Cardio Flashcards
(95 cards)
1
Q
Dilated Cardiomyopathy:
Pathophys, Etiology & Epidemiology
A
- Def: systolic dysfunction (S3 gallop) leading to a dilated, weak heart with EF <40%
-
Pathophys:
- increased heart size & weight, ventricular dilation, thinned ventricular walls (usually due to increased volume)
-
Etiology:
- Idiopathic = most common cause
- alcohol (#2)
- myocarditis (#3)
- cocaine
- doxorubicin
- infection (viruses eg coxsackie, HSV 6, adenovirus)
-
Epidem:
- age 20-60
- most COMMON type of cardiomyopathy
2
Q
Dilated Cardiomyopathy: S/sxs
A
-
Sxs:
- pulm congestion (Left HF): dyspnea, orthopnea, rales
- systemic congestion (Right HF): peripheral edema, JVD, nausea, abdominal pain, nocturia, enlarged liver
- Low CO: fatigue, weakness
-
Other:
- HTN or hypotension
- tachycardia, tachypnea
- S3 gallop
- mitral/tricuspid regurg: papillary muscles stretches with dilation -→ valvular dysnfunction
- PMI shifted laterally
3
Q
Dilated Cardiomyopathy: Dx
A
-
Diagnostic Criteria:
- inclusion: EF <40%
- LVEDD >177% of predicted
- inclusion: EF <40%
-
Labs to order:
- BNP
- Na, Mg, K
- BUN, Cr (CMP)
- Hemoglobin (CBC with diff)
-
CXR:
- cardiomegaly
- pulmonary edema
- pleural effusion
-
EKG:
- wide QRS
- LBBB
-
Echocardiogram:
- L ventricular dilation
- thin ventricle walls
- decreased ejection fraction (<50%, but often <30%)
4
Q
Dilated Cardiomyopathy: Dx
A
-
Diagnostic Criteria:
- inclusion: EF <40%
- LVEDD >117% of predicted
- inclusion: EF <40%
-
Labs to order:
- BNP
- Na, Mg, K
- BUN, Cr (CMP)
- Hemoglobin (CBC with diff)
-
CXR:
- cardiomegaly
- pulmonary edema
- pleural effusion
-
EKG:
- wide QRS
- LBBB
-
Echocardiogram:
- L ventricular dilation
- thin ventricle walls
- decreased ejection fraction (<50%, but often <30%)
5
Q
Dilated Cardiomyopathy: Tx
A
- tx just like systolic heart failure
- beta-blockers (metoprolol, carvedilol) + [ACE-I (lisinopril, captopril, enalapril) =mainstay of tx] + Loop diuretic (furosemide)
- Anticoag if EF <30%
- if you need increased contractility = digoxin (digitalis)
- Pt education:
- limit activity
- salt restriction <2g/day
- fluid restriction <2L/day
- extreme cases = heart transplant or L ventricular assist device
6
Q
Canadian Cardiovascular Society Classification System: Angina
A
- Stage I: angina with strenuous activity
- Stage II: slight limitation of ordinary activity; angina walking 2 blocks, up stairs rapidly
- Stage III: marked limitation of ordinary activity; angina walking 1-2 blocks
- Stage IV: Angina at rest
7
Q
Major Risk Factors of Coronary Artery Disease (CAD)
A
- Diabetes Mellitus (Worst risk factor, considered a CAD equivalent)
- Smoking (Most important modifiable risk factor)
- Hyperlipidemia, HTN
- Men >45yo, Women >55yo
- Fam Hx of CAD: (first degree relative – father or brother before age 55, mother or sister before age 65)
8
Q
Etiology of Acute Coronary Syndrome
A
-
Etiology:
- atherosclerosis = most common cause -→ acute coronary artery thrombosis with platelet adhesion with fibrin formation
- coronary artery vasospasm: prinzmetal variant angina, cocaine induced
-
Silent MI:
- 25% are atypical, more common in women, elderly, diabetics, obese patients; sxs include: dyspnea, epigastric pain, syncope, or sudden death
9
Q
NSTEMI: def, s/sxs, dx, & tx
A
- Definition: myocardial necrosis (evidenced by elevated troponins & cK-MB) without acute ST segment elevation; coronary artery not completely blocked, subendocardial infarct
-
S/sxs:
- Chest pain, SOB
-
Dx:
- EKG: ST-depression, T-wave inversion
- Troponins: positive, usually need 2+ draws on this, troponins take up to 3 hours to become elevated
-
Tx:
-
First line: oxygen of o2 <95%
- sublingual nitroglycerin (1-2 sprays Q5 min, max of 3)
- Aspirin (inhibits platelet activation)
- either IV unfractionated heparin (inhibits factor IIa (thrombin, and factor Xa) OR SQ enoxaparin (low molecular weight heparin, only inhibits factor Xa)
- clopidogrel 300mg
- if going for PCI → high dose statin prior to angiography
- Then eventually: BAAAS (b-blocker, ace-i or ARB, stain)
- ***Do NOT use Thrombolytics***
- “go to cath lab if not responding to treatment and still having chest pain, significant ST changes etc. Not all NSTEMI go to Cath emergently, many do not need to. Can cath semi-electively” -Dr Pearl
-
First line: oxygen of o2 <95%
10
Q
STEMI: def, s/sxs, dx & Tx
A
- Definition: myocardial necrosis (evidenced by elevated troponin & CK-MB) with acute ST-segment elevation or Q-waves; coronary artery completely blocked; full thickness infarct
-
S/sxs:
- Chest pain
- SOB
- pain radiating to jaw and/or arm
-
PE:
-
Inferior Wall MI:
- bradycardia or heart block (R. coronary artery supplies the AV node)
- epigastric pain
- may have S4
-
Triad of R ventricle MI:
- JVD
- Clear lungs
- positive Kussmaul sign : paradoxical JVP that occurs during inspiration -→ heart cannot accommodate extra blood that returns via the venous system when the intrathoracic pressure becomes negative during inspiration
-
Inferior Wall MI:
-
Dx:
-
EKG: new ST-elevation in two contiguous leads of >1mm
- reciprocal changes in opposite leads
- **progression: hyperacute T-waves → ST elevations → Q waves
-
Troponin:
- positive → returns to baseline in 7-10 days
- **may be falsely positive in pts with renal failure, advanced heart failure, acute PE, or CVA**
-
EKG: new ST-elevation in two contiguous leads of >1mm
-
Tx: a) prevent further clot formation by inhibiting platelet function- Aspirin and Clopidogrel
- b) Prevent thrombus formation by blocking Fibrin with Heparin
- c) Decrease Myocardial Oxygen demand (while working to improve supply)- Beta Blockers
- d) Vasodilate coronaries (spasm may occur as well with ischemia) and decreases preload as well by vasodilation- NTG
- e) Oxygen- only if sats below about 95%
- f) Morphine-used less frequent now- need a good BP, avoid in right ventricular infarction
- g) ACE inhibitor may be added later for remodeling and for afterload reduction, can use sooner if hypertensive
-
Definitive care:
- If < 3-5 hours and having STEMI go emergently to Cath lab for PTCA ( Balloon and Stent). Goal is 90 minutes door to reperfusion.
