exam 2 final content

what are the signs of heart attack in women

- indigestion

- choking sensation (esp with exertion)

- constant fatigue

- shoulder pain

what are the signs of heart attack in older adults

- SOB

- may have no pain

- acute onset altered LOC

what is troponin

• sensitive serum biomarkers of myocardial injury/ cardiac cell necrosis

• draw it at bedside (point of care)

• obtained q6hrs up to 3x - mon for elevations

when do serum troponin levels rise 

• within 2-24 hrs

• can stay elevated up to 14 days post injury

• if levels stay elevated → could be another underlying cause 

what are the different imaging studies that are done to assess for myocardial injury

- chest xray: rules out things → aortic dissection (do within 30 mins of arrival)

- thallium scans (nuclear stress test)

- echocardiography

- contrast enhanced cardiovascular magnetic resonance (CMR)

- CT coronary angiography (CTCA)

what are some other diagnostic tests that can be done when assessing for myocardial injury

- ECG: 12 lead (get within 10 mins of arrival) → determine pathway of where and what interventions needed → looks for ST depression, T wave inversion, or ST elevation 

- exercise tolerance test (stress test)

- cardiac cath (percutaneous coronary intervention)

what does ST depression and T wave inversion indicate

ischemia w/in heart muscle

what does ST elevation indicate

injury and infarction → cell death and necrosis

what is ischemia of the heart

• insufficient O2 supply to meet myocardial demand

• reversible → no permanent damage if timely

• chest pain/tightness as warning sign

what is infarction of the heart

• necrosis when severe ischemia is prolonged w/ complete blockage

• irreversible

what are the risk factors for angina

increase metabolism/demand

- physical exertion

- stress

- temp extremes

- a heavy meal

- smoking

what is the tx for CSA pectoris

- pain relieved with rest or nitroglycerin (NTG)

- often managed with drug therapy (Aspirin (ASA), Statins, NTG) → manages atherosclerosis & clot formation

what occurs in acute coronary syndrome (ACS)

atherosclerotic plaque ruptures

what does a rupture in an atherosclerosis plaque result in

- platelet aggregation: occurs because the platelets are trying to fix injured site

- thrombus formation

- vasoconstriction

what are the types of ACS

unstable angina and acute MI

what is the characteristic of new onset angina

presents with the first episode of s/s

what causes vasospastic/ variant/ prinzmetal angina

• caused by vasospasm

• unpredictable → typ at rest

• not bc of atherosclerotic plaque

what is pre infarction angina

pain occurs days/ wks prior to heart attack (warning signs)

what are the s/s of unstable angina

- pain occurs at rest OR with exertion

- # of episodes (attacks) increase with greater intensity

- pain causes severe activity limitation

- ST "changes" without elevated cardiac enzymes (troponin): reflect as an inverted t wave or ST segment depression

how does a MI occur

• atherosclerotic plaque ruptures

• results in occlusive thrombus formation

• ischemia → injury → necrosis of cells

what is the zone of ischemia

• reduced blood flow but if corrected in a timely manner it can fully recover

• t wave & ST inversion

what is the zone of injury

• significant lack of blood that injures cardiac cells

• ST elevation & troponin starts elevating

what is the zone of necrosis

• area of dead cardiac muscle that no longer functions due to lack of blood supply

• abnormal/ pathologic Q wave

what is NSTEMI

• not complete obstruction → little bit of perfusion

• ST depression and/or t wave changes

• initial troponin is neg (norm) but elevates over next 3-12 hrs

• changes on ECG AND elevated troponin indicates myocardial cell death

• damage does not extend through the ventricular wall/ → partial thickness injury

what is STEMI

• ST elevation at the J point in at least 2 contiguous leads of >0.1mV → more elevated = more severe

• troponin is immediately elevated → more elevated = more severe

• 100% occlusion of coronary artery

• medical EMERGENCY

what is a 12 lead used for

locate ischemia or infarction on an EKG (need at least 2 leads in each lead group to confirm this)

what is a 18 lead used for

determines if ischemia or infarction has occurred on the right side of the ventricle

what are the inferior leads

looking at LV and R coronary artery

- II

- III

- aVF

what are the lateral leads

- I

- aVL

- V5

- V6

what are septal leads

• V1

• V2

what are the anterior leads

- V1

- V2

- V3

- V4

what is the process of ventricular remodeling

1. “Pre” MI - no s/s of HF, healthy structure, high rx factors

2. Early MI - expansion of infarct → hrs to days → myocardium starts expanding and thinning

3. Late MI - global remodeling → days to mths → myocardium is extremely expanded and thin

what are the interventions for managing acute pain

- decrease pain

- decrease myocardial O2 demand

- increase perfusion

- provide a position of comfort → semi-fowlers

- decrease pts movement → decrease workload of heart

- provide a quiet and calm environment

- MONA meds and O2

what are the MONA meds used for controlling acute pain

- morphine, oxygen, nitroglycerin, aspirin

- O2 (given first → do not use unless sats are <90% → hyper oxygenation can constrict vessels)

what does NTG do

- increases collateral blood flow

- redistributes blood flow toward the sub endocardium

- dilates coronary arteries

- decreases myocardial O2 demand

- decreases preload and afterload

what should you do before and after administering NTG

- assess pain and VS 5 mins before and after: only administer if they are stable and in pain

