module 3 nurs 3366

signs of good perfusion

normal BP

capillary refill < 2 secs

good mentation

skin pink

skin warm/dry

good UO

good cardiac output

cardiac output

average amount of blood left ventricle ejects per minute

formula: HR * SV

stroke volume

amount of blood ejected per CONTRACTION

Ex.) 70 ml/beat

good cardiac output

HR + heart rhythm

contractility (pump) (part of SV)

preload (vol) (part of SV)

afterload (res) (

SA node

switch that generates electrical activity allow heart to beat 60-100 impulses/min

systole

ejects blood from right & left ventricle

diastole

right & left ventricle receive blood from right & left atrium

fills will blood

preload

volume of blood before contraction 

contractility

how well the heart pumps blood

afterload

resistance to ejection of blood from a heart

inotropic

effect of different factors of contractility

positive contractility effect 

enhances contractility of heart 

negative contractility effect 

decreases contractility of heart 

right ventricle afterload

normal status of pulmonary artery and its branches through lungs (pulmonary vascular resistance or PVR)

pumps blood into pulmonary artery

left ventricle afterload

normal status of aorta & systemic arterial system (systemic vascular resistance or SVR)

pumps blood into aorta & systemic arterial system

high afterload

more res in blood vessel

more work for ventricle

neither resistance good

low afterload

less res in blood vessel

less work for ventricle 

neither resistance good 

palpable pulse

difficult to feel/weak pulse

bounding pulse

very easy to feel/strong

desired arterial BP

110/60 to 115/70 (normal is under 120/80)

normal arterial organ function

skin pink

heart good cardiac function

brain good MENTATION

kidneys good urine output

arterial insufficiency

cause ischemia

from atherosclerosis

atherosclerosis

arteries become stiffer (sclerosis) and collect fat (athero) and other things in their walls

related to aging from arterial vessels increase dmg by hypertension, smoking, diabetes,infection, high blood levels of cholesterol, genetics, free radicals

arteriosclerosis

chronic disease from aging where arterial vessels increase dmg by hypertension, smoking, diabetes, infection, high blood lvls of cholesterol, genetics, free radicals 

arteries become thick & hardened

arterial diseases 

alteration in vasomotor tone (lose flexibility of muscle wall)

non-patent lumen (build up of fat causing blockage)

S & S of arterial disease

ischemia (less O2 to blood)

decreased perfusion

ischemic pain (pain with increasing exertion & diminishing rest) 

skin pale

delayed capillary refill > 2 sec

pulse diminished/absent

delayed healing (ischemic skin ulcer)

heart less cardiac output

brain altered consciousness (stroke) 

kidneys diminished urine output

non-modifiable risk factors of arterial disease

family history (genetics)

aging

modifiable risk factors of arterial disease

diet, obesity, sedentary lifestyle

heavy alcohol consumption

type 2 diabetes

smoking

S & S of PAD 

pain

numbness of feet (paresthesia)

pale (pallor) 

prolonged cap refill (>2 sec) (pulselessness) 

feet cool to touch (poikilothermia)

no hair grows on legs (skin shiny)

ischemic skin ulcers

arterial thromboembolic S & S

pain

paresthesia 

pallor 

pulselessness

poikilothermia

hypertension BP 

130/80

hypotension BP

90/60

secondary HTN

uncommon type caused by hemodynamics with disease process

primary/essential/idiopathic HTN

caused by complex factors with 92-95% have primary HTN

widespread effect on almost all body organs

same risk factors as atherosclerosis

tachycardia

HR faster than normal

>100 beats/min

possible causes of tachycardia

neurohormonal influence of SNS (secrete epinephrine cause bind with beta receptors of heart & increases HR)

hyperkalemia causing hypopolarization

glitches with SA node & AV node

bradycardia

HR slower than normal 

<60 beats/min

possible causes of bradycardia

neurohormonal influence of PNS (vagus nerve secretes acetylcholine cause decrease HR) 

hypokalemia causing hyperpolarization 

ischemia from right coronary artery narrow blockage

glitch in SA node & AV node

dysrhythmia/arrhythmia

irregular sinus rhythm pattern

dysrhythmia/arrhythmia causes 

ischemic or infarcted tissue interferes 

electrolyte imbalances

aging

atrial fibrilation (afib)

example of atrial dysrhythmia

unorganized contraction of atria

common in elders

2 sequelae of afib

decrease in CO (lose 25% of blood)

pooling of blood in atria (either in arterial or venous thrombi)

arterial thrombi pooling of blood 

form in left atrium become emboli to brain arteries 

cause stroke (weakness on 1 side of body, confusion from ischemia in brain)

venous thrombi pooling of blood 

form in right atrium become emboli in lungs

cause pulmonary embolus (SOB, hemoptysis, chest pain, possible shock)

stroke S&S

weakness on 1 side of body

confusion from ischemia in brain

pulmonary embolus S&S

SOB

hemoptysis

chest pain

possible shock

ventricular fibrillation (Vfib)

unorganized contraction on ventricles

DEADLY dysrhythmia no CO (no blood flow —> no pulse = dead) 

negative inotropic change to contractility for SV

ischemia (blocks coronary arteries from heart muscles)

changes from preload that affects SV

increased preload = increased blood volume causing increase workload on heart

decreased preload = decreased blood volume causing CO & BP

changes from afterload that affects SV

increased afterload = harder for ventricles eject blood

decreased afterload = arterial vasodilation in LV result in shock

increased afterload for RV

pulmonary vascular resistance (PVR)

chronic bronchitis can cause PVR increasing PVR

increased afterload for LV

aorta & systemic arterial system

systemic vascular resistance (SVR)

