihydropyridine CCBs

\-do not significantly affect heart rate

\-relax smooth muscles in vasculature

Vasodilators

-direct vasodilation of arteriolar smooth muscle
-highly effective but many adverse effects
-i.e. hydralazine, nitroprusside, nitroglycerine

Hydralazine

-vasodilator
-acts primarily on arterial relaxation
-IV available for rapid lowering in hypertensive emergencies
-adverse reactions: dizziness, headache, reflex tachycardia, edema, dyspnea, SLE, rash

Nitroprusside

-vasodilator
-similar to hydralazine but only used acutely IV (very quick action)
-adverse effects: headache, methemoglobinemia, cyanide toxicity

Nitroglycerine

-vasodilator used to treat angina and lower blood pressure
-adverse effects: headache, hypotension, dizziness, tolerance

Diuretics

-increase urine secretion in order to rid the body of excess water and salt
-also affect renal excretion of other ions

Types of diuretics

-loop
-thiazide
-potassium sparing

Loop diuretics

\-block sodium reabsorption in the ascending loop of Henle

\-large effects due to abundance of sodium in loop of Henle

\-should be given in the morning to avoid nocturia

Loop diuretics adverse effects

-GI effects
-headache, dizziness, tinnitus
-hypokalemia, hypocalcemia, hyponatremia
-metabolic alkalosis
-renal failure

Potassium sparing diuretics

\-blocks the effects of aldosterone in the distal tubules and collecting ducts

\-aldosterone dumps potassium into the collecting ducts and reabsorbs sodium

\-mild diuresis but can affect BP

Potassium sparing diuretics adverse effects

-GI effects
-dizziness
-altered menses
-hyperkalemia, hyponatremia

Thiazide diuretics

-inhibit distal tubular reabsorption of sodium, chloride, and potassium
-minimal diuresis effect, but effects blood pressure