Cardiovascular Flashcards
(149 cards)
1
Q
name the arteries of the heart
A
Right coronary artery
Left coronary artery - breaks into the circumflex and left anterior descending artery
2
Q
The right coronary artery supplies what area
A
the R atrium, R ventricle, bottom portion of the L ventricle and back of the septum
3
Q
The circumflex artery supplies what area
A
The L atrium, side and back of the L ventricle
4
Q
The left anterior descending artery supplies what area
A
front and bottom of the L ventricle, and front of the septum
5
Q
what is hyperlipidemia
A
high cholesterol
6
Q
what is high cholesterol related with
A
increase risk of coronary artery disease such as angina (moderate), or myocardial infarction MI (severe)
7
Q
What is atherosclerosis
A
Cholesterol accumulation in the vessel wall
8
Q
What is the progression of atherosclerosis
A
fatty streaks to a fibrous stage leading into lesions involving calcification, ulceration, hemorrhage and eventually thrombosis and occlusion of a vessel
9
Q
risk factors for atherosclerotic coronary artery disease
A
DISLIPIDEMIA - high LDL (bad), low HDL (good) hypertension diabetes mellitus smoking family history obesity and lack of exercise male gender and advanced age
10
Q
what are the three parts to cholesterol
A
LDL - low density lipoprotein
HDL - high density lipoprotein
TG - triglyceride
11
Q
the skinny of LDL - low density lipoprotein
A
Known as the ‘Bad’ cholesterol
60-70% of total serum cholesterol
LDL transports cholesterol from the liver to peripheral tissue. excessive LDL may deposit onto the walls of the arteries
Forms atherosclerotic plaque which increase risks of CVA
12
Q
the skinny on HDL - high density lipoprotein
A
known as the ‘Good’ cholesterol
20-30% of total serum cholesterol
HDL transports cholesterol from periphery to the liver for removal from circulation
high HDL is associated with low risk of developing CAD. conversly low HDL increases risk of developing HDL
13
Q
the skinny on TG - triglycerides
A
10-15% of total serum cholesterol
positive relationship between TG and incidence of coronary artery disease (CAD)
14
Q
desirable Cholesterol levels
A
Total < 5.2 mmol/L
LDL < 2.6 mmol/L
HDL > 1.5 mmol/L
TG < 1.7 mmol/L
15
Q
Poor cholesterol levels
A
Total > 6.2 mmol/L
LDL > 4.1 mmol/L
HDL < 1.0/1.3 mmol/L (men/women)
TG > 2.3 mmol/L (up to 5.6mmol/L)
16
Q
what is the Framingham Risk Score (FRS)
A
risk assessment on when to initiate treatment for hyperlipidemia
High > 20% - consider treatment
Moderste 10-20% - lower LDL < 2 mmol/L (or 50%)
Low < 10%
17
Q
Statin mechanism of action and therapeutic uses
A
inhibits an enzyme called HMG-CoA reductase which is needed for the final step of cholesterol production
Therapeutic uses: reduce cholesterol, primarily before 1st heart attack, secondly to prevent a 2nd heart attack.
18
Q
Adverse effects of statins
A
Myopathy (muscle pain/breakdown)
liver dysfunction
nausea
if used in conjunction with fibrates it increases the risk of myopathies
19
Q
List of the Statin drugs generic names
A
atorvastatin fluvastatin lovastatin pravastatin rosuvastatin simvastatin
20
Q
risk factors that should be considered for prevention of myopathies when administering statins
A
> 80 years of age (especially women) small body frame / frailty high dose of statin multiple disease polypharmacy hypothyroidism alcohol abuse Note: increase risk of myopathy when mixing statin with fibrates
21
Q
Fibrates mechanism of action
A
primarily to decrease triglyceride production in the liverby interacting with specific receptors in the liver and fat tissues
- significantly reduces TG’d
- significantly increases HDL
- slightly reduces LDL
22
Q
Therapeutic uses and A/E’s for Fibrates
A
Use: reduce triglycerides A/E: nausea, headaches liver dysfunction Gallstones insomnia rash
23
Q
Fibrates important drug interactions, dosing and administration
A
interacts with statins - increases risk of myopathies
dosing: Oral and take with food
