CV Flashcards
List your DANGER SIGNALS
Acute MI AAA (Dissecting Abdominal Aortic Aneurysm) CHF Bacterial Endocarditis
DS-Acute MI Classic Case
- Mid age or older male c/o midsternal chest pain that feels like heavy pressure on chest. Pain a/w numbness and/or tingling in the left jaw and the left arm. Pt diaphoretic with cool, clammy skin.
- Women p/w nonspecific symptoms such as dyspnea, fatigue, back pain and nausea.
DS-AAA Classic Case
- Elderly white male c/o PULSATING type sensation in abdomen and or LBP.
- With impending rupture, sudden onset of severe chest and LBP that steadily becomes SHARP and EXCRUCIATING.
- pt with HTN and Smokers are at higher risk.
DS-CHF Classic Case
- Elderly pt c/o acute or gradual dyspnea, fatigue, DRY cough, and swollen feets and cankles.
- pt has sudden or gradual increase in weight
- Lung exam will reveal crackles on both the lunch bases (bibasilar crackles) along with an S3 heart sound.
- Hx preexisting CAD, prior MI, or previous episode of CHF is possible. - This pt is usually taking diuretics, digoxin, and antihypertensives.
DS-Bacterial Endocarditis Classic case
- Pt presents with fever, chills, and malaise a/w NEW murmur and the abrupt onset of CHF
- Associated skin findings are found mostly on the fingers, hands, and toes/feet.
- Subungal hemorrhages (splinter hemorrhages on nailbed), petechiae on palate, painful violet colored nodes on fingers or feet (OSLER NODES). - Tender red spots on palms/soles (JANEWAY LESIONS)
Mneumonic for remembering valves
MOTIVATED APPLES
AV Valves
Mitral and Tricuspid
SemiLunar Valves
Aortic and Pulmonic
S1
“LUB” SYSTOLE
-Closure of the AV valves (MT)
S2
“DUB” DIASTOLE
-CLosure of the semilunar valves (Aortic/Pulmonic)
S3
- CHF or heart failure
- occurs during early diastole
- ventricular gallop
- sounds like kentucky
- always considered abnl if occurs after age 35
- this may be normal in some kids or young adults if there are no s/s of heart or valvular disease
S4
- caused by increased resistane due to STIFF left ventricle
- usually indicates LVH; considered normal in some elderly
- sounds like tenesee
- best heard at apex or apical area (mitral area) using the bell of the steth
Summation Gallop
- Pathologic finding
- all heart sounds are present from S1-S4 and sounds like a galloping horse
Bell
- Low tones such as the extra heart sounds (S3 or S4) sounds
- Mitral Stenosis
Diaphragm
- Mid to High pitch tones such as LUNG sounds
- MR which is SYSTOLIC
- AS which is SYSTOLIC
Benign Split S2
- Best heard over pulmonic area (2nd ICD left side of sternum)
- Due to splitting of the aortic and pulmonic components; - Its only normal if it appears during inspiration and disappears at expiration
Benign S4 in Elderly
- Some healthy elderly pt have S4 (late diastolic) heart sound aka “atrial kick” (the atria have to squeeze harder to overcome resistance of a stiff left ventricle)
Heart Mumurs. its all about…
Timing (systole or diastole)
and
Location (aortic or mital)
Systolic Murmurs Mneum
MR. AS
Diastolic Murmur Mneum
MS. AR
DARMS
Auscultatory Areas
Mitral and Aortic
Mitral Area
- AKA Apical area or Apex
- 5th left ICS midclavicular
Aortic Area
-2nd ICS to the right side of the upper border of the sternum at the base of the heart
Systolic MR. ASH.
- Occur during S1 or as a HOLOsytolic, PANsystolic, early systolic, late systolic, or midsystolic murmurs.