- IF > 3 hours before one can get to a cath lab then use Thrombolytic Therapy TPA or TKI etc. for STEMI
11
Q
Post MI Complications
A
- Pericarditis: 1-3 weeks post MI (Dressler Syndrome)
- VSD (ventricular septal defect: 1-5 days post MI: shock, new murmur, pulmonary edema
- Acute Mitral Regurg: shock, apical murmur, pulmonary edema
- new or recurrent MI: chest pain, new ECG changes possible, new bump in troponins
12
Q
Stable Angina
A
Coronary Artery Disease
- predictable and occuring with exertion → typically same distance each time
- relieved with rest or NTG
-
Workup:
- EKG: Normal, q-waves (if prior MI)
-
Cardiac Stress Test: pt should be able to walk 6 min on treadmill or else unreliable, goal is 85% of max predicted HR
- bruce protocol (increase by 2% grade & 0.8mph q 3 minutes)
- monitor: BP, EKG, Echo, sxs (CP, SOB)
-
coronary angiography:
- provides a definitive dx → defines location and extent of CAD but only used if:
- pt is severely symptomatic despite medical therapy and being considered for PCI
- pt with sxs difficult to dx
- angina sxs in pts who have survived cardiac death event and ots with ischemia on non-invasive testing
- provides a definitive dx → defines location and extent of CAD but only used if:
-
Tx:
- NBC (mnemonic to remember)
- beta blockers: decrease HR, contractility, blood pressure → decreased demand (metoprolol, carvedilol)
- nitroglycerin: sublingual or IV: decrease preload/afterload, vasodilate coronary arteries
- Calcium channel blockers: decrease afterload/blood pressure (velocity) , may dilate coronary arteries (non-dihydropyridine CCBs → diltiazem, verapamil)
- Statins: improve endothelial function
- aspirin: prevent thrombus formation (anti-platelet activation)
- NBC (mnemonic to remember)
13
Q
Unstable Angina
A
- Definition: occurs at rest (Canadian Angina Classification Level 4), or not relieved by rest or NTG. Some include exertional angina that is occurring more frequently, with lesser exertion, more intense, lasting longer (Crescendo Angina
-
Dx:
- EKG = ST segment depression >1 mm
- Troponins: Negative (no cell death)
- angiography = gold standard for diagnosing CAD but only used when revascularization is being considered
-
Tx:
- antiplatelet drugs (aspirin and/or clopidogrel (plavix) ticagrelor)
- beta-blockers (metoprolol, carvedilol)
- nitroglycerin & Ca channel blockers for symptom control
- Revascularization if sxs persist despite medical therapy
- ACE-I + statins
14
Q
Stress Test (Exercise Testing)
A
- Pt must be able to walk 6 min on a treadmill: goal is 85% of max predicted HR
-
initial test in pts who are stable and able to exercise
- Bruce Protocol: increase grade by 2% and speed by 0.8mph q 3 minutes
- Monitor: BP, EKG, symptoms (CP, SOB)
- Duke Treadmill Score: (duration of exercise in min) - (ST segment depression in mm)x (5) - (angina score)x(4)
-
if patient cannot exercise:
- can use adenosine for myocardial perfusion imaging
- can use dobutamine for a stress echo
15
Q
Angina- Prinzmetal Variant
A
-
Definition:
- Coronary artery vasospasm causing transient ST-segment elevations, not associated with clot. Usually happens at night or early morning
- risks: COCAINE ABUSE, female >50yo, hx of vasospastic disorders
- triggers: cold weather, exercise, alpha-agonists, hyperventilation
-
S/sxs:
- chest pain at rest (usually midnight to early morning, non-exertional & not relieved with rest)
- Preserved exercise capacity
-
Dx:
-
EKG: transient ST-elevation that resolves with symptom resolution
- inverted U-waves
-
EKG: transient ST-elevation that resolves with symptom resolution
-
Tx:
-
calcium channel blockers: first line monotherapy -→ given at NIGHT (Non-dihydropyridine: diltiazem, verapamil Qday)
- → can add long acting nitrate (Isosorbide mononitrate ER 30-60mg QAM: SEs: Methemoglobinemia, severe hypotension)
- Nitroglycerin IR for sx relief (1-2 sprays sublingual Q5 min PRN, max of 3 doses)
- AVOID BETA-Blockers! → may cause unopposed vasospasm
-
calcium channel blockers: first line monotherapy -→ given at NIGHT (Non-dihydropyridine: diltiazem, verapamil Qday)
16
Q
Acute vs. Chronic Heart Failure
A
-
S/sxs:
-
Chronic Heart Failure (compensated):
- congestion
- laterally displaced apical impulse
-
Acute Heart Failure:
- breathlessness
- rapid weight gain
- fluid build-up in the lungs and around the body
- inadequate time for compensation: largely systolic (HTN crisis, acute MI, papillary muscle rupture); often fatal
-
Chronic Heart Failure (compensated):
17
Q
Systolic Heart Failure
A
-
Definition: heart failure with decreased ejection fraction
- impaired contractility
- thin ventricular walls (DILATED)
- S3 gallop (sys-tol-ic)
-
Etiology:
- ischemic heart disease, rapid HTN, dilated cardiomyopathy (LEADING CAUSE), myocarditis, congenital, post-surgical, PE, sepsis
18
Q
Diastolic Heart Failure
A
-
Definition: Heart failure with preserved ejection fraction
- impaired filling/relaxation
- thick ventricular walls (**Hypertrophied**)
- S4 gallop (Di-a-stol-ic)
-
Etiology:
- HTN, aortic stenosis, restrictive & hypertrophic cardiomyopathy, fibrosis, amyloidosis, sarcoidosis, constrictive pericarditis, normal aging, CAD scarring
19
Q
Management goals of Heart Failure
A
- Afterload: make it easier for the heart to empty
- preload: appropriate stretch, get the heart back on the proper part of the Sterling curve
- contractility: help the heart function better (pump, squeeze, relaxation, rate & rhythm)
**Uncompensated heart failure: diuretics, afterload reduction, inotropes, mechanical support, transplantation
**Compensated heart failure: diuretics, afterload reduction, beta-blockers
20
Q
Tx of Heart Failure
A
- **initial management usually consists of an ACEI & (maybe a beta blocker) + diuretic (for sxs)**
-
Long Term Tx (Afterload reduction:
- ACE Inhibitors (Captopril, Enalapril, Lisinopril): reduce afterload by vasodilation & BP reduction, useful in pts with EF <35%,mainstay of tx, (adverse effects: hyperkalemia, cough, angioedema, & elevated creatinine)
- Angiotensin II Receptor Blockers (Losartan, Valsartan): blocks effects of angiotensin II, indicated in pts who cannot tolerate ACEI (cough)
- Angiotensin Receptor Neprilysin Inhibitor (Sacubitril/Valsartan): inhibits breakdown of BNP so BNP no longer becomes a reliable marker in pts taking this
- Beta-Blockers (Carvedilol, Metoprolol, Bisprolol): usually added after ACEI or AR
-
Long Term Tx (Preload Reduction)
- Loop Diuretics (furosemide, bumetanide, torsemide): inhibit water transport across the Loop of Henle, effective for sx tx.