24
Q
Fibrates - drug names
A
Gemfibrozil
Fenofibrate
25
Bile Acid Sequestrants (Resin)
cholestyramine
26
cholestyramine mechanism of action
a large bile acid resin that converts cholesterol to bile acids which lowers blood LDL. Also, slightly increases HDL
27
cholestyramine therapeutic use and A/E's
USE: hypercholesterolemia
A/E: horrible taste (disliked by Pt's)
GI discomfort (bloating, indigestion, steatorrhea - fatty pooh)
causes deficiency in lipid soluble vitamins A/D/E/K
CONTRAINDICATED WITH HYPERTRIGLYCERIDEMIA
28
Nicotinic Acid (Niacin) for hyperlipidemia - mechanism of action and therapeutic uses
Mechanism: appears to alter lipid level by inhibiting lipoprotein synthesis
USES: reduce triglycerides
low doses of nicotinic acid are sufficient to raise HDL, unfortunately larger doses are needed to lower LDL
reduces TG 20-40%, reduces LDL 20-35%, elevates HDL 10-20%
29
Nicotinic acid A/E's and important drug interactions
A/E's: flushing, rash, pruritis, hepatoxicity
IMPORTANT interaction:
1. Statins - increases risk of liver damage
2. Fibrates - increase risk of gall stones
30
Ezetimibe mechanism of action
Blocks absorption of cholesterol
31
Ezetimibe therapeatuic uses
for elevated LDL
Used alone or in combination with Statins
Reduces LDL by about 20%
32
Ezetimibe A/E's
Nausea, bloating
33
What is angina and it causes
- sudden pain beneath the sternum often radiating to the left shoulder and arm.
- causes by insufficient blood flow to the heart muscle from narrowing of coronary arteries
- often occurs secondary to athersclerosis which blocks the coronary arteries
34
goals of therapy for angina
to prevent myocardial infarction
| to prevent pain
35
what are the main three families of drugs used to treat angina
1. Nitrates
2. Beta-Blockers (BB)
3. Calcium Channel Blockers
36
what are the three types of angina
1. Stable - usually triggered by increase in physical activity, emotional excitement, large meals, and cold air
2. Unstable - Present at rest, intensification of existing angina (greater risk of death compared to stable) This is the urgent medical emergency type
3. Variant (Vasospastic) - coronary artery spasm, can occur at rest or on exertion. Vessels are clean and clear
37
What are nitrates mechanism of action
nitroglycerin acts directly on vascular smooth muscle to promote vasodilation.
38
Three therapeutic uses of nitrates (nitroglycerin) for angina
1. relieves the attack by using when the attack begins
2. prevents attacks by using just before an attack is expected to occur
3. to reduce the number of attacks by using the drug regularly on a long term basis
39
Nitrates (nitroglycerin) A/E's (think about it… vasodilator)
headache (diminishes over time, or take acetominophen)
hypotension
reflex tachycardia
40
Nitroglycerin dosing and ways of admin
```
sublingual / oral tablets
spray
patch (on for 12, off for 12)
paste
intravenous infusion
```
41
IMPORTANT drug interaction of nitrates
Sildenifil (Viagra) - intensifies the nitrates and causes severe vasodilation which can invoke a heart attack due to life threatening hypotension
42
nursing implications for nitrates (nitroglycerin)
monitor for tolerability, blood pressure and response
43
types of Beta blockers for angina
Beta blocker receptors (several types B1 and B2)
blockade of the receptors cause: 1. reduction in HR and contractility. 2. bronchconstriction
NOTE: B1 is more specific for the heart so it reduces the risk of bronchoconstriction
44
Beta 1 blockers affect...
The heart as they cause decrease in HR and contractility
45
Beta 2 blockers affect
the lungs as they cause bronchconstriction
46
Therapeutic uses for Beta-blockers
```
Angina
Myocardial infarction
hypertension
dysrhythmias
heart failure
hyperthyroidism
pre/eclampsia (high BP during pregnancy)
```
47
A/E's for beta blockers
bradycardia and heart block
hypotension
bronchconstriction
fatigue
48
Beta blockers dosing and administration
Various IV and oral doses.