- compared to diastolic murmurs, these are LOUDER and can radiate to the neck or axillae
- Mitral Regurg
- Aortic Stenosis
Mitral Regurgitation
- PANsystolic (or HOLOsystolic) murmur
- heard best at the apex of the heart
- radiates to the axilla
- LOUD blowing and HIGH pitched murmur
Aortic Stenosis
MIDsystolic ejection murmur
- best heard at the second ICS at right side sternum
- radiates to the neck
- harsh and noisy murmur (diaphragm)
- These pt should avoid physical overexertion, as there is increased risk of sudden death…Really? just euthanize me
- Valve replacement candidates
Diastolic murmurs are always indicative of
-Heart disease, unlike systolic murmurs
Diastolic: MS. ART
Mitral Stenosis
- LOW pitched diastolic rumbling murmur
- Heard best at the apex of heart
- AKA “Opening Snap” (use bell)
Diastolic: MS. ART
Aortic Regurgitation
- High pitched diastolic murmur
- Best heard at the second ICS at right of the sternum
- High pitched blowing murmur (use diaphragm)
ACS
ACUTE CORONARY SYNDROME: An ischemic chest pain syndrome usually associated with coronary artery plaque rupture. Encompasses STEMI, NSTEMI, and UA.
Unstable Angina
UNSTABLE ANGINA: An acute coronary syndrome in which chest pain is of new onset, increasing severity, or occurs at rest, and cardiac biomarkers are not elevated.
NSTEMI
NON-ST ELEVATION MYOCARDIAL INFARCTION: An acute coronary syndrome in which cardiac biomarkers are eventually elevated but which lacks new ST elevation on ECG.
STEMI
ST ELEVATION MYOCARDIAL INFARCTION: An acute coronary syndrome in which significant ST elevation is found in two or more contiguous ECG leads. It is typically associated with epicardial coronary artery occlusion and transmural infarction, resulting in myocardial cell death evidenced by Q waves if perfusion is not soon restored.
Key ECG Findings in ACS
STEMI: indications for immediate reperfusion therapy
ST elevation >1 mV (1 mm) in two contiguous leads and <12 h since pain onset
Left bundle-branch block not known to be old with a history suggestive of acute MI
ST elevations in posterior leads (V7, V8, and V9) or ST depression in V1-V3 with a prominent R wave and upright T-wave suggestive of posterior STEMI
Typical ECG findings in NSTEMI and UA
Horizontal ST-segment depression
ECG findings change in accord with symptoms
Deep T-wave inversions
Therapies Proven Benefit for MI
Aspirin (162 mg, chewed immediately, then continued daily for life)
PCI (angioplasty or stenting the blocked artery)
Thrombolysis (if primary PCI not available; most regimens require heparin therapy)
β-blockers (immediate IV use and started orally within 24 hours; if no contraindications then continued daily)
ACE (started within 1-3 days and continued for life)
STATIN Cholesterol-lowering drugs (started within 1-3 days and continued daily for life)
Enoxaparin (dosage given prior to thrombolysis or PCI, for patients <75 years of age)
Clopidogrel (75 mg daily with or without reperfusion therapy)
Potential Complications from Acute MI
VFIB
VTACH
HBlock
RV Infarction
FWR Free wall rupture
Ventricular aneurysm
Hemorrhage secondary to therapy
Cardiogenic pulmonary edema
Ventricular septal defect
Cardiogenic shock
Mitral regurgitation
Pericarditis
Thromboembolism
Anterior MI
A new systolic murmur may be heard if cardiogenic pulmonary edema is caused by papillary muscle dysfunction and acute mitral regurgitation. Right ventricular infarction from an inferior MI usually presents as hypotension without pulmonary congestion. Treatment is aggressive volume loading. Nitroglycerine will decrease preload and must be avoided in patients with right ventricular infarction.
