Cardiac Flashcards
(29 cards)
What are the most common cardiac reflexes?
Decreased Contractility causes Increased Heart Rate
Hypoxia causes pulmonary artery constriction and thereby pulmonary hypertension
Decreased systemic perfusion causes vasoconstriction except in neurogenic, spinal, septic, and anaphylactic shock
Increased systemic vasoconstriction causes decreased CO
How are afterload, contractility, preload, stroke volume, and cardiac output related?
Cardiac output is heart rate x stroke volume, typically 4-8 L/min. Stroke volume is the amount of blood pumped from the left ventricle per beat which is affected by preload (the load that stretches cardiac tissue before contraction which includes the amount of blood returned to the right heart from the body and the left heart from the lungs), contractility (heart’s intrinsic ability to contract which involves the Frank-Starling law of the heart which states that the stroke volume of the heart increases in response to an increase in volume of blood filling the heart because the increased volume stretches the ventricular wall creating a more forceful contraction), and afterload (the degree of vascular resistance to ventricular contraction which involves right heart afterload which is connected to the pulmonary arteries and left heart afterload which is tied to systemic vascular resistance).
What are pulmonary vascular resistance and systemic vascular resistance?
Pulmonary Vascular Resistance (PVR): right heart afterload measurement (50-250). Increased PVR indicates acidosis hypercapnia, hypoxia, atelectasis, ARDS. Decreased PVR indicates alkalosis, hypocapnia, vasodilator med use
Systemic Vascular Resistance (SVR): left heart afterload measurement (800-1200). Increased SVR indicates hypothermia, hypovolemic shock, decreased CO. Decreased SVR indicates anaphylaxis, neurogenic shock, septic shock, vasodilator Med use
What are the heart sounds?
S1: Lub -bicuspid/tricuspid valve closure (NORMAL)
S2: Dub -aortic/pulmonic valve closure (NORMAL)
S3: Kentucky -excess ventricle filling which can be from CHF or chordae tendinae (heart string) dysfunction (S1-ken/S2-tuck/S3-Y) (ABNORMAL)
S4: Tennessee -blood being forced into stiff ventricle which can be from hypertrophic cardiomyopathy, HTN, and often connected with an MI (S4-ten/S1-e/S2-see) (ABNORMAL)
How are heart murmurs graded?
Grade 1-5 (1=barely audible, 5=loud)
What are the main components of coronary circulation?
Right Coronary Artery (RCA) supplies right ventricle and in 60% of population the SA Node. Blockage causes Inferior MI and bradycardia due to SA Node being connected
Posterior Descending Artery (PDA) is a branch of the RCA in 85% of population. Supplies inferior wall, ventricular septum, and papillary muscles (heart strings)
Left Coronary Artery (LCA) feeds the LAD and LCX sometimes called the Left Main Artery. A blockage of this is at times referred to as the widow maker
Left Anterior Descending (LAD) supplies anterior left ventricle and anterior septum. Blockage results in Anterior MI/Septal MI/Anteroseptal MI.
Left Circumflex (LCX) supplies lateral left ventricle and the posterior left ventricle in 45% of the population. Sometimes referred to as Circumflex Artery. Blockage creates Lateral MI/ Posterior MI
What are the 3 main Acute Coronary Syndromes?
STEMI: ST Segment Elevation Myocardial Infarction evidences by ST Elevation of greater than 2 mm in 2 contiguous leads. Often connected with LBBB. Cardiac markers/enzymes are positive.
Non-STEMI: ST depression or dynamic T wave changes in 2 contiguous leads. ST Depression caused by lack of O2 to cardiac tissue. Dynamic T wave changes are inversion of the T wave. Cardiac markers/enzymes are positive.
Unstable Angina: Angina that is different in quality to normal chest pain of a pt of is not relieved with nitroglycerin or rest. ST depression could be present.
What is the progression of a Myocardial Infarction on an EKG?
