Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NUR370 Pathophysiology and Pharmacology > Cardiovascular Disorders > Flashcards

Cardiovascular Disorders Flashcards

1
Q

Blood pressure (BP)

A

pressure exerted by circulating blood on walls of blood vessels: CO x SVR

SBP: 90-140 mmHg
DBP: 60-90 mmHg

Clinical significance
++BP: exercise, disease, medications
–BP: pregnancy, hypovolemia, medications, bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mean arterial pressure (MAP)

A

average arterial pressure during a single cardiac cycle: (SBP + 2 x DBP) / 3

70-100 mmHg

Clinical significance
++MAP: primary HTN
–MAP: cardiac failure, sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cardiac output (CO)

A

volume of blood pumped by the heart per minute: SV x HR

4-8 L/min

Clinical significance
++CO: increased circulating volume
–CO: decreased circulating volume or strength of ventricular contraction, heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

End diastolic volume (EDV)

A

volume of blood in the ventricles immediately before contraction (the preload)

100-160 mL

Clinical significance
++EDV: increased preload
–DEV: decreased preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Stroke volume (SV)

A

amount of blood pumped by the heart per cardiac cycle

50-100 mL

Clinical significance
++SV: increased circulating volume, + inotropes
–SV: impaired contractility, valve dysfunction, heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Systemic vascular resistance (SVR)

A

measurement of resistance or impediment of the systemic vascular bed to blood flow: 80 x (MAP - RAP) / CO

770-1500 dynes sec/cm5

Clinical significance
++SVR: vasoconstrictors, hypovolemic shock
–SVR: vasodilators, morphine, late septic shock, anaphylactic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Frank-Starling Mechanism (heart action)

A

Increased blood volume&raquo_space; increased stretch of myocardium = increased force of contraction

  • after prolonged stretching, contractility decreases over time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Laplace’s Law

A

describes the relationship between the transmural pressure differences and the tension, radius and thickness of the vessel wall

Wall tension = (intraventricular pressure x internal radius)/wall thickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Aneurysm

A

weakening of an artery wall that creates bulge or distension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Factors affecting cardiac performance

A

Vascular system

a. preload (pressure at end of diastole)
b. afterload (resistance to ejection during systole)

Cardiac Tissue

a. heart rate
b. myocardial contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Preload

A

= pressure generated at the end of diastole, end of ventricle filling
= determined by 2 primary factors
a. amount of venous return to the ventricle
b. blood left in the ventricle after systole or end-systolic volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Implications of Preload

A

Increased preload
- any factor that significantly increases venous return
i.e. fluid overload
= therapeutic measures that ++ preload: fluids, blood products

Normal preload
++preload > ++ stretching of cardiac muscles > ++ cardiac output (Frank-Starling Law)

Decreased preload
- any factor that decreases venous return or limits ventricular filling
i.e. hemorrhage, cardiac tamponade
meds that – preload: vasodilators, diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Afterload

A 
= resistance to ejection during systole
= the force that the contracting heart must generate to eject blood from the filled heart
= depends mainly on
a. ventricular wall tension
b. peripheral vascular resistance

++ afterload = ++ pressure&raquo_space; – CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Implications of Afterload

A

Increased afterload
= caused by ++ aortic pressure and ++ SVR
= may impair ventricular ejection if ventricles cannot generate sufficient pressure
*vasopressors enhance afterload

Decreased afterload
= caused by decreased SVR, vasodilation, decreased BP, nitrates
*arterial dilators decrease afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Conditions that increase Heart Rate

A 
increased temperature
digestion
exercise
stress
hypoxia (anemia, hypovolemia)
pregnancy
stimulants
hormones (epi, NE, thyroid)
SNS activation (pain)
interventions that ++ heart rate:
pacing
atropine
dopamine
dobutamine
epinephrine, norepinephrine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Conditions that decrease Heart Rate