Late complications of MI that tend to occur several hours to days after presentation include left ventricular free wall rupture causing tamponade, ventricular septal defect, pericarditis, left ventricular aneurysm, and thromboembolism. Finally, iatrogenic complications of MI therapy can occur. Heparin and antiplatelet therapies lead to significant bleeding in up to 10% of patients. Intracranial hemorrhage occurs in 0.5% to 0.7% of patients who receive thrombolytics for STEMI. These bleeds are usually fatal.
Left ventricular dysfunction that occurs with anterior MI usually causes pulmonary edema or cardiogenic shock. Signs of cardiogenic shock range from frank hypotension to indicators of impaired perfusion such as cool moist skin, oliguria, and confusion. Treatment includes emergent PCI, pressor agents, and, if necessary, an intra-aortic balloon pump.
Classification of HTN
JNC7 Classification of HypertensionClass
Systolic BP (mm Hg) Diastolic BP (mm Hg)
Normal <120 and <80
Prehypertension 120–139 or 80–89
Stage 1 140–159 or 90–99
Stage 2 ≥160 o r≥100
Hypertensive Emergency
Hypertensive emergency is an acute elevation of blood pressure (≥180/120 mm Hg) associated with end-organ damage; the targeted end organs include the brain, heart, aorta, kidneys, or eyes
The key is to seek acute end organ involvement
Target End Organs
brain,
heart,
aorta,
kidneys,
eyes
Brain
- ischemic brain damage
- Hemorrhagic stroke CVA
Heart/Aorta
- ECG changes in acute MI
- Diastolic murmur in AA
- Aortic dissection
Kidneys
- Acute Renal Failure: Elevated serum creatinine confirms the diagnosis, and urinary sediment is also abnormal
- HELLP: Pre-eclampsia is associated with hypertension, peripheral edema, and proteinuria. These patients may also develop hemolysis, elevated liver enzyme levels, and low platelet counts (HELLP syndrome)
Eyes
- Papilledema (encephelopathy)
- Hypertensive retinopathy: Scattered flame (splinter) hemorrhages and cotton-wool spots
Labs
Commonly ordered tests include basic metabolic panel (73%), ECG (53%), chest radiograph (46%), and urinalysis (43%).3
Kidneys: creatinine, urinalysis
Endocrine: thyroid profile, fasting bg
Electrolyte: K, Na, Ca
Heart: Cholesterol, HDL, LDL, Tri
Baseline EKG CXR to r/o cardiomegaly
target organs
Pt can have htn caused by 3 other things:
- Causes classified into three groups
1. Renal: renal artery stenosis, polycystic kidneys, chronic kidney disease
2. Endocrine: hyperthryoidism, hyperaldosteronism, pheochromoctyoma
3. Other causes: OSA, coarctation of aorta
Sympathetomimetic HTN Emergency
In particular, obtaining history about the use of cocaine or other sympathomimetic substances (phenylephrine and monoamine oxidase inhibitors) is crucial, as it significantly alters the treatment regimen (beta-blockers must be avoided in the setting of sympathomimetic use).
