Unit 4B: Alterations In Perfusion

Front 1

A severe and abrupt elevation in BP, arbitrarily defined as a DBP >140 mm Hg
-rate of rise of BP is more important than the absolute value in determining the need for emergency treatment
-occurs most commonly in patients with a history of hypertension who have failed to comply with their prescribed meds or who have been undermedicated

Back 1

-Hypertensive crisis

**Patients with chronic HTN can tolerate much higher BP than those previously normotensive

Front 2

In this setting, rise in BP is thought to trigger endothelial damage and the release of vasoconstrictor substances which then ensues leading to life-threatening damage to target organs
-also can be caused by cocaine or crack use, amphetamines, PCP, LSD aslo

Back 2

-Hypertensive crisis

Front 3

This class of hypertensive crisis develops over hours to days, is a situation in which a patient's BP is severely elevated (>180/120 mm Hg) with evidence of acute target organ damage, especially damage to the CNS
-can precipitate encephalopathy, intracranial or subarachnoid hemorrhage, acute left ventricular failure with pulmonary edema, MI, renal failure, dissecting aortic aneurysm, and retinopathy:

Back 3

-Hypertensive emergency

Front 4

This class of hypertensive crisis which develops over days to weeks, is a situation in which a patient's BP is severely elevated but there is no clinical evidence of target organ damage:

Back 4

-Hypertensive urgency

Front 5

Describe a treatment for a patient experiencing a hypertensive emergency:

Back 5

-BP level alone is a poor indicator and is not the major factor in deciding the treatment
-Requires hospitalization
-IV admin of antiHTN dugs
-Intensive care monitoring
-MAP readings guide and evaluate therapy
-Treatment goal is to decrease MAP by no more than 25% within min to 1 hour

Front 6

What is the formula for determining a patient's MAP?

Back 6

-MAP = (SBP + 2 DBP)
_____________
3

Front 7

During a hypertensive crisis, lowering the BP excessively may cause what?

Back 7

-Decrease cerebral, coronary, or renal perfusion and could precipitate a stroke, acute MI, or renal failure

Front 8

What drug is the most effective against hypertensive emergencies?

Back 8

-Sodium Nitroprusside

Front 9

Antihypertensive drugs admin IV have a rapid onset of action (within seconds to minutes). The patient's BP and pulse should be taken every ___ to ___ _____ during the initial admin of these drugs.

Back 9

-2-3 minutes

Front 10

When the heart fails to pump enough blood to meet systemic metabolic needs
-characterized by ventricular dysfunction, reduced exercise tolerance, diminished quality of life, and shortened life expectancy

Back 10

-Heart failure

Front 11

What are risk factors for the development of HF?

Back 11

-CAD and advancing age (both primary)
-HTN
-Diabetes
-Smoking
-Obesity
-High cholesterol

Front 12

The most common cause of HF, results from an inability of the heart to pump blood
-defect in the ability of the ventricles to contract or pump
-LV loses its ability to generate enough pressure to eject blood forward through the aorta
-decrease LV EF is seen
-caused by impaired contractile function (MI), increased afterload (HTN), cardiomyopathy, and mechanical abnormalities (valvular heart disease)

Back 12

-Systolic failure

Front 13

An impaired ability of the ventricles to relax and fill during diastole
-can have normal EF
-results in decreased stroke volume and CO
-characterized by high filling pressures due to stiff or noncompliant ventricles and results in venous engorgement in both the pulmonary and systemic vascular systems
-diagnosis is make on the basis of the presence of pulmonary congestion, pulmonary HTN, ventricular hypertrophy, and a normal EF
-usually the result of LV hypertrophy from chronic systemic HTN, aortic stenosis, or hypertrophic cardiomyopathy

Back 13

-Diastolic failure

Front 14

Name the 4 compensatory mechanisms the body uses when in HF:

Back 14

1.) Sympathetic Nervous System Activation
2.) Neurohormonal Response
3.) Dilation
4.) Hypertrophy

Front 15

This compensatory mechanism of HF:
-first mechanism triggered
-least effective
-release of catecholamines (increases HR and myocardial contractility and peripheral vasoconstriction)
-Negative: increases the myocardium's need for O2 and the workload of the already failing heart

Back 15

-Sympathetic Nervous System Activation

Front 16

This compensatory mechanism of HF:
-because of decreased volume, the kidneys release renin, activates the RAAS which in then end, results in Na and H2O retention and increased BP
-ADH is secreted which increases H2O retention ad increasing blood volume
-ventricular remodeling