A

decreased temperature
parasympathetic NS activation
hypothyroidism
severe malnutrition

interventions that -- heart rate:
beta blockers
calcium channel blockers
digoxin
adenosine
antiarrhythmics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Contractility

A

how hard myocardium contracts for a given preload

increasing contractility results in increased stroke volume up to the point at which increased myocardial oxygen consumptions becomes a limiting factor

3 factors:

  • preload
  • innervation to ventricles
  • oxygen supply
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Medications that affect contractility

A

++
inotropes (dobutamine, dopamine, digoxin)

–
beta blockers, calcium channel blockers, antiarrhythmics, anesthetics, chemotherapeutic agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Factors affecting BP

A

a. baroreceptors and chemoreceptors
b. renin-angiotensin pathway
c. regulation of body fluid volume
d. vascular autoregulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Baroreceptors

A

= pressure sensitive receptors in the carotid sinus and aorta
= respond to changes in the stretch of vessel wall, sends impulse to brain to regulate
- decrease via vagus nerve (parasympathetic)
- increase via sympathetic chain

i.e. blood loss due to trauma > –BP > ++HR and vasoconstriction and ++ contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Chemoreceptors

A

= sensory receptors in the medulla oblongata, carotid and aortic bodies
= detect changes in the concentration of O2, CO2 and pH in arterial blood

i.e. respiratory illness > – arterial O2 concentration/++ CO2 concentration > ++HR, ++SV and ++BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Renin-Angiotensin Pathway

A

a. renin is released by kidney when arterial pressure falls too low
b. renin acts enzymatically on angiotensinogen to release angiotensin I
c. angiotensin I travels to lungs and is converted to angiotensin II by Angiotensin Converting Enzyme (ACE)

RESULT: elevate arterial pressure by

  1. vasoconstriction (arterioles and veins)
    - acute effect
  2. aldosterone secretion, which leads to water and sodium retention (++ extracellular fluid volume)
    - long term effect that takes place over hours to days
23
Q

Retention of Body Fluid Volume

A

increasing blood volume increases blood pressure

therefore:
to decrease BP, diuresis
to increase BP, sodium retaining hormones such as aldosterone

24
Q

Vascular Autoregulation

A

= intrinsic ability of arteries to adjust blood flow according to tissue needs
= explained by metabolic hypothesis: ++ metabolism > vasodilation > relaxation of smooth muscle encircling the vessel

25
Q

Hypertension

A

= a persistent elevation of systemic arterial blood pressure; CO x SVR

Stage 1: systolic 140-159 or diastolic 90-99
Stage 2: systolic 160 or higher or diastolic 100 or higher

26
Q

Primary HTN

A
  • 90-95% of all HTN is primary
  • no known cause, result of a complicated interaction between genetics and the environment
  • increased peripheral resistance AND increased blood volume causes sustained hypertension

contributing factors:
++SNS activity, ++ sodium-retaining hormones, diabetes, overweight, ++sodium intake

27
Q

Secondary HTN

A
  • 5-10% of cases
  • > 80% in children
  • altered hemodynamics associated with a primary disease (renal, endocrine, identifiable cause)
28
Q

Isolated systolic HTN

A
  • sustained elevation of SBP of > 140 mmHg
  • common in older adults related to loss of elasticity of large arteries
  • can cause damage to organs such as kidneys, brain, heart or eyes
29
Q

Malignant HTN

A

EMERGENCY

  • rapidly progressing SBP of > 180 or DBP > 120
  • can lead to profound cerebral edema and death
  • can lead to cardiac failure, uremia, retinopathy
30
Q

Any factor that produces an alteration in these 3 things affects systemic arterial blood pressure

A

systemic vascular resistance
heart rate
stroke volume

31
Q

How does the Sympathetic Nervous System cause HTN?

