Cardiovascular system

÷ RA LA

tricuspid valve %hi%%%awe

☐ ☐

RV LV
filled w/ blood
-

Aortic Valve
Pulmonic

✗
valve Aorta
02

Congestive Heart Failure

conge!%
•

much blood volume " "" "

• Heart

-
Failure

heart can't
pump
} blood stays
in heart

congestion HF

Inotropic Agents Unloaded

1.) cardiac glycosides 1.) Diuretics
2.) B agonist, 2.) Vasodilators
3.) PDE } f) ACE /
Aa RBS
3.) Mixed BB

congestion

cardiac Glycosides
-
from digitalis

>
Digoxin -

exc .
in urine ; cannot be given to Px w/ renal
problems
1
Digitoxin - " "
feces

MOA : f) NAIK Atpase

N'a / ca exchange
"

f)
↓
f) No + f) ca
influx efflux
↓
↑ la
intracellularly
↓
↑ contraction

Effects : CI :
1.) t.HR
1) ↑ contraction
" "" " " " " "*
Calcium

]
2.) ↑ GIT disturbance
3.) ↓ k 1.)
3) ↓ HR 4.) ↓ Mg 2.) color blindness &

5) is blurring of vision
↑ Vago mimetic Px
taking 3.) arrhythmia
-
AV nodal f) Quinidine
4) ↓ K ↳ ↑ GG absorption Bea : DOC for CG induced
-

arrhythmia :

↑ Blood level OF GG lidocaine

5.) ↓, Mg
CG has Ntl =
toxicity * Phenytoin / alternative)
Fibric Acid derivatives tholes tyramine
& Antacids

↳ ↓ GG absorption

faithgsb
 & PDE } Inhibitors
B , agonists

ATP B,
↑B , / t) / adenylate cyclase ↑ 1.) Dopamine
↓ PDE } / 2.) Dobutamine
↑ CAMP , Amp
PDE } t)
↓
PDE } metabolizes
↑ pµµ
+
1.) Amrinone
CAMP to AMP
↓
i. must be inhibited 2.) Milrinone
↑ Ca influx
↓
Tca intracellular
↓
↑ contraction

heart failure
-

Blood SIE :
MOA
site of Action uses
" ^ / ◦ Ad " glaucoma ; mountain sickness
disease
BAD Brtnvolamide Acetollolamiae Dorzolamide
, ↓Nq1↓k ; metabolic acidosis
1.) GA , pqt ,

Diuretics ↑ Ndexc f) Nalklclcotransport Aca / CHF

/ ¥m%gency
[ OH Furosemide torsemide.Bumetanide.t-thacrynioacidtiwaltiklt.mg/4Ca Pulmory Edema

t.UA/Ototoxicit t,Na1t.K1tiM91XC9
↑ H2O exc 2.) loop Fun TO BE ,

ascending ( thick)
.

f) Na / 201 wtransportt.ca / maintenance

chbrothiau.de/HCT2i1ndapamideiCh10rthatid0nepuA lipid /* glucose for BP

kidney tubules
3.) thiazide , DfT CHIC /↑

acidosis Digoxin
Kimetabolic tox
P" "t
spirinolactone.t-prelenone.Amwride.triamler.net/Na/t'
.

4.) K sparing CT ( cortical) SEAT

Gynecomastia ; impotence
↑ Aldosterone ( Cottus)

/
-

"

an
"a "
0T
1C → HC * ICP
PCT
LOH Urine
g.) Osmotic SUM Sorbitol , Urea Mannitol 1- Brain Mannitol
LOH
, :
Blood ↑Na / H2O
descending ( thin ) hypovotemict lithium
tox
H2O -1 plasma
.

Osmosis

loop & Thiazide K -

sparing
MOA ! Carbonic Anhydrase Inhibitors
I Blood

}
lumen
lumen tubules Blood Aldosterone antagonist
-

Aldo / tenne

.it#zf-p.*i;
Blood " Na retention
Lumen
Tubular Cell
µ,
[ ✗ ex , ,
" "" " > µ,
↑ "" "
"
¥
"
"
"☐ " " "" " " ° "
K K ×
A Naexc -4

}
Ht
> K K -

sparing
1- INA Channel
* % , , µ,
* * +
retention

Hiko } ↑ # 01 > Cl T
> c,
Halo } SE :

I
×
# ↑ 1.) Metabolic Acidosis Urine
H2O
-iC④→ ☒ + H2O 2.) Hyponatremia Ng ING
3.) 4K k
tuk
urine
CI Angiotensin II also triggers your adrenal glands to release aldosterone
↑Na ⇒ hypernatriuria and your pituitary gland to release antidiuretic hormone (ADH, or
vasopressin).
Carbonic Anhydrase -

catalyzes formation of
carbonic Acid from carbon Aldosterone and ADH cause your kidneys to retain sodium.
dioxide in water
Aldosterone also causes your kidneys to release (excrete) potassium
CA Inhibitors -
↑ Natin urine through your urine.

