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Cardio 2

Terms in this set (129)

Blood pressure
Force applied to artery walls. Determined by:
Force
Amount of blood
Size and flexibility of arteries
Essential (primary) HTN
Most common and usually no know cause

Gradual onset, >40 years, FH, s/s years after onset
Secondary HTN
Caused by another medical condition.
Less common, more dramatic onset, can happen at any age

Suspect secondary if:
Severe or refractory HTP
Acute rise in BP although previously was stable
Onset before puberty
Onset <30, non-obese, non-black, negative FH

Can be caused by:
OSA, drugs, thyroid dz, CKD, RAS, Cushings/steroids, pheochromocytoma, coarctation
Pathophysiology of HTN
multifactoral-genetics, environment, increased vascular tone, increased blood volume.
RAAS and HTN
Over activation of RAAS causes salt and water retention which raises BP
SNS and HTN
increased catecholamine production increases SNS which increases systemic vasoconstriction which raises BP
Factors that influence arterial pressure
stroke volume, distensibility of large arteries, PVR, volume, life, OSA, kidneys, adrenals, thyroid, congenital defects, meds, chronic alcohol use
Pulse pressure
the difference between systolic and diastolic blood pressure

The change between the two causes the pulse

Narrow PP <30:
Tachycardia, Severe AS, constrictive pericarditis, pericardial effusion, ascites

Wide PP >40:
Aortic dissection, atherosclerosis, AR, anemia, thyrotoxicosis
HTN screening guidelines
Annual screening for adults >40 and those at risk for high BP

Adults 18-39 without risk factors should be screened every 3 - 5 years
HTN symptoms
Usually is already pretty bad when symptoms appear

HA, fatigue, visual disturbances, TIA, angina, dyspnea, irregular heartbeat, nosebleeds, tinnitus, frequent urination, foamy urination and edema, hematuria, changes in urine color.

Most symptoms are related to end-organ damage (heart, stroke, kidney, PAD, retinopathy)

If these symptoms are present, rule out secondary cause:
tachy/sweating/tremor (pheo), thin skin (steroids), flank pain (kidneys), daytime somnolence (OSA)
Family history and HTN
Family history of these will increase HTN risk:
premature CVD or death, renal disease, diabetes, pheo
Physical exam for HTN
Should look at the following:

General: distribution of fat, alertness
EENT: fundoscopic, examine thyroid
CV: size, rhythm, sounds
Pulmonary: rhonchi, rales
Abdomen: renal masses, aortic/renal bruits, femoral pulses
Extremities: peripheral pulses, edema
MSK: strength
Skin: lesions
Neuro: visual disturbances
Measuring blood pressure
In office: 2 readings, 5 minutes apart with feet flat on ground. Confirm in opposite arm

Ambulatory: Q 30 minutes for 24 hours. Typically rule out "white coat HTN" and a great way to diagnose, but rarely done

Patient self-check: improves adherence to treatment, make sure to "calibrate" their home monitor

**Ensure you're using the right size cuff
Ascultatory gap
Silent interval that MAY be present between SBP and DBP. If unrecognized can lead to underestimation of SBP (false low) or over estimation of DBP (false high)

Avoid this gap by obtaining the pulse obliteration point OR inflate to >200
Hypertensive retinopathy
looks similar to diabetic, but presence of disc edema, lack of neovascularization and history (SUPER high BP) can help differentiate

exam: Flame shaped hemorrhages, dot-blot hemorrhages, exudates, cotton-wool spots, subtle blurring of disc marginally (papilledema), AV nicking (Gunn sign)
Labs and imaging for HTN
CBC- rule out hemolysis and thrombocytopenia
BMP- look at kidneys
Thyroid- if suspected thyroid dz
Urinalysis- look for proteinuria and hematuria
Lipid profile (yearly)- monitor for hyperlipidemia
EKG (2-4 year intervals)- rule out heart disease
Hypertension definitions (JNC8)
TARGETS
>60 years: 150/90
<60 years: 140/90
>18 w/CKD: 140/90
>18 w/DM: 140/90
Lifestyle modifications for HTN
#1 treatment for everyone:
DASH diet (healthy diet)
Decrease Sodium to 2400 mg/day
Increase Potassium to 4,700 mg/day
Moderate Alcohol Men <2 Women <1
Stop smoking
Increase daily activity/exercise (30 min daily)
Lose weight (healthy BMI)
Control stress
Pharma treatment of HTN
1. Select antihypertensive medication
1. ACEI or ARB (lisinopril/losartan)(unless black then choose amlodipine)
2. Thiazide diuretic (hydrochlorothiazide)
3. DHP CCB (amlodipine)