A

= SNS is regulated by the sympathetic vasomotor centre located in the medulla
= NE activates receptors in the SA node, myocardium and vascular smooth muscles

result:
++ HR and contractility
vasoconstriction in peripheral arterioles
release of renin by the kidneys
++ arterial pressure due to increased CO and SVR

32
Q

Activation of SNS causes

A

a. increased HR and peripheral resistance
b. increased insulin resistance
c. vascular remodelling
d. procoagulant effects

33
Q

How does the Renin and Angiotensin Mechanism cause HTN?

A

= angiotensin II acts as a vasoconstrictor and stimulates aldosterone secretion by the adrenal cortex
= increased renin secretion causes increase in peripheral vascular resistance

34
Q

How do Natriuretic peptides cause HTN?

A

Atrial natriuretic peptide (ANP)

  • secreted by the atria in response to ++ in blood volume
  • targets kidneys and decreases sodium reabsorption
  • promotes vasodilation in blood vessels

Brain natriuretic peptide (BNP)

  • secreted by cardiomyocytes in the ventricles in response to stretching
  • similar effect as ANP

C-type natriuretic peptides (CNP)

  • produced in endothelium
  • complements ANP and BNP functions

= excessive sodium intake, inadequate dietary intake of potassium, magnesium and calcium and obesity can affect their function
= renal injury can lead to dysfunction of this regulatory system

35
Q

What is the significance of endothelial dysfunction?

A

= decrease production of vasodilators and increase production of vascoconstrictors
= inability to regulate

inflammation, obesity and insulin resistance contribute to endothelial injury and dysfunction, and renal sodium retention

36
Q

Clinical Manifestations of HTN

A

= majority are symptomatic until complications develop

a. elevated BP
b. suboccipital pulsating headache (starts in AM)
c. dizziness/lightheadedness
d. S4 related to left ventricular hypertrophy

37
Q

Diagnosis of HTN

A

= not usually based upon one single elevated BP reading
= history and physical
= all patients with treated HTN need to be monitored for diabetes

Diagnostic tests:

a. routine urinalysis (kidney disease, diabetes)
b. blood chemistry: Na+, K+, Cr, BUN (kidney disease)
c. fasting blood glucose (diabetes)
d. fasting cholesterol (HDL, LDL and triglycerides)
e. ECG (dysrhythmias, left ventricular hypertrophy
f. urinary albumin excretion in patients with diabetes

38
Q

Non-pharmacologic Management of HTN

A

a. weight reduction
b. nutritional: low sodium diet, fresh fruits and vegetables, low-fat diary products, reduced saturated fat and cholesterol
c. cessation of smoking
d. avoidance or reduction of alcohol intake
e. stress management
f. exercise (30-60 mins, 4-7 days/week)

39
Q

Pharmacologic Management of HTN

A

a. diuretics (blocking reabsorption in distal tubule > decrease blood volume)
b. beta-blockers (decrease HR and contractility > reduce CO)
c. ACE inhibitors (inhibit conversion of angiotensin I to angiotensin II > blocks vasoconstriction and aldosterone effect)
d. calcium channel blockers (calcium channel blockers regulate contraction > prevent contraction)
e. vasodilators

40
Q

Complications of HTN

A

a. stroke, dementia (damage to blood vessels in the brain)
b. retinopathy, blindness (damage to arteries in the eyes)
c. aortic aneurysm or dissection
d. CAD, angina, MI, heart failure
e. Kidney injury and dysfunction, end stage renal disease

41
Q

Heart Failure

A

= not a disease but a syndrome
= associated with persistent HTN, CAD and MI
= failure of the heart to pump enough blood to maintain tissue demand

Acute: abrupt onset, following acute MI or valve rupture

Chronic: develops as a result of inadequate compensatory mechanisms that have been employed over time to improve cardiac output

42
Q

Etiology of heart failure

A

Primary risk factors

  • CAD
  • advancing age

Contributing factors

  • HTN
  • diabetes
  • tobacco use
  • obesity
  • high serum cholesterol
43
Q

Compensatory Mechanisms of HF

A

= ways in which the heart compensates to maintain cardiac reserve
can cause problems when employed over prolonged periods of time

a. frank-starling mechanism
b. SNS activity
c. neurohormonal responses
d. ventricular dilation and hypertrophy

