NUR 239: Cardiovascular Study Guide

NUR 239: Cardiovascular Study Guide

N 239: Pathphysiology and Pharmacotherapeutics I

Cardiovascular Study Guide

Pulmonary (Central) Circulation: moves blood through lungs; low pressure

-Left side—Systemic (Peripheral) Circulation: supplies all other tissues of the body; high pressure

 

Valves prevent backflow—

Valve	Location	Closes during____	Sound produced
Tricuspid v			lub sound or S1
Mitral v
Pulmonic			dup sound or S2
Aortic

 

3 layers of cardiac tissue:

Layer	Location	Function
Pericardium	outside	Tough fibrous
Myocardium	middle	Muscle layer
Epicardium	inside	Epithelial cells lining heart and valves and blood vessels

Cardiac Muscle (Myocardial) function

Striated muscle with intercalated disks (full of calcium) & gap junctions

–allows impulse to spread rapidly and entire muscle layer to contract together

–very dependant on ECF calcium ion changes for contraction

 

Electrical Stimulation & contraction: 

–involuntary contractions

• Normal Impulse starts in SA node (atrial pacemaker cells)  —  AV node (ventricular pacemaker cells)— bundle of His — bundle branches —   purkinje  fibers

 

–Regulated by ANS–Neural control

• SNS stimulation (Beta 1 receptors)—speeds up heart rate and contractility
  • Epinephrine and norepinephrine: epinephrine stimulates Beta 1 receptors in heart causing increased heart rate and contractility
• PaNS stimulation (vagal nerve)—slows down heart rate
  • Acetycholine: Vagal nerve release of ACH causes heart rate to slow

Heart rate is due to balance between “sympathetic tone” and “vagal tone” on SA node

EKG: Electrocardiography—click  for review of basic EKG tracings

Shows depolarization and repolarization of cardiac muscle cells

P wave = depolarization of atria

QRS complex = depolarization of ventricles

T wave = repolarization of ventrilces

St segment: alerts to MI

Lub: av valves closing; dub: closing of semilunar valves or aortic pulmonic

Cardiac Cycle:   click here to read more about this

See graphic of cardiac cycle

 

Systole: ventricles contract and blood ejected from heart.

 

Diastole: Ventricles relax and blood fills heart.

 

 

Cardiac output:

= amount of blood heart pumps each minute or volume of blood ejected by ventricle into the circulation per minute

CO= stroke volume * heart rate.

CO = SV x HR

–Ave. adult = 3.5 – 8.0 L/min.

–Cardiac reserve: maximum percentage of increase in CO that can be achieved above normal resting level.

–either >HR or >SV or both will >cardiac output

 

CO = SV x HR

HR = Heart Rate = frequency of ejecting blood

• Increasing HR will increase CO if the SV stays constant or increases
• BUT–an increased heart rate causes decreased ventricular filling time so  very rapid tachyarrythmias will lead to decreased cardiac output
• Chronotropic effect:  modifies heart rate

• Parasympathetic NS has a neg. chronotropic effect (slows heart rate)
  • Anti-arrythmic drugs for tachycardias have a neg. chronotropic effect
• SNS has a + chronotropic effect (speeds heart rate)

 

Stroke Volume = volume of blood ejected from ventricle with a contraction

= end-diastolic volume  minus  end-systolic volume

-is usually about 70 mL

-affected by heart;s workload and power

-power=contractility

-workload=preload and afterload

***LOOK AT CV PICTURES***

Ejection Fraction = fraction (%) of diastolic volume that is ejected from the heart during systole—is an index of left ventricular function. Normal = 65%

 

Stroke volume (and therefore cardiac output) determined by:

 

Preload = volume of blood in ventricle at end diastole

• mainly determined by venous return [amount of blood coming back to heart from venous system]

• this volume of blood causes a stretch on myocardial fibrils
• Frank-Starling Law states that the more myocardial stretch (up to a point) the harder the force of contraction
• Conditions which increase venous return: fluid overload (kidney failure), laying horizontal (not working against gravity), heart valve regurgitation
• Conditions which decrease venous return: dehydration, hemorrhages
• As > preload, >SV & CO to a point (Ex: stretched rubber band)

 

Afterload = pressure ventricles must exert to eject blood, resistance to LV ejection; pressure LV must overcome to pump out blood

• Pressure is due to  systemic vascular resistance [SVR] or total peripheral resistance [TPR] (L side) and resistance to pulmonary flow (R side)
• largely determined by BP—BP is a function of arteriolar resistance and reflects SVR or TPR
• afterload also increased with stenotic [narrowed] aortic or pulmonic valves
• Example: pushing
• As > afterload, <SV and <CO
• Conditions with Increased afterload: heart valve stenosis, high peripheral resistance, hypertension
• Conditions with Decreased afterload: arteriolar dilation

Contractility = force of myocardial contraction (intensity of myofibril contraction) regardless of blood volume in ventricle (preload)

• ability of heart to change force of contraction without changing the myocardial fiber length
• Inotropic effect—modifies contractility without changes in end-diastolic volume

• + inotropic effect—increases contractility: SNS stimulation has a + inotropic effect
• inotropic effect—decreases contractility: hypoxia has a – inotropic effect

 

• >contractility, >SV & CO
• Conditions that increase contractility: >SNS stimulation (B receptors)
• Conditions that decrease contractility: Heart muscle diseases

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Dynamics of Blood Flow to the periphery:

 

Blood vessels are dynamic—constrict and dilate to control BP and blood flow

Arteries and veins have 3 layers:

1. tunica externa
2. tunica media: muscle layer, much thicker than one of veins. Helps contain and resist pressure in the arteries, helps control the shape, and contraction and relaxation of it determines the resistance to blood flow
3. tunica intima: endothelial layer

 

Arteries:

• have thick smooth muscle layer in tunica media
• are higher pressure vessels & able to constrict & dilate

3 types of arteries:

• Large elastic arteries (aorta and distal branches)
• Medium-sized arteries (coronaries and renal)
• Small arteries and arterioles pass through the tissues—these are main controllers of systemic vascular resistance (SVR) by vasoconstricting and vasodilating

 

Veins:

• are thin walled with little smooth muscle
• very distensible (stretchable) & are low pressure vessels
• carry about 60% of blood volume and may expand to store more
• valves & leg muscle pump help propel the blood back up to heart

 

Capillaries:

• very thin walled with no muscle layer
• slower flow allows diffusion & osmosis so get delivery of nutrients and fluid to cells and removal of wastes

 

Hemodynamics = physics of blood flow

–looks at entire circulatory system & relates to pressure gradients, flow and resistance

 

–Flow is a rate—measured as mL per second and is affected by the pressure pushing the blood forward, & resistance to blood flow [velocity [speed of blood flow] & blood vessel radius]

–Factors impacting blood flow :

• Blood volume—must be enough to fill vessels
  • What are ways we can have decreased blood volume?
    Lose a lot of excess water and salt through sweating, vomiting.. or we can hemorrhage.
• Pressure—the difference in pressure between in and outflow
  • The driving force to blood flow in the body is ventricular contraction (ejection of blood out of heart)
  • This pressure is higher in the arteries than the veins
• Resistance to blood flow
  • Terms = systemic vascular resistance [SVR] or total peripheral resistance [TPR] or peripheral vascular resistance [PVR]
  • Due to blood vessels and the blood itself
  • Blood vessels:
    • length of vessels
    • **size of blood vessel (radius) – more resistance in smaller diameter vessel**main thing that determines resistance!!!!!
    • main source of resistance to blood flow in body = small arterioles
      • can contract [smaller radius] – effect on pressure=
      • can dilate [larger radius]—effect on pressure =
    • Viscosity of blood
      • more resistance with more viscous blood ( Increased HCT or polycythemia)

 

Blood has laminar flow:                formed elements in middle of stream and plasma near periphery or vessel wall–reduces frictional forces and prevents clotting factors from coming in contact with vessel wall.

 

Turbulent flow (creates murmurs and bruits)— can feel or hear, if feel then is THRILL, if hear then BRUIT.

Bruit are at arteries and murmurs are at valves. Can also get turbulence if blood is more watery (decrease in RBC)

• disordered flow where blood moves crosswise and lengthwise in vessels.
• can be created by:

• decreased viscosity of blood (decreased HCT as in anemia)
• increased velocity due to rapid HR or larger diameter vessel

 

Compliance = how easily a vessel is distended

= change in volume / change in distention pressure needed to cause this change in volume

–vessels with high compliance allow a large increase in volume with little increase in distention pressure

–vessels with low compliance allow a small increase in volume with a large increase in distention pressure—they are stiffer

 

Which type of vessels are more compliant—arteries or veins?

 

Blood Pressure

Arterial blood pressure = force exerted on arterial walls by blood flow

BP usually remains constant due to homeostasis mechanisms that adjust blood flow to meet tissue needs

Systolic: exerted right after contraction

Diastolic: exerted by the blood against the walls of arteries during diastole, when it is at rest and filling

 

Blood pressure determined by:

1. Cardiac output = volume of blood pumped into circulation per minute
2. Systemic vascular resistance (SVR)
   1. = degree of vasoconstriction and vasodilation (in arterioles)
   2. = “vascular tone”
   3. = resistance to blood flow

 

Blood pressure regulation:

1–Short-term blood pressure regulation:

• Involves neural and hormonal mechanisms
• Occurs over minutes and hours
• Is intended to correct temporary imbalances in BP: hypotension due to postural changes, exercise, hemorrhage

Neural Control of BP

Central Nervous System (CNS):

• Reticular formation of Pons and medulla à cardiovascular center
• Integrates info from hypothalamus
• Stimulated by
  • Baroreceptors: located in carotid sinus (c. artery) and arch of aorta
    • Sensitive to pressure / stretch

 

• Chemoreceptors: located in carotid body (by c. artery) and aortic body (by aorta)
  • Sensitive to changes in O2, CO2, H+
  • Main role is to regulate respiration but also can increase BP
• Stimulation of cardiovascular center causes stimulation of Autonomic Nervous System (ANS)
  • Sympathetic NS:
    • Neurotransmitter: norepinephrine, epinephrine
    • 2 types of adrenergic (SNS) receptors: alpha (a) and beta (b) receptors.
      • Stimulation of a1 receptors in vascular smooth muscle produces ______________  Effect on BP à_______________________
      • Stimulation of b1 receptors affects heart: causes increased HR & ____________ Effect on BP àincreases
    • Parasympathetic NS—vagal nerve
      • Neurotransmitter: acetylcholine
      • Vagal nerve stimulation causes decreased heart rate. Effect on BP à lower

 

Renal control of BP:

• Through balancing water and sodium in blood and urine
• Renin-angiotensin-aldosterone cycle (RAA) – see chart in Porth
  • Kidneys release renin due to low blood flow to kidneys (low BP, low blood volume) or SNS stimulation
  • Renin à conversion of angiotensin I to angiotensin II by angiotensin converting enzyme (ACE) in lungs and endothelial lining of blood vessel
  • Angiotensin II: powerful vasoconstrictor
    • à fast and potent vasoconstriction: effect on BP: increased (increased the afterload)

 

• à release of aldosterone by adrenal gland (cortex)
  • Aldosterone causes kidney to retain Na and water: increases blood volume
  • effect on BP: decreases (increases preload)

 

 

2–Long-term blood pressure regulation:

• Controls daily, weekly, monthly regulation of BP.
• Kidneys are main organ involved
  1. Changes excretion of salt and water by kidneys
  2. RAA  cycle
  3. Pressure natriuesis—
• Collateral circulation—mechanism for long-term regulation of local blood flow involving development of collateral vessels.