Exam #2 Prep

Página 1

Blood Pressure

Mean Arterial Pressure(MAP) = Cardiac Output (CO) x Total Peripheral Resistance (TPR)

CO: amount of blood ejected by each ventricle in one min: CO = SV x HR

TPR aka Peripheral Vascular Resistance (PVR): force that must overcome to push blood through the circulatory system/F vessel wall tension. sympathetic --> constrictxn

MAP = CO x TPR

CO: determined through Heart Rate (HR) & Stroke Volume (SV) --> generates central perfusion

HR: + SNS -PNS

SV: contractility & volume

TPR: determined by diameter of vessels and viscosity of blood

Diameter; thickening of vessel wall & plaque buildup

Viscosity; polycythemia (increased RBC count), dehydration (decreased plasma vol)

decrease in volume leads to increased [blood]

Determinants:

Blood Volume: Sodium ingestion/excretion,RAAS

Beats per minute: preload ventricles, afterload/ejection,

Volume per beat: cardiac contractility from myosin/actin & heart rate

Vessel Radius: influences flow vaomotor tone

Vasoconstriction: smaller diameter : increases pressure --> decreases flow

Vasodilation: larger diameter : decreases pressure --> increased flow

Blood Viscosity: the higher the viscosity, the greater the resistance to blood flow

[RBC] --> too much = thicker b/c bulky, too little =thinner & not as capable of gas exchange

[Plasma] --> more = less dense & better flow , less= more dense & worse flow

What is the difference between pathophysiology and pathology?

pathophysiology:

pathology:

What is etiology and what are some examples of etiologic agents?

etiology:

​​​​​​​ex)

What is pathogenesis?

​​​​​​​

What is a:

sign:

symptom:

syndrome:

complication:

sequela:

If someone has significantly fewer glomeruli than normal, could that affect fluid and electrolyte excretion, blood volume, or cardiac output? If so, how?

How could that impact blood pressure?

​​​​​​​microcirculation: affected at the glomeruli because it is a (small structure) & becomes damaged from sustained constant pressure (no relief/opportunity to recoil)

compromise tissue perfusion (adapts to changes) --> remodelling --> decreased integrity tisssue/organs & functional impairment

abrupt/spontaneous change is not constant and can therefore be reversed ie) one high blood pressure reading body can adapt & recoil

​​​​​​​macrocirculation: large structures (arteries/veins) arterial pressure increases:

damage : atherosclerosis --> weakening of vessel walls & increases risk anyeurisms

increases resistance --> harder working heart

Hypertension

Primary aka essential

cause of BP elevation is unclear

Factors:

poor kidney functxn

high dietary sodium

Symptoms: none

​​​​​​​headaches, nosebleeds, tiredness & dizziness

Secondary

​​​​​​​resulting effect from identifiable cause ie) gestational hypertension

Causes:

​​​​​​​kidney disease: vessel structure changes -->further damage to kidneys

tumours; secrete homones--> increase BP

atherosclerosis; narrowing vessels b/c plaque

Complications:

​​​​​​​Kidney: nephrosclerosis

​​​​​​​smalll, rough, granular pitted scarred surface

Brain: hemorragic stroke

Eyes: retinopathy

​​​​​​​impaired --> loss vision b/c microcirculation damage/ hemorrhage

Heart& Vessels: work of heart increases over time/ways to overcome resistance to blood flow

​​​​​​​L ventricular hypertrophy: thickening of muscularis to accomodate pressure --> diameter decrease

athersclerosis

aneurysm

Página 2

Perfusion

Perfusion: flow of blood through arteries and capillaries to tissues, delivery of nutrients O2 to cells. Blood flow per kg of unit mass. Sufficient CO is required for transport decreased CO --> shock

all cells in body depend on perfusion to carry O2 & nutrients to the cells: interrelated to all other physiological concepts

flow of blood through arteries & capillaries

delivering nutrients oxygen

ml/min/kg

Factors:

Blood Volume pmped by heart (BPM)

Radius of blood vessels

Viscosity(density) blood

Velocity(rate) of flow

Blood Pressure

Central: generated by CO; Tissue/Peripheral: volume of blood that flows through target tissues

Optimal: good flow = good delivery: good vitals, NO SOB, edema, anxiety, altered mentation, or sweating, strong peripheral pulses, skin: normal, warm & dry,

Impaired: ischemia --> injury @ cell/tissue (potentially reversible) hypoxia @ tissues: cold & pale, extremmeties first (nail beds, lips, ears.) decreased CO therefore low HR & or low SV (dizziness, fainting, dyspnea, pain, arrhythmia, hypertension, MI, heart failure, shock: hemmor, cardio or anaphylactic.