- potassium sparing diuretics (spironolactone, eplerenone): aldosterone antagonist, decreased mortality
- Thiazides (hydrochlorothiazide, Metolazone): inhibits DCT reabsorption of Na+
-
Long Term Tx (Positive Inotropes):
- Digoxin: positive inotrope; 2nd line for pts in CHF with sinus rhythm, 1st line for pts with afib + CHF
21
Q
Left-Sided Heart Failure: Pathophys, Etiology, S/sxs, PE
A
-
Pathophys: leads to increased pulmonary venous pressure from fluid backing up into the lungs. Increased hydrostatic pressure drives protein-poor fluid into alveoli through an intact barrier
- → resolution depends on Na+ reabsorption and lymphatic drainage
-
Etiology:
- Coronary artery disease, HTN = most common
-
S/sxs:
- dyspnea: exertional, paroxysmal nocturnal dyspnea, orthopnea
- fatigue
- cough with frothy sputum
- activity intolerance
-
PE:
- pulmonary edema & congestion → crackles, rhonchi, wheezing, tachypnea
- cheyne-stokes breathing: deep, fast breathing with gradual decrease in episodes of apnea
- cyanosis
- S3 or S4 gallop
22
Q
Right-Sided Heart Failure: Pathophys, Etiology, S/sxs, PE
A
-
Pathophys:
- leads to increased systemic venous pressure from fluid backing up into the IVC, SVC, and hepatic circulation
-
Etiology:
- left sided heart failure = most common
- pulmonary disease (COPD, pulmonary HTN), mitral stenosis
-
S/sxs/Pe:
-
inferior vena cava:
- peripheral edema
-
Superior Vena Cava:
- jugular vein distention
- hepatic: anorexia, weight loss, n/v, hepatojugular reflex
- hepatosplenomegaly
-
inferior vena cava:
23
Q
Hypercholesterolemia: primary vs secondary, etiology, risk factors
A
- primary: WITHOUT known CV disease (carotid, heart, arteries)
- Secondary: with known clinical CV disease
-
Etiology:
- hypothyroidism, pregnancy, kidney failure
-
Risk Factors:
- sex, age, HTN, DM, smoking, family hx of coronary heart disease
- 1st degree male relative with CHD before age 55
- 1st degree female relative with CHD before age 65
- sex, age, HTN, DM, smoking, family hx of coronary heart disease
24
Q
Primary Prevention of ASCVD in age 0-19 years
A
- lifestyle to prevent or reduce ASCVD risk
- Diagnosis of familial hypercholesterolemia?
- statin
25
Primary Prevention of ASCVD in Age 20-39
* **Estimate lifetime risk** to encourage lifestyle to reduce ASCVD risk
* Consider statin if family hx, premature ASCVD and **LDL-C ≥ 160mg/**dL
26
Primary Prevention of ASCVD in Age 40-75 and LDL-C ≥ 70 to \<190 mg/dL without diabetes mellitus
10-year ASCVD risk percent begins risk discussion:
* _\<5%: “low risk”_
* emphasize lifestyle to reduce risk factors
* _5-\<7.5%: “borderline risk”_:
* If risk enhancers present then risk discussion regarding moderate-intensity statin therapy
* _≥7.5-\<20%_: “Intermediate Risk”
* Risk discussion:
* if risk estimate + risk enhancers favor statin, initiate **moderate-intensity** statin to reduce LDL-C by 30-49%
* if unsure, can use CAC score
* _≥ 20%: “high risk”_:
* initiate statin to reduce LDL-C ≥ 50%
27
At what LDL-C level do you initiate high intensity statin with no risk assessment?
LDL-C ≥ **190** mg/dL
28
What population do you initiate a moderate-intensity statin regardless of risk factors?
Diabetes Mellitus age 40-75yo
Risk assessment to consider high-intensity statin
29
CAC
Coronary Artery Calcium Score
* if risk decision is uncertain in age 40-75yo with intermediate risk (≥7-\<20%)
* **_CAC = zero_**
* (lower risk; consider no statin unless diabetes, family hx of premature CHD, or cigarette smoking are present)
* **_CAC = 1-99_**
* favors statin (esp. after age 55)
* **_CAC = 100+ and/or ≥75th percentile:_**
* initiate statin therapy
* Calculate MESA score with CAC, will give you a percentage by which to evaluate whether to initiate statin
30
Best meds to lower elevated LDL
* **Statins** (**Rosuvastatin, atorvastatin, etc****)** → inhibit HMG Co-A reductase
* impair production of cholesterol in the liver → upregulation of LDL receptors
* **Bile Acid Sequestrants (****Cholestyramine, colesevelam, colestipol****) & Cholesterol absorption inhibitors (****Ezetimibe****)**
* impair enterohepatic recirculation and gut absorption → less hepatic cholesterol → upregulation of LDL receptors
31
Best Meds to Lower Triglycerides
* **Fibrates** **(fenofibrate, gemfibrozil****)**: inhibit triglyceride synthesis = Drug of Choice;**gemfibrozil should NOT be given with statins**
* **Niacin**
32
Best Meds to Increase HDL
* **Niacin**
* **Fibrates** **(feno**_fibr_**ate, gem**_fibr_**ozil****)**: inhibit triglyceride synthesis = Drug of Choice;**gemfibrozil should NOT be given with statins**
33
Treatment of Secondary Hypercholesterolemia without high-risk (clinically stable)
_secondary hypercholesterolemia_ = **WITH** known clinical CV disease
* **high-intensity statin**
* can add **ezetimibe** if inadequate response (\<50% LDL reduction); goal is LDL \<70 mg/dL
34
Treatment of Secondary Hypercholesterolemia with High Risk (unstable)
_secondary hypercholesterolemia_ = **WITH** known clinical CV disease
* **high-intensity statin**
* can add **ezetimibe**
* can also add **PCSK9 monoclonal antibody (****Alirocumab, Evolocumab****)** : blocks PCSK9 binding to LDL receptor → direct upregulation of LDL receptors → lowers LDL 30-60%; injections Q2-3 weeks
* goal is LDL \<55 mg/dL
35
Abnormal Lipid Values
* Low HDL \<40 mg/dL
* High LDL \> 190 mg/dL
* high LDL in diabetic \>70 mg/dL
* high total cholesterol \>250 mg/dL
* high fasting triglyceride \>150 mg/dL
36
Hypertriglyceridemia
* _Definition_: fasting blood triglyceride level of **\>150 mg/dL**
* _Etiology_:
* diabetes mellitus, EtOH, obesity, steroids, estrogen
* _S/sxs_:
* **pancreatitis**, eruptive xanthomas, lipemia retinalis (creamy white discoloration of the retinal vessels), corneal arcus (grey arc of deposit on outer iris)
* _Dx_:
* **fasting lipid panel**
* Severity:
* 150-499: mild
* 500-886: moderate
* \>886: severe
* _Tx_:
* **Best meds to lower elevated triglycerides → Fibrates (****fenofibrate, gemfibrozil****)**, niacin
* **Best meds to lower elevated LDL → Statins**, bile acid sequestration
* **Best meds to increase HDL → Niacin (****Nicotinic Acid****)**, fibrates
* Type II DM → statins, fibrates
* **Fibrates** **(fenofibrate, gemfibrozil****)**: inhibit triglyceride synthesis = Drug of Choice;**gemfibrozil should NOT be given with statins**
* **Nicotinic Acid (Niacin)**: increases HDL levels, causes flushing
* **fish oil supplements**
* **Lifestyle modification:** avoid alcohol & refined sugars, lower caloric intake, exercise
37
Essential HTN: definition, PE, and diagnosis
* _Definition_:
* resting **systolic ≥ 130** or **diastolic ≥ 80** on at least **2 readings** on at least **2 separate visits** with **no identifiable cause**
* \*\*need to measure BP in **Both Arms**\*\*
* _PE:_
* fundoscopic exam: hypertensive retinopathy → AV nicking
* _Diagnosis_:
* see above definition
* **BP\>15 mmHg higher in one arm** than the other is **associated with a higher mortality** **→** eval of upper vasculature is required!!