Hyperactive T wave
ST Elevation
Q wave
ST Depression
What are the Cardiac Enzymes?
Troponin I: High Specificity/ Detectable at 2 hours/ Peak levels at 12 hours
Creatinine Kinase Myoglobin (CK-MB): Moderate Specificity/ Detectable at 4-8hrs/ Peak levels at 12-24 hours
Myoglobin (MB): Low Specificity/ Detectable at 3 hours/ Peak levels at 4-9 hours
Which EKG Leads are affected by which MI’s?
Posterior MI: Reciprocal changes to V1, V2, V3, V4 (predominantly V1 and V2). Vessel affected is LCX.
Anterior MI: V2, V3, V4. Vessel affected is LAD.
Inferior MI: II, III, aVF. Vessel affected is RCA.
Lateral MI: I, aVL, V5, V6. Vessel affected is LCX.
Septal MI: V1, V2. Vessel affected is LAD.
Anteroseptal MI: V1, V2, V3, V4. Left ventricle and septum affected. Papillary muscle dysfunction leads to cardiogenic shock.
What are the Bundle Branch Blocks?
Bundle Branch Blocks are caused by a defect in electrical impulse conduction (slows conduction). Wife QRS or rabbit ears. V1 will show weather bundle branch block is right or left.
Right Bundle Branch Block has an amplitude that is up.
Left Bundle Branch Block has an amplitude that is down (typically connected with new onset acute MI)
What is involved in AMI treatment?
Reduce Preload/Pain (MONA)
Reduce HR/O2 demand (Beta and Calcium Channel Blockers)
Clot Prevention (ASA)
Reperfusion (Chemical or Surgical)
What are Heparin and ACEi?
Heparin prevents fibrinogen conversion to fibrin to decrease clot formation in the coronary arteries
Angiotensin Converting Enzyme Inhibitors prevent ventricular remodeling in the Post-MI patient (keeps heart muscle from growing too much to make up for lost tissue from MI)
What are the antidysrythmic classes?
Class I: Sodium Channel Blockers
Class II: Beta Blockers
Class III: Miscellaneous (Amiodarone/Affects K efflux)
Class IV: Calcium Channel Blockers (Affects AV node)
Class V: Other
What are the Neurovascular system mechanisms?
Alpha 1: Vasoconstriction
Beta 1: Increase Heart Rate, Contractility
Beta 2: Dilate bronchioles/blood vessels
Dopaminergic: gut kidney vessel dilation
Cholinergic: decrease HR
What are the vasoactive drugs?
Increased SVR: Dopamine, Neo-synephrine, Epinephrine, Levophed, NorEpi (Levophed)
Decreased SVR: Nitroprusside (reduces preload and afterload by dilation/can cause cyanide toxicity) , High dose NTG, CCBs, ACEi, alpha Blockers, dobutrex, natrecor, Nicardipine (reduces afterload/does not cause cyanide toxicity)
Increase Preload: vasoconstrictors (drugs that increase SVR), fluids
Decrease Preload: vasodilators, morphine, Lasix, drugs that decrease SVR
What are Fibrinolytics?
Chemical reperfusion breaks the clot
Indications: Clinical presentation consistent with AMI within 12hrs of symptom onset EKG showing STEMI or LBBB Absence of contraindications Absence of cardiogenic shock
Absolute Contraindications: Prior intracranial hemorrhage Known structural cerebral vascular lesion Known malignant intracranial neoplasm Ischemic stroke within 3 months Suspected aortic dissection
What are the main methods of achieving reperfusion surgically?
PTCA (Percutaneous Trans luminal Coronary Angioplasty): Cardiac Cath
- Administer GP2B3A Inhibitors: this class of medication prevents platelet activity (differs from aspirin because aspirin cannot be titrated)
- keep leg straight during transport and hold direct pressure for 30 min after cardiac catheter removal
CABG (Coronary Artery Bypass Graft): Cardiac Bypass
- Right Coronary Artery repaired using Saphenous vein
- Left Anterior Descending repaired using Inferior Mammary Artery
What are the 5 most common other coronary problems?