}
ACEI
Vasodilators
Vasodilators
BEQ : mixed BB with CG increases
ARBS in pxwl CHF
lifespan

mixed BB

✗ BIBB

faithgsb
?⃝
y­
 disease
coronary ar tery

Myocardial Infarction
"
atherosclerosis
"
Disease ⇒
coronary Artery
↓ oxygenation ⇒ chest pain full
↑ Troponin
>
I
blockage
> ECG
is -1 Elevation
•

402 to partial
Angina pectoris
blockage
→ imbalance bet .
02 supply 40 , demand
stable angina
Morphine → Doc analgesia
☐ →
fastest
-

triggered by work ; relieved by rest Effects :

nitrates Depression CNS -
sedation
Doc : of
Histamine
-

-
release it Git antidiarrheal
angina
-

☐ Printz metal Emesis "

Cough center antitussive
vasodilation followed by vasoconstriction
-

series of
-

cardiovascular
Respiratory depression
-
DOC :( CBs hypotension
Euphoria
☐ unstable angina of Analgesia
-
atherosclerosis A Miosis
-

pre MI
-

02
Doc : BBS
Ñlitrates
-

hospital : nitrates _

Anti platelets
strategies :
platelet aggregation
-

- inhibit
1.) ↑ 02 supply promoters of Aggregation
2.) ↓ 02 demand 1) TXA , 2.) ADP 3.) PDE 4.) Glycoprotein Ia / Ib
a) efficiency oxygen utilisation
÷
↑ of -
irreversible
WXII aspirin)

Phospholipid ADP
µ
clopidogrel
pm ,ugre, CAMP TAMP
Nitrates ↓ PIA2 Ticlapidine
app
Arachidonic 131121 ↳ prevent
aggregation

411
Nitrate , Nitric Acid Guanylate goy ,
→

Cyclase
Algid ↑gp
Abxicimab Dypirinidone
× PGH , Eptifibatide ciloltazol
IM
↓ 1lb / "a tiropibian
←
cgmp * GMP -1×1-24
relaxation PDEs
↓
/ vasodilation ~ SIE :

↑bÉod supply
,
HiPR*7↓BP Anticoagulants Mechanism Of Action :
a.) Headache _

+ 02
supply warfarin 110972 )
3.) tolerance
warfarin
Heparin
Heparin 1.) Regular act on inactive of ✗ 11×1 " " /
"

}
-

g, :

Parenteral Oral
1AM
1.) Viagra ( hypertensive shock / = death 2.) Unpraotionated
↳ PDEs inhibitor small indirect
large acidic
-

lipid soluble -

( t) antithrombin #
→ 1-111--91×9
polysaccharide
-

Clubs & BB
liver
Blood

very slow
Rapid
"
02
Nitrates
app -1
PT / INR 3.) t.MN -
not for pregnancy
↓
" " ʳᵈᵗ "
02
" B' ↑ guppy demand CCBS 1-
I Activated
( Prothrombin Time /
international Normalized
direct -

f) IF # a
angina
-

BB ,
Ratio ) ✗a

t.no/aparinFraxiparin#Dalteparin
pregnancy ×

}
200Mt Vitamin K
200mi Antidote : protamine

⇒
D sulfate
100Mt/ beat
50M / beat

= 4 beats =L beats

↓ activity
↑ activity
, , , , man , , , ,, man ,

Thrombolytic cascade :
- "
coagulation
fibrinolytics
"
-
a.k.a
Intrinsic Extrinsic
-
MOA : increase conversion OF
to plasmin V11 V19
plasminogen ✗
llyxlla
-

plasmin dissolves Fibrin

⇒

chest pain
✗I
"YX1a
give w/ in 14hm after '
Ha t I
µ
-
-

↓
1st Gen 2nd Gen X④ ,

I 1
Rete Plate
streptokinase Plasminogen
•
•
protrombin Protrombin
Alternate ±
Fa MOAH)
↓
•

•
urokjnase
•
Tenecteplase , ,

Fibrinogen Fibrin > ↑ Plasmin

Ia
SE :
bleeding I

f) ✗ a : t-ordaparinux.Apixaba.nl?ivaroxaban
Desimdin
f) Ila : Bivahmain , Argatroban Dabigatran
,
,

faithgsb
 arrhythmia
-

R
Prob : conduction

Normal Whdh ①
:

pathway p
sa node ( pacemaker) i Avnode /
> Atrial Depolarization / > bundle of T