Can use these alone or in combo

2. Titration strategy
-Maximize 1 med before adding another
-add second med before at max dose
-start with 2 med classes
-consider reducing meds in patients with excellent BP control over the past several years

3. Monitor appropriately
- Recheck 1 month after staring meds, once at goal recheck every 6 months to a year
Side effects of antihypertensvies
Thiazides :hyperglycemia, hypokalemia, reduced uric acid clearing (gout)

ACEI and ARB: hyperkalemia and/or decreased GFR

DHP CCB- Edema from arterial vasodilation (Consider adding ACEI to help with edema)
Resistant (refractory) HTN
Measurements are still above goal despite concurrent use of 3+ types (classes) of antihypertensives (one of these 3 should be a diuretic)

OR

BP is controlled with 4+ types (classes) of antihypertensives

CONSIDER: improper measurements, excessive sodium/caffeine, inadequate diuretic, drug interactions, excessive alcohol, secondary causes
Antihypertensive dosing
HCTZ: 12.5 - 25 mg daily
Lisinopril: 10 - 40 mg daily
Losartan: 25 - 100 mg daily/BID
Amlodipine: 2.5 - 20 mg daily
Hypertensive urgency vs emergency
URGENCY: SBP >180 OR DBP >120 acute elevations with risk of end organ damage (no other symptoms).
Treat: Outpatient with Clonidine. Lower slowly over 24-48 hours (no more than 25% in 24 hours). Adjust current meds. F/U in 1 week

EMERGENCY: SBP >180 OR DBP >120 acute elevation with acute impairment of one or more organ systems (chest pain, vision changes, HA, AKI, etc.)
Treat: Hospital admission for continuous cardiac monitoring. Treat with IV Sodium Nitroprusside. Lower BP slowly (except with aortic dissection), then when risk of end organ damage has dissipated, convert to oral therapy
Hypertensive cardiomyopathy
Hypertrophy of LV and RB that will cause CHF (late stage)

Early symptoms: cough, weakness, fatigue

Later symptoms: edema, weight gain, dyspnea with exertion, and PND
Hypertensive nephropathy
Seen after 5-20 years of HTN

Symptoms: frequent urination, foamy urination and edema (proteinuria), hematuria, changes in urine color (dark brown)

Black patients have 8-fold increase of risk of HTN-induced_ ESRD
Hypertensive CV disease
Causes a variety of changes in vasculature and myocardium and conduction which leads to increased risk for:
Stroke, PAD, CAD/MI, systolic/diastolic dysfunction, conduction system diseases (a.fib)
Hypotension considerations
Symptomatic?
Acute hypotensive episode?
Is this normal for patient?
Is the reading correct?
Is patient stable?
Are other vitals abnormal?
What is the CC?
Types of hypotension
Absolute:
SBP <90mmHg MAP <65mmHg (vital organs will become hypoxic)

Relative:
Drop in SBP of >40mmHg

Orthostatic:
>20mmHg drop in SBP within 3 minutes of standing
>10mmHg drop in DBP within 3 minutes of standing
**Measure in at least 2 positions (Lying to sitting and sitting to standing)
Causes of hypotension
Orthostatic
Cardiogenic
Sepsis
Drug induced
Endocrine
Hypovolemia
Vascular
Neurological
Hypotension symptoms
Depends on underlying cause, comorbidities, age, etc.

