Cardiovascular Disorders Flashcards
Blood pressure (BP)
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
Mean arterial pressure (MAP)
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
Cardiac output (CO)
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
End diastolic volume (EDV)
volume of blood in the ventricles immediately before contraction (the preload)
100-160 mL
Clinical significance
++EDV: increased preload
–DEV: decreased preload
Stroke volume (SV)
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
Systemic vascular resistance (SVR)
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
Frank-Starling Mechanism (heart action)
Increased blood volume»_space; increased stretch of myocardium = increased force of contraction
- after prolonged stretching, contractility decreases over time
Laplace’s Law
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
Aneurysm
weakening of an artery wall that creates bulge or distension
Factors affecting cardiac performance
Vascular system
a. preload (pressure at end of diastole)
b. afterload (resistance to ejection during systole)
Cardiac Tissue
a. heart rate
b. myocardial contractility
Preload
= 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
Implications of Preload
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
Afterload
= 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»_space; – CO
Implications of Afterload
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
Conditions that increase Heart Rate
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
Conditions that decrease Heart Rate
decreased temperature
parasympathetic NS activation
hypothyroidism
severe malnutrition
interventions that -- heart rate: beta blockers calcium channel blockers digoxin adenosine antiarrhythmics
Contractility
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
Medications that affect contractility
++
inotropes (dobutamine, dopamine, digoxin)
–
beta blockers, calcium channel blockers, antiarrhythmics, anesthetics, chemotherapeutic agents
Factors affecting BP
a. baroreceptors and chemoreceptors
b. renin-angiotensin pathway
c. regulation of body fluid volume
d. vascular autoregulation
Baroreceptors
= 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
Chemoreceptors
= 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
Renin-Angiotensin Pathway
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
- vasoconstriction (arterioles and veins)
- acute effect - aldosterone secretion, which leads to water and sodium retention (++ extracellular fluid volume)
- long term effect that takes place over hours to days
Retention of Body Fluid Volume
increasing blood volume increases blood pressure
therefore:
to decrease BP, diuresis
to increase BP, sodium retaining hormones such as aldosterone
Vascular Autoregulation
= 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
Hypertension
= 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
Primary HTN
- 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
Secondary HTN
- 5-10% of cases
- > 80% in children
- altered hemodynamics associated with a primary disease (renal, endocrine, identifiable cause)
Isolated systolic HTN
- 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
Malignant HTN
EMERGENCY
- rapidly progressing SBP of > 180 or DBP > 120
- can lead to profound cerebral edema and death
- can lead to cardiac failure, uremia, retinopathy
Any factor that produces an alteration in these 3 things affects systemic arterial blood pressure
systemic vascular resistance
heart rate
stroke volume
How does the Sympathetic Nervous System cause HTN?
= 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
Activation of SNS causes
a. increased HR and peripheral resistance
b. increased insulin resistance
c. vascular remodelling
d. procoagulant effects
How does the Renin and Angiotensin Mechanism cause HTN?
= angiotensin II acts as a vasoconstrictor and stimulates aldosterone secretion by the adrenal cortex
= increased renin secretion causes increase in peripheral vascular resistance
How do Natriuretic peptides cause HTN?
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
What is the significance of endothelial dysfunction?
= 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
Clinical Manifestations of HTN
= 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
Diagnosis of HTN
= 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
Non-pharmacologic Management of HTN
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)
Pharmacologic Management of HTN
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
Complications of HTN
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
Heart Failure
= 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
Etiology of heart failure
Primary risk factors
- CAD
- advancing age
Contributing factors
- HTN
- diabetes
- tobacco use
- obesity
- high serum cholesterol
Compensatory Mechanisms of HF
= 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
SNS activity as a compensatory mechanism for heart failure
= 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
Neurohormonal responses as a compensatory mechanism for heart failure
= RAAS, ADH, stimulated endothelium, proinflammatory cytokines
..depress cardiac function, cardiac wasting, muscle myopathy and fatigue
Ventricular dilation and hypertrophy
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
Left-sided heart failure
congestive heart failure
- 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
Right-sided heart failure
lung disease
- 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
Clinical Manifestations of Left-sided HF
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
Clinical Manifestations of Right-sided HF
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)
HF Complications
++ 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
Diagnostic Assessments
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
Management of heart failure
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
Functions of drug therapy for heart failure
- 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
