cardiac exam 2

exposure to cold--> inc SVR
eating a heavy meal stimulates vagus nerve and decr HR
HTN,
Arrythmias
valve disfunction
fever: increases metabolic demand
low bp: SVR dec cant perfuse well
Anemia

Predicatable, observable s/s
relieved by rest and nitro

changed from previous patten, mor eintense, not
relieved by rest and NItro
You can give 1 tab nitro, q5min x3
if not relievd=unstable, call EMS

spasms of coronary artery
happens when pt is resting
caused by nicotine, alcohol, cocaine
TX: nitro (vasodilator)
and Cal channel blocker (vasodilates, tx tachy)

EKG shows ST depression
asymptomatic
Most dangerous, silent killer

t wave inversion
st wave depression

st seg elevation

necrotic tissue
Q wave got bigger, taller
or if there previously was not a q wave, now there is

dyspnea
n/v
profound weakness
dizziness /dec CO
palpitations

tachypnea
SOB, crackles
Sa02, < 90%
need to sit upright to breathe well
color pale dusky grey

Increase blood supply back to heart
decrease demand b/c want to dec 02 consumption
pain relief
modify risk factors
OVERALL GOAL is to save muscle from going to zone of infarction/necrosis

Arrythmias: most common is PVC which can lead to Pulseless vtach or vfib
dont treat PVC unless symptomatic & pt cant tolerate
pump failure
Cardiogenic shock
Right sided MI: prob w/ oxygenation
Left sided Mi: problem w/ perfussion to tissues

MONA
Oxygen 1st 4L NC
Aspirin 2nd, give immediately 325 mg
GET VITAL
Nitroglycerin 3rd (vasodilator)
wear gloves
Morphine 4th arterial venous dilator

LOW DOSE 2-5: DILATES THE RENAL ARTERY
Med dose 5-10: pos inotropic
High dose: 10-20 vasoconstriction

given to avoid high doses of dopamine that could increase b/p
can give together or seperate

vasodilator: retain na and h20,
cyanide poison, watch out fro low b/p

venous dilation, decreases preload volume (atria blood going in r/l atria)
doses higher than 30mcg/kg/min dilate the arteries
start at 5mcg/kg/min for effect increase til you get the desired effect
decreases volume going into the heart to decrease the workload

1st generation: non selective (propanolol) heart and lung
Newer: BETA 1 only,
dec HR, dec contractility, dec automaticity= heart wont work hard
can cause depression
will have decrease hr and b/p

lowers 02 requirements by dec HR
Arterial vasodilation, dec afterload (SVR)
diliatezem (common)
verapamil, nifedipine
USED for lowering b/p or HR

blocks formation of angiotensin
decreases afterload
improves contractility
decreases malignant arrythmias
vasodilates

increases diuresis and natriuresis (gets rid of water and sodium)
decreases aldosterone
vasodilates
ONLY use when pt has sever CHF

fibrinolitycs:
break down clots, early
treatment decreases mortality
give within 12 hrs
BLEEDING PRECAUTIONS

fibrin-selective, less systemic
tpa, activase
reteplase

contractility of the heart

heart rate
pulse

conduction throught the heart
duration of the QRS complex

heparin antidote

warfarin

What to do when theres Pulseless Elctrical acitivity?
Or pulseless a-fib

shock
CPR
SHOCK HIGHER
EVERYBODY SHOCK: EPI/VASOPRESSIN DEFIB
LITTLE SHOCK-LIDOCAINE, DEFIB
AMPLE SHOCK; AMIODARONE SHOCK
MEGA SHOCK: MAGNESIUM SHOCK

Atropine or pacemaker
dopamine if hypotensive
epinephrine drip if no improvement
factors-consider causes

asystole/pulseless electrical activity

What to do when theres Pulseless Elctrical acitivity?
Or pulseless a-fib

shock
CPR
SHOCK HIGHER
EVERYBODY SHOCK: EPI/VASOPRESSIN DEFIB
LITTLE SHOCK-LIDOCAINE, DEFIB
AMPLE SHOCK; AMIODARONE SHOCK
MEGA SHOCK: MAGNESIUM SHOCK

Atropine or pacemaker
dopamine if hypotensive
epinephrine drip if no improvement
factors-consider causes

asystole/pulseless electrical activity

causes:
ripped aorta
retroperitoneal duodenum, tears and end up with peritonitis

tensile stress, stretch on the splenic capsule

compressive stress, pressed together eg comminuted bone fracture

shearing stress from a tangetial source tearing of the aorta

trying to reduce the incidence of trauma

prevent injury from occuring and decreasing the severity of the injury

mvc
motorcycle crashes
guns
falls
crush injuries
machine
humans(bites, assaults, battery)

heat
steam
fire

drugs
insects/snakes
posions

rays of sunlight
sound waves (explosion)
electromagnetic waves (x-ray exposure)
nuclear leak

Clots in Left main cuts off Left descending and circumflex and wont allow heart to pump blood out to body

2/3 of coronary blood supply occurs during ____

20-40 beats per minute

40-60 beats per minute

60-100 beats per minute

Contraction of the heart is affected in large part by ___________

This phase is due to the opening of the fast Na+ channels causing a rapid increase in the membrane conductance

action potential occurs with the inactivation of the fast Na+ channels. the movement of K+ and Cl- ions moves out

This "plateau" phase of the cardiac action potential is sustained by a balance between inward movement of Ca2+ outward movement of K+.

During phase 3 (the "rapid repolarization" phase) of the action potential, Ca2+ channels close, while K+ channels are still open. This ensures a net outward current, corresponding to negative change in membrane potential, thus allowing more types of K+ channels to open.

resting membrane potential. This is the period that the cell remains in until it is stimulated by an external electrical stimulus (typically an adjacent cell). This phase of the action potential is associated with diastole of the chamber of the heart.

The phlebostatic axis is located at the fourth intercostal space and 1/2 the anterior-posterior (AP) diameter of the chest. This approximates the location of the right atrium.