🫀Cardiac Flashcards
Acute Coronary Syndrome
results from damage/disease of coronary artery (CAD)
Cannot supply blood or o2 to heart :(
When do the coronary arteries fill?
During diastole
What is the main purpose of coronary artery?
supply blood and oxygen to heart
ECG shows:
damage to coronary arteries
Angina Pectoris
chest pain caused by decreased cardiac blood flow
(oxygen imbalance)
Stable Angina
pain with activity which improves with rest
Unstable Angina
pain that does not improve with rest
EMERGENT
risk AMI, dysrhythmia/SCD
Which patients might have atypical angina
women
>65
diabetic
Gold standard diagnostic for MI
ECG
ST elevation is indicative of:
STEMI
What finding could you see on an ECG of a patient with a previous history of MI
Q wave
Treatment goals for acute MI (4)
Maintenance of cardiac output
Minimize workload
Prevent complication (DYSRHYTHMIA)
Education
Immediate assessment Cardiac MI
ECG, pain, v/s, history, cardiac bios, cxray
Immediate treatment Cardiac MI
O2 therapy if under 90%
NITRO
DAPT
Morphine
Pain score for chest pain should be
ZERO
Three components of stroke volume
Preload
Afterload
Contractility
Pain assessment
Normal
Onset
Relieving factors
Quality
Region/radiation
Severity/other sx
Timing
Understanding/perception
Initial treatment cardiac
Bedrest
Semi/High fowlers
avoid valsalva maneuver
Nitroglycerin
Potent art vasodilator, decreases preload/afterload/o2 demand
What vital sign should you obtain before Nitro administration
Blood pressure
DO NOT ADMIN IF SYS <90
Nitro is fatal when combined with
Viagra, slidenifil 🍆🍆🍆🍆🍆
48hr+ d/c
Morphine
pain relief
preload/afterload reduction
decrease o2 demand
ACE-I
Vasodilation, afterload reduction
inhibits renin, aldosterone
limits sodium reabsorption
Selective Beta Blocker (Metoprolol)
Blocks Beta ONE
decreases dromo, chrono, inotropic action
Calcium Channel Blockers (Diltiazem and Verapamil)
decrease o2 demand
Preload Reduction Meds (CVP/Wedge pressure)
NITRO
Morphine
Afterload Reduction Meds (SVR)
ACE-I/ARBS
Nitro, morph, ccb
Contractility Meds (HR)
Beta Blockers
ccb
Anti-Thrombotic Therapy
prevention
Antiplatelet/Anticoagulation
Fibrinolytic Therapy
STEMI ONLY
Lyse/Destroy
Anti-Platelet
Aspirin
P2y12 inhibitor (Clopidogrel, Ticagrelor)
**risk for bleeding
Anti-Platelet GCP11 inhibitor
Post cath lab intervention
Eptifibatide, Tirofiban
Anti-Coagulants
Heparin - alters clotting cascade
Lovenox - low weight, more effective, less control, half life is longer
Labs for Heparin
PTT,APTT
IV continuous monitoring
Desired effect of heparin PTT
increase! more time to clot
Reversal agent for heparin
Protamine sulfate
Drugs for thrombocytopenia
c/b heparin
Bivalrudin, Argatroban
MONA BASH
Morphine
Oxygen
Nitrates
Aspirin
Beta Blocker
ACE-I
Statin
Heparin
Reperfusion therapy Medical
Fibrinoloytic therapy (STEMI patients)
Reperfusion therapy Interventional
PCI
CABG
Successful reperfusion findings
0/10 angina
ST returned to baseline
Reperfusion dysrhythmia –> still have to treat but reassuring
Early and marked peaking of troponin
Fibrinolytic Therapy
Goal : Limit MI, clot bust, 30min of arrival reperfusion
Criteria: STEMI, when cath lab not accessible
t-PA
Nursing management: Fibrinolytic therapy (3)
IV access
reperfusion (AxO)
prevent/monitor for complications
Cardiac Cath
Coronary
Angiography, Percutaneous Coronary Intervention, Stents
Complications post PCI
Coronary spasm, artery dissection, thrombosis
bleeding, low perfusion to extremity
abd/back pain
contrast induced renal failure
ventricular dysrhytmia
vasovagal response –> brady, loc, hypotension
Nursing management: Post PCI
head-to-toe
<30 degrees HOB
prevent/minimize complications –> pain? site check? compression device? renal protection
Coronary Artery Bypass Graft (CABG)
reroute piping (radial or mammary)
indicated when multiple arteries are occluded (multi vessel disease)
seen with: NSTEMI, unstable angina diagnose via: cath
Patient Teaching: Post PCI
bedrest 4-6hr
HOB under 30 degrees if femoral
straight extremity
report pain, numbness, angina
