By Jenny R. Sheriff, EMT-P, I/C Heart Blocks and CVD

Heart Blocks Can happen anywhere in the electrical system Delays conduction The lower in the conduction system, the more deadly the block can be. Blocks will cause EKG abnormalities.

AV Blocks Delay in AV conduction and relay First degree Second degree type I (Wenckenbach) Second degree type 2 Third degree The higher the degree of the heart block, the more severe it is.

First Degree AV Block Prolonged PRI 1:1 P:QRS Regular rhythm Benign, no treatment required PRI will be > or = 0.20 seconds. P will be upright, rhythm will be regular. Caused by a delay in the AV node relay.

Mobitz type I AKA, 2nd degree type 1 or Wenckenbach Regularly irregular PRI lengthens then drops a beat R-R shortens The last heart block that atropine may work with (in cases of bradycardia). The PRI will get longer and longer until a beat is dropped, then the cycle will repeat.

Mobitz type II In conducted beats, PRI is the same Several, uniform P waves for every QRS Happens further down in the AV When measuring PRI, those that produce a QRS will all be the same (unlike Wenckenbach, in which the PRI widens until a beat is dropped). The P waves will be uniform in appearance. This block may also produce widened QRS’s if the block occurs close to or in the bundle of His.

3rd degree AV block AKA complete heart block Normal P-P interval Normal R-R interval Varying PRI No communication In this block, the atria and ventricles are doing their own thing, separately. The atria are marching along at a steady pace, thus the regular P-P interval. The ventricles are marching along at their own steady pace, thus the regular R-R interval. But the AV node is completely blocked, so there is no communication at all between the two.

Bundle Branch Blocks One branch has a block Changes on EKG When one branch is blocked, the other conducts normally, however, the muscle on the blocked side receives only cell-to-cell stimulation until the impulse gets past the block. This slows ventricular conduction on that side, producing 2 separate ventricular contractions.

Right Bundle Branch Block (RBBB) V1 and V2 show the right side of the heart, so a RBBB will be most easily seen in those leads.

Left Bundle Branch Block (LBBB) V5 and V6 show the left side of the heart, so LBBB will be most easily seen in these leads.

All together now…

Cardiovascular Diseases Hypertension CAD Arteriosclerosis Atherosclerosis Angina CHF Cardiogenic Shock AMI In 2006, CVD was the COD for 34.3% of all deaths nationwide (http://www.americanheart.org/presenter.jhtml?identifier=4478).

Hypertension Many causes Systolic >130, diastolic >90 Signs and symptoms Flushed appearance Headache Common meds Diuretics ACE inhibitors Beta Blockers Calcium Channel blockers Pre-cursor or symptom of thrombolic stroke. HCTZ, furosemide, lisinopril, enelapril, captopril, metoprolol, atenolol, verapamil

Coronary Artery Disease (CAD) Arteriosclerosis Thickening of the artery wall (hardening of the arteries) Causes loss of elasticity Can be caused by atherosclerosis or hypertension Atherosclerosis Fatty deposits or plaque that lines the inside wall of the arteries Caused by high cholesterol and fat intake Treatment includes that for underlying conditions. Cholesterol meds include statins (lipitor, zocor, lovastatin). ASA is also a common med. Surgical intervention may be necessary (endarterectomy, angioplasty).Causes also include diabetes and obesity, there can be a genetic predisposition.

Angina Pectoris Stable Unstable Prinzmetals’s AKA chest pain. Can include radiation to jaw or upper extremities and/or nausea/vomiting. May also be accompanied by pallor/diaphoresis. Tx includes O2, ASA, NTG.

Stable Angina Exertional Eases or resolves with rest Caused by increased blood pressure through already diseased arteries

Unstable Angina Can happen for no reason Non-exertional Usually lasts longer than stable angina Does not resolve w/ rest Caused by decreased blood flow to the heart due to a clot or other blockage

Prinzmetal’s Angina A form of unstable angina Caused by arterial spasms

Congestive Heart Failure Heart is not pumping effectively Back pressure of blood Caused by AMI, HTN S & S Pedal edema SOB Pillow therapy HTN Rales or wheezes may be heard in the lungs. A back-pressure in the pulmonary veins causes increased capillary pressure until fluid leaks through the capillaries and into the alveoli. Treatment includes O2, IV, furosemide, NTG, CPAP. V/S very important, both baseline and repeat. Is common after MI.

Cardiogenic Shock Shock d/t low cardiac output CHF will eventually lead to cardiogenic shock if not treated SAMPLE history is very important Same signs of shock as hypovolemic shock (change in mentation, diaphoresis, pallor, cyanosis). Will see pitting edema, hear rales or no lung sounds at all. Hypotension, tachycardia (then, later, bradycardia), labored breathing. Reassess often. NO NTG or CPAP for hypotension! Careful w/ fluids! Call ALS and/or med control.

Acute Myocardial Infarction AKA heart attack STEMI Can be diagnosed w/ 12 lead EKG NSTEMI Does not produce EKG changes AKA chemical heart attacki Tissue injury (ischemia) leads to tissue death (necrosis or infarction) ST segment elevation can indicate MI. All 12 leads should be xmitted to the hospital. Pre-hospital treatment includes O2, V/S, SAMPLE hx, OPQRST, IV, 12 lead, ASA, NTG. Frequent reassessment. MONA

Sudden Cardiac Arrest AHA Chain of Survival Early recognition Early and effective CPR Early defibrillation Meds The first 3 steps are the most important in cardiac arrest.