Hypertension (HTN) increases SVR

decreased afterload 

caused in LV related to vasodilation result in shock (low BP) 

cause septic shock & anaphylaxis

coronary artery disease (CAD)

coronary arteries are narrowed or occluded by plaques (ischemia)

risk factors that cause CAD

HTN & atherosclerosis

other risk factors of getting CAD

elevated serum levels of homocysteine & C-reactive protein (CRP)

if CAD not reversed

ischemia lead to cell death (necrosis) in heart

myocardial infarction

cell death from no O2 in heart

common symptom of CAD

angina (painful constriction or tightness on heart)

S&S of angina

SOB

chest pain

sweating

pain in jaw, back, or left arm

burning, indigestion

2 categories of CAD 

stable angina 

acute coronary syndrome (ACS) 

stable angina

pain pattern predictable & well controlled

patho of stable angina

slow development of plaque so no dramatic changes stimulating arteriogenesis or collateral circulation

arteriogenesis

new blood vessel creation

treatment of stable angina

maximize coronary patency = increase perfusion to myocardium

decrease workload of heart

nitroglycerin (NTG) under tongue or patch to dilate coronary arteries

Aspirin acts as anti-inflammatory to decrease platelet adhesion 

acute coronary syndrome (ACS)

existing plaque ruptures

clot develop to fill up with lumen

arterial embolus flow to narrow coronary artery

ACS can manifest to 2 subcategories

unstable angina

myocardial infarction (MI)

myocardial infarction (MI)

total blockage of coronary artery from plaque rupture causing cell death (necrosis)

unstable angina 

causes partial blockage (occlusion) of artery 

S&S of myocardial infarction

severe unrelenting pain

EKG changes 

dx based on lab test of myocardial infarction

troponin can be used to detect dead cells

creatine kinase released from dying cells

tx for myocardial infarction

clot-busting drugs 

S&S for ACS

chest pain at rest

diaphoresis (sweating)

tachycardia

bradycardia

dysrhythmias (afib, Vfib)

outcomes of CAD 

ACS 

valve problems

shock

heart failure

failure of heart to eject blood FOWARD effectively

diagnosis from physician

epidemic in U.S

has a spectrum

left heart failure (LHF)

LV decreased contractility from ischemia or myocardia infarction

LV struggle from high afterload (SVR) from hypertension (HTN)

LV increased preload from fluid overload

decreased CO

RAAS up involvement

3 major causes of HF

pump problem

increased resistance

increased preload

right heart failure (RHF) 

RV has decreased contractility from ischemia or myocardial infarction 

RV struggle with high after load (PVR)

RV has increased preload from fluid overload 

decreased CO

RAAS involvement

2 general sequelae of HF 

diminished CO equals RAAS kicks in 

huge backup of fluid causing fluid overload

S&S of LHF

fluid backup into lungs

decreased CO

fatigue weakness

mental change

hypotension

dyspnea

prolonged capillary refill

low urine output

S&S of fluid backup into lungs

pulmonary edema

S&S of pulmonary edema

crackles with auscultation of lungs

cough up frothy blood sputum (hemoptysis)

orthopnea (SOB when lying down)

increased RR

decreased

S&S of RHF

decreased CO

fluid back into periphery

S&S of fluid backup into peripheral vein

jugular venous distention (JVD)

liver congestion (enlarged liver)

ascites (extra fluid pushed out of abdominal veins)

edema of legs & feet

cor pulmonale

RHF caused by pulmonary vascular resistance problem

caused by lung problem not heart problem

HF treatments

increase pump with positive inotropic drugs (digoxin)

decrease afterload with vasodilator drug (NTG) 

inhibit RAAS (ACE inhibitors) 

decrease preload (diuretics) 

blood test confirmation of HF

elevated BNP (b-type natriuretic peptide) confirms HF

normal PO2

80-100mmHg

normal SO2

97-100%

SO2

measured by oximeter

saturation of oxygen

normal PCO2 

35-45mmHg

PCO2 

if not normal number then respiratory problem 

normal HCO3

22-28 mEq/L

HCO3

if not normal then caused by metabolic problem 

respiratory acidosis

low pH

patient usually unconscious —> slow breathing —> retain CO2 —> blood CO2 high —> makes pH low

typical ABG: pH <7.35

PO2 <80

PCO2 >45

HCO3 normal

hypercapnia

high PCO2

respiratory acidosis compensation

kidneys will increase amount of HCO3 they make to excrete to urine to decrease PCO2

respiratory alkalosis

high pH 

patient has hyperventilation —> breathing fast —> breathing out TOO much CO2 —> blood CO2 low —> making high pH

typical ABGs: pH >7.45

PO2 normal 

PCO2 <35

HCO3 normal 

respiratory alkalosis compensation

kidneys decrease amount of HCO3 make

metabolic acidosis

low HCO3

patient with diabetic ketoacidosis (DKA) attain byproducts of glucogenesis —> acid ketone —> blood acid level high —> make pH low

typical ABGs: pH < 7.35

PO2 normal

PCO2 normal

HCO3 <22