Common Antihypertensive Agents in HTN EMERGENCY
Sam Needs Cheese w/her L E F E H
Sodium nitroprusside
Nitroglycerin
Nicardipine
Labetalol
Esmolol
Fenoldopam
Enalaprilat
Hydralazine
Sodium Nitroprusside
Hypertensive encephalopathy
and
Aortic dissection
SE/Con: Reflex tachycardia, coronary steal, methemoglobinemia, metabolized to cyanide
Nitroglycerin
Gtt works great for:
Myocardial infarction
and
CHF
and LVD
SE/Cont: Hypotension: contraindicated in severe aortic stenosis, left ventricular outflow obstruction and inferior MI
Nicardipine
Great for:
Hypertensive encephalopathy
and then
MI
and then
CHF
and thennnnn
Cerebral infarction/hemorrhage
5 mg/h IV gtt, increasing by 2.5 mg/h IV every 5 minutes to a max of 30 mg/h IV gtt
SE/Con: Hypotension: contraindicated in severe aortic stenosis. Reflex tachycardia
Labetalol
Great for: Hypertensive encephalopathy, myocardial infarction, preeclampsia/eclampsia, cerebral infarction/hemorrhage
SE/Con: Hypotension: contraindicated in acute asthma, COPD, acute CHF, heart block, and sympathomimetic intoxication (eg, cocaine)
Esmolol
Great for: Hypertensive encephalopathy, myocardial infarction, eclampsia, cerebral infarction/hemorrhage
Loading dose 500 μg/kg IV over 1 min, 25-50 μg/kg/min IV gtt titrated every 10-20 min
Fenoldopam
Great for:
ARF
and
CHF
SE/Con: in increased intraocular pressure
Enalaprilat
Great for:
CHF
SE/Con: in pregnancy and ACE I-related angioedema
Hydralazine
Great for:
Preeclampsia/eclampsia
SE/Con: Reflex tachycardia, CNS and myocardial ischemia
Tx of Hypertensive Emergencies by Diagnosis:
AORTIC DISSECTION
Goal is to:
-Reduce shear forces by ↓ BP and PR; lower SBP to 100–120 mm Hg or lower SBP to <140 mm Hg23; ↓ PR <60 beats/min.
-Measure BP in both arms and treat higher BP
Labetalol, IV continuous infusion
or esmolol IV bolus, then continuous infusion
Respiratory distress in COPD, asthma patients; test dose of esmolol recommended, switch to diltiazem if esmolol intolerant.
Always use β-blocker prior to vasodilators!!!
Nicardipine IV continuous infusion (after β-blocker)
Nitroprusside continuous infusion (after β-blocker); nitroprusside alone increases wall stress from reflex tachycardia; cyanide and thiocyanate toxicity in patients with reduced renal function or therapy >24–48 h
Tx of Hypertensive Emergencies by Diagnosis:
ACUTE MI
Goal: Reduce ischemia; avoid ≤25% reduction of MAP.
BP >180/110 mm Hg is a relative contraindication for thrombolytics.
Meds: Nitroglycerin SL, topical, or IV continuous infusion (((Do not give nitrates in patients who have taken phosphodiesterase inhibitors for erectile dysfunction ≤24 h (48 h for tadalafil)))
Metoprolol or labetalol IV bolus ((Do not give β-blockers in CHF, low-output states, or other contraindications to β-blockers. Monitor for hypotension; consider RV infarct and volume depletion)))
Nitro.cardene. labetalol. esmolol
Tx of Hypertensive Emergencies by Diagnosis:
Acute Renal Failure
Reduce BP by no more than 20% acutely
(((Do not give nitroprusside, as it results in cyanide and thiocyanate toxicity; avoid ACE)))
Nicardipine IV gtt
Clevidipine IV gtt
Fenoldopam IV gtt****
Tx of Hypertensive Emergencies by Diagnosis:
HYPERTENSIVE ENCEPHALOPATHY
Decrease that MAP 20%–25% in the first hour of presentation; You cant be more aggressive than that bc youll cause ischemic infarction.
*****The goal is not to normalize the blood pressure because this can lead to cerebral ischemia secondary to hypoperfusion. Instead, the goal is to reduce the MAP by 20% to 25% over the first hour.****
Nicardipine and labetalol are potential first-line agents for lowering blood pressure in the setting of hypertensive encephalopathy
Autoregulation of cerebral perfusion may be significantly impaired, so avoid rapid BP lowering; NO NITRO
Nicardipine gtt
Labetalol gtt...Avoid in sympathetic crisis from drugs
Sodium Nitroprusside
Esmolol
Clevidipine gtt
Recommended Treatment Protocol for ED Patients with Increased Blood Pressure (BP)
FOR NONBLACK…
-Initial therapy recommendations for nonblack individuals:
THIAZIDE (e.g., hydrochlorothiazide, 25 milligrams daily)
ACE (e.g., lisinopril, 10 milligrams daily),
OR CCB
Reccommended Tx Protocol for ED Pt with High BP
FOR BLACKS…
-In blacks, initiate a thiazide diuretic or a calcium channel blocker, alone or in combination.