Lightheadedness, dizziness, syncope, N/V, confusion, fatigue, reflex tachy, flushing, diaphoresis, clammy, pallor, prolonged capillary refill, altered LOC
Orthostatic hypotension etiology/risk factors
Volume depletion (diuretics, hemorrhage, vomiting, DI, etc.), medications, age (elderly), vasodilation (prolonged standing, fever), neurologic (failure of ANS), neurodegenerative dz (Parkinson's, dementia with Lewy bodies), neuropathies, cardiac impairment (bradycardia, AS, tachycardia, MI, pericarditis), carotid stenosis
Labs and imaging for hypotension
Focus on identifying underlying cause (anemia, dehydration, heart disease, etc.)
CBC
BMP
EKG
EMG
Urine drug screen
Head CT
Echo
Management of hypotension
Asymptomatic: no treatment. Consider lifestyle modifications and continued monitoring

Hypovolemic: fluid resuscitation (IV bolus NS)

Septic: fluid, fluid, fluids

Over medicated: stop offending agents

Non-pharm treatments: get up slowly, avoid straining/large meals/exertion in hot weather, maintained hydrated, compression stockings, increase salt and water intake

Pharma treatments:
-Fludrocortisone (fake aldosterone) promotes salt reabsorption and potassium excretion
-Midodrine (alpha 1 agonist) increases PVR and thus blood pressure
"atherosclerosis"
athero: porridge- soft lipid material in center of atheroma

sclerosis: scarring (connective tissues in plaques)
Atherosclerosis
sub-type of arterioscerlosis primarily affecting the intima. Involves lesions/plaques/atheromas

Veins do not develop atheromata

Most common locations for plaques are regions of turbulent blood flow (bifurcation of vessels-carotid)
Response to injury theory
1. endothelial injury
2. LDL infiltration
3. Fatty streak formation
4. Formation of fibrous plaque
5. Rupture of fibrous cap leading to thrombus
Endothelial injury
HTN and hyperlipidemia are two major risk factors. Damaged endothelium releases vWF (von Willebrand factor-clotting protein) which leads to a platelet plug, inflammation, and macrophage accumulation in the area
LDL infliltration
LDLs infiltrate endothelium at site of injury and build-up in the tunica intima. LDLs oxidize and trigger further inflammation. Macrophages are drawn into the area and distend becoming foam cells. Foam cell death contributes to growth and formation of atheroma
Chylomicrons and VLDL
Transport TGs, are much more buoyant
LDL and HDL
Carry mostly cholesterol and apoproteins, are more dense
Fatty streatks
accumulation of foam cells in intima develops into fatty streaks which are precursor lesions to atherosclerotic plaques.

1st grossly visible lesions in development of atherosclerosis. Seen in most people by age 20

These can remain stable, regress or evolve into atherosclerotic plaques
Fibrous caps
Stable plaques form fibrous caps that become calcified over a lesion. Remodeling of the vessel then occurs and ultimately lumen may become narrowed.

Cap provides stability to plaque and walls off the lesion from coming in contact with blood

These can remain stable or progress slowly over decades
Arterial remodeling during athrerogeneiss
initially growth is outward preserving caliber of lumen. "compensatory enlargement" accounts for tendency to underestimate degree of atherosclerosis on angiogram

Stenosis is a late even which is result of repeated plaque rupture and healing

Prior to plaque rupture there may have been no narrowing or aneurysmal enlargement of the atheroma

Narrowing of ~75% is necessary to produce detectable abnormalities on stress test
Thrombus formation
If the cap ruptures and blood comes in contact with thrombotic core blood flow becomes turbulent and culminates in intravascular thrombosis

Plaque disruptions vary from tiny fissures/erosions to deep intimal tears
Partial vs complete occulsion
Partial: stable angina/ischemia, claudication, TIA

Complete: ACS (unstable angina, STEMI, NSTEMI), claudication, stroke
Atherosclerosis risk factors
age, male, race (AA, mexican, indian, hawaiian), FH (male <55, female <65), hyperlipidemia, HTN, smoking, DM, obesity, physical inactivity, unhealthy diet

High levels CRP, high TG, OSA, stress, alcoholism
Hyperlipidemia and atherosclerosis
direct proportional relationship with atherosclerosis and IHD.

Plaques are derived from lipoproteins.

Increased risk with increased LDL
Decreased risk with increased HDL
Coronary heart disease risk equivalents
Stroke, PAD, AAA, DM, metabolic syndrome, 10 year ASCVD risk of >20%
Ischemic heart disease
FIXED STENOSIS:
Stable angina

ACUTE CORONARY SYNDROME (ACS)
Unstable angina
MI
NSTEMI
STEMI
Angina
chest discomfort related to inadequate blood supply to heart. Is a symptom of ischemic heart disease.