Angina
- Stable: pain or discomfort 1-5min relieved with rest and/or nitroglycerin
- Variant (Prinzmetals): chest pain at rest has a circadian rhythm/commonly in early morning/commonly in women/treatment is nitroglycerin and CCBs
- Silent: painless but with EKG ischemia/ST depression
Heart Transplant
- Immediately cardiovert if decompensating
- dopamine and NS bolus (or neosynephrine, but not atropine) when bradycardic
WPW
- Heart condition in which extra electrical circuit in the heart is present and leads to tachycardia
- One of the top heart rate issues in pediatrics
- Treated with surgical ablation of extra circuit
- Delta wave is caused
Endocarditis
- Inflammation/infection on inside of heart
- top cause of endocarditis is IV drug use
- Infection with sudden onset and development of new murmur
- Osler Nodes: fingertips red and painful
- Janeway Lesions (palms of hands and soles of feet with red lesions)
- treatment often includes antibiotics via IV and potentially heart valve replacement
Pericarditis
- Inflammation/infection to outside of heart
- Substernal chest pain upon breathing or supine which is the pericardium rubbing against the sternum
- 80% of cases cant be identified
- Uremic pericarditis: can be seen in dialysis pt due to renal failure
- Dressler’s Syndrome: pericarditis in person after MI or cardiac surgery
- commonly see with ST Elevation everywhere
- treat with NSAIDS (typically Indocin) but Colchicine (also used for gout) is quickly becoming the choice treatment
What are the key points of Congestive Heart Failure?
- Difficulty breathing, frothy sputum
- Left heart failure is the most common cause of right heart failure
- Bilateral diffuse infiltrates and butterfly pattern or Kerley B lines
- The heart is greater than 50% width of chest
- BNP or B-type Natriuretic Peptide elevated as it is released by ventricles in response to stretching and leads to diuresis, Preload and afterload reduction
- BNP level less than 100=no heart failure, greater than 300=mild heart failure, greater than 600=moderate heart failure, greater than 900=severe heart failure
- Treatments include Lasix, Nitroglycerin, CPAP/BiPap, ACEi, Beta Blockers
What are the key aspects of Aortic Dissection?
- Ripping or tearing feeling between shoulder blades (sensation can also be in chest or abdomen, common in marfan’s syndrome, ascending aorta most common site of dissection, CXR shows widened mediastinum, loss of aortic knob, and pleural effusion
- difference of 20 in systolic BP between arms is common
- first line treatment is Beta Blockers (Labetalol) followed by Vasodilators (Nipride), pain medications (morphine, fentanyl, ketamine), and fluid restriction unless hypotension occurs
What are the key points of an Aortic Aneurysm?
An out pouching of abdominal or cardiac aorta which is typically found on routine CT scan for other medical problems or during physical exam in case of abdominal aortic aneurysm which can be palpated when greater than 5cm. Typically repair is done surgically when aneurysm becomes symptomatic or when greater than 5cm
What are the key attributes of Swan Ganz monitoring?
Swan-Ganz Catheter measures amount of pressure blood is under when it goes into the pulmonary artery. Measurements of right heart afterload and left heart Preload are also provided. Access site is subclavian vein. The distal tip is used to to measure pressures and the distal cuff should not be inflated with more than 1.5ml air. Wedge pressure readings should not be taken for longer than 3 breaths or 15 seconds. Readings should be taken at end of exhalation. PA port is not to be used for anything other than monitoring and lab sample draw. DEFLATE balloon when transporting or with PA catheter.
What is the progression of the swan ganz catheter?
Right atrium to right ventricle to pulmonary artery then balloon inflation to obtain PAWP.