No Perfusion: infarction/death: cyanosis, DLOC, low/no RR, HR, BP or Pulse, edema, infarction, hypoexemia, damage potentially not reversible

Modifiable Risks:

smoking CRAP (anything but air & water)

elevated serum lipids --> atherosclerosis (plaque)

sedentary lifestyle

obesity; comorbidity- diabetes & atherosclerosis

hypertension

Non-Modifiable Risks:

age: increases over time

gender: men > women

genetics; family hx

LEARNING OUTCOMES

Define the concept of perfusion.

Describe the scope of perfusion.

Describe the normal physiological processes that determine central and tissue perfusion.

Identify the determinants of blood pressure.

Describe the relationship between blood pressure and perfusion.

Identify the determinants of impaired perfusion and describe the possible physiological consequences.

Identify risk factors for impaired perfusion in the older adult.

Describe the pathophysiology of hypertension.

Describe the clinical complications of hypertension and the effects on perfusion.

Identify the components of an assessment.

Identify methods used to assess perfusion.

Describe the signs and symptoms of optimal and impaired perfusion.

Describe the theory behind measuring blood pressure and factors that impact blood pressure readings.

Describe the signs and symptoms of hypertension.

Identify examples of target organ damage due to uncontrolled hypertension.

Describe the primary, secondary, and tertiary management of hypertension.

Identify strategies to lower blood pressure and manage hypertension

Página 3

GAS EXCHANGE

Gas Transport; movement of oxygen and carbon dioxide in the blood through the body

-impaired when: inadequate [hemoglobin] = anemia

Gas Exchange: transportation of oxygen to cells ad removal of carbon dioxide from cells

lungs --> O2 --> pulmonry capillaries --> hemoglobin--> cells--> drops O2 & p/u CO2 --> lungs to be exhaled

Mechanics:

Ventilation = inhalation(move O2 in) + exhalation(move CO2 out)

-regulated by chemoreceptors in medulla ONLY RESPOND TO CO2 levels / [CO2] determines RR: incr CO --> incr RR

Diffusion: process by which oxygen and carbon dioxide move between alveolar air and pulmoary capillary blood.

-impairment occurs in conditions that decrease ventilation (obstructxn, neuromusc functxn, restrictve lung disease) or decreased diffusion ( diffusion b/c edema)

Impairments:

Anoxia: total depletion of O2 in body, gas exchange stops --> death

Hypoxemia: insufficient O2 @ blood

Hypoxia: insufficient O2 @ tissues

Anemia: insufficient iron & therefore insufficient hemoglobin --> decreased diffusions & exchnage

LEARNING OUTCOMES

Define the concept of gas exchange.

Describe the scope of gas exchange.

Describe the normal physiological processes of ventilation, alveolar-capillary diffusion, and pulmonary perfusion.

Identify the determinants of impaired gas exchange and describe the possible physiological consequences.

Identify risk factors for impaired gas exchange in an older adult.

tobacco use, allergies, air pollutxn exposure, immunosuppression, immobility, neurlogic/neuromuscular, alcohol/drug abuse, anesthesia, intubation, COPD, asthma, cystic fibrosis(CF), heart failure, pneumonia, chest trauma, lung cancer & pleural effusion(water on the lungs).

Describe the pathophysiology of chronic obstructive pulmonary disease (COPD).

Describe the effects of COPD on gas exchange.

Identify complications of COPD.

Identify methods used to assess gas exchange.

HX: cough, fatigue, SOB, chest pain when breathing

Examination: altered mental status(anxiety, restlessness, confusion), increased RR & HR, low SPO2, elevated temp, lung sounds, increased work of breathing, skin: pale & cyanotic, muscle weakness.

Diagnostic studies: blood gases & sputum tests, radiographic (MRI, CT, Xray) lung function tests, endoscopy/bronchoscopy, V/Q (ecg) scan

Describe the signs and symptoms of optimal and impaired gas exchange.

Describe the signs and symptoms of COPD.

Describe how pulmonary functions tests are used to diagnose and monitor COPD.

Describe the theory behind pulse oximetry.

Describe the management of COPD:

primary: infectxn control, smoking cessation, immunizatins, prevent post-op complicatxn

secondary: mantoux skin test/screening

tertiary: airway management, pharmacotherapy, oxygen therapy, breathing support, chest physiotherapy, postural drainage, positioning, chest tubes/thoracentesis, nutritional therapy, ambulatin, rest period during activity

Identify strategies to prevent COPD, manage symptoms, and slow progression.