Cardiology 2 Flashcards
Right Heart
Thinner wall
Tricuspid valve
Pumps into pulmonary circulation via pulmonary arteries
Receives blood from IVC and SVC
Innervated with RBB no fascicels
Location of SA and AV node
Atrium
Left Heart
thicker wall
Mitral valve
Pumps into systemic circulation via aorta and great vessels
Innervated with LBB
MAP
Average pressure over one full cardiac cycle
2/3 diastolic + 1/3 systolic
Normal MAp
70-100
Perfusion MAP
60-65 to perfuse coronary arteries, kidneys, brain
Weights MAP not used
Pts <12 or <20kg
Factors affecting MAP
Vascular tone
Fluid Status
Drugs
Cardiovascular and Neurogenic status
Preload
RV wall stress at end diastole
Increase Preload
NS/RL bolus
RBC bolus
Releasing intrathoracic pressure
Supine position
Vasopressors
Decrease preload
Nitroglycerin
Morphine
Furosemide
PPV, AutoPEEP, increased intrathoracic pressure
Sitting
Contractility
Squeeze or inotropy of cardiac muscle
Increases of contractility
Increased preload
Reducing tension in cardiac muscle caused by ischemia
Correcting electrolyte abnormalities
Reversing acidosis
Giving drugs that stimulate Beta I
Afterload
Resistance against which ventricles contract
Increased Afterload
Alpha agonists
PSNS Effect on Heart
Innervates SA and AV node
Stimulation decreases HR by decreasing conduction velocity
Reduces contractile force of atrial and ventricular cardiac muscle
SNS Effect on Heart
Innervates all aspects of heart
Stimulation causes increased HR and contractility
Blockade decreases HR and contractility
PSNS Stimulation of SA node
Releases acetylcholine at both nerve terminals
Dominate activity at SA node
Decreased Ca channels increasing efflux of K, decreases HR and conduction through AV
Sympathetic Stimulation
Increase Na and Ca influx
Able to reach threshold quicker
Sodium
Influx increases charge towards threshold for AP
Potassium
Increased K decreases membrane potential, decreases intensity of AP and decreases contractions
Calcium
Increases contractions
Aortic Arch Baroreceptors
Responds to increased Bp
Transmits via vagus nerve to medulla
Carotid Body Baroreceptors
Transmit via glossopharyngeal nerve to medulla
Response to all Bp changes
Increased Carotid pressure
Increase stretch
Increase PSNS decrease SNS
Vasodilation and decreased HR
Decreased carotid pressure
Decreases arterial pressure, decreased stretch, increased sympathetic outflow and decreased PSNS
Vasoconstriction, increased HR, increased contractility, increased BP
Central Chemoreceptors
Respond to changes in pH and pCO2 in brain
Peripheral Chemoreceptors
Carotid and aortic bodies respond to decreased pO2 increased pCO2, and decreased pH
Chemoreceptors
Activation increases sympathetic outflow to compensate for vasodilation effects of hypoxia to redistribute blood flow
RAAS
Renin from juxtaglomerular cells (kidneys)
Renin turns angiotensinogen to angiotensin I
Angiotensin I to Angiotensin II by ACE from lungs
Angiotensin II
Vasoconstriction
Decreased excretion of salt + water
Increased BP
Hormones impacting Vasoconstriction
NE and Epi
ANgiotensin
Vasopressin
Endothelia
Ion Changes to Vasoconstriction
Increased calcion
Decrease in H
Decrease BP Hormones
Bradykinin
Histamine
Ion Changes to Decrease BP
Increase K
Increase Mg
Increase acetate and citrate
Changes in H
Increased CO2
Unstable Angina
No myocardial injury
T wave abnormality/ST depression
NSTEMI
Subendocardial injury with +ve troponin
TI > 99th percentile
STEMI
Transmural injury with ST elevation on ECG
3 Types of troponin
Troponin C (skeletal)
Troponin I (cardiac)
Troponin T ( cardiac)
Other causes of increased troponin
Myocarditis
Pericarditis
Heart failure
Valvular disease
Aortic dissection
Sepsis
Renal failure
PE
Primary Hemostasis
Utilizes platelets to form a plug at site of injured blood vessel
Secondary Hemostasis
Fibrin mesh formed by multiple coagulation factors to stabililze the plug
5 Phases of Primary Hemostasis
Endothelial injury
Exposure: underlying collagen release vWF
Adhesion: platelets bind to vWF
Activation: platelets become active
Aggregation: platelet cluster
Secondary Hemostasis Patho
Thrombin binds with receptor activating more platelets
Fibrinogen -> fibrin -> fibrin mesh
Stabilizing factor
Primary Hemostasis Treatments
ASA
Antiplatelets
ASA
Inhibits thromboxane A2 production (inhibits COX-1 and COX-2)
Decreases ability for clot to form
Antiplatelets
Prevent platelet aggregation and thrombus formation
Inhibit GP IIB/IIIA receptors
Secondary Hemostasis Treatments
Heparin
Coumadin
Direct Thrombin Inhibitors
Direct Factor Xa Inhibitors
Heparin
Binds to enzyme inhibitor anti-thrombin III
Inactivates thrombin, factor Xa and other proteases
Coumadin
Decreases active vitamin K
Decrease clotting ability
Direct Thrombin INhibitors
Bind to thrombin in circulation and those already forming clot
When is direct thrombin inhibitor useful