1006pm
His ②
60
③
-

③ ②
ventricular
↓
ventricular p Q S
, bundle branches
Repolarilatioh Depolaritationt bundles
s

Mt : Elevated IT

Depolarilatiun -
inside is more positive
I
0

f
' Na influx

✗ Kt

kefflux
outside it more Positive
Repolarization I
-

0 1
2 (a influx

µ
Nat

K I Ng
0 3k efflux
efflux influx

Plateau phase 4
4
-

0 1

↑
"

Kth
> gainful

BB → Class # → Phase 4
NACB Propanol "
SIE

} hypoglycemia
-

ESMOIOI
5/ E : -

DOB
IA -
I -10 Acebutolol
Quinidine
-
cinchonism
Procainamide -
SLE
3
Tdpltorsadesdepointes) Class # →
KCB -

Dysopyramide -

SIE :

}
Amiodarone
idp
Bretylium
•

liver, pulmonary, thyroid toxicity

/
IB -
l -10 best to give -

☐ ofe.fi/ide
1- ocainide MI
to P×w / POH Ibutilide
phenytoin
Lidocaine 501-9101
Mexeletene
CCB , -
Class IV -1>4,0 ; Prolong 3 sie :

/
If -1-10

)
Diltiaem
} both Bvlrheart edema
•

"" " " "

Moriciiine " " " Verapamil "
'

constipation
"
dipine only act
piecanide *

propafenone on BV

Adenosine ; Alt : verapamil

1) supra ventricular tachycardia -
Doc :

Tachycardia
2.) ventricular
} Doo Amiodarone
:

3.) Atrial Fibrillation

Alt : Propafenone
DOC lidocaine ; Alt : Phenytoin
4) CG Arrhythmia
-
-
:

5.) CI :(G
→ Quinidine
SLE
6.) Hydra/ azine
-

SLE
procainamide -

faithgsb
?⃝
 hyperlipidemia
prob : ↑ LDL
hypercholesterolemia → DOC : HMG-COA reductase c- )
↓ HDL Alt : acid requestrants
bile

LDL -

goes to BV

HDL -
removesfat from vessel ; transfers to liver
from monounsaturated fatty acids
-

Doc : fibril acid derivatives

Prob : ↑ TAG Tait : Niacin
Niacin / Nicotinic Acid
- ↑ intake OF Processed food
-
Vitamin B}
CHOLESTEROL SYNTHESIS available hyperlipidemia agent
most widely
-

" Ma wa -

-
multiple beneficial effect on lipoproteins ; least expensive & least tolerated
HMG-CoA
reductase
ennsmye Mevalonate
ti

¥ MOA :

Adipose tissue
Cho terol
-

tissue respiration REDOX rxns ( ↓ hepatic LDL & VLDL prod'n)

"
bit ! acid -

f) of adipose tissue hormonal sensitive blocked

✗
-

emutsityt.at ↓ hepatic TG esterification

× lipase by niacin
SÉ :
-

YAG
2-
liver
-
↑ lipoprotein lipase activity glycerol -1
FFA s FFA
the
>
happens in the liver , in evening
'
cholesterol is used to Hn
their
brie acid side Effects : TAG

>
bile acid emulsifies fat Blood
• GI effects '
KD , → 1- Dl

I reduced compliance )
•
flushing
antihyperlipi-demi.at 2x daily & increasing the dose by 50010
1000mg / day
- >
250mg
3000 /
- agents to a maximum of day
staking aspirin 30 mins before meat needed to reduce
HMG-CoA Reductase Inhibitors "
/ flushing
LDL receptors express in surface of liver
¥ er

skin / build up of bile skin)

-

13100¥ : ↓ LDL
•
itchy on

CSGPT, saot ) liver

toxicity ( esp @ ↑ doses)
for liver function
•
must test Px
.

•
hyperglycemia & dec glucose tolerance
.