* Other tests you can order: -**urinalysis and spot urine albumin: creatinine ratio**
* **blood tests** (creatinine, K, Na, fasting plasma glucose, lipid profile, and TSH
* **ECG**
38
Essential HTN: Tx
* _ACC/AHA_:
* **goals**: \<130/80
* AntiHTN therapy initiated in the following populations:
1. **all pts with stage 2 HTN** (baseline ≥140/90)
2. **pts with stage 1 HTN** (130-139/80-89 mmHg) who have **1+ of the following**:
* ASCVD
* Type II DM
* CKD
* 10-year calculated ASCVD risk ≥ 10%
* **Lifestyle Modifications**:
* DASH diet, increase fruits and veggies
* **Sodium** reduction **\<2.3grams/day** (1 tsp)
* **reduce alcohol** intake:
* **→ Men: 1-2 drinks daily max**
* **→ Women: 1 drink daily max**
* _Exercise goals_:
* → **\>150 minutes** of moderate intensity/week
* → **\>75 minutes** of vigorous intensity/week
* **ONE drug given initially**:
* for **non-black pts, including DM** give either:
* → **ACE-I** or **ARB**
* **→** long acting **CCB** (often a dihydropyridine like amlodipine)
* → or a **thiazide-like diuretic** (chlorthalidone, or indapamide)
* **for stage 2 HTN or a black adults:**
* recommendation is
* → **2 BP-lowering meds** from **different classes**
* If **Target BP is not achieved in 1 month**, dose of drug can be increased or a second drug added → BP should be checked monthly until the target is met
39
ACC/AHA Classification of BP
40
Hypertensive Emergency: definition, Dx, & Tx
* _Definition_: **\>180 systolic and/or \>120 diastolic** **_WITH_** signs of **damage to target organs** (except papilledema = hypertensive retinopathy) → encephalopathy, nephropathy, intracranial hemorrhage, aortic dissection, pulmonary edema, unstable angina or MI
* _Diagnosis_:
* **BP measurement**
* ECG
* urinalysis
* ophthalmic exam
* serum BUN
* serum creatinine
* _Tx_:
* **sodium nitroprusside** = drug of choice
* pt should be admitted to ICU
* If pt has: Aortic dissection, severe pre-eclampsia or eclampsia or pheochromocytoma crisis
* → **reduce SBP to _\<140mmHg_ during first hour and then to \<120 mmHg in aortic dissection**
* If pt does NOT have any of the above:
* **Reduce BP by** (10-20%) **max 25% over first hour, then to 160/100-110 mm/Hg over next 2-6 hours, then to normal over next 24-48 hours**
41
Hypertensive Urgency: Definition, Dx, & Tx
* _Definition_: **SBP \>180 and/or DBP \>120** without target-end organ damage
* _Dx_:
* BP measurement
* ECG
* urinalysis
* ophthalmic exam
* serum BUN, serum creatinine
* _Tx_:
* **immediate BP reduction is NOT required**
* **Clonidine** = drug of choice
42
Secondary HTN Definition and Causes
* _Definition_: **SBP ≥130 and/or DBP ≥80 WITH identifiable cause**
* _Causes_:
* **Primary aldosteronism** = MOST COMMON
* renal vascular disease
* pheochromocytoma
* adrenal tumor that secretes catecholamines (ie norepi and epi)
* Cushing's Syndrome
* activation of the renin-angiotensin system
* Congenital Adrenal Hyperplasia
* Hyperthyroidism
* Myxedema
* associated with hypothyroidism
* Coarctation of the Aorta
* Excessive alcohol intake
* Use of Oral Contraceptives
43
Secondary HTN Red Flags, Dx, & Tx
* _Red Flags_:
* HTN at an early age \<25 without a family hx
* HTN first develops \>50 yo
* previously controlled now refractor
* **Pt is refractory on antihypertensive medications** or has severe BP
* _Dx_:
* when HTN is newly diagnosed consider ordering:
* **urinalysis**
* s**pot urine albumin: creatinine ratio** → albuminuria ratio = \>30mg/day
* indicative of CKD
* **Blood tests**
* creatinine, K, Na, fasting glucose = _BMP_
* lipid panel
* TSH
* **EKG**
* _Tx_:
* tx the underlying condition and aim for **BP \<130/80**
44
Mixed Venous O2 vs A-VO2 difference
* _Mixed Venous O2_:
* amount of oxygen that is in the venous blood upon return to the heart
* Normal:
* Superior Vena Cava = 65% (brain uses most oxygen)
* Inferior Vena Cava = 75%
* Abnormal: **\<65%**
* **\<50% = danger zone**
* _A-VO2 difference_:
* arterial O2 (~98%) - venous O2 saturation
* **normal \<30%**
* **higher the difference = the WORSE the situation**
* As mixed venous O2 drops, AVO2 difference will increase (inverse relationship)
45
Delivery of oxygen is affected by
DO2 = CO x CaCO2
delivery of oxygen is affected by cardiac output and arterial oxygen content
46
Hypovolemic Shock: Definition, Etiologies, Pathophys, S/sxs
* _Definition_:
* **reduction in intravascular volume/preload** → decreased CO → insufficient perfusion
* _Etiologies_:
* **hemorrhagic**: trauma, GI bleed, ruptured aneurysm, post-operative, open central line
* **non-blood fluid loss**: vomiting, diarrhea, 3rd spacing, burns, dehydration, DKA, over-diuresis
* _Pathophys_:
* loss of blood/fluid volume → increased HR & vasoconstriction, increased epi, vasopressin, & angiotensin
* _S/sxs_:
* **tachycardia/tachypnea**
* **narrowed pulse pressure (d/t vasoconstriction)**
* **oliguria (d/t decreased CO)**
* hypotension
* pale, cool dry skin and extremities
* cap refill \>3 sec
* decreased skin turgor
* dry mucous membranes
* AMS
47
Features of Hypovolemic Shock
* _Preload_: decreased (volume depletion)
* _Cardiac Output_: decreased
* _Afterload_: increased (vasoconstriction)
* _BP_: low
* _Organ perfusion_: decreased
* _AVO2 Difference_: high (b/c heart is delivering less blood so tissues are using more O2 from the available blood)
48
Normal Blood Volume
* _Adults_: 7% IBW (75ml/kg)
* → 70kg adult = 5.5 Liters or approx 15 units
* _Children_: 9% IBW (90 ml/kg)
IBW = ideal body weight
49
Phases of Hypovolemic Shock
* **_Compensated_**: **0-24.9% blood loss** (500-1250cc)
* normal SBP/pulse pressure/ pulse, alert
* **_Uncompensated_**: **25-40%** (1250-2000cc)
* decreased SBP/ pulse pressure, tachycardic, anxious