| IV route faster onset
49
types of beta blockers
```
Acebutolol
Atenolol
Bisoprolol ***
Esmolol
Metaprolol ***
Nadolol
Oxprenolol
Pindolol
Propranolol
Timolol
***most common
```
50
Calcium channel blockers for angina. mechanism of action
calcium channels help regulate function of the myocardium, the sinoatrial node, and the atrioventricular node
-CCB's prevent calcium ions from entering the cell thus reducing BP, HR, electrical conduction, and force of contraction
51
Therapeutic uses for Calcium Channel Blockers (CCB's)
Angina
Myocardial infarction
hypertension
dysrhythmias
52
A/E's for CCB's
bradycardia and heart block
hypotension
dizziness
flushing
53
nursing implication for CCB's
Contraindicated with heart dysfunction
Monitor BP, HR, ECG and response
Various IV and oral doses
54
Two CCB agents
Dihydropyridines
| Nondihydropyridines
55
list the three CCB dihydropyridines
Amlodipine
Felodpine
Nifedipine
56
list the two CCB nondihydropyridines
Diltiazem
| Verapamil
57
What is acute coronary syndrome (ACS)
term used to cover a range of clinical symptoms associated with acute myocardial ischemia
58
ACS includes these three categories
1. unstable angina
2. Non-ST-elevation myocardial infarction (NSTEMI)
3. ST-elevation myocardial infarction (STEMI)
59
What is an ECG (electrocardiogram) used for
to view the PQRST Wave voltage of the heart during contraction.
-it can identify angina, NSTEMI, and STEMI
60
what are caridac biomarkers
Cardiac biomarkers are substances that are released into the blood when the heart is damaged or stressed. Measurement of these biomarkers is used to help diagnose, risk stratify, monitor and manage people with suspected acute coronary syndrome (ACS) and cardiac ischemia.
Troponin
Creatine kinase-MB
LDH
61
signs and symptoms of myocardial infarction (MI)
- asymptomatic in 25% (mostly women and those with diabetes)
- chest pain similar to Angina except, more intense, more persistent, and not releived by palliative measures (nitroglycerin)
- nausea, sweating, apprehension
- Pallor
- Tachycardia
- signs of congestive heart failure CHF - shortness of breath, swelling, cough
62
List three 'clot busters' thromolytics
TPA (alteplase)
RPA (Retevase)
TNK (TNKase)
63
what are anti-thrombotic agents (plateletes)
ASA (Asparin)
Clopidogrel (plavix)
IIb-IIIa antagonists
-Eptifibitide, Tirofiban, Abciximab
64
list the three anticoagulant agents
Warfarin
Heparin
Low molecular weight heparin (LMWH ex. Enoxaparin)
65
drugs used to treat acute coronary syndrome
```
Thrombolytics
Anti-thrombotic agents
anti-coagulant agents
Beta-Blockers
Calcium Channel Blockers
ACE inhibitors
Statins
```
66
ACS thrombolytics dosing and administration
Parental - all IV
TPA - loading dose then infusion
RPA - 2 bolus dose thirty minutes apart (don't forget the 2nd dose!!!)
TNK - 1 bolus dose (most common now and cost approx. $2500/shot
67
therapeutic uses for thrombolytics in ACS
```
myocardial infarction (heart attack)
Stroke (brain attack) - TPA ONLY!!
```
68
Adverse effects for thrombolytics
BLEEDING (caution for bleed in head)
repurfusion dysrhythmias (stunned heart when the artery opens up after the blockage)
hypotension
69
Anti-thrombotic agents dosing and administration
Oral - ASA, Clopidogrel, Ticlopidine
Parenteral: Eptifibitide, Tirofiban, Abciximab
-loading doses and infusions
70
anti-thrombotic agents mechanism of action
decreases the function of plateletes (so they can't clog the artery)
71
therapeutic use for anti-thrombotic agents
Prevents myocardial infarction
| prevent stroke - ASA, Clopidogrel, Ticlopidine only
72
Adverse effects for anti-thrombotic agents
Bleeding
Nausea
Thrombocytopenia (low WBC count)
73
anticoagulant names
```
Warfarin
Heparin
low molecular weight heparin (LMWH)
Rivaroxiban
Dabigatran
```
74
mechanism of action for anticoagulants
inhibits clotting factors
| -prevents the production of Fibrin
75
Therapeutic uses for anticoagulants
Various clotting disorders
- prevents/treats myocardial infarction
- treat pulmonary embolism
- prevent/treat DVT (deep vein thrombosis)
- prevent stroke
- atrial fibrillation (ineffective = clots = stroke)
76
Warfarin dosing and administration
Oral
takes about 5 days to kick in (need to be on heparin/LMWH until warfarin kicks in
need to carry/wear a bracelet "on blood thinner"
CONTRAINDICATED in pregnant women