- ensure adequate CO and hemodynamic stability

- ask if they have taken PDE4 inhibitors within the past 24 to 48 hrs: cause profound hypotension when mixed with NTGs

- can cause severe h/a → put cold washcloth on forehead and back of neck after

what are parameters of NTG

Hold NTG if:

• SBP <90

• if SBP drops 30 below baseline

• HR <50 or >100

• pt is pain free

how often can you give NTG**

0.4 mg q5mins and up to 3 doses only

what should you do with the dose of NTG

titrate it

what med is used if pt is unresponsive to NTG

morphine

how does morphine work

- decreases pain

- decreases myocardial O2 demand

- relaxes smooth muscle

- reduces circulating catecholamine's/ epinephrine

how should you administer morphine

slowly through IV

what are the expected outcomes of increasing myocardial tissue perfusion

- adequate CO

- normal sinus rhythm

- VS within normal limits

what are drugs for increasing myocardial tissue perfusion

• antiplatelets

• anticoagulants

• beta blockers

• ace inhibitors or ARBS

• calcium channel blockers

• statins

aspirin for tissue perfusion

• 325 mg 

• have pt chew to get into system faster

• reduces congregation of platelets

anticoagulants for perfusion

• heparin

• if clot is suspected → prev from worsening

beta blockers for perfusion

- decreases workload of heart

- reduces occurrence of ventricular dysrhythmias

ACEIs and ARBs for perfusion

• reduces chance of ventricular remodeling

• given w/in 48 hrs to ACS w/ evidence of HF

calcium channel blockers for perfusion

• promotes vasodilation and myocardial perfusion

• used in chronic stable angina and coronary vasospasms

when are statins implemented

to reduce risk factors of atherosclerosis

what is the reperfusion drug used to increase myocardial perfusion

fibrinolytic (thrombolytic) IV → dissolves clot → given secondary if PCI or Cath-lab isn’t available

what are the different fibrinolytics (thrombolytics)

- tissue plasminogen activator (tPA, alteplase)

- reteplase (activase)

- tenecteplase (TNK)

what is disease criteria for receiving fibrinolytics (thrombolytics)

only for STEMI & within 30 minutes of arrival**

when are fibrinolytics given

• onset of s/s w/in prior 12 hours and ST elevation AND if PCI is not available w/in 90 minutes of first medical contact

what is the door to needle time once arrived in ED for reperfusion therapies

30 min of ED arrival**

when should you not give fibrinolytics

- pts who present more than 24 hrs after the onset of s/s

- pts with ST segment depression, unless a true posterior MI is suspected

- there is an absolute contraindication

reporting immediate indications of bleeding

Assess - Neuro Status -> establish baseline and observe for changes

Observe - All IV sites for bleeding and patency

Monitor - Clotting studies -> PT/PTT/INR

Observe - For signs of internal bleeding -> V/S, Hgb/Hct, stools, urine, emesis for occult blood

what are some indications that a clot has dissolved and the artery is reprefused after fibrinolytic therapy

- abrupt cessation of pain or discomfort

- sudden onset of ventricular dsyrhythmias

- resolution of ST segment depression/ elevation or T wave inversion: monitor but it is a good sign because it indicates the heart is waking back up

- a peak at 12 hrs of markers of myocardial damage

what are some indications that an artery has reclotted after fibrinolytic therapy

- return of chest pain/ discomfort or previous s/s

- worsening or return of ST elevation

what is a PCI

percutaneous procedure in the cath lab to return blood flow to obstructed areas via a balloon expansion of the occluded artery

what is the time frame goal to get a PCI done upon arrival in ED if someone has a STEMI

door to balloon within 90 mins of ED Arrival of STEMI**

for doing a PCI, what should you assess for

allergies (contrast media, anesthetics) and surgical hx (kidney function)

what are the different interventions when it comes to a PCI

- atherectomy - go in and break thru occlusion → rx for perforation

- angioplasty with stent placement - more comm

what do you need to monitor post op for a PCI

- acute vessel closure

- bleeding

- reaction to contrast dye - allergies

- hypotension - excessive bleeding

- hypokalemia (<3.5 mEq/ L) - result of lots of fluid/solution

- dysrhythmias

- infection - pink, warm, dry w/ sensation distally to access site

what is a CABG

occluded coronary arteries are bypassed by harvesting a vein in the leg and using it to replace a damaged artery in the heart