1.) nepatotoxio
2) My otitis ttyporurioemia
3.) rhabdomyolysis

☐ lovastatin
☐ simrastatin SA ; @ bedtime
☐ Atorvastatin ( most potent)
☐ Prava statin
☐ Flava statin

MOA :

coenzyme A ( HMG-CoA
) reductase
inhibit 3-
hydroxy -3 methyl glutaryl
-
-
,

biosynthesis wk converts
the rate-limiting enzyme in
cholesterol ,

HMG-CoA to me valonia acid

Fibrio Acid Derivatives

☐ CIO fib rate >

-
Fenofibrate Gemfibrozil ,

FAD :

-
PPAR agonist 1 Peroxisomal Proliferation Activated Receptor ) ①
Bu

pap

-1ft
' " '"
↑ transcription of lipoprotein lipase ( IPL) that
"

f) lipoprotein
•

pptap
⇒

lipase
catabolite HDL
triglyceride , ,
↑ FFA & 2 MAG
excess : {
•
↓ decreased transcription of the apolipoprotein C gene snored in

fatty tissue
( inhibition of LPL activity )
lipoprotein Ii pose
② APO GII - inhibit destruction of
-

inhibit cholesterol synthesis 1-1

↑ HDL HI Apo
{¥ }
⇒
" HDL
-

↑ activity of LPL
↓ LDL
-

effects : ↓ LDL ; ↓ -14 ;

I /E : GI disturbance , my otitis , & erectile dysfunction

Cclofibrate)

faithgsb
?⃝
Bile Acid Binding Resins -

-
bite -
acid request rants
↳ anion exchange resins that remain in the gut bind , liver

intestinal bile acids ,

prevents their reabsorption
Ba >
¥
'

↑ BAS
& greatly ↑ their fecal absorption ↓ cholesterol is
insoluble ✗ feces

to feedback inhibition
op 7- alpha hydroxylase → Blood
↑ LDL
↑ synthesis of new bile salts →
↓ liver cholesterol →

↑ LDL receptors → b. plasma LDL

alternative for px intolerant to a statin

0 Cholettyramine ,
Coletti pot Colesevelam
,

effect :
↓ LDL (20-254)
NOTE : Resins can increase TG ! !

SIE :
constipation ↓ absorption , of many
other
drugs ( should be taken at
least 1hr 4-6 hrs after
before or

the resin
-

( t) statin . → safe !! 150% LDL reduction

)

Intestines
Cholesterol Absorption Inhibitors

☐ Eletimibe
c.not
"
a¥p%
-
inhibits the intestinal absorption of cholesterol & related

Ñ?\
phyto sterols
-

effects : ↓ LDL , ↓ TG , ↑ HDL

-
in combination µ, HMG-CoA reductase inhibitors :

1.) NPGL 1
A P2
2.) Clathrin
liver
cholesterol s

↓
Da

PGSK 9 Inhibitor

↳ destroys LDL receptors

DEVAIOCUM Ab .

☐ Aliraoumab

faithgsb
-
antihypertensives
Note : 22-7 Pas

6.) Vasodilators ↓TPR↓BP 7) CCBS

5) BB Blown
-

2.) 0 3.) 2 , blockers 4) da agonists "

BV
1.) Diuretics dipine
" -

↓ Dihydro pyridine
-

Hydra / Aline HE
*
↓
↓ dihydnpiridinc verapamil
' -

, of µ , ↓BP But
↑¥a
-

↓" Non
-

↓¥R
* -

Diaxoside
- -

c- INE release -

vasodilation p;µ;azem
-

exc "
! ↓
t.HR .↓Bp
-

Na Nitropmside
↑H↓aOexc ↓¥pp
↓wnd
!ᵗjdema
-

↓NE DOC : HTN crisis

↓NE
(cyanide toxicity)
.

.
, ↓ ↓
↓ t.co ↓BP
↓ CACB
-

↓ ↓ˢA i. cont
-
.

MOA :

↓ ,a
.
Minoxidil ↓
↓ Plasma V01
↓
↓
↓BP
↓¥pp ,
( hirsutism ) ca intracellular
I
↓HRt↓TPR
↓ ¥BP
¥p smyyelaxation
↓BP
Reflex tachycardia vasodilation
↓
vasodilators
-

* TPR

↓
1.) ACE inhibitors BP
"
pril
-
"

ACE RAAS
bradykinin >
inhibit PROBLEM :
1.) ↓BP
SE :
coughing >

2.) ↓Na
3.) ↓BV

Renin
8) ARB Angiotensin ogen > Angiotensin I

-
"
Sartan
" ↓ ABE

Angiotensin ICMOIT potent 1 Angiotensin 11

Vasoconstrictor receptor
↓ "
"
Sartan
↑ TPR -

AARB
↓
TBP

Aldosterone

lumen blood

> Na
↑
Angiotensin II also triggers your adrenal glands to release aldosterone.
ret .

Aldosterone causes your kidneys to retain sodium. Aldosterone also causes your kidneys
K
< to release (excrete) potassium through your urine.
excretion

HW↑

↑BV

faithgsb
Trust in the Lord with
all your heart
Proverbs 3:5-6