Monitor blood work - INR (international normalization ration) target is 2-3 (>3 is too thin. = way too much bleeding)
REVERSE EFFECTS with Vitamin K
77
Adverse effects for warfarin
Bleeding
Purple toe
-this syndrome is thought to be secondary to cholesterol crystal emboli released as a result of warfarin-induced bleeding into atherosclerotic plaques
-if warfarin therapy is discontinued, the toe pain will resolve, but the purple discolouration will persist
78
Heparin and LMWH (low molecular weight Heparin) dosing and administration
Heparin is Parenteral IV or S/C
-Heparin - IV loading dose and infusion (very short acting)
Monitoring - Use aPTT (activated partial thromboplastin time) - NOT the same as INR
LMWH is S/C injections (no infusion)
Monitoring - no monitoring of clotting times required
79
Adverse effects for Heparin and LMWH
Bleeding
| Heparin-induced thrombocytopenia (HIT)
80
Anticoagulants - Dabigatran and Rivaroxiban dosing and administration
Good alternate to Warfarin as its hard to stabilize patients or poor compliance with monitoring
Oral treatment. - No lab test required
Note: costs lots more than warfarin
81
Adverse effects to Dabigatran and Rivaroxiban
bleeding
| GI upset
82
Cardiac interventions
```
Coronary Artery Bypass (artery added around blocked area)
Balloon Angioplasty (balloon inflation to open up artery)
Stent (wire mesh inside artery)
```
83
What is hypertension
high blood pressure
| The force against the blood vessel walls
84
what can cause hypertension - risk factors
```
sedimentary lifestyle
smoking
excess abdominal weight
fatty diet
alcohol consumption
and STRESS
Non-modifiable: family history, heart disease, stroke >45 for men, >55 for women, ethnicity
```
85
ways to reduce hypertension
reduced sodium (intake <88cm)
86
usual blood pressure threshold values for initiation of pharmacotherapy treatment
if Diabetic = 130/80
high risk = 140/90 (if CV risk)
low risk = 160/100 (if no CV risk)
very elderly = 160/na
87
Therapeutic uses for Ace inhibitors
hypertension
heart failure
myocardial infarction
diabetic nephropathy
88
Adverse effects of ACE inhibitors
```
hypotension
dizziness
electrolyte abnormalities (may need to increase K)
Cough
Angioedema (swelling of the throat)
```
89
list some ACE inhibitors (PRIL's)
```
Benazepril
Captopril
Cilazapril
Enalapril
Fosinopril
Lisinopril
Perindopril
Ramipril
Tandolapril
```
90
Therapeutic uses for diuretics
hypertension
| heart failure
91
Adverse effects for diuretics
hypotension/dizziness
Metabolic/Electrolyte abnormalities
-increase Uric Acid levels (Thiazides) will form crystals that lead to gout in the joints
-increase Na+
-increase/decrease of Potassium (usually decreases except with K-sparing)
Gynecomastia (Spironolactone) = man boobs
NSAIDS reduce the effectiveness of diuretics as they cause the body to retain salt
92
what needs monitoring when on diuretics
Electrolytes
Kidney function
Blood pressure
93
mechanism of action for Thiazides (diuretics)
Causes diuresis (decreased plasma volume)
Reduce peripheral vascular resistance
Works in the distal part of the kidney
94
mechanism of action for Loop diuretics
Causes more profound diuresis than thiazides
not generally used for chronic management of hypertension
works in the Loop of Henle in the kidney
95
mechanism of action for Potassium sparing diuretics
Weak diuresis
| usually combined with a thiazide to prevent potassium loss
96
List the generic thiazides diuretics
Chlorthalidone
Hydrochlorothiszide
Indapamide
Metolazone
97
List the generic Loop diuretics
Ethacrynic Acid
| Furosemide **most common
98
List the generic Potassium Sparing diuretics
Amiloride
Spironolactone
Triamterene
99
List the generic Angiotensin Receptor Blockers (ARB's) (SARTAN's)
```
Candesartan
Eprosartan
Irbesartan
Losartan
Telmisartan
Valsartan
```
100
Alpha 1 Antagonists (blockers) mechanism of action
- prevents stimulation of alpha1 receptors on the blood vessels thereby preventing vasoconstriction
- relaxes smooth muscle in the prostate and the bladder neck, thus decreasing the blockage of urine flow
101
Therapeutic uses for Alpha 1 antagonists
```
Hypertension
Prostatic hypertrophy (enlarged prostate in men)
```
102
Adverse effects of alpha 1 antagonists
hypotension
dizziness
fluid retension
nasal congestion
103
list the 3 alpha 1 antagonists generic names
Prazocin
Doxazocin
Terazocin
104
Mechanism of action for Alpha 2 agonists