Back 16

-Neurohormonal Response

Front 17

This compensatory mechanism of HF:
-an enlargement of the chambers of the heart
-occurs when pressure in the heart chambers (usually LV) is elevated over time
-muscle fibers of the heart stretch in response to the volume of blood in the heart at the end of diastole
-degree of stretch is directly related to the force of the contraction
-initially this increases CO and maintenance of arterial BP and perfusion, but eventually becomes overstretched and can no longer contract effectively, thereby decreasing the CO

Back 17

-Dilation

Front 18

This compensatory mechanism of HF:
-an increase in the muscle mass and cardiac wall thickness in response to overwork and strain
-occurs slowly
-generally follows persistent or chronic dilation and thus further increases the contractile power of the muscle fibers
-lead to an increase in CO and maintenance of tissue perfusion but this muscle now has poor contractility, requires more O2 to perform work, has poor coronary artery circulation and is prone to ventricular dysrhythmias:

Back 18

-Hypertrophy

Front 19

These counterregulatory hormones are produced by the heart muscle that promote venous and arterial vasodilation (thus reducing afterload and preload)
-enhance diuresis and reduce preload and volume stress
-block the effects of the RAAS

Back 19

-Atrial natriuretic peptides (ANP)

-b-type natriuretic peptides (BNP)

Front 20

-Most common form of HF
-Results from LV dysfunction, which prevents normal blood flow and causes blood to back up into the left atrium and into the pulmonary veins
-Manifested as pulmonary congestion and edema

Back 20

-Left-sided HF

Front 21

-Causes a backup of blood into the right atrium and venous circulation
-Manifested as jugular venous distention, hepatomegaly, splenomegaly, vascular congestion of the GI tract, and peripheral edema
-Eventually results in chronic pulmonary hypertension (increase RV afterload), cor pulmonale (RV dilation and hypertrophy causes by pulmonary dz), and RV infarction

Back 21

-Right-sided HF

Front 22

What is the primary cause of right-sided heart failure?

Back 22

-Left-sided HF

Front 23

Describe s&s of HF:

Back 23

-Fatigue (one of the earliest symptoms)
-Dyspnea (common, may have persistent dry cough, unrelieved)
-Tachycardia (early sign)
-Edema (common)
-Nocturia (when HF patient lies down at night, interstitial edema is pulled back into vascular system and perfused to the kidneys)
-Skin Changes: dusky, cool, clammy, swollen, diminished hair growth
-Behavioral Changes: restlessness, confusion
-Chest Pain
-Weight Changes

Front 24

Describe complications of HF:

Back 24

-Pleural Effusion
-Dysrhythmias
-LV Thrombus
-Hepatomegaly
-Renal Failure

Front 25

One of the many goals for the treatment of HF includes decreasing intravascular volume, which interventions and medications would you choose to do this?

Back 25

-Diuretics

** By decreasing venous return to the LV and thereby reducing preload, the overfilled LV may contract more efficiently and improve CO which in return increases LV function, decreases pulmonary vascular pressures, and improves gas exchange

Front 26

One of the many goals for the treatment of HF includes decreasing preload, which medications and interventions would you choose to do this?

Back 26

-Placing pt in High Fowler's position with the feet horizontal in the bed or dangling at the bedside
-Diuretics
-Nitroglycerin
-Sodium nitroprusside
-Morphine Sulfate

Front 27

One of the many goals for the treatment of HF includes decreasing afterload, which medications and interventions would you choose to do this?

Back 27

-Sodium nitroprusside
-Morphine Sulfate
-Nesiritide

Front 28

One of the many goals for the treatment of HF includes improving gas exchange and oxygenation, which medications and interventions would you choose to do this?

Back 28

-Morphine Sulfate (decreases pain and anxiety)
-O2

Front 29

One of the many goals for the treatment of HF is improving cardiac function, what medications and interventions would you choose to do this?