* **_Irreversible_**: **\>40%** **blood loss**
* decreased SBP/ pulse pressure, very tachycardic, lethargic
50
Tx of Hypovolemic Shock
* ABCs
* **Volume resuscitation: Crystalloids (LR or NS)**
* usually 3-4 liters:
* initially **1-2 NS boluses** to restore tissue perfusion and continued at rapid rate until clinical signs of hypovolemia improve
* control the source of hemorrhage +/- packed RBCs if severe
* **maintain body temp** (prevent hypothermia)
51
Distributive Shock: Definition, Pathophys, & Etiologies
* _Definition_: **excessive vasodilation in small vessels** & altered distribution of blood flow with shunting from vital organs to non-vital tissues
* _Pathophys_:
* dilation of all blood vessels so the “tank” becomes too big
* _Etiologies_:
* **Septic**: overwhelming infx → systemic inflammatory response → systemic vasodilation
* **Anaphylactic**: severe rxn to allergen → systemic histamine release → widespread vasodilation
* **Neurogenic**: acute spinal injury that results in loss of sympathetic tone that normally keeps vessels constricted → vessel walls veno/vasodilate
* **Endocrine**: adrenal insufficiency
52
Distributive Shock: S/sxs of Sepsis, Anaphylaxis, and Neurogenic Shock
* _Sepsis_: “Warm shock" “warm shock”
* **warm, flushed extremities** (d/t systemic vasodilation of capillaries)
* **wide pulse pressure**
* bounding pulses
* hypotension
* _Anaphylactic Shock_:
* pruritus, urticaria
* angioedema
* hoarseness
* _Neurogenic_:
* warm skin
* bradycardia or normal HR
* wide pulse pressure
53
Features of Septic Shock
Type of Distributive Shock
* _Preload_: decreased
* _Afterload_: decreased
* _Cardiac Output_: decreased
* _BP_: low
* _Organ perfusion_: decreased
* **Mixed venous O2: HIGH** (oxygen is not reaching tissues and is not getting used due to loss of vascular tone)
* **AVO2 difference**: **LOW** (oxygen is not reaching tissues and is not getting used due to loss of vascular tone)
* so mixed venous o2 is high and arterial o2 is also high
54
Features of Neurogenic Shock
Type of Distributive Shock
* _Preload_: decreased
* _Afterload_: decreased
* _Cardiac Output_: **increased**
* _BP_: low
* _Organ Perfusion_: normal (b/c of good cardiac output so normal organ perfusion)
* _AVO2 difference_: normal
55
Tx of Distributive Shocks
* **_Septic Shock_**:
* broad spectrum IV abx
* IV fluid resuscitation, then a vasopressor (vasoconstrictor: **epinephrine, norepi/phenylephrine)**
* **_Anaphylactic Shock_**:
* -Epi
* -Airway management
* -antihistamines
* **_Neurogenic Shock_**:
* IV fluid resuscitation
* vasopressors +/- corticosteroids
* **_Endocrine Shock_**:
* hydrocortisone
56
Obstructive Shock: Definition, Etiology & Tx
* _Definition_: **mechanical block to heart's outflow or inflow**
* _Etiology_:
* very large PE
* pericardial tamponade
* tension pneumo
* aortic dissection
* _Tx_: **Tx the underlying cause**
* PE: heparin, thrombolytics (TPA, TKI)
* Tamponade: pericardiocentesis
* Tension Pneumo: needle decompression
* oxygen, isotonic fluids, inotropic support (**dobutamine, epi, milrinone)**
57
Cardiogenic Shock: Definition, Etiology, & S/sxs
* _Definition_: **primary myocardial dysfunction** (pump failure) → low cardiac output → inadequate tissue perfusion
* _Etiology_:
* **Pump Failure**:
* ischemia (CAD), acute MI, myocarditis, valve dysfunction (mitral regurg secondary to papillary rupture), cardiomyopathy, post-operative, myocardial contusion, acute ventricular septal or L ventricular rupture
* Arrhythmia, toxic/metabolic
* _S/sxs_:
* **Acute hypotension** (you can only compensate with increasing afterload [vasoconstriction) **BP \<90/60**
* tachycardia, tachypnea
* weak pulses
* mottled skin
* diaphoretic
* AMS
* anxiety/restlessness
* **Elevated JVP**
* oliguria
58
Features of Cardiogenic Shock
* _Preload_: **increased** (due to decreased stroke volume)
* _Afterload_: increased
* _Cardiac Output_: decreased
* _BP_: low
* _Organ Perfusion_: decreased
* _AVO2 difference_: **high** (b/c heart is delivering less blood, so tissues are using more O2 from the blood available)
59
Tx of Cardiogenic Shock
**Tx the underlying cause**
* if acute MI: revascularize
* **i****notropic Support****(****dobutamine, epinephrine, milrinone****)**
* can use a vasodilator if BP is okay (**dobutamine, milrinone**)
* if hypotensive then use vasopressor (**Epi, norepi/phenylephrine**)
* intra-aortic balloon counterpulsation
* oxygen
* isotonic fluids: AVOID large amounts of fluid
* if you use fluids, will eventually need to diurese (**Lasix [furosemide])**
60
Hypertrophic obstructive Cardiomyopathy: Pathophys & Risk Factors
**autosomal dominant**
* _Pathophys_:
* subaortic **outflow obstruction** d/t **asymmetrical septal hypertrophy** & systolic **anterior motion of the mitral valve**
* \*\*Hypercontractile\*\*
* can have myocardial ischemia d/t increased muscle mass and increased demand for O2
* _Risk Factors_:
* young age, fam hx of sudden death, gene mutations prone to SCD, sustained VT or SVT, recurrent syncope, brady arrhythmias
* **#1 cause of sudden death in competitive athletes \<35 yo**
61
Hypertrophic Cardiomyopathy: S/sxs & PE
* _S/sxs_:
* **dyspnea, syncope**
* angina
* palpitations
* dizziness
* fatigue
* **sudden cardiac death**
* _PE_:
* _Hypertrophic Obstructive Cardiomyopathy Murmur:_ **Crescendo-decrescendo systolic murmur** (best heard at R sternal border)
* **increased with decreased venous return** (valsalva or standing)
* → d/t less volume in L ventricle meaning that the obstruction from the septum is more severe, (vs when it has more volume it pushes the septum to its “normal” place making the murmur less severe)
* loud S4 (di-a-stol-ic)