THIAZIDE DIURETIC
AND/OR
CCB
Reccommended Tx Protocol for ED pt with High BP
CKD with or w/o DM
-initiate ACE or ARB
Compelling Indications:
CHF
- BP goal <140/90
- First Line: Diuretic + ACE
- Second Line: BB
Compelling Indications:
Post MI
BP Goal: <140/90
First Line: BB or ACE
Second Line: Aldosterone Antagonist
Compelling Indications:
DM NB v Black
FIRST LINE:
- Nonblack: Thiazide diuretic, ACE inhibitor, ARB or CCB
- Black: Thiazide diuretic or CCB
Compelling Indications:
Recurent Stroke Prevention
First Line:
-Diuretic + ACE inhibitor or ARB
Compelling Indications:
High CAD risk
First Line: BB
2nd: ACE, CC, BB, or Diuretic
BETA BLOCKERS
- Avoid abrupt discontiunation after chronic use. Wean slowly bc may precipitate REBOUND HTN
- IV labetalol with ACS and PO Labetalol for hyp emergency.
- Esmolol has a short duration of action and is titrable, an advantage in patients at risk for the adverse effects of β-blockers, such as those with severe asthma and chronic obstructive pulmonary disease.
SE:
CALCIUM CHANNEL BLOCKERS
Clevidipine is a third-generation dihydropyridine calcium channel blocker with ultra-short-acting selective arteriolar vasodilator properties, good for patients with renal dysfunction. Its advantage is its ability to be titrated with a half-life less than a minute.
Nicardipine has an onset of action of 5 to 15 minutes and can be titrated at 15-minute intervals. It has been found to be safe and effective in neurologic hypertensive emergencies and has a favorable effect on myocardial oxygen balance increasing both stroke index and coronary blood flow. Nicardipine worked quicker then lab drip.
Nifedipine use (10 milligrams PO) is discouraged in hypertensive emergencies except in peripartum patients. For the preggers only.
The NONDIHYDROpyridines depress the muscles of the heart (inotropic effect). The DIHYDROpyridines slow down heart rate (chronotropic effect). The di-pines are chronotropic…nifedipine,amlodipine..call them
DI-CHRONO-PINES
ALDOSTERONE RECEPTOR ANTAGONIST DIURETICS
Action:
- antagonizes the action of aldosterone. increases elimination of water in kidneys and conserves potassium
- AKA mineralcorticoid receptor antagonists
Indications:
- HTN, Heart failure, hirsuitism, precocious puberty
- Avoid combining with K sparing diuretics, ACE, or K supps
Side Effects: gynecomastia, hyperkalemia, GI (vomitting, diarrhea, stomach cramps), ED, postmenopausal bleeding
Ex: SPIRINOLACTONE, EPLERENONE
Loop Duretics
Action:
Inhibit Na K Cl pump of the kidney in the loop of Henle
Side Effects:
- Electrolyte imbalance
- Hypokalemia (potentiates dig tox, increased risk of arrythmia) torsades
- Hyponatremia (hold diuertic, restrict water intake, replace K lost)
- Hypomagnesemia
Contraindications:
-Sensitivity
Ex: Furosemide, Bumetanide
ACE INHIBITORS AND ANGIOTENSIN RECEPTOR BLOCKERS
- Blocks conversion of angiotensin 1 to 2 (more potent vasoconstriction)
- DM: drug of choice (protects kidneys) for diabtes
Pregnancy Category C (1st trimester) Category D (2nd and 3rd trimester)-fetal kidney malformations and fetal hypotension
Side Effects: dry hacking cough, hyperkalemia angioedema
Contraindicated: RENAL ARTERY STENOSIS, MOD to SEVERE KIDNEY DISEASE
ALPHA 1 BLOCKER/AGONIST
- AKA alpha adrenergic blockers “zosin” A potent vasodilator. Give at bedtime at very low dose and titrate up, SE dizziness and hypotension.