STABLE (fixed stenosis):
typical predictable pattern (when heart is stressed), lasts 1-15 minutes then goes away with rest or nitro, may continue without change for years

UNSTABLE(transient formation/dissolution of thrombus):
unexpected or a change to usual pattern, occurs when blood is suddenly slowed through narrowed vessels/thrombus, does not go away with rest/nitro, may be warning sign of MI
Cardiac Ischemia
reduced O2 to myocardium. Heart can tolerate a short time with decreased flow.

IF flow returns within a reasonable time, cells will usually recover
Cardiac Injury
Severe or prolonged ischemia. Damage to cells may be reversible
Cardiac infarction
Sever ischemia that continues until there is myocardial tissue death (heart attack/MI).

Cells will sustain irreversible injury and die

"Acute" infarct is <3-5 days old
NSTEMI
Subendocardial infarct
involves a small ares in the sub-endocardial wall

Will present with ST depression, T wave inversion, or no EKG changes
STEMI
Transmural infarct
Extends through whole thickness of heart muscle caused by complete occlusion of blood supply.

Will present with ST elevation and sometimes a new onset LBBB
t-wave inversion
characteristic sign of ischemia and may show ischemia without infarction.

Usually most pronounced in chest leads (V2-V6)
Things that cause ST elevation
STEMI
Prinzmetal's angina (absence of infarct)
Ventricular aneurysm (can cause persistent ST elevation in chest leads)
Pericarditis (unique ST elevation with elevated T waves)
Brugada
BER
Brugada Syndrome
Resembles RBBB and ST elevation in leads V1-V3

Elevated ST segments have peculiar downsloping appearance (coved). May have inverted T wave after ST elevation

Young man (<40) with fainting spells or sudden cardiac death.

Treatment: ICD
Pericarditis
Can elevate the ST segment creating a flat or concave middle (saddleback). May elevate the entire T wave

Any age person with pleuritic chest pain, worse when leaning forwards and deep breathing, may have pericardial friction rub
ST segment depression
NSTEMI (usually depressed AND flat- horizontal or downsloping)
angina attack (ischemia only)
positive stress test
LVH with strain
Digitalis
Low potassium
Significant Q waves
At least 0.04 seconds long (1 box) or 1/3 of entire QRS amplitude

Significant Q waves indicate necrosis. Can be an old (prior) MI
Insignificant q waves
Less than 0.04 seconds (1 box)
LV hypertrophy
Very tall R wave in V5

Deep S wave in V1

Often will have inverted T wave with asymmetry (gradual downslope, but quick return to baseline)

Presentation: patient with long-standing poorly controlled HTN
Q wave
Q wave is the first downward stoke and will never be preceded by anything else in the QRS complex. If there is a tiny spike before the "Q" the spike will be an "R" and the down stroke will be an "S"

If there is no "R" the downward deflection will be called a "QS"
ST segment considerations
ST segment deviation >1mm from baseline in limb leads

ST segment deviation >2mm from baseline in chest leads
J point
Where QRS ends and ST segment begins (directional change between depolarization and beginning of repolarization)
Inferior
Leads II, III, aVF

Fed by RCA
Septal
Leads V1 and V2

Fed by LAD
High lateral
Leads I and aVL

fed by LCX
Lateral
Leads V5 and V6

Fed by LCX
Anterior
Leads V1, V2, V3, V4

Fed by LAD
Age of a STEMI
minutes to hours: ST elevation
Days: ST elevation, Q waves develop, T waves invert
Weeks: ST flattening, Q waves present
Months: ST normalization, persistent Q wave
Upsloping vs downsloping
Upsloping: Smiley face, more reassuring

Downsloping: Frowny face, more worrisome
Prinzmetal (variant) angina
Younger patient who smokes, complains of chest pain at rest during morning hours

Transient coronary spasms. Usually younger and have fewer risk factors

Occur in clusters at rest and in the morning. Rarely causes a heart attack.

This ischemia will cause ST elevation but changes are transient and will resolve when chest pain resolves. Can only diagnose while symptoms are present
Ventricular aneurysm
Recurrent chest pain about >2 weeks after an MI.

Bulge where MI (or CM, infection, congenital abnormality) weakened heart wall

Increased risk of: ventricular arrhythmia, sudden cardiac death, CHF, mural thrombus + embolus

EKG shows ST elevation (concave or convex) >2 weeks following acute MI
Benign Early Repolarization (BER)
Incidental finding in young healthy males with no symptoms and a healthy heart.