- Acts within the brainstem to suppress sympathetic (norepinephrine) outflow to the heart and blood vesssels
- Results in vasodilation and reduced cardiac output
105
Therapeutic uses for Alpha 2 Agonists
hypertension
| Pre/Eclampsia (methyldopa) - hypertension plus protenuria after 20 weeks gestation
106
Alpha 2 agonists adverse effects
hyoptension / dizziness (do not withdraw Clonidine abruptly as it will lead to rebound hypertension)
fluid retention
dry mouth
sedation
107
list the two alpha 2 agonists
Clonidine and Methyldopa
108
Mechanism of action for Direct Acting Vasodilators (Minoxidil and Hydralazine)
primarily causes vasodilation in the arteriole
| Limited effect on the veins (therefore minimal orthostatic hypotension)
109
Therapeutic uses for Direct Acting Vasodilators (Minoxidil and Hydralazine)
Hypertension
Baldness (Minoxidil = Rogaine)
Pre/Eclampsia (Hydralazine)
110
adverse effects for Direct Acting Vasodilators (Minoxidil and Hydralazine)
hypotension
dizziness
fluid retention
Hydralazine - systemic lupus erythromatosis SLE - arthritis autoimmune disease that attacks the joints in the body
Minoxidil - hypertrichosis (excessive hair growth)
111
list the generic names of the two Direct Acting Vasodilators
Minoxidil
| Hydralazine
112
what is heart failure
condition in which the heart is unable to adequately pump blood throughout the body
generally, heart failure is a process that occurs over time, when an underlying condition damages the heart or makes it work too hard, weakening the organ
113
Stats for heart failure
affects 1% of people aged 50 and older and about another 5% of those aged 75 years and older
about 10% of patients diagnosed with heart failure die within 1 year, and about 50% die within 5 years of diagnosis
114
top 4 causes for heart failure (in order)
1. myocardial infarction
2. Coronary artery disease
3. Valve disease
4. Idiopathic cardiomyopathy
others: viral/bacterial cardiomyopathy, myocarditis, pericarditis, arrhythmias, chronic hypertension
115
what is ejection fraction
the percentage of blood pumped out of the left ventricle with each contraction
measuring the ejection fraction using Echocardiography is a way to determine left ventricle function
116
what are normal ejection fraction amounts and abnormal
normal is about 60%
40-45% indicates mild dysfunction
30-40% indicates moderate dysfunction
10-25% indicates severe dysfunction
117
List some symptoms of heart failure
```
Fatigue
Heart palpitations
Loss of appetite
Memory loss, confusion
Nausea
Persistent coughing/wheezing
Shortness of breathe (dyspnea)
Swelling (edema) of the feet, legs, or abdomen
```
118
Mechanism of action for Digoxin
increases the pumping force of the heart (positive inotrope) - Binds to the NA-K-ATPase (sodium pump)
slows conduction through the heart
Comes from the Fox Glove Plant (Latin: Digitalis)
119
Therapeutic uses for Digoxin
Congestive Heart Failure
| Dysrhythmia's
120
Adverse effects to Digoxin
Bradycardia
Nausea
Vision disturbances
**Amiodarone and Verapamil - significantly increases Digoxin blood levels
NOTE: measure serum blood concentration and chech HR prior to administration (must be >60bpm)
121
what is a dysrhythmia
abnormal rhythm of the heart
| The atriums and ventricles are not contracting in sync
122
how does the normal rhythm of the heart work
normally generated by the pacemaker cells within the sinoatrial (SA) node, which is located within the wall of the right atrium.
The SA node governs the rhythm of the atria and ventricles. Atrial contraction is always followed by ventricular contraction.
123
types of dysrhythmias
```
too fast (tachycardia)
too slow (bradycardia)
frequency of the atrial and ventricular beats are different
```
124
what can cause dysrhythmias
changes in the pacemaker cells
abnormal generation of impulse at sites other than the SA node - (Ectopic Foci - a tissue in the heart becomes hyperactive and triggers the muscle to fire/contract out of rhythm)
125
types of tachy-dysrhythmias
Supraventricular (above the ventricles)
-Atrial fibrillation / flutter
Ventricular
- Premature Ventricular Contractions (PVC's)
- Tachycardia or Fibrilation
126
types of brady-dysrhythmias
atrioventricular block
- first degree
- second degree = type I and type II
- third degree (will lead to death)
127
what do anti-dysrhythmic drugs do
act primarily by altering ion fluxes within tissue of the myocardium.