- Not first line med unless pt is a male with HTN and BPH
- Alpha blockers relax smooth muscle found on bladder neck and prostate glad and relieve obstructive voiding symptoms such as weak urianry stream, urgency, and nocturia.
Ex: Terazosin used for HTN and BPH, or Tamsulosin used for BPH only
Lifestyle Reccomendations
First line therapy in HTN, hyperlipidemia, and diabetes:
- Lose weight if overweight BMI 25-29-2.9 or obese BMI >30
- Nl weight is a bmi of 18.5 to 24.9
- Stop smoking
- Reduce stress level
- Reduce sodium less than 2.4g/day
- Maintain adequate intake of K, Ca, Mg
- Limit ETOH 30ml or less a day for men
- Eat fatty cold water fish (salmon) 3x a week
- Exercise moderately 30-45 min most days of week
Dash Diet
Goal: eat foods rich in K, mg, ca
- Reduce Na intake, red meat, procesed food
- Eat more whole grains, fish, poultry
THIAZIDES and women
Women with HTN and osteopenia/osteoporosis shoud recieve thiazides
thiazides help bone loss by slowing down calium loss from the bone and stimulating osteoclasts
***Most common causes of CHF
CAD and HTN
**Most Common Cause of CHF Exacerbation
Myocardial infarction, myocardial ischemia, and noncompliance
CHF General Tx
- Obvi oxygenate em
- correct the underlying shit
- Relieve the symtoms by REDUCING PRELOAD AND AFTERLOAD and DIUERSING
- Might possily need some inotropic support depending on how bad the case is
MILD CHF EXAC + trace pulm edema
-with trace pulm edema and fluid overload may only need diuresis!
Systolic Heart Failure
rEF REDUCED EF
EF<50%
Ventricle has trouble ejecting blood which leads to increaded intracardiac volume and afterload sensitivity.
Diastolic HF
pEF. PRESERVED EF, Preload Sensitivty
- Youre ventricle just cant relax
- characterized by impaired ventricular relaxation, causing an abnormal relation between diastolic pressure and volume.
- As a result, LV has trouble receiving blood and your atria has to work harder.
-Decreased LV compliance necessitates higher atrial pressures to ensure adequate left ventricular diastolic filling, creating a preload sensitivity.
AHF Clinical Presentation
- The symptom with the highest sensitivity for diagnosis is DOE
- The most specific symptoms are paroxysmal nocturnal dyspnea, orthopnea, and edema.
- On exam, an S3 has the highest LR+ for acute heart failure
- Abdominojugular reflux and JVD are the only other two physical examination findings
Diagnosing AHF
CXR
CXR: pulmonary venous congestion, cardiomegaly, and interstitial edema are most specific for a final diagnosis of acute heart failure.
Diagnosing AHF
Biomarkers
BIOMARKER: BNP
- correlating with cardiac filling pressures and ventricular stretch. As a result, B-type natriuretic peptide or N-terminal pro-B-type natriuretic peptide testing is recommended and helpful when the cause of dyspnea is unclear after standard evaluation
- BNP <100 youre in the clear, no HF
- BNP >500…Youre HF A-F
Diagnosing AHF:
POC US
1) Are there signs of pulmonary congestion? (2) Are there signs of volume overload by measuring the size of the inferior vena cava and its collapsibility? (3) Is the left ventricular ejection fraction low or normal?
- Pulmonary US is used first to determine if pulmonary congestion is present by looking for B lines. >2 B lines=Insterstitial edema
- Sonographic B lines are ring-down artifacts that arise from the interface of the visceral and parietal pleura when there is swelling of the lung’s interlobular septa due to lymphatic congestion as is seen in pulmonary edema.