Back 29

-Morphine sulfate
-Diuretics
-Vasodilators
-Positive inotrope (digitalis, dopamine, dobutamine, epinephrine, norepinephrine)

Front 30

Constitutes a groups of diseases that directly affect the structural or functional ability of the myocardium
-can be classified as primary or secondary
-3 major types: dilated, hypertrophic, restrictive

Back 30

-Cardiomyopathy (CMP)

Front 31

This class of cardiomyopathy refers to those conditions in which the etiology of the heart disease is unknown or idiopathic
-heart muscle in this case is the only portion of the heart involved, and other cardiac structures are unaffected

Back 31

-Primary CMP

Front 32

This class of CMP, the cause of the myocardial disease is known and is secondary to another disease process

Back 32

-Secondary CMP

Front 33

This is the most common type of CMP
-characterized by a diffuse inflammation and rapid degeneration of myocardial fiber that result in ventricular dilation, impairment of systolic function, atrial enlargement, and stasis of blood in the left ventricle
-cardiomegaly results
-often follows an infectious myocarditis

Back 33

-Dilated cardiomyopathy

Front 34

Describe s&s of dilated CMP:

Back 34

-may develop acutely after and infectious process or insidiously over a period of time
-Decreased exercise capacity, fatigue, dyspnea at rest, paroxysmal nocturnal dyspnea, orthopnea
-dry cough, palpitations, abdominal bleeding, N&V, anorexia
-irregular heart rate, abnormal S3 and/or S4, tachycardia or bradycardia, pulmonary crackles, edema, weak peripheral pulses, pallor, hepatomegaly, jugular venous distention
-heart murmurs and dysrhythmias
-at risk for blood clot formation

Front 35

Name some causes of secondary cardiomyopathy:

Back 35

-Cardiotoxic agents- alcohol, cocaine
-Genetic
-HTN
-Ischemia
-Metabolic disorders
-Muscular dystrophy
-Myocarditis
-Pregnancy
-Valve disease

Front 36

Describe treatment for a patient experiencing dilated CMP:

Back 36

-similar to the treatment of chronic HF
-Nitrate and loop diuretics to decrease preload
-ACE inhibitors to reduce afterload
-B-blockers and aldosterone antagonists to control the neurohormonal stimulation
-Digoxin to treat a-fib (increased susceptibility to dig toxicity)
-Antidysrhythmics
-Anticoagulation therapy

-dilated CMP does not respond well to therapy
-VAD to allow the heart to rest and recover
-Heart transplant

Front 37

This type of CMP is asymmetric left ventricular hypertrophy without ventricular dilation

-4 main characteristics are:
1.) massive ventricular hypertrophy
2.) rapid, forceful contraction of the left ventricle
3.) impaired relaxation (diastole)
4.) obstruction to aortic outflow

-Associated with a thickened intraventricular septum and ventricular wall
-End result is impaired ventricular filling as the ventricle becomes noncompliant and unable to relax
-primary defect is diastolic dysfunction from LV stiffness

Back 37

-Hypertrophic CMP

Front 38

Describe s&s for a patient experiencing hypertrophic CMP:

Back 38

-may be asymptomatic or may have exertional dyspnea (most common), fatigue, angina, and syncope

Front 39

Describe treatment for a patient experiencing hypertrophic CMP:

Back 39

-goals of intervention are to improve ventricular filling by reducing ventricular contractility and relieving LV outflow obstruction by using b-blockers or Ca channel blockers
-digitalis are contraindicated
-antidysrhythmics
-cardioverterdefibrillator implanted
-atrioventricular pacing
-surgical resection of the hypertrophied ventricular muscle
-alcohol ablation
-any activity or procedure that causes an increase in SVR is dangerous and should be avoided
-patients who experience chest pain (from lack of blood flow to the heart) are managed by rest and elevation of the feet to improve venous return to the heart

Front 40

Describe some causes of secondary hypertrophic CMP:

Back 40

-Aortic stenosis
-Genetic
-HTN

Front 41

This type of CMP is the least common; it is a disease of the heart muscle that impairs diastolic filling and stretch; systolic function remains unaffected; the ventricles are resistant to filling and therefore demand high diastolic filling pressures to maintain CO

Back 41

-Restrictive CMP

Front 42

Describe s&s for a patient experiencing restrictive CMP:

Back 42

-fatigue
-exercise intolerance
-dyspnea
-angina
-orthopnea
-syncope
-palpitation
-may have signs of HF (pulmonary and systemic)

Front 43

Describe treatment for a patient experiencing restrictive CMP:

Back 43

-no specific treatment exists
-conventional therapy for HF and dysrhythmias
-Heart transplant

Front 44

Name causes of secondary restrictive CMP:

Back 44

-Amyloidosis
-Endomyocardial fibrosis
-Neoplastic tumor
-Post-radiation therapy
-Sarcoidosis
-Ventricular thrombosis