44
Q

SNS activity as a compensatory mechanism for heart failure

A

= first and least effective mechanism
= release of catecholamines (epi and NE) to ++ HR, contractility and peripheral vasoconstriction

..increases workload of the failing myocardium and the need for O2

45
Q

Neurohormonal responses as a compensatory mechanism for heart failure

A

= RAAS, ADH, stimulated endothelium, proinflammatory cytokines

..depress cardiac function, cardiac wasting, muscle myopathy and fatigue

46
Q

Ventricular dilation and hypertrophy

A

Ventricular dilation
= enlargement of chambers that occurs when pressure in the left ventricle is elevated
= an adaptive mechanism to pump blood to body but cannot be sustained for long, CO decreases

Hypertrophy
= increase in muscle mass and cardiac wall thickness in response to chronic dilation, need more muscle mass to pump harder
= results in poor contractility, ++ O2 needs, poor coronary artery circulation and risk for ventricular dysrhythmias

47
Q

Left-sided heart failure

congestive heart failure

A
  • most common type
  • results from left ventricular dysfunction, leading to backup of blood into the left atrium and pulmonary veins

SUBTYPES

Systolic: impaired contractile or pump function
Diastolic: impaired ventricular relaxation, compliance or filling

48
Q

Right-sided heart failure

lung disease

A
  • primary cause is L-sided HF, also caused by pulmonary diseases resulting in high pulmonary resistance and right ventricular infarction (ineffective R ventricular contractility)
  • causes backward flow of blood to R atrium and venous circulation > venous distension > hepatomegaly, splenomegaly, congestion of GI tract, peripheral edema
49
Q

Clinical Manifestations of Left-sided HF

A

pulmonary congestion
- dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough and crackles

peripheral constriction
- cool, pale skin

sympathetic stimulation
- tachycardia

rapid ventricular filling
- S3

atrial contraction against the non-compliant ventricle
- S4

50
Q

Clinical Manifestations of Right-sided HF

A

venous congestion
» elevated jugular vein distention, hepatomegaly, splenomegaly

liver engorgement
» RUQ pain

congestion of liver and intestines
» anorexia, fullness and nausea

fluid retention
» weight fain, edema, ascites

impaired renal perfusion
» oliguria (abnormally small amount of urine)

51
Q

HF Complications

A

++ pressure in the pleural capillaries
» pleural effusion

cardiac enlargement may alter normal electrical pathways, esp in atria
promotes thrombus/embolus formation, risk of stroke
» dysrhythmias: atrial fibrillation, fatal dysrhythmias

liver lobes become congested with venous blood, impair liver function
» hepatomegaly

decreased CO and perfusion to kidneys
» renal insufficiency or failure

52
Q

Diagnostic Assessments

A

a. history and physical exam

b. chest x-ray
- pulmonary vascular markings, interstitial edema, pleural effusion, cardiomegaly

c. labs
- cardiac enzymes, BNP, renal and liver functions

d. ECG
- acute MI, dysrhythmia

e. hemodynamic assessment, stress testing, cardiac catheterization, ejection fraction, echocardiogram
- assess abnormalities and limitations of cardiac function

53
Q

Management of heart failure

A

a. reduction of metabolic demands with rest and O2 therapy
b. monitor daily weight to detect peripheral edema and S/S of fluid overload
c. frequently monitor BUN, cr, serum K+, Na+, Cl-
d. reduction in preload and afterload
e. salt and water restriction
f. augmentation of cardiac functions with drug therapy

54
Q

Functions of drug therapy for heart failure

A
  • diuretics and vasodilators to reduce preload
  • agents to enhance contractility
  • b-blocking agents to reduce myocardial oxygen demands and prevent inappropriate stimulation of b-adrenergic receptors
  • ACE inhibitors to suppress formation of angiotensin II

NUR370 Pathophysiology and Pharmacology (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions