NURS 115/Pathophysiology
Test 3 Study Guide
Disorders of Blood Flow & Blood Pressure Control
Know all arterial disorder material starting from Raynauds on
Venous flow and insufficiency
●Raynaud’s Disease
○Caused by intense vasospasm
○Most often occurs in healthy young women (we love our
ashlynn)
○Cause is unknown (some tie to tobacco use)
○Often seen in fingers (bilaterally) after drastic temperature
changes
○S/S
■Pallor → cyanosis
■treatment : 1. RELAX vasospasm (vasodilator) 2. Last
resort--calcium channel blockers
●Arterial Embolism
○Acute arterial embolism
■Pistol shot (acute onset)
■Pallor
■Polar (cold)
■Pulselessness
■Pain
■Paresthesia
■Paralysis
○Diagnosis
■Duplex doppler
■Arteriography--catheter
■Echocardiogram
○Treatment
■Thromboaspiration (clot aspiration)
■Embolectomy (clot removal via balloon catheter or
open surgery)
■Blood vessel bypass
■Medications
●Thrombolytics (streptokinase and TPA)
●Anticoagulants (warfarin or heparin)
●Antiplatelet meds (aspirin or plavix)
●Pain medication (for ischemia)
●Aneurysm
○Berry
■Often in circle of Willis
■Small, spherical dilation
○Fusiform (bulge on both sides) and Saccular (bulge on one
side)
■Often in thoracic and abdominal aorta
■Gradual and progressive enlargement of the aorta
○Dissecting Aneurysms
■Acute, life threatening
●Hemorrhage into vessel wall (longitudinal tearing)
■Diagnosis
●Px exam, CT, and MRI
■Treatment
●Surgery
●Medications to reduce BP
Virchow’s Triad and DVT prevention measures
●Virchow’s Triad
○Three factors that contribute to thrombosis
■Stasis of blood
■Increased blood coagulability
■Vessel wall injury
○Results in → thrombus (DVT)
●DVT prevention
○Early mobility
○Exercising legs (ROM, PT)
○Support stockings (need proper fit!)
○Sequential compression device (SCDs)
○Prophylactic anticoagulation (i.e. Heparin)
Mechanics of blood flow and pressure alterations
●Blood flow requirees
○Arterial pressure > venous pressure
○Arterial, venous, & capillary pressures are GREATER than the
pressures surrounding the vessels
Compartment syndrome
●Increased pressure in anatomic space that cannot expand
●Caused by decreases in compartment size or increase in
compartment volume
●May need fasciotomy
●Common in soft tissue injury, burns or excessive edema
Medications associated with heart disease
●Diuretics
○Remove excess fluids
●Nitroglycerin (NTG)
○Vasodilator (coronary arteries; every 5 min x 3)
●digitalis//digoxin
○Therapy for CHF
○Positive inotrope
■Greater squeeze
○negative chronotrope
■Slower HR
○Apical HR prior to administration, if lower than 60
(bradycardia) do NOT administer
●ACE Inhibitors (renin/angiotensin/aldosterone)
○Inhibits action of Angiotensin II (which is to constrict)
●Beta adrenergic blocking agents
○Relax smooth muscles, better breathing
●For STEMIs: MONA B (morphine, oxygen, nitroglycerin, ace
inhibitors, beta blockers) & aspirin
Venous/arterial disorders
●Arterial
○Decreased blood flow to tissues
○Impaired delivery of oxygen and nutrients
●Venous
○Interference with the outflow of blood from the capillaries
○Interference with removal of tissue wastes and return of
blood to the heart
○Incompetent veins/valves (backflow)
BP control
●Short term
○Neural
○Humoral
■Renin
●Converts angiotensinogen to angiotensin I then to
angiotensin II by ACE
●Also acts on adrenal cortex to release
aldosterone which causes reabsorption of water
●Long term (Daily, weekly, monthly, etc)
○Parasympathetic
Hypertension: classifications, causes, management
●Factors
○Age
■More common in younger men than younger women
■*more common in the elderly
○Race
■More blacks than whites
○Socioeconomic group
■More common in lower socioeconomic groups
●(cheaper food are processed--containing a lot of
salt)
●Less compliant (lack of education)
●Categories
○Primary
■Essential HTN
●systolic/diastolic HTN
○BOTH systolic and diastolic numbers
elevated
●Diastolic HTN
○Only diastolic number elevated
●Systolic HTN
○Only systolic number elevated
■Chronic elevation without evidence of other disease
○Secondary
■Elevation of BP that results from other disorder--such
as kidney disease, pheochromocytoma, contraction of
the aorta, sleep apnea
○Malignant
■Accelerated form
■Sudden elevation (diastolic > 120)
■Organ damage
■Presents with
●Massive HA
●Motor effects
●Progress to coma
●Risk factors
○Family history
○Age-related changes in BP
○Race
○Insulin resistance and metabolic abnormalities
○Circadian variations
○Lifestyle factors
■High salt intake
■Obesity
■Excess alcohol//illegal drugs
■Oral contraceptive drugs
■Stress
●Treatment
○Weight control
○Low salt diet
○Exercise
○Medications
■Diuretics
■Beta blockers
■Calcium channel blockers (dilate arteries)
■ACE inhibitors
●Classifications of BP
○Normal--S: <120 AND D: <80
○pre-HTN--S:120-129 AND D: <80
○Stage 1 HTN--S: 130-139 OR D: 80-89
○Stage 2 HTN--S: greater than 140 OR greater than/equal to 90
Shock
Know and understand the different types of shock, contributing
factors, treatment
●Cardiogenic shock
○Causes
■Damage to heart from MI
■Ineffective pumping caused by cardiac arrhythmias
■physical/structural problems
●Ventricular septal defects
●Ventricular aneurysm
●Acute disruption of valvular function
■Problems associated with open heart surgery
○Symptoms
■Similar to extreme heart failure
■Cyanotic--lips, nail beds, skin
○Treatment
■Improve cardiac output
■reduce workload on heart and O2 demand of the heart
■By:
●O2 administration (monitoring O2 sat)
●Strict I & O, daily weights
●VASODILATORS--NTG (IV), nitroprusside
●Intra-aortic balloon pump (to increase aortic
diastolic pressure), ventricular assistive device,
heart transplant
●Monitor
○VS
○Fluid and electrolytes
○Heart pressures (Swan-Ganz catheter)
●Circulatory shock
○Hypovolemic
■Causes
●Loss of whole blood
○Acute loss of 15-20% of the circulating
blood volume
○Internal hemorrhage or from 3rd space
losses
●Loss of plasma (*often seen in burns)
●Loss of extracellular fluid
■Stages
●Initial
○Circulatory blood volume decreased, not
serious effects
●Second
○Compensatory mechanisms are able to
maintain BP and tissue perfusion
(preventing cell damage)
●Third (*needs intervention)
○BP begins to fall
○Blood flow to brain and heart impaired
○Capillary permeability is increased→ fluid
leaves capillaries
○Blood flow becomes sluggish
○Thee cells and their enzyme systems are
damaged
●Fourth
○Irreversible shock, even though blood
volume may be restored and vital signs
stabilized
○Death ensues eventually
■S&S
●Polydipsia
●Tachycardia
●Pulse weak and thready
●Possibly acidosis
●Respirations may become deep and rapid
●Cool clammy skin, may have ~pallor~ due to blood
loss
●Decreased urine output (20 mL/hour or less)
■Treatment
●Treat the cause--check hemoglobin and
hematocrit
●Increase fluid, blood--IV
●Give vasopressors (constrict vessels-->elevate BP)
●Give O2
●May need heart meds
○Obstructive
■Causes
●Inability of the heart to fill properly
●Obstruction to outflow from the heart
○Which could be a result of:
■Dissecting aneurysm
■Cardiac tamponade
■Pneumothorax
■***pulmonary embolism--DVT
■Signs/Symptoms
●Signs of right heart failure
○Fatigue
○Increased peripheral venous pressure
○ASCITES
○Enlarged liver and spleen
○Distended jugular veins
○Anorexia (lack of appetite) and complaints
of GI distress
○Swelling in hands and fingers
○Dependent pitting edema
●Jugular vein distention
●Impaired venous return to the heart
■Treatment
●Embolectomy
●Pericardiocentesis
●Thrombolytic therapy
○Distributive//vasodilatory//vasogenic shock
■Causes
●Loss of sympathetic vasomotor tone
●Presence of vasodilating substance in the blood
●Presence of inflammatory mediators (histamine)
■Types
●Neurogenic
○Loss or decrease in sympathetic control of
vessel tone
○Cause
■Defect in vasomotor center in the
brain stem (*often related to spinal
cord injury)
○Signs/Symptoms
■WARM shock
■Hypotension
■bradycardia*
■Warm but DRY skin*
■Peripheral vasodilation
■Decreased cardiac/urine output--low
volume
■Altered mental status
○Treatment
■Large volumes!!!
■Atropine--to increase HR
■vasopressor --NOR Epi
■Treat the underlying cause
●Anaphylactic
○Severe allergic reaction--histamine release
(vasodilatory effect)
○Signs//symptoms
■Increased cellular permeability
■Vascular response may lead to
laryngeal edema and bronchospasm,
difficult breathing
■Abdominal cramps
■Apprehension
■Wheezing and coughing
■Circulatory collapse
■Often RAPID onset
■Warm and burning sensation to skin,
itching
○Treatment
■O2 Administration
■Meds
●Epi
●Steroids (inhibits inflammatory
response)
●antihistamine --benadryl
■Discontinue agent (whatever it is)
■Monitor of CV and respiratory status
●Septic
○Associated with severe infection (systemic
response)
○Bacteremia more common
○Endotoxins and inflammatory response
○Associated with complications--organ
failure, pulmonary insufficiency
○S/S
■Fever
■Warm, initially flushed
skin--prostaglandins
■Mild hyperventilation
■Respiratory alkalosis
■Altered state of mind
■Initially a warm shock
●May progress to cold shock
○Low cardiac output→ cold
extremities
■Poor outcome (70% die)
○Treatments
■Control bacteria/fungus, etc
■Aggressive fluid administration
■Monitor VS, labs (CBC/differential)
■Vasopressors
■Antipyretics
■May need insulin--for hyperglycemia
○Complications
■Acute respiratory distress syndrome
(ARDS)
■Acute renal failure--happens quickly
■Dyspnea
■GI complications
■Disseminated intravascular
coagulation (DIC)
■Multiple organ dysfunction syndrome
(MODS)
Cardiac conduction and Rhythm
Know the cardiac cycle, including systole and diastole and the
relationship to depolarization and repolarization and ECG tracings, also
know what valves are open and closed during the cardiac cycle
●Cardiac cycle (electrical flow and blood flow through heart--i'm
guessing)
○1st heart sound is the mitral and tricuspid valves closing
○2nd heart sound is the aortic and pulmonary valves closing
●Systole
○Ventricular contraction
●Diastole
○Ventricular relaxation
●P Wave
○SA node through atrium
○Atrial depolarization
○Atrial contraction follows P wave
●QRS Complex
○Ventricular depolarization
○--atrial repolarization is not seen but occurs here--
○Ventricular contraction (systole) follows the QRS complex
●T wave
○Ventricular repolarization
○(peaked T’s associated with hyperkalemia)
○Ventricular relaxation and filling (diastole) follows T wave
Know sinus, Atrial and ventricular Arrhythmias (only common ones)
●Normal Sinus Rhythms (NSR)
○Sinus bradycardia
○Sinus tachycardia
●Atrial Rhythms
○Atrial fibrillation
○Atrial flutter
○Paroxysmal atrial tachycardia
●Ventricular Rhythms
○Premature ventricular contractions (PVC)
○Ventricular tachycardia
○Ventricular fibrillation
Know ECG tracings including normal PR intervals, P, Q, R, S, T;
calculating HR
●Normal duration
○P → 0.08-0.12 seconds
○PR → 0.12-0.20 seconds
○QRS → 0.06 (0.04)-0.10 seconds
●Normal ECG tracings
○T wave should be smooth
○QT interval should be less than 0.40 seconds
○ST segment should not be depressed or elevated--associated
with ischemia or MI
●Calculating HR
○Count number of blocks (T wave to next T wave)
○Divide 300 by the number of blocks
○Answer is the pt’s HR
●Normal HR
○WNL: 60-100bpm
○Tachycardia: greater than 100bpm
○Bradycardia: less than 60bpm
Know about cardiac tamponade
●Slow or rapid compression of heart due to the accumulation of
fluid, pus or blood in the pericardial sac (obstructive shock)
Know about stable vs unstable angina, and prinzmetal's angina (acute
vs chronic Coronary artery disease)
●Stable Angina
○Relieved with meds/rest
○Chronic stable angina
■Associated with a fixed coronary obstruction that
produces a disparity b/t coronary flood flow and
metabolic demands of the myocardium
○Stable angina
■The initial manifestation of ischemic heart disease (in
approx. half of persons with CHD)
●Unstable Angina
○Causes (slow flow)
■Atherosclerotic plaque disruption--> fissure
■Platelet aggregation
■Secondary hemostasis
●Blood not moving
○Characteristics of pain in unstable angina
■Occurs at rest (or with minimal exertion), lasting more
than 20 minutes
■It is severe; described as frank pain and new onset (pain
they haven’t experienced before)
■It occurs with a pattern that is more severe, prolonged,
or frequent than previously experienced
○Diagnosis
■INCREASED pain severity and presenting symptoms
■Hemodynamically unstable
■Changes in ECG findings
■Serum cardiac markers
●Troponin
○Rises immediately following ischemia in
heart
○Healthy person should have 0 troponin
●CK-MB
●Prinzmetal’s//Variant Angina
○Temporary increase in coronary vascular tone
Know about Myocardial Infarction, signs and symptoms, complications
and patient teaching post MI, including medications
●Manifestations
○ABRUPT onset
○severe/crushing pain, usually substernal, radiating to the left
arm, neck or jaw
○GI complaints (N&V)--especially in females
○Complaints of fatigue and weakness
○Tachycardia, anxiety, restlessness, feelings of doom (“I just
knew I was going to die”)
○Pale, cool and moist skin
●Factors determining extent
○Location and extent of occlusion
○Amount of heart tissue supplied by the vessel
○Duration of the occlusion
○Metabolic needs of the affected tissue
○Extent of the collated circulation
○HR, BP and cardiac rhythm
●Heart Muscle Involvement
○Transmural infarcts
■Involve full thickness of the ventricular wall
■Occur when there is an obstruction of single artery
○Subendocardial
■Involves inner ⅓-½ of the ventricular wall
■Occur more frequently in the presence of severely
narrowed but still patent arteries
●Diagnosis
○Exam (EKG) & labs (looking for troponin) and studies
●Treatment
○Thrombolytic therapy/digoxin/beta blockers
○Revascularization interventions
■Coronary artery bypass grafting (CABG)
■Percutaneous coronary intervention (PCI)--stents
■Artherectomy (VERY rare)
○Cardiac rehabilitation programs
●Complications
○Post infarction recovery period
○Others
■Pump doesn’t work well (CHF)
■Reperfusion dysrhythmias
■Cardiogenic shock
■DVT
Hematology and Anemias
Know about the signs and symptoms of anemia
●Abnormally low hemoglobin level or circulating RBC level or BOTH
●Three categories
○Impaired O2 transport
■SOB
■dizziness/faint
■weakness/fatigue
■Angina
■Compensatory mechanism--tachycardia, palpitations
■Cyanosis--nail beds and mouth
○Reduction in Red Cell Indices and/or Hgb levels
■Decreased RBC, Hgb, Hct lab values
■Pallor
○S/S of the process causing anemia
■Severity--acute (much more severe symptoms) vs
chronic (has adapted)
Know the function of blood components, RBC, WBC, Platelets
●RBC
○M 4.7-6.1
○F 4.2-5.4
○Increase
■Congenital heart disease
■Polycythemia vera
■dehydration/hemoconcentration
○Decrease
■Hemorrhage
■Hemolysis
■Anemia
■Cancer
■Leukemia
■Renal failure
■Overhydration
■Dietary deficiency
●WBC
○5,000-10,000
○Increase
■Infection
■Trauma
■Stress
■Inflammation
○Decrease
■Bone marrow failure
■Overwhelming infection
■Drug toxicity
■Dietary deficiency
●Platelet
○150,000-400,000
○Increase
■Malignant disorder
■Polycythemia vera
■Post-splenectomy syndrome
○Decrease
■Hemorrhage
■Hypersplenism
■Leukemia
■Thrombocytopenia
●White Blood Differentials
○Neutrophils (55-70%) // 2500-8000
○Lymphocytes (20-40%) // 1000-4000
○Monocytes (2-8%) // 100-700
○Eosinophils (1-4%) // 50-500
○Basophils (0.5-1%) // 25-100
Know the RBC indices, characteristics, and relationships to anemia
types, signs and symptomology
●Slide 7 on Hemostasis PPT
●Mean Corpuscular Volume (MCV)
○Normal: 80-95 micrometers cubed
○Measure of average volume/size of a single RBC
○Used to categorize anemias
○Increase:
■Alcoholism, pernicious anemia (B12 deficiency)
■Folic acid deficiency
○Decrease:
■Iron deficiency
■Anemia
■Thalassemia (abnormal form or inadequate amount of
Hgb)
●Mean Corpuscular Hemoglobin (MCH)
○Normal: 27-31 pg
○Measure of avg amount (weight) of Hgb within an RBC
○Increase
■Macrocytic anemia
○Decrease
■Microcytic anemia
●Mean Corpuscular Hemoglobin Concentration (MCHC)
○Normal: 32-36g/dL or 32-36%
○Measure of avg concentration/percentage of Hgb within a
single RBC
○Increase
■Intravascular hemolysis
○Decrease
■Iron deficiency
■Anemia
■Thalassemia
●Red blood cell distribution width (RDW)
○Normal: 11-14.5%
○Indication of variations in RBC size
○Increase
■Iron deficiency anemias
■B12 or folate deficiency anemia
■Sickle cell disease
■Hemolytic anemias
Clotting cascade
●Vessel spasm
○Reduces blood flow
●Platelet plug
●Fibrin clot and blood coagulation
○Intrinsic pathway (slow)
○Extrinsic pathway (faster)
■Both interact with calcium ions--conversion of factor X
to factor Xa
■Prothrombin to thrombin
■Fibrinogen to fibrin clot
●Clot retraction
○Vessel wall edges seal
●Clot dissolution -- fibrinolysis
○Allows blood flow to continue
○Controlled by series of activators and inhibitors
■Plasminogen to plasmin
■Breaks down clot