- They are the sonographic equivalent of Kerley B lines seen on chest radiography.
- More than two B lines in any one sonographic window along the anterior and anterolateral chest are pathologic and highly specific for alveolar and interstitial edema.
Management of Hypertensive Acute Heart Failure
Step 1: Administer oxygen as needed for saturation 95%;
-give sublingual nitroglycerin. Sublingual nitroglycerin may be repeated up to one per minute.
Step2: If severe dyspnea, consider NIV or intubation.
Step3: If BP >150/100 mm Hg, add IV nitroglycerin or nitroprusside; if BP falls below 100 mm Hg, stop nitrates, and monitor for persistent hypotension or symptoms. If BP <150/100 mm Hg after sublingual administration and if improved, consider transdermal nitroglycerin.S
Step4: Start IV loop diuretic (furosemide or bumetanide) in the setting of volume overload. Initiate nitrates before diuretics.
Step5: Assess for severity of illness/high risk: altered mental status persistent, hypoxia despite NIV, hypotension, troponin elevation, ischemic ECG changes, blood urea nitrogen >43, creatinine >2.75, tachycardia, tachypnea, or inadequate urine output.
Step6: Admit to intensive care unit if high severity of illness or risk of decompensation.
Vasodilators for AHF
Vasodilators for Acute Heart Failure
VasodilatorDoseTitration End PointComplications
Sublingual NTG-0.4 milligram every 1–5 min Complication: hypotension
IV NTG-0.2–0.4 microgram/kg/min (starting dose) Symptoms: Headache, hypotension
Nitroprusside-0.3 microgram/kg/min (starting dose), 10 micrograms/kg/min (maximum) Complications: Hypotension, cyanide/thiocyanate toxicity, coronary steal
Diuertics for AHF
Diuretics for Heart Failure
DiureticDose (IV)EffectComplications
Furosemide
-No prior use: 20–40 milligrams IVP.
- Diuresis starts within 15–20 min
- Complications: ↓ K+, ↓ Mg2+, hyperuricemia, hypovolemia
- If prior use: total daily IV dose 1 to 2.5 times the patient’s previous total daily oral dose, divided in half and given IV bolus every 12 h Duration of action is 4–6 h
SE: Ototoxicity, prerenal azotemia
If no effect by 20–30 min, increase subsequent dose
Bumetanide
-1–3 milligrams IVDiuresis starts within 10 min
Peak action at 60 min
Torsemide
10–20 milligrams IV
-Diuresis starts within 10 min
Peak action in 1–2 h
Drugs to Avoid in Acute Heart Failure
CCB (po)
Oral calcium channel blockers have myocardial depressant activity and are not routine treatment for acute heart failure, with trials demonstrating either no benefit or worse outcomes. If necessary, amlodipine may be used for compelling clinical reasons (e.g., as an antianginal agent despite maximal therapy with nitrates and β-blockers).
NSAIDS
Avoid selective or nonselective nonsteroidal anti-inflammatory drugs in patients with acute heart failure. They can cause sodium and water retention and blunt the effects of diuretics,2 and may increase morbidity and mortality.
AHF PE-LEFT
Left Ventricular Failure (Diminished ventricular systolic empyting)
- Crackles, babasilar rales (rales on lower lobes of the lungs), cough, dyspnea, decreased breath sounds, dullness to percusion
- Paraxosymal nocturnal dyspnea, orthopnea, nocturnal nonprodcutive cough, wheezing (cardiac asthma)
CHF-RIGHT
RIGHT GI
Right Ventricular Failure
- Jugular venous distention (JVD), normal jvd 3-4cm or less
- Enlarged spleen, enlarged liver causes anorexia, nausea, and abd pain
- Lower extremity edema with cool skin
Other PE
-Presence of S3 gallop, which can be accompanied by anasarca (severe generalized edema due to effusion of fluid into the extracellular space)
CHF LABS
CXR: will show increased heart size, intersitital and alveolar edema, KERLEY B lines, and other signs of pulmonary edema
ECG, CPK, TROP, BNP
ECHO with Doppler study
Bacterial Endocarditis AKA Infective Endocarditis
Bacterial pathogens are gram POSITIVES (Viridians streptococcus, Staphyloccus aureus
VIRIDDIANS STREP
STAPH AUREUS
Classic Endocarditis Case
-Middle aged male p/w fever, chills, and malaise that are a/w subungal hemorrhages (splinter hemorrhages on nailbed) OSLER. Palms soles may have tender spots on skin JANEWAY. Some may have heart murmur.