-the three main ions are: Na+, Ca2+, K+
Anti-dysrhythmic drugs can be classified by their ability to directly or indirectly block flux of one of these ions
128
types of antidysrhythmic agents
Class 1a - atrial fibrilation
Class 1b - ventricular dysrhythmias
Class 1c - Severe ventricular dysrhythmias
Class II - general myocardial depressants for both supra-v and ventricular dysrhythmias
Class III - Life threatening ventricular tachycardia
Class IV - Paroxysmal supraventricular tachycardia
129
Class I Antidysrhythmic agent
Procainamide
130
Therapeutic uses for Procainamide (class 1 antidysrhythmic agent)
atrial and ventricular dysrhythmias
131
Adverse effects of Procainamide
```
Dizziness
Hypotension
Rash (Systemic Lupus Erythromatosis SLE - same as hydralazine)
bradycardia
vision disturbances
```
132
Procainamide (antidysrhythmic agent) dosing and nursing implications
Oral or Parenteral
Measure serum blood concentration
Monitor for tolerability, HR and response (ECG)
133
Class Ib Antidysrhythmic agent
Lidocaine
134
therapeutic use for Lidocaine (class Ib antidysrhythmic agent
Ventricular dysrhythmias
135
Adverse effects of Lidocaine (class 1b antidysrhythmic agent)
Dizziness
hypotension
bradycardia
136
Lidocaine (antidysrhythmic agent) dosing and nursing implications
Parenteral
| Monitor for tolerability, HR and responses (ECG)
137
Class Ic antidysrhythmic agent
Propafenone
138
Therapeutic uses for Propafenone
atrial dysrhythmias
139
Adverse effects for Propafenone (antidysrhythmic agent)
dizziness
hypotension
bradycardia
SOB (shortness of breath) in asthma Pt's
140
Propafenone dosing, administration and nursing implications
Oral, and loading does for conversion out of atrial fibrillation
CAUTION in patients with CHF and asthma
Monitor for tolerability, HR and response (ECG)
141
IMPORTANT drug interactions with Propafenone (antidysrhythmic agent)
Digoxin - significantly increases the digoxin blood levels
| Warfarin - significantly increases the warfarin levels (increases risk of bleeding) - check the INR
142
Class III antidysrhythmic agent
Amiodarone
143
Therapeutic use for Amiodarone
Atrial and ventricular dysrhythmias
144
Adverse effects for Amiodarone (antidyshythmic agent)
```
dizziness / hypotension / bradycardia
HYPO/HYPERthyroidism
BLUE SKIN (Smurf drug)
Pulmonary fibrosis (scars in the lungs)
Liver toxicity
nausea
```
145
Amiodarone dosing, administration and nursing implications
Oral and parenteral. Loading dose for conversion out of atrial fibrillation
- may be used safely in patients with CHF.
- Monitor for tolerability, HR and response (ECG)
- Thyroid function tests
- Chest X-ray
146
What is acute ischemic stroke and the two types
Brain attack where a blood vessel breaks or clogs
1. Ischemic (most common 85%)
a. Thrombotics - clot in a brain blood vessel
b. Embolic - clot between heart and brain
2. Hemorrhagic (bleed in brain)
a. intracerebral (inside) or subarachnoid (outside)
147
goal of therapy for acute ischemic stroke
minimize brain damage
prevent complications
reduce the risk of recurrence
restore function of the individual
148
signs/symptoms of Acute Ischemic Stroke
Weakness - sudden loss of strength, numbness, tingling
Trouble speaking - sudden confusion (even if temporary)
Vision problems - sudden (and sometimes temporary)
Headache - sudden, severe and unusual
Dizziness - sudden loss of balance with any of the above signs
149
goal of care for those experiencing a stroke
4hr window from signs to drug administration or threshhold would have passed for benefits from meds
1. identify signs
2. EMS assessment
3. Immediate general assessment and stabilization (CT scan of brain)
4. Immediate neurologic assessment by stroke team
5. review CT scan for hemorrhage
6. no bleed = consider fibrinolytic therapy (TPA)
- Bleed = consider transfer to neurosurgeon
