331 test 2 Flashcards
nervous system can be separated into
central and peripheral
central nervous system
brain and spinal cord
peripheral nervous system broken down into
somatic and autonomic
somatic
skeletal muscle
autonomic nervous system can be broken down into
parasympathetic and sympathetic
parasympathetic
rest and digest. cholinergic receptors
sympathetic
fight or flight. adrenergic receptors with alpha and beta receptors
what does parasympathetic do to your eyes, SA node, bronchial muscle, arteriole, and gastric motility
constriction in eyes and brachial muscles, SA node decrease, arteriole dilation, increase in gastric motility
what neurotransmitter is connected with parasympathetic
acetylcholine
inotropic
contractibility of the heart
chronotropic
effect heart rate
dromotropic
electrical conduction of the heart
glycogenolysis
breaking down of glycogen into glucose
sympathetic neurotransmitter
norepinephrine and epinephrine
what is epinephrine? and what does it do?
nonselective adrenergic agonist for both beta 1&2 and alpha 1. vasoconstrictor, bronchodilator, and increases inotropic, chronotropic, and dromotropic
PEA
pulseless electrical activity
indications for epinephrine
PEA, asystole, bradycardia
asystole
cardiac arrest rhythm with no discernible electrical activity on the EKG monitor. It is a flatline EKG, P Waves and QRS complexes are not present The heart is not functioning.
miosis
pupillary constriction
what can increase chances of hypertenstion
age, diabetes, being African American, and diet (obesity)
what diseases are associated with hypertension
MI, renal disease, stroke
what 2 systems are involved in hypertension
RAAS (renal) and central nervous system
what is the most common primary diagnosis in the US
hypertension
what can lead to an increase in circulating volume
an increase in intake of Na and/or decrease excretion of Na and K, Ca, Mg deficiency
ANP
Atrial Natriuretic Peptide
BNP
Brain natriuretic peptide
CNP
C-type natriuretic peptide still need to figure out what this does
urodilatin
hormone that causes natriuresis through increasing renal blood flow
natriuretic hormones
ANP, BNP, CNP, urodilatin
what causes hypertension?
sustained increase in peripheral resistance and cardiac output
SVR
systemic vascular resistance. reflects changes in the arterioles, which can affect emptying of the left ventricle
increase in RAAS leads to
decreased renal salt excretion so increase salt retention
what does sympathetic nervous system do to you HR and vessels
increase heart rate and vasoconstrict
what can prolonged hypertension do to your body?
vascular remodeling, increase renin/angiotensin, renal sodium retention, and procoagulant
primary hypertension
due to genetics and environment
secondary hypertension
usually from disease process. Is reversible
complicated hypertension
leads to target organ damage such as LVH, HF, CAD
LVH
left ventricular hypertrophy
CAD
coronary artery disease
CVA
cerebral vascular accident (stroke)
TIA
Transient ischemic attack (mini stroke)
what can complicated hypertension do to your body?
LVH, HF, CAD, kidney damage with microalbuminuria, stroke, vascular sclerosis
microalbuminuria
albumin in urine – sign of kidney damage (something bad is going to happen)
hypertensive crisis
BP 180/110+, rapid onset. can cause organ damage, CVA, or stroke
what can cause a hypertensive crisis
alcohol withdrawal, stimulant drugs, or pregnancy
High blood pressure guidelines
Normal: Less than 120/80 mm Hg;
Elevated: Systolic between 120-129 and diastolic less than 80;
Stage 1: Systolic between 130-139 or diastolic between 80-89;
Stage 2: Systolic at least 140 or diastolic at least 90 mm Hg;
Hypertensive crisis: Systolic over 180 and/or diastolic over 120, with patients needing prompt changes in medication if there are no other indications of problems, or immediate hospitalization if there are signs of organ damage
Microvascular
arteries, veins, capillaries
microvascular dysfunctions stems from?
stems from constant state of increased volume and increased vasoconstriction
adipokines
inflammatory mediators released by adipocytes
adipokines release
leptin and adiponectin
leptin control what in the body?
appetite suppression and increase metabolic rate
what happens to leptin and adiponectin when you are obese?
increase in leptin and decrease in adiponectin
what do adiponectins deal with
insulin
what do increased levels of leptin do?
cause resistance by increases SNS, decreasing renal sodium excretion, and causing inflammation
what does a decreased amount of adiponectin do to your body?
increases SNS, increases RAAS, and decreases nitric oxide
Bariatric surgery
weight loss surgery. usually beings hypertension back to secondary
what does microvascular dysfunction lead to?