education –> if bleeding provide pressure
Complications with AMI
Ventricular Dysrhythmia ***
HF
Pulmonary Edema
Cariogenic Shock
Discharge meds MI
Beta Blocker
Statin (decrease plaque)
Aspirin
ACE-I
Nitro
Heart Failure
inability of ventricle to fill or eject blood effectively
**pump issue
Ventricle Remodeling
heart stiffens and enlarges post MI
Left sided heart failure
Lungs
SOB, crackles, S3. elevated PAWP, PAOP, PAP
Right sided heart failure
Body
lower extremity edema
JVD
HJR
Elevated CVP
B-Type Natriuretic Peptide (BNP)
Marker of cardiac dysfunction, LV preload
compensatory mechanism responding to excessive cardiac stretch
Increases GFR, decreases sodium, inhibits renin and aldosterone secretion
Heart Failure Med: Hydralazine
strict arterial vasodilator
Heart Failure Med: Diuretics
decrease preload
Heart Failure Med: Digoxin
decrease HR to increase contractility
Heart Failure Med: Statin
decrease plaque formation
Implantable cardioverter defibrillator
senses lethal rhythm and shocks cardiac tissue to reset
Heart Failure: Self management
Drug compliance
Daily weights
Low Na+ diet
Exercise
Smoking and alc cessation
Nursing Management Acute Heart Failure
NO BETA BLOCKER
Preload/afterload reduction
+Inotropic meds
Intraaortic Balloon Pump
decrease afterload, increase arterial blood flow
Left ventricular assistive devices (LVAD)
sits in aorta to help pump blood
bridge to transplant
Preload Reduction Med therapy Acute Heart Failure
Diuretic
Nitrates
Afterload reduction Med therapy Acute Heart Failure
Nitroprusside –> IV monitor BP
ACE-I
Hydralazine
Inotropic Support Med therapy Acute Heart Failure
Dobutamine (B1 agonist)
Dopamine
Milrinone (decrease afterload)
Goals for Heart Failure Therapy
Cardiac output will be maximized
Patient’s symptoms will be managed
Euvolemia achieved
Prevent rehospitalization
Abdominal Aortic Aneurysm (AAA)
localized dilation of aorta >1.5
AAA risks
smoking, age, HTN, lipid disorders, atherosclerosis, MARFAN SYNDROME
Staple AAA symptoms
palpable, pulsatile mass at umbilical
ABD/lower back pain
Acute AAA rupture
SEVERE ABD PAIN
Hypotensive with loss of consciousness
Surgical repair AAA
rapidly expanding, >4.5-5.5cm, symptomatic aneurysm
Stent prefered
Aortic Dissection
weakened aortic medial layer causes tear creating false channel of blood
SX aortic dissection
SEVERE HTN
Pain between shoulder blades, ripping and tearing sensation, unequal pulses
Management of aortic dissection
Reduce with IV beta blockers (Esmolol) or B+A combo labetalol
IV Nitroprusside
Post op Aortic dissection repair
IV Nitroprusside to keep sys <120mmHg
Strict monitoring (labs, v/s, i/o)
Complication monitoring (Acute renal failure, ischemic colon, spinal cord ischemia)
Peripheral Artery Disease
Processes obstruct blood supply to lower/upper extremities
Risks for peripheral artery disease
atherosclerosis, smoking, diabetes, >70, male gender, hypertension, hyperlipidemia, family hx, history MI, heart failure, TIA/Stroke
Clinical manifestations of PAD
Pain intermittent claudication cramping , burning aching relieved with rest
pulseless, pallor, paresthesia, paralysis
intermittent claudication PAD SX
Early
Cramping, burning, aching pain in the legs, activity relieved with rest
Late
pain at rest is sign anoxic limb
Pulse strength
0-Absent
1-Palpable, thready, weak
2-normal
3- bounding
NONPALP=DOPPLER
Pallor skin PAD
lower extremity
cool, atrophic, alopecia, red (more when dependent), thick brittle nails, ulcers not healing
delayed cap refill
Paralysis and paresthesia
limb threatening ischemia and mandate emergent evaluation consultation
PAD Bedside diagnostic evaluation
Ankle brachial index
Apply blood pressure cuff to upper arm and above ankle
systolic ankle pressure divided by systolic brachial pressure
Managing PAD
Antiplatelets
– pentoxifylline, cilostazol aspirin and clopidogrel
— statins
PTCA and stenting
Surgical vascular bypass for severe/diffuse arterial obstruction
Chronic Venous Insufficency
Pooling of blood to legs
brown pigmentation, edema, thick flaky skin, ulcerations