EKG shows widespread ST elevation (may mimic pericarditis or acute MI) with tall peaked T-waves with J-point notching
Hypokalemia
K <3.5 but usually doesn't show symptoms until K <2.7

Hypokalemia increases myocardial excitability and can lead to reentrant arrhythmias

EKG: prominent U waves (usually precordial leads) increased amplitude/width of P wave, T flattening and inversion.

Present with history of N/V/D, muscle cramps, palpitations, and have low K

Treatment: replace Mg and K
Hyperkalemia
K > 5.5

High potassium decreased myocardial excitability and can depress pacemaking

Present with fatigue, muscle weakness, tingling. History of renal failure, on K-sparing diuretic, K replacement, or ACEI. Slow HR with weak pulse and high K

EKG: peaked T waves, prolonged PR interval, Broad/bizzare QRS complexes that merge with P and T waves
Digitalis effect
Caused by digoxin toxicity

Presents as older person taking digoxin with Green halo vision, vomiting, and confusion

EKG: ST sagging/slurring/scooping best seen in V4-V6
Pulmonary embolism
Presentation: SOB, pleuritic chest pain (worse with inhalation), pre-syncope, leg pain/swelling. Common complication of hospitalized patients

EKG: Classic triad (S1Q3T3)
S1- S wave is large in lead I
Q3- pathological Q wave in lead III
T3- Inverted T wave in lead III
Tachycardia, RBBB, many others
Pacemaker
Symptomatic bradycardia, high-grave AV block, SSS with pauses, A-fib with pauses

Will show pacer spikes on EKG. Impossible do diagnose STEMI from EKG of patient with ventricular pacer

Types:
Single chamber-RA or RV
Dual chamber- RA and RV
BiV-RV and LV (with or without RA)
ICD or AICD
Primary and secondary prevention of sudden cardiac death

(V-fib, etc)
How to diagnose ischemic heart disease
History
Physical exam
Risk factors (to determine probability of IHD)
History for IHD
Quality: aching, burning, pressure, squeezing

Location: substernal, radiating (neck/jaw/arms)

Duration: minutes

Timing: intermittent or gradual

Severity: variable

Provocative factors: exercise, meals, stress/emotions, cold, morning, supine position

Palliative factors: nitro, cessation fo activity, rest

Associated S/S: SOB, N/V, diaphoresis, fatigue, weakness, feeling of impending doom, paresthesias, dizziness, fever
Typical angina
Must meet all 3. Atypical meets 2, non-cardiac meets <1

1. substernal chest discomfort with characteristic quality that is...
2. provoked by exertion or emotional stress...
3. Relieved by rest or nitroglycerine
Atypical presentation for women with heart disease
Pressure or pain in lower chest, upper abdomen, or upper back
Dizziness
Extreme fatigue
lightheadedness/fainting
Physical exam for IHD
Vitals: hypo/hypertension, tachy/brady
General; anxious, diaphoretic, confused
Neck: JVD
CV: arrhythmia, muffled sounds, new murmur, diminished pulses
Resp: rales, wheezing, labored breathing
Neuro: signs of stroke
TIMI risk score
>65
>3 CAD risk factors
Prior CAD (>50% stenosis)
ASA in last 7 days
Severe angina (>2 angina episodes in 24 hours)
ST deviation
Elevated cardiac markers
Non-coronary causes of chest pain
Hypotension, HTN, HOCM, severe AS/AR, pericarditis, hyperthyroid, etc.

Differentials:
MI, GI, psychiatric, pulmonary, chest wall (costochondritis)
Diagnostic 12-lead EKG
in patients with chest pain or other symptoms suggesting ACS, 12-lead EKG should be collected within 10 minutes of patient's arrival to the ED

If EKG is not diagnostic, but the patient remains symptomatic and there is a high clinical suspicion for ACS, you can do serial EKGs (15, 30 minutes)
Cardiac biomarkers
How we differentiate unstable angina from a NSTEMI, also needed to make a diagnosis of STEMI

These are only drawn inpatient

Myoglobin: earliest released (as early as 2 hours)
Troponin-I: Preferred biomarker

Biomarkers rise with: MI, post-PCI, post-CABG, CHF, sepsis, PE, CKD, myocarditis, aortic dissection, etc.
Diagnosis of acute myocardial necrosis
Must determine peak troponin value and serial changes