Diagnosing Endocarditis
-Blood cx. Staphylococcus aureus and Streptococcus species
-ECHO. Obtain echocardiography as soon as possible, because (1) echocardiographic abnormalities represent one of the two major criteria required for definitive diagnosis of endocarditis and (2) evaluation of the cardiac valves and surrounding structures provides critical information for management decision.
-Common findings are anemia (70% to 90% of cases), hematuria, and elevated erythrocyte sedimentation rate (>90% of cases), C-reactive protein, and procalcitonin.
Endocarditis Empiric Tx
Uncomplicated
EASY: VANC/GENT or NAFCILLIN
Ceftriaxone, 1–2 grams IV
or
Nafcillin, 2 grams IV
or
Oxacillin, 2 grams IV
or
Vancomycin, 15 milligrams/kg plus Gentamicin, 1–3 milligrams/kg IV
or
Tobramycin, 1 milligram/kg IV
Endocarditis Empiric Tx:
IV drug use, congenital heart disease, hospital-acquired, suspected methicillin-resistant Staphylococcus aureus, or already on PO abx
NAF, VANC/GENT
Nafcillin, 2 grams IV
plus
Gentamicin, 1–3 milligrams/kg IV
plus
Vancomycin, 15 milligrams/kg IV
Endocarditis Empiric Tx:
Prosthetic Heart Valve
VANC/GENT/NAF
Nafcillin, 2 grams IV
+
Gentamicin, 1–3 milligrams/kg IV
+
Vancomycin, 15 milligrams/kg IV
Bacterial Endocarditis Complications
-Valvular destruction, myocardial abcess, emboli
Endocarditis Prophylaxis
For highest risk patients, provide antibiotic prophylaxis before dental procedures that involve manipulation of gingival tissue, the periapical region of teeth, or perforation of the oral mucosa.
- Prosthetic heart valves
- Prosthetic material used for valve repair
- Hx of previous infective endocarditis
- Unrepaired cyanotic congenital heart disease
- Repaired congenital heart defect with prosthetic material or device
- Repaired congenital heart disease with residual defects
- Cardiac transplant recipients with valve regurgitation due to a structurally abnormal valve
Mitral Valve Prolapse Classic Findings
- S2 “click” followed by a systolic murmur. Some patients with MVP are at higher risk of thromboemboli, TIA’s, Afib, and ruptured chordae tendinae.
- Diagnosed by cardiac echo with doppler flow study
MVP Classic Case
- Adult tall and thin FEMALE pt c/o fatigue, palpitations, and lightheadedness (orthostatic hypotension) that is aggravated by heavy exertion. May be asymptomatic.
- A/w pectus excavatum, hypermobility of the joints, arm span greater than height (r/o marfans syndrome)
MVP tx plan
- If its asymptomaitic dont treat it
- MVP with palpitations is treated with BB, avoidance of caffeine, ETOH, and cigarettes. Holter monitoring is useful in detecting significant arrythmia
Pt p/w hypotension AND poor perfusion
- Think CARDIOGENIC SHOCK, may require inotropic support (dobutamine or milrinone to enhance contractility)
- Vasopressor support (LEVO to increase coronary diastoli perfusion)
- Maybe a fluid bolus to increase preload