what should you do preop CABG

- verify allergies; diagnostic tests; type and cross match; review meds

- anticipate incisions, ETT/ ventilator, mediastinal chest tubes, urinary cath, pacemaker wires

what should you teach someone about CABG

- splint incisions, TCDB

- arms/ leg exercise

- expected pain

- early ambulation

- anxiety is common

what should you do postop CABG

- sterile technique with dressing changes

- connect and monitor mediastinal tube to water seal drainage system

- pacer wires, monitor for dysrhythmias

- manage symptomatic dysrhythmias

- monitor, report and document CABG complications

what occurs in fluid and electrolyte imbalances post CABG

- edema is common

- serum electrolytes may be low → check electrolytes frequently

what is hypotension after a CABG 

• r/t collapsed coronary graft, hypovolemia, or vasodilation

• report to provider if pt activity induces

  • ↓ SBP >20mm Hg

  • 20 beats/min change in HR

  • c/o dyspnea, chest pain

hypothermia after CABG

• if temp <96.8 F

• promotes constriction and HTN

• re-warm at are no faster than 1.8 F/hr

HTN after CABG

• systolic >140-150s

• promotes leakage of suture lines and increased bleeding

bleeding after CABG

• measure drainage hourly

• report if >150 mL/ hr or abrupt cessation of previously heavy drainage

cardiac tamponade after CABG

• fluid around heart sac that causes compression

• s/s - JVD, distant muffled heart sounds, hypotension

decreased LOC after CABG

• neuro checks q30-60 mins until anesthesia has worn off → then q2-4 hrs

• increased transient neuro deficits in older adults

• suspect stroke if

  • abnormal pupillary response

  • failure to awaken

  • seizures

  • absence of sensory or motor function

anginal pain after CABG

• Sternotomy pain is expected

• Anginal pain indicates graft failure

sternal wound infection after CABG

• Fever 4 days post op

• Bogginess of sternum - DON’T WANT

• Redness, induration, swelling, drainage from suture sites

how many sec are 5 boxes on a ECG

0.20 s

how many sec is 1 box on a ECG

0.04 s

what does a p wave represent

SA node fired and atrial depolarized (contracted)

what does a PR segment represent

atrial kick (last squeeze from atria)

what does a PRI represent

- contains P wave and PR segment

- full length of time for atrial depolarization

what is the normal time of a PRI

0.12-0.20 s

what does a QRS complex represent

• ventricular depolarization (contraction)

what is the normal time of a QRS complex

0.04-0.10 s

what time frame of a QRS complex starts to become concerning

>0.12 s

what does a ST segment represent

- early ventricular repolarization (relaxation) starts

- starts from J point and goes to the beginning of the T wave

which part of a ECG do most lethal dysrhythmias occur

t wave (esp electrolyte imbalances like K which causes a peaked t wave)

what does a t wave represent

completing ventricular repolarization (relaxation)

how tall is a t wave usually

<10 mm

what does a QTI represent

- full time for ventricular depolarize and repolarize

- starts at the beginning of QRS and ends at the end of the T wave

what is the normal time of a QTI

0.32-0.44 s

U wave

• never supposed to be part of ECG

• opposite of T wave

• indicates hypokalemia → bc slowing ventricular repolorization

• occurs after T wave

sinus bradycardia

∙ Rate: < 60 beats/min

∙ Regularity of rhythm: regular

∙ P wave: round, upright, and symmetrical

∙ P:QRS = 1:1

∙ PRI: 0.12 to 0.20 sec and constant

∙ QRS: 0.06 to .10 sec and constant

what are the causes of sinus bradycardia

- decreased automaticity

- increased parasympathetic (rest and digest) activity: vagal response

when do you tx someone with sinus bradycardia

• if they are symptomatic and HR is <50 bpm

• need to know if acute/chronic → if it’s something that is baseline w/ no s/s → no tx

what are the s/s of sinus bradycardia

- syncope

- dizziness

- hypotension

- confusion

what is the first line tx for sinus bradycardia

atropine - 1mg q3-5 mins w/max of 3 mg → bolus

what are some other tx options for sinus bradycardia

• transcutaneous pacemaker - deliveers smaller stimulus to try and generate pace that is effective

• dopamine or epinephrine IV infusions

• transvenous pacing: continuous pacemaker used for symptomatic bradycardia

what is a permanent pacemaker

• battery powered device that delivers electrical stimulus to the right myocardium which causes a contraction

• always sending little stimulus 

• indicated for symptomatic bradycardia