Measure at presentation, 3 hours, 6 hours after symptom onset (X3)

Only measure beyond 6 hours in patients with normal troponin with EKG changes that suggest high index of suspicion for ACS
Other potential labs for IHD
CBC: anemia, leukocytosis
BMP
Fasting lipid panel: required in all patients with MI
PT/INR
CRP: elevated CRP may increase risk of subsequent MI
ESR: elevates within 3 days and may stay increased for weeks
Myocardial infarction diagnosis
Rise in cardiac biomarkers PLUS (at least one of the following)

Symptoms of ischemia
EKG changes of new ischemia
new Q waves
Imaging with evidence of new loss of viable myocardium or new wall motion abnormality (echo)
Stress test
Recommended initial non-invasive procedure for evaluating inducible ischemia in patients with angina
(exercise or pharmacologic)
Exercise stress test
Preferred form of stress test if not contraindicated

Positive test: ST-segment depression of 1mm

Will work to get patients to ~70% of max HR

Contraindications:
Abnormal resting EKG (WPW, Ventricle paced rhythm, >1mm ST depression on rest, Complete LBBB, LVH with ST-T abnormalities, Digoxin use with associated ST-T abnormalities)
Acute MI within last 2 days
High-risk unstable angina
Severe symptomatic AS
PE, myocarditis, aortic dissection
HF
Pharmacologic stress test
Used when a patient is unable to do exercise test.

ALWAYS combined with imaging

1. Vasodilators (adenosine)- contraindicated in bronchospasm

2. adrenergic stimulating (dobutamine): contraindicated in recent MI, unstable angina, aortic dissection, resting SBP >180)
Coronary angiogram
Prevent contrast-induced nephropathy (D/C metformin and HCTZ + hold for 48 hours after) Hydrate well before and after
Other imaging for angina
Chest x-ray: identify potential chest pain causes and can see widened mediastinum (aortic dissection)

Chest CT with contrast: exclude PE and aortic dissection (HR must be <50)

TTE: pericardial effusion, tamponade, wall motion abnormalities, proximal aortic dissection
Primary prevention of ACS
Educate about risk factors, clinical presentation, symptoms.

Older persons, those with DM, women, and post-op patients my have atypical symptoms

Decrease CAD risk factors
When presenting to ED for ACS what should they be given?
MONA
Morphine: pain and anxiety relief in STEMI. Use caution with hypotension, resp depression
Oxygen: if O2 <90
Nitro: 1st line for chest pain (besides RB infarct). Can use IV NTG
Antiplatets (DAPT)
ASA (162-325 mg) chewed then 81 mg/day long term
P2Y12 antagonist (loading dose of 600 prior to PCI). If given and they need CABG, but wait 5-7 days. Continue 75 mg for a year
GLP IIb/IIIa inhibitor can also be used

Beta Blocker: 1st line therapy for ACS, start within 24 hours.

Anticoagulant: for minimum of 48 hours up to 8 days
BB and ACS
1st line therapy, start within 24 hours unless contraindicated.

Improves mortality and morbidity
ACEI/ARB and ACS
Start within 24 hours unless contraindicated. Use especially if HF, anterior STEMI, or EF <40%

Preserve myocardium in MI
High intensity statin and ACS
Should be given to stabilize plaque even if cholesterol levels aren't high
Reperfusion considerations
Most important factor defining short and long term outcomes. Should be started within 12 hours of symptom onset

Facility PCI capable?
Time required to transfer to PCI site?
Time since symptom onset?
Shock?
PCI
percutaneous coronary intervention
(balloon angioplasty, stent angioplasty, atherectomy)

Stent angioplasty is most effective therapy, should be on DAPT. No benefit for stable CAD.

PCI is recommenced reperfusion method for STEMI)

D2B: door to balloon goals for STEMI
90 minutes if PCI capable hospital
120 minutes for non-PCI capable hospital (need to transfer)
Stents
BMS (bare metal stent): high rates of restenosis at one year. Does not have coating

DES (drug-eluting stent): drugs block cell proliferation
Atherectomy
Roto-rooter
TIMI grade flow
0: no perfusion

1: penetration without perfusion

2: partial reperfusion

3: complete reperfusion
Fibrinolytics
"clot busters" Should be started if device time to transfer and perform PCI exceeds 120 minutes. Do not give if symptoms are >12 hours. Goal is to initiate within 30 minutes of arrival (D2N door to needle)

ONLY used in STEMI, stroke, DVT/PE

Side effects: bleeding, hemorrhagic stroke, dystrhythmias

Contraindicated in: previous hemorrhagic stroke, any intracranial hemorrhage
NSTEMI treatment
Ischemia guided strategy: Stabilized patients with lower risk scores. Can decide if PCI or CABG is best

Early invasive strategy: Stable patients with high risk of coronary event.

