Cardio 1

Aortic stenosis

1. Calcification of the trileaflet valve (typically in those presenting at sixty years of age or older)

2. A congenital unicuspid or fused bicuspid valve (typically in those presenting in the teens and early twenties)

3. Rheumatic disease damage

Exertional angina, dyspnea, and syncope.

Cresendo-decrescendo systolic ejection urmur in the right 2nd intercostal space that radiates to the carotids.

Pulsus parvus et tardus, a weak S2, and an S4 may be noted.

In the later stage of AS, the LV may dilate, resulting in a displaced PMI and overt symptoms of heart failure.

Extracellular deposit of insoluble poymeric protein fibrils in tissues and organs.

Can be primary (AL type) or secondary (AA) to chronic inflammatory conditions such as:

- Inflammatory arthritis (RA)

- Chronic infections (bronchiectasis, TB, osteomyelitis)

- Inflammatory bowel disease (Crohn's disease)

- Malignancy

- Vasculitis

- Asymptomatic proteinuria or nephrotic syndrome

- Restrictive cardiomyopathy

- Hepatomegaly

- Peripheral neuropathy and/or autonomic neuropathy

- Visible organ enlargement (macroglossia)

- Bleeding diathesis

- Waxy thickening, easy bruising of skin

Tissue biopsy (abdominal fat pad)

Can develop dilated cardiomyopathy w/ left ventricular cavity dilation, impaired systolic function, and/or overt CHF.

Other findings:

- Liver disease (hepatomegaly, elevated liver enzymes, cirrhosis)

- Arthropathy

- Skin pigmentation

- DM

- Hypogonadism with decreased libido

- Erectile dsyfunction

Can cause granulomatous infiltration of the myocardium and lead to HF w/ both systolic and/or diastolic dysfunction.

Affects younger adults and involves the lung (bilateral hillier adenopathy and/or reticular opacities), skin (erythema opossum), or eye (uveitis).

Sarcoidosis does not cause proteinuria.

Secreted in response to ventricular stretch and wall tension when cardiac filling pressures are elevated.

It is common practice in the ED to measure the BNP level to differentiate dyspnea of heart failure from dyspnea of non-cardiac etiology.

The level of BNP correlates both with the severity of left ventricular filling pressure elevation as well with mortality.

argues against acute HF

Intravenous diuretics

Due to its negative inotropic effects, diltiazem is not beneficial in the treatment of patients with decompensated heart failure.

Pericardiocentesis is indicated in SOME patients!

Tricyclic antidepressant

Clinical features:

- Sympathetic hyperactivity- tachycardia, HTN, dilated pupils

- CP due to coronary vasoconstriction

- Psychomotor agitation, seizures

Complications:

- Acute MI

- Aortic dissection

- Intracranial hemorrhage

Management of CP:

- Benzodiazepines for BP and anxiety***

- Asprin

- Nitroglycerin and CCP for pain

- BB are CONTRAINDICATED

- Fibrinolytics not preferred d/t increased risk of intracranial hemorrhage

- Immediate cardiac cath with repercussion when indicated

Cardiac output- Decreased

Pulmonary capillary wedge pressure- Decreased

Systemic vascular resistance- Increased

Blood pressure- Decreased

Renal artery stenosis!!!

Could indicate renal artery stenosis.

Warmth, erythema, swelling, and tenderness.

Cold leg with mottled appearance, minimal swelling, absence of distal pulses.

Typically occurs 5-10 days after initiation of heparin therapy.

Possible arterial embolus f/ left ventricular (LV) thrombus.

Management includes anticoagulation, vascular surgery consultation, and transthoracic echocardiogram to screen for LV thrombus and evaluate LV function.

1. Left ventricular thrombus ***

2. Thrombus (usually left atrial) formation duet o atrial fibrillation

3. Aortic atherosclerosis

Released from the cardiac ventricles in response to volume overload.

In a patient with CHF, sodium is reabsorbed via the kidneys in response to simulated renin-angiotensin-aldosterone system; therefore, the patient's urine sodium levels are most likely low.

Used only for patients with serious ventricular arrhythmias! Like A. fib.

About 50% of pts on long-term amiodarone therapy will develop significant side effects!

Cardiac:

- Sinus bradycardia, heart block

- Risk of proarrhythmias- QT prolongation & risk of tornadoes de pointes

Pulmonary:

- Chronic interstitial pneumonitis (cough, fever, dyspnea, pulmonary infiltrates) MC

Endocrine:

- Hypothyroidism

- Hyperthyroidism

GI/Hepatic:

- Elevated transaminases, hepatitis

Ocular:

- Corneal microdeposits

- Optic neuropathy

Dermatologic:

- Blue-gray skin discoloration

Neurologic:

- Peripheral neuropathy

N/V, diarrhea, anorexia, confusion, visual disturbances, and a variety of cardiac arrhythmias.

Thyroid and hepatic effects are significantly less common than with amiodarone.

Vasodilator/Nitrite

Can cause salt and fluid retention, peripheral edema, palpations, orthostatic hypotension, and a drug-induced lupus-like syndrome.

Antiarrhythmic and HTN

Constipation and impaired cardiac conduction and contractility, with potential worsening of bradyarrhythmias and CHF

Paroxysmal supraventricular tachycardia (PSVT).

Attacks begin abruptly and are characterized by heart rates between 160-220 bpm. MC mechanism underlying PST is re-entry into the AV node.

Mechanical and medical therapies for PSVT decrease AV node conductivity.

Vagal maneuvers, such as Valsalva, carotid sinus massage, and immersion in cold water increase vagal tone and decrease conduction through the AV node. This slows the HR and can often break the rhythm.

Adenosine is a very short acting AV-nodal blocker that is often used well.

MC results f/ accessory conduction pathways through the AV node. Vagal maneuvers and medications that decrease conduction through the AV node often resolve the PSVT.

Hypotension.

ST elevation in inferior leads, which strongly suggests an inferior infarct.