* mitral regurg
* _Dx_:
* Echo:
* **asymmetrical ventricular wall thickness**
* systolic anterior motion of the mitral valve
* small LV chamber
* EKG:
* **Left ventricular hypertrophy**
* Septal Q-waves
* R. atrial enlargement
62
Tx of Hypertrophic Cardiomyopathy
* _Tx_:
* **Beta-blockers** = 1st line, or CCB
* Diuretics if CHF symptoms
* surgery (if gradient \>50 mmHg at rest or class III-IV heart murmur)
* alcohol septal ablation
* dual chamber pacing
* cardiac transplant
* Pt should avoid dehydration, extreme activity, **& competitive sports** (low-risk older pts can speak with a cardiologist)
* _Complications_:
* can progress to dilated cardiomyopathy
* a.fib, stroke
* clinical deterioration is slow
63
Restrictive Cardiomyopathy: Definition, Etiology, & S/sxs
* _Definition_:
* rigid ventricular wall with impaired ventricular filling & **reduced diastolic fnx** in a non-dilated ventricle. No change in contractility
* Least common form of cardiomyopathy
* _Etiology_:
* **amyloidosis = most common**
* Sarcoidosis
* Scleroderma
* Hemochromatosis
* _S/sxs_:
* R & L HF:
* R: peripheral edema, **JVD**, hepatomegaly, ascites, GI sxs
* L: dyspnea, fatigue
* Other: Kussmaul sign, S4
64
Restrictive Cardiomyopathy: Dx & Tx
* _Dx_:
* Echo:
* non-dilated ventricles with normal thickness
* marked dilation of both atria
* **abnormal mitral flow** (LA to LV)
* **\*\*Endomyocardial biopsy = definitive diagnosis\*\***
* amyloid on biopsy may be d/t primary amyloidosis or secondary to **multiple myeloma** & **hypergammaglobulinemia**
* _Tx_:
* Tx the underlying disorder
* use drugs with caution: diuretics, vasodilators, CCB
* **DO NOT USE DIGITALIS (DIGOXIN)** & other inotropic agents
* Tx of **hemochromatosis**: phlebotomy & chelation therapy → cardiac fnx may normalize
65
HEART Score
For Acute Coronary syndrome to tell you if the patient is low, medium, or high risk
* H: History
* E: EKG
* A: Age
* R: Risk factors (DM, dyslipidemia, HTN, smoking, CKD, prior CAD or PAD)
* T: Troponin
66
Acute Bacterial Endocarditis Definition and organism
* _Definition_: infection of a **normal valve** with a virulent organism (usually **S. Aureus**).
* **Rapidly destructive** (fatal \< 6 weeks if untreated)
67
Subacute Bacterial Endocarditis: Definition & Organism
* _Definition_: indolent infection (causing little or no pain) of **abnormal valves** with less virulent organisms (**S. Viridians** = normal oral flora)
* **slower onset**, longer duration (may continue for weeks-months before fatal)
68
Bacterial Endocarditis: General Definition, Risk factors, & Sxs
* _General Definition_:
* **infx of the _endocardium_** (usually the valve) secondary to colonization. **Mitral valve** = most common valve involved (M\> A\> T \>P)
* _Risk Factors_:
* **\>60 yo**, males, **IV drug abusers, poor dentition**
* pre-existing structural cardiac abnormality, prosthetic heart valve, prior episode, intravascular device (**indwelling catheter**), congenital heart disease, hemodialysis, HIV, co-morbidities
* _S/sxs_:
* **Fever**
* Chills/sweats
* Anorexia & weight loss
* Malaise, fatigue
* Arthralgias & myalgias
69
Types of Endocarditis
1. **_Native Valve Endocarditis_:** \*\***majority of cases\*\***, infx of mitral & aortic valves with streptococci, enterococci (GI/GU), staphylococci, or normal mouth organisms
2. _._**_Prosthetic valve endocarditis_:** 10-20% of cases, **S. epidermidis** = most common
3. **_.IV Drug Associated endocarditis_**: infx of right-sided valves (**tricuspid**, pulmonic) with **S. aureus (acute bacterial endocarditis)** (or fungi, gram -)
70
Community Associated vs Healthcare Associated Endocarditis
* _Community associated:_
* if diagnosed **within 48 hours** of hospital admission
* _Healthcare Associated_:
* if recent contact with healthcare setting with **onset of symptoms \> 48 hours** after hospitalization (25-30% of cases)
71
Bacterial Endocarditis: PE and tests to order
* _PE_:
* **murmur** → **new or worse** **regurg murmur**
* splenomegaly
* arterial **emboli**
* **petechiae** (appear in crops then disappear in 2-3 days)
* neurological features, clubbing, arrhythmia, scleral hemorrhage
* **Osler’s nodes** (small, painful, purple-red SQ nodules on digits and palms)
* **Roth’s spots** (oval retinal hemorrhages with pale center)
* **Janeway Lesions** (small, non-tender hemorrhagic macules or nodules on palms & soles)
* **Splinter hemorrhages** (linear reddish brown lesions under the nail bed)
* _Tests to Order_:
* Labs:
* **BLOOD CXs** : 3 sets \> 1 hour apart
* ESR or CROP: elevated
* Rheumatoid factor: positive
* Leukocytosis
* Anemia
* Proteinuria, microscopic hematuria
* _Transesophageal Echocardiogram_:
* more sensitive than TTE but obtain TTE first → looking for endocardial vegetations
72
Diagnosis of Bacterial Endocarditis
**DUKE CRITERIA**
* _Duke Criteria-_**_Major_:**
1. **Sustained bacteremia**: 2 positive blood cultures by organism known to cause endocarditis
2. **Echocardiogram** showing vegetation, dehiscence, or abscess
3. **New** valvular **regurgitation**
* _Duke Criteria_ **_Minor_**:
1. Predisposition (heart condition or IVDA)
2. Fever \>38C (100.4F)
3. Vascular: emboli to organs/brain hemorrhages
4. Immunologic: glomerulonephritis, Osler’s nodes, Roth spots, RF
5. Positive blood culture not meeting major criteria (1 positive)
6. Echocardiogram not meeting major criteria
* \***Definitive Endocarditis**: 2 major criteria; 1 major + 3 minor criteria; 5 minor criteria or histological findings
* \***Possible Endocarditis**: 1 major + 1-2 minor, 3 minor
* \***Rejected Endocarditis**: resolution within \<4 days of abx, alternate dx made, no evidence of IE at surgery or autopsy, definite or possible criteria not met