Both recommend DAPT and anticoagulation
CABG
Preferred method when:
LM is stenosed >50%
Poor LVEF
Significant 3 vessel CAD
2 vessel CAD involving proximal LAD
DM with focal stenosis in more than 1 vessel
Need concomitant valve surgery
Diffuse disease not amenable to treatment with PCI
Dressler's syndrome
Type of pericarditis believed to be an immune response following damage to heart/pericardium after MI, surgery, or traumatic injury

Occurs 2 weeks post MI or CABG

S/S: ischemic type chest pain, fever, pericardial friction rub

Treatment: Colchicine+ NSADIS (indomethacin) +GI prophylaxis
Tachyarrhythmias post ASC
PVCs
VT and VF
Sustained VT: amiodarone, cardioversion
Accelerated idioventricular
A.fib
Free-wall ventricular rupture
Permanent damage to portion of heart wall can lead to myocardial scarring and ventricular aneurysm that can rupture
VSD
ventricular septal defect can be caused by an MI
MR
Mitral regurgitation can occur post-MI if the MI ruptures a papillary muscle
Secondary ACS prevention
change in diet
new exercise program
new medications
more frequent doctor's visits
ACS discharge
Labs: Blood glucose, lipids

Imaging: EKG, follow-up stress test

F/U:
1-2 weeks with PCP
4-6 weeks with cardiologist/surgeon
PCP every 6 months to year
Psychosocial considerations post ACS
debility/decreased exercise tolerance

activity/recreation: should exercise 3-5 x per week. Can do cardiac rehab

depression: "cardiac blues" Very common and increases risk of another MI

sexual activity: can return to normal in 2 weeks after non-complicated MI, or at 6 weeks post-MI (when they can walk up 2 flights of stairs)

work
Cardiac rehab
1. exercise training
2. education to reduce risk factors
3. counseling to deal with stress, anxiety, depression

phase 1: inpatient
phase 2: outpatient
phase 3-4: outpatient and in groups at the gym, etc.
Shock
Inadequate tissue perfusion with oxygenated blood

Shock occurs when something causes dysfunction in the circulatory system
Cardiogenic shock
most common cause is MI with reduction of myocardial contractility (pump failure).

Leading cause of death in patients with acute MI who make it to hospital alive
Pathophysiology of cardiogenic shock
Decreased contractility due to LV damage (LVEF <40%)

Pump failure

Reduced CO

Reduced BP

Coronary artery hypoperfusion...start again (vicious cycle)
Cardiogenic shock presentation
Chest pain, SOB, nausea, etc.

Patient may often be confused/obtunded

Altered mental status, decreased urine output, hypotension (<90 SBP), tachycardia, tachypnea, cool/mottled extremities, acute HF (rales, JVD)
New murmurs post MI
"mechanical catastrophes"

MR from papillary muscle rupture: new holosytolic murmur at apex radiates to axilla

VSD: holosystolic murmur at left sternal border, often with thrills

Free wall rupture: fast death
Diagnosis of cardiogenic shock
EKG (usually shows STEMI)
Labs: CBC, CMP, Cardiac biomarkers, BNP, Lactate (elevated in hypoperfusion)
Imaging: CXR (pulmonary congestion/edema), Echo (assess for wall abnormalities, reduced EF, etc)
Treatment of cardiogenic shock
Airway: Oxygen
Breathing: Trach/intubation

Meds:
Vasopressors (noreninephrine)
Inotropes (dobutamine)
*Be careful with fluid, may already be overloaded

Treat blockage and any mechanical defects (CABG usually if mechanical complications)
Long-term management post ACS
Antiplatelets (DAPT)
ACEI/ARB
Anti-anginal (NTG)
Beta-blocker
Cholesterol meds
Diet
Exercise
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