vascular remodeling, endothelial dysfunction, decrease in vasodilator release, and sustained HTN
salt retention and increased volume =
vascular resistance
what causes salt retention
increased Na intake, renin secretions which would stimulate RAAS, and decrease of K, Ca, and Mg
what does angiotensin do?
stimulates the release of aldosterone from the adrenal cortex to promote sodium retention by the kidneys
Atherogenesis
plaque formation. a disorder of the artery wall that involves adhesion of monocytes and lymphocytes to the endothelial cell surface
Atherosclerosis
plaque with the addition of inflammation around vessel
what does increased angiotensin 2 do?
systemic vasoconstriction, arteriolar remodeling, endothelial dysfunction, insulin resistance, platelet aggregation, Hypertension end-organ damage
Increases platelet aggregation =
increase risk of blood clot
what can cause increased volume?
renal injury that causes renal vasoconstriction, tissue ischemia that causes inflammation and sodium retention
tissue ischemia
a restriction in blood supply to tissues, causing a shortage of oxygen
proper function of natriuretic hormones
vasodilation, sodium excretion, decrease BP
improper function of natriuretic hormones
increase vascular tone, sodium retention that increases blood volume, and increase in BP
BNP test
blood test that measures levels of a protein called BPN that is made by your heart and blood vessels.
what does higher levels of BNP mean? what is considered normal?
less than 100 = normal. higher than 100 = heart failure, increase in volume, or ventricle stretch
decrease in venous return =
decrease preload
increased ANP/BNP levels linked to
heart failure, ventricular hypertrophy, atherosclerosis
ANP linked to
right atrium
two things that affect cardiac output
stroke volume and heart rate
what affects stroke volume and heart rate
preload, after load, and contractility
how does the body compensate when BP drops
increase HR, increase contractility, increase preload, vasoconstriction by SNS and RAAS
dysfunction of the natriuretic hormones can be due to
low levels of Ca, K, or Mg
vomiting and diarrhea may cause toxicity for which drug?
digoxin cause vomit and diarrhea can make you lose potassium and hypokalemia increases potential digoxin toxicity
most common reason for people over 65 years old to be admitted into hospital
heart failure
what does left heart failure (systolic) do to CO and EF?
decrease CO and EF is less than 40%
what is EF?
EF is the ejection fraction. a measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction
what affects Stroke volume
contractility, preload, and after load
what happens with contractility and preload during left systolic heart failure?
decrease in contractility and increase in pre load
why would preload increase during left heart failure?
decrease contractility and increased vascular volume
what leads to decreased contractility during left sided heart failure
myocyte disfunction
constant ischemia in the heart leads to
increase workload which causes hypertrophy, increase RAAS and SNS and myocardial remodeling
what does decrease CO lead to?
decrease in renal percussion, increase in RAAS which increases after load and preload. Also activates bars-receptors which increase ADH which increase SNS which increase after load and preload.
LVH
Left ventricular hypertrophy is enlargement and thickening (hypertrophy) of the walls of your heart’s main pumping chamber (left ventricle)
LVEDV
Left Ventricular End-Diastolic Volume.
effects of decrease contractility
increase preload - stretching of myocardium and decrease of lumen coronary arteries - myocardial ischemia - leads right back to more decreased contractility
effects of increased afterload
increases left ventricle workload - increase RAAS and SNS which causes hypertrophy causes increases demand for oxygen causes ventricular remolding which leads to decrease in contractility which increases RAAS and SNS and leads to more vascular resistance
how does a patient present with left systolic heart failure
fatigue, pulmonary edema, dyspnea, orthopnea, cough with frothy sputum, S3 heart sound
orthopnea
shortness of breath while laying down
what tests should you run with heart failure
echocardiogram and BNP
ASA
aspirin which is an anti platelet
Ace inhibitors and ARBs
reduce preload and after load, decrease volume and PVR, are cardio and renal protective
diuretics do what to preload
reduce preload by reducing volume
treatment for heart failure
beta blocker, anti platelet, salt restriction, diuretic, ACE inhibitor or ARB
what is a first line treatment for HTN if no other comorbidities exist?
diuretic - decrease BP, CO, and preload
what should you do when administering diuretic
monitor electrolytes, BUN, and creatine
lasix
Furosemide - antihypertensive and diuretic
adverse affects of lasix
vertigo, hypotension, hypokalemia, fatal skin rash
Cardiac glycosides Mechanism of actions and what do they do to inotrope, chronotrpe, and dromotrope
increase sodium and calcium (positive inotrope), augments parasympathetic stimulation (negative chronotrope), prolongs conduction (negative dromotrope)
what cardiac glycoside did we learn
Digoxin
what do you have to be careful with when using digoxin?
toxicity = bradycardia, confusion, and visual disturbances
what do you use to reverse digoxin toxicity?
digoxin immune FAB (digifab)
if someone presents with hyperkalemia and life threatening cardiac dysrhythmias what do you give them?
digoxin immune FAB (digifab)
if calcium is not leaving the cells within the heart what happens
there’s an inability to relax the heart
DOE
dyspnea on exertion
Left heart diastolic failure
filling problem with normal EF and CO
patient presentation with Left heart diastolic failure
DOE, fatigue, S4 heart sound, pulmonary edema and hypertension
right heart failure
seen with CHF and pulmonary hypertension because there is inadequate blood flow to the lungs
what will you see with right heart failure
peripheral edema, hepatosplenomegaly, venous congestion, COPD, pulmonary endothelial remodeling, hypoxic vasoconstriction
hepatosplenomegaly
enlarged liver and spleen
High output failure
ineffective tachycardia but CO in normal
what can cause high output failure?
anemia by decreasing oxygen carrying capability or sepsis by vasodilation and anaerobic metabolism
LLMs
lipid - laden macrophages
what do LLMs release?
inflammatory cytokines which causes oxidation of LDL
stages of atherosclerosis
damaged endothelium, cholesterol sticks to vessel to “repair”, leads to a fatty streak, foam cells, and platelets attach to endothelium, fibrous tissue encapsulates lipid areas and causes plaque buildup. then thinning of college cap leads to rupture and capsule breaking off and forming a blood clot
inflammatory cytokines
interleukins, interferons
risk factors to atherosclerosis
Poor diet High cholesterol Smoking Sedentary lifestyle Hypertension (biggest risk factor)
intermittent claudication
pain with walking
how does peripheral artery disease present?
can be asymptomatic but if not will show as intermittent claudication, severe color change, loss of pulse, severe pain
how do you test and treat peripheral artery disease?
test with ankle/brachial index and treat with anti platelets and reducing risk factors
coronary artery disease
hardening or narrowing of arteries which impairs heart pumping ability
risk factors for coronary artery disease
Hypertension
Endothelial injury from a constant state of high pressure
Hypertrophy – vascular remodeling from constant pressure and stretch
path from HTN to ischemia
HTN-endothelial injury-hypertrophy-increased oxygen demand-increased SNS-increased RAAS - ischemia
first line drug therapy for hypercholesterolemia
antilipemics HMG-CoA reductase inhibitor, also known as statins. reduces LDL and plasma triglycerides and increases HDL
Statin Adverse effects
elevated liver enzymes, myopathy, rhabdomyolysis
what is dark urine a sign of while taking statin
sign of rhabdomyolysis
what is rhabdomyolysis
muscle breakdown and myoglobin protein end up in urine
process of going from atherosclerosis to myocardial ischemia
plague-thrombus formation-ischemia
what happens after ischemia to the heart
there is glucose deprivation which lead to aerobic metabolism which causes lactic acid to build up and cause pain
after myocardial ischemia how lung do you have until MI?
20 minutes
fatal arrhythmias
V fib and V tac
types of angina
stable, prinzmetal, and unstable
stable angina
predictable shows a lot like MI
prinzmetal angina
unpredictable and occurs at rest, usually at night.
unstable angina
results from reversible myocardial ischemia but on your way to MI
silent ischemia
mental stress induced ischemia
STEMI
ST elevation = infarction = tissue death
non-STEMI
ST segment depression = ischemia = lack of blood flow
CPK-MB
creatine phosphokinase MB
what happens when you go through myocardial infarction
decrease contractibility, altered LV compliance, decrease stroke volume and ejection fraction, SA node malfunction, increased left ventricular end diastolic volume, inflammation, and angiotensin 2 release, myocyte remodeling
CRP
A plasma protein that rises in the blood with the inflammation
what can be signs of inflammation
CRP and leukocytosis
you get a surge of what during MI?
catecholamines
what tests should you use for MI
CPK-MB, troponin, CRP
MI does what to contractibility?
decreases it
what does decreased contractibility do?
decrease EF and renal perfusion (increase preload), increase LVEDV and renin/angiotensin (increase after load)
how will a patient present with MI?
depends on stage of progression, but will have pain, SOB, impending doom, could look pale and be cool
MONA
Morphine, oxygen, nitroglycerin, and aspirin
you do not want to use what with nitroglycerin?
erectile dysfunction meds
Nitroglycerin
anti anginas therapy - decreases preload and after load. coronary artery dilation
nitroglycerin contraindicated for
anemia and ED drugs
adverse effects of nitroglycerin
headache, hypotension, tachycardia
when is preload increased?
hypervolemia, regurgitation of cardiac valves, and heart failure
when is after load increased
hypertension and vasoconstriction
calcium channel blockers
inhibit calcium entry into cardiac/smooth muscle cells and promotes muscle relaxation
what calcium channel blockers did we learn
amlodipine and diltiazem
what does amlodipine do?
decreases after load, reduced cardiac workload, reduces oxygen demand
what does diltiazem do?
negative inotrope, dromotrope, and chronotrope
when and how should you take amlodipine
orally for angina or HTN
when and how should you take diltizem
IV for a-fib, A-flutters, or SVT
SVT
Supraventricular tachycardia
when is troponin considered elevated
when its over 0.04 and we usually want to test every 3 hours
beta blockers
end in “olol” decrease contractibility, decrease HR
what can beta blockers mask
hypoglycemia so be careful when giving to diabetics
ACE inhibitors
end in “pril” decrease preload and after load and stops the conversion of angiotensin 1 to angiotensin 2
ARBS
“artan” decrease preload and after load
all ACE inhibitors have a black box warning of
fetal toxicity
phentalomine
causes vasodilation
first dose phenomenon
causes orthostatic hypertension
first dose phenomenon
fall in blood pressure
decreased mg, ca, and K can lead to
high BP
when is troponin released
with cardiac cell death
an echocardiogram shows us what
EF
what does your blood concentration look like during Heart failure?
diluted so your sodium looks low due to all the fluid retention
what happens with renin during HF
renin is recreated due to low blood flow to kidneys due to vasoconstriction
what happens with renin during HF
renin is recreated due to low blood flow to kidneys due to vasoconstriction
epinephrin
alpha and beta agonist
tamsulosin (flomax)
alpha 1 blocker
clonidine (catapres)
alpha 2 agonist
metaprolol (lopressor)
beta 1 blocker
carvedilol (coreg)
nonselective beta and alpha blocker
lisinopril
ace inhibitor
losartan (cozaar)
ARB
enalopril
ACE INHIBITOR
hydralazine
vasodilator
amlodipine (norvasc)
calcium channel blocker
diltiazem
calcium channel blocker
Lipitor
Statin
furosemide (lasix)
loop diuretic
nitroglycerin (nitrostat)
nitrate
Digoxin
cardiac glycoside
what do alpha receptors do
vasoconstrict cardiovascular, bladder constriction, promote glycogenolysis, mydriasis
what do beta 1 receptors do
increase contractility in heart, increase HR, promote renin secretion
what do beta 2 receptors do
bronchodilate, glycogenolysis, vasodilation
adrenergic agonist (alpha and beta)
promote SNS. low dose beta, high dose alpha
alpha 1 blocker
smooth muscle relaxation, vasodilation. used for men with enlarged prostates and rhaynaud’s disease
rhaynaud’s disease
fingertips and toes start to turn blue due to low perfusion.
alpha 2 agonist
centrally acting, blocks SNS activity, decreases PVR, BP, and HR. used for opioid withdraws and hypertension
alpha 2 agonist adverse effects
bradycardia, hypotension, or rebound hypertension if stopped abruptly,
Beta 1 blocker
negative ionotrope (SNS blocked), negative chronotrope (SNS blocked), and negative domotrope (fills ventricle), brings workload of heart down, O2 demand down, and renin secretion down
beta 1 blocker indication
MI and angina
Nonselective beta and alpha blocker
blocks glycogenolysis, inhibits insulin secretion, brings workload of heart down so can mask hypoglycemia symptoms so be careful when giving to diabetic patients
indication for Nonselective beta and alpha blocker
heart failure, beneficial for hypertension and angina
Ace inhibitor
blocks AG1 to AG2, brings SVR down which decreases after load, blocks aldosterone which prevents sodium and water retention which brings volume down and decreases preload
ace inhibitor indicator and what do they protect
hypertension or heart failure, protect both heart and renal
adverse effects of ACE inhibitors
dry cough, hyperkalemia, acute renal injury, angio edema
what is a serious concern for ACE inhibitors
black box warning of fetal toxicity
ARBs
blocks vasoconstriction of vascular smooth muscle, and blocks production of aldosterone. with being a vasodilator is decreases SVR which brings afterload down
ARBs indication
hypertension and heart failure, lowers mortality after MI
Vasodilator drugs
directly causes arteriolar and venous smooth muscle relaxation, decreases SVR which decreases afterload
Vasodilator drug indication and contraindication
used for hypertension. do not use with CAD or diastolic dysfunction
what do nitrates do
coronary vasodilator and antianginal can cause headache
what do calcium channel blockers do
relax vascular smooth muscle, effective in treating angina
what are cardiac glycosides used for
heart failure
what are statins used for
to bring cholesterol down