73
Prophylaxis of Bacterial Endocarditis: Indicated cardiac conditions, Procedures, & Regimen
\*\*Recommended prior to procedures which may introduce bacteria into the bloodstream of patients who are at high risk of developing bacterial endocarditis\*\*
* _Indicated Cardiac Conditions_:
* Prosthetic Cardiac Valve, heart repairs with prosthetic material, prior endocarditis, Cyanotic congenital heart disease, cardiac transplant
* _Procedures_:
* dental:
* (manipulation of gums, roots of teeth, oral mucosa perforation)
* respiratory:
* respiratory mucosa manipulation, rigid bronchoscopy
* Skin/MSK tissue procedures
* including abscess I&D
* GI/GU → NO longer recommended
* _Regimen_:
* **2g amoxicillin PO 1H before procedure** (if allergic: 500mg Azithro, 2g cephalexin, 600mg clinda)
74
Indications for Surgery in Bacterial Endocarditis
* Refractory CHF
* **persistent/ uncontrolled infx (sepsis**)
* recurrent emboli
* endocarditis-associated valve dysfunction causing HF
* **invasive infection (causing development of abscess, fistula, heart block**)
* fungal infx
* **pedunculated vegetation \>1-2cm in size**
75
Tx of Bacterial Endocarditis
* **Duration: 4-6 weeks of high dose therapy** (indwelling catheter often used)
* _Native:_
* anti-staph penicillin (nafcillin, oxacillin) **+** ceftriaxone or gentamicin
* _Prosthetic_:
* vancomycin + gentamicin + rifampin
* _Fungal_:
* Amphotericin B
76
Acute Pericarditis: Definition, Etiology, Classification, & Types
* _Definition_:
* inflammation or infection of the pericardium (outer layer of the heart)
* Pericardium has 3 layers: fibrous pericardium, parietal pericardium (lines fibrous pericardium), and visceral pericardium (lines the epicardium)
* _Etiology_:
* infectious: viral, bacterial (**TB**), fungal
* noninfectious: **secondary to MI (DRESSLER SYNDROME), neoplastic**, uremic, traumatic
* Hypersensitivity/autoimmune: rheumatic fever, SLE, RA, scleroderma, drug-induced (phenytoin, INH, procainamide, hydralazine)
* _Classification:_
* **Acute pericarditis: \<6 weeks**
* subacute pericarditis: 6wks -6months
* Chronic pericarditis: \> 6 months
* _Types_:
* serous: surface of heart look rough
* fibrinous: “junk” stuck between layers
* adhesive
* hemorrhagic
* purulent
* constrictive
77
Acute Pericarditis: S/sxs & PE
* _S/sxs_:
* **chest pain: sudden onset of pleuritic, persistent, postural CP** (\*\*Worse when supine, relieved by sitting up & leaning forward)
* aggravated with cough, breathing
* may radiate to back, shoulder, or neck
* _PE_:
* **Pericardial friction rub**:
* heard during both systole & diastole, high-pitched scratching/grating, loudest during inspiration, 2-3 components, may come and go
78
Acute Pericarditis: Diagnosis
* _EKG_:
* **diffuse ST segment elevation (concave)** in most limb leads & precordial v2-v6
* **ST depression in aVR +/- V1**
* sinus tach common d/t pain or infx
* _Stage 1_: widespread ST elevation with reciprocal changes in aVR
* _Stage 2_: Normalization of ST changes, T wave flattening
* _Stage 3:_ flattened T-waves or inverted
* _Stage 4_: EKG returns to normal
* _Echo_:
* useful for showing pericardial effusion +/- tamponade → can be performed at bedside
* _Diagnosis_ (**2 criteria must be met for diagnosis)**:
* typical CP
* pericardial friction rub
* typical EKG changes
* new/worse pericardial effusion
* elevated CRP
* \*\*no biomarkers for pericarditis → BUT 30% of pats have troponin elevation d/t **myopericarditis**
79
Acute Pericarditis: Tx & Admit factors
tx the underlying disorder
* _Tx_:
* Anti-inflammatory: **NSAIDs x 2 weeks**: aspirin 600-900mg QID, or indomethacin
* **Colchicine x 3 months**
* possibly steroids
* **AVOID anticoags** (system is irritated so it is likely to bleed) **& activity**
* _Admission Factors_:
* fever \> 38C
* subacute course
* large pericardial effusion (\>20mm)
* immunosuppressed pts
* use of anticoags
* acute trauma
* **failure to improve** **after 7 days of NSAIDs + Colchicine**
* elevated cardiac troponin (suggest myopericarditis)
80
Myocarditis: Definition, Pathophys, Etiology, Epidemiology, Classifications
* _Definition_: **inflammation of the myocardium** caused by infectious & noninfectious conditions. Focal or diffuse involvement
* _Pathophys_: myocellular damage leads to myocardial necrosis & dysfunction → **heart failure**
* _Etiology_:
* 1st world = **parvovirus B19, herpes virus 6**, coxsackie B (enterovirus)– used to be the most cause, adenovirus, hepatitis C, COVID-19, lymphocytic, giant cell
* 3rd world: HIV, chagas disease, rheumatic fever
* _Epidemiology_:
* most common in **20-50yo with \*\*\*_hx of recent viral infx\*\*\*_**
* _Classifications_:
* acute \< 3 months
* chronic \> 3 months
81
Myocarditis: S/sxs, PE, and Profiles
* _S/sxs_:
* \*many cases go undetected due to subclinical signs
* **chest pain, myalgia, fever, fatigue**
* CHF: dyspnea, fatigue
* **arrhythmia**, sudden death
* megacolon
* _PE_:
* **S3 or S4**
* mitral/tricuspid regurg
* edema (hepatic & peripheral)
* low cardiac output (shock)
* tachycardia
* _Profiles_:
1. **Acute Coronary Syndrome-Like**:
1. severe, recurrent acute CP 1-4 weeks after viral illness, ST elevation or depression, T-wave inversion, global or regional LV +/- RV dysfunction, +/- troponin elevated
2. **New onset or worsening HF:**
1. new onset or progressive HF over 2weeks - 3months with symptoms, impaired LV +/- RV systolic function
3. **Life-threatening Condition:**
1. life threatening arrhythmias or aborted sudden death, cardiogenic shock
82
Myocarditis: Dx & DDx
* _Dx_:
* Labs: CBC, BMP, acute phase reactants (CRP, sed rate), **troponin (may be elevated**), BNP (**increased**)
* _CXR_:
* **congestion (not usually cardiomegaly yet)**
* _EKG_: nonspecific ST changes, PACs/PVCs
* _Echo_:
* LV dilation, wall motion abnormalities, decreased systolic dysfunction
* _MRI_:
* inflammatory hyperemia, edema, wall motion abnormalities, global function, size/geometry
* **_Endomyocardial Biopsy_**: **definitive diagnosis**
* infiltration of lymphocytes with necrosis of myocardial tissue
* Nasal swab: PCR for viruses
* _DDx_:
* ischemic heart disease, valvular heart disease, other causes of cardiomyopathy, congenital heart disease, pulmonary disease, takotsubo, pericarditis
83
Myocarditis: When to suspect & Tx
* _When to suspect_:
* onset of otherwise unexplained cardiac abnormality such as CHF, shock, arrhythmia, in a **20-50 yo with a hx of viral illness**
* LV dysfunction without apparent etiology
* pericarditis with accompanying troponin elevation
* Acute Mi presentation without hx of CAD & negative angiogram
* ECG changes
* _Management_:
* **supportive care**: oxygen, inotropes, diuretics, antiarrhythmics, afterload reduction (ACEI), anticoag, mechanism support
* _Steroids:_ anti-inflammatory but suppresses the immune system
* IVIG
* Antivirals (if documented)
* plasmapheresis: takes out immunoglobulins that are attacking the heart
* immunosuppression
84
Pericardial Effusion: Definition & Etiology
* _Definition_: **Accumulation of fluid in the pericardial space** (normal pericardial space has about 5-50cc)
* _Etiology_:
* **Acute pericarditis** (viral, bacterial, TB, idiopathic) serous or purulent
* autoimmune disease
* Post Mi or cardiac surgery → serous or hemorrhagic
* blunt or sharp chest trauma → hemorrhagic
* **Mediastinal radiation (d/t Hodgkin's or breast cancer)**
* **Renal failure with uremia**
* Myxedema (hyperthyroidism)
* aortic dissection extending into the pericarium
* Drugs
85
Pericardial Effusion: S/sxs, PE, & Dx
* _S/sxs_: chest pain, dyspnea, fatigue
* _PE_:
* **decreased (muffled) heart sounds** d/t fluid → as fluid increases friction rub may disappear & heart sounds may become faint
* _Dx_:
* EKG: **electrical alternans** (alternating amplitudes of the QRS complexes)
* **low QRS voltage** (something b/w the heart & EKG leads → fluid)
* Echo: **Diagnostic test of choice**
* increased fluid in the pericardial space
* CXR: “water bottle appearance”
* Labs: gram stain & bacterial/fungal culture, cytology, AFB stain, PCR
86
Pericardial Effusion: When to suspect & Tx
* _When to suspect_:
* in all cases of acute pericarditis
* unexplained **new radiographic cardiomegaly without pulmonary congestion**
* presence of isolated left pleural effusion
* fever of hemodynamic deterioration in a pt with another disease process involving the pericadium
* _Tx_:
* if _minimal (_**_\<20mm_**_)_ or no evidence of hemodynamic compromise: **no immediate intervention** needed but may treat conservatively with therapy aimed at underlying cause & hemodynamic monitoring
* if **_progressively_** _enlarging_ or symptoms suggest cardiac tamponade then **pericardiocentesis** is indicated
* if _related to pericarditis_ treat with **NSAIDS (2weeks) & Colchicine (x3mo)**
* if _chronic_ consider surgery: **pericardial window**
87
Cardiac Tamponade: Definition, Etiology, S/sxs, & PE
* _Definition_:
* **pericardial effusion causing significant pressure on the heart, impeding cardiac filling, leading to decreased cardiac output and shock.** The **Rate of accumulation of fluid is more critical than volume.** (slow accumulation of large volume is OKAY if pericardium is compliant)
* _Etiology_:
* **Malignancy**, idiopathic pericarditis, & uremia (renal failure) are the most common causes
* _S/sxs_:
* Dyspnea
* Fatigue
* peripheral Edema
* **BECK's Triad**:
* distant (muffled) heart sounds
* increased JVP
* systemic hypotension
* _PE_:
* EKG:
* **Electrical Alternans** (alternating amplitudes of the QRS complexes)
* **low QRS voltage**
* Echo:
* pericardial effusion & diastolic collapse of teh cardiac champers
* CXR:
* “water bottle” appearance
88
Cardiac Tamponade: Tx
* immediate: oxygen, IV fluids, type & culture
* **Don’t give pain meds**, **sedate, or intubate** (causes vasodilation which will lower BP even further)
* **Pericardiocentesis**
89
“water bottle” appearance
associated with pericardial effusion/ cardiac tamponade
90
Beck's Triad
Associated with Cardiac Tamponade
1. elevated JVP
2. muffled heart sounds
3. systemic hypotension
91
Mnemonic to Remember Medical Tx of STEMI
**MOAN & BASH**
**Morphine**, **oxygen** if O2 \<90%, **Aspirin** 162 mg, **Nitro** q 5 min (don't give to pts with systolic \<90, or to inferior MI with R ventricular involvement → dependent on preload and nitro decreases preload)
**Beta blockers** (Decrease remodeling, decrease oxygen demand of heart, decreases HR, improve L ventricular hemodynamic funx, reduce incidence of ventricular arrhythmias; *Contraindication in Heart block, high risk for cardiogenic shock*) **, ACE-I/ARB** (more for long term use → improve L ventricular EF, mortality rate)**, Statin, Heparin** (antithrombotic therapy → impede progression of thrombus in coronary artery)
**TPA** if pt cannot have reperfusion from cath lab in \<90minutes from door to lab
92
Dressler's Syndrome
Post-MI pericarditis
tx = aspirin or colchicine
93
Triad of R Ventricular Infarction
1. **JVD**
2. **Clear Lungs**
3. **Positive Kussmaul Sign**
1. paradoxical rise of JVP with inspiration (blood backs up into vein during inspiration due to failure of R ventricle)
94
3 populations with atypical sxs for acute MI
elderly, women, diabetics
95
Which cardio biomarker peaks the fastest?
Myoglobin
## Footnote
**My O My you are fast**