Heparin induced thrombocytopenia
Side effects of direct thrombin inhibitors
GI symptoms, dyspepsia, gastritis
Direct Factor Xa inhibitors
Act on factor X of coagulation cascade
International Normalized Ratio
Lab value of how long it takes for blood to clot
Therapeutic iNR
2-3s
Nitroglycerin Action
Converted to NO in cell
Causes vascular smooth muscle relaxation and vasodialtion
Reduces oxygen demand
Decreases preload, afterload, and dilates coronary arteries
Phosphodiesterase Inhibitors
Inhibit phosphodiesterase III -> cAMP breakdown
Unable to activate platelets
MOA Morphine
Binds with opiate receptors throughout CNS
Hyperpolarization of nerve cells, inhiibitions of nerve firing
Pain relief decreases sympathetic outflow, catecholamine release, MVO2, MI progression
Morphine effects of inhibition of nerve firing
Alter’s brain perception of pain
Decreases pain perception at spinal cord
Binds to perihheral terminals to decrease pain stimuli
Reduces sensitivity of respiratory centre to CO2
Histamine release causing hypotension
Enhances PNS stimulus
Stimulates chemoreceptor trigger for vomiting
Cardiogenic Shock
Acute physiological condition caused by inability of heart to pump blood for needs of body
S/Sx of Cardiogenic Shock
Rapid breathing
Severe shortness of breath
Sudden tachycardia
LoC
Weak pulse
Low BP
Sweating
Pale skin
Cold hands or feet
Urinating less than normal
Causes of Cardiogenic Shock
Decreased function or performance of myocardium
Abnormalities leading to decrease in LV EDV
Structural defects or obstructions leading to shock
Dopamine Classifications
Sympathomimetic
Alpha Adrenergic Agonist
Beta Adrenergic Agonist
Dopaminergic Agent
Dopamine 2-5mcg/kg/min
Dopaminergic stimulation
Dilation vessels in mesentery and kidney
Increased blood flow to kidney and gut
5-10mcg/kg/min dopamine
Beta I stimulant
Positive inotropic
Positive chronotropic
10-20mcg/kg/min dopamine
Alpha I stimulant
Peripheral vasoconstriction
Beta I stimulation
Reversal of dopaminergic effects
ACS definitive treatment
Antiplatelets, antithrombins, abtianginal
Primary PCI for balloon angioplasty
Thrombolysis (TNK)
Atropine Classification
Parasympatholytic
Anticholinergic
Antimuscarinic
Antidote for cholinergic OD, cholinesterase inhibitors and amanita muscaria
Diagnostic agent
Belladonna alkaloid
Antiparksonian
MOA Atropine
Competitively blocks effects of AcH at muscarinic receptors of PNS
Inhibits vagal influence of HR
Depresses salivation and bronchiole secretion, relaxes GI
Relaxes pupils
Atropine Precautions
Can cause paradoxical bradycardia if administered slowly
May not work in heart blocks
Increases workload of heart
Transcutaneous Pacemaker
External
Non-invasive
Pacing through skin
Transvenous Pacemaker
Electrodes via large central vessels to right chambers of the heart
Epicardial Pacemaker
Internal implanted
Electrodes on surface of heart
Permanent Pacemaker
Venous or epicardial
Implanted
Electrodes on surface of heart
Fixed Rate Pacemaker
Fires constantly at preset rate without regard for inherent beats
Demand Pacemakers
Sensing device that will only discharge when natural rate of heart falls below present value established for pacer
Single Chamber Pacemaker
Either ventricle or atria
Dual chamber Pacemaker
Stimulate atria then ventricles
Pacemaker Failure to Sense
Inability to identify ECG waveforms
Paced beats early, late, or not at all
Failure to Fire
Pacing spike fails to appear when it should
failure to Capture (electrical)
Waveform fails to appear after pacing spike and depolarization of heart does not occur
Failure to Capture (mechanical)
Spike appears, no mechanical output
Pulse doesn’t match
Adenosine Class
Anti-arrhythmic
Diagnostic agent
MOA Adenosine
Endogenous nucleoside acting at adenosine A receptors in heart
Decrease adenylyl cyclase, resulting in decreased SA discharge and AV conduction
Efflux of potassium from cell, hyper polarization of cell
Decreases automaticity of AV node, causing complete AV bock
Adenosine Half life
<10s
Lidocaine Class
Anti-arrhythmic Class Ib
Sodium channel blocker
Local anesthetic
Indications lidocaine
Cardiac irritability
Refractory VF or VT
Topical administration pre ETT
MOA Lidocaine
Shortens phase 3 decreasing myocardial excitability
Decreases slope of phase 0
Increases fibrillation threshold
Decreases conduction in ischemic cardiac tissue without adversely affecting normal conduction
Precautions Lidocaine
Pt with perfusion disorder, hepatic disease, elderly
Lidocaine toxicity
3.0mg/kg
S/Sx of lidocaine toxicity
Drowsiness
Slurred speech
Dysrhythmias
CNS depression
Seizure
Coma
Death
Amiodarone Class
Class III antiarrhythmic
Adrenergic blocker
Na, K, Ca blocker
Acts on all cardiac tissue
Indications Amiodarone
Refractory VF VT
Refractory PSVT or A-fib
Symptomatic atrial flutter
MOA Amiodarone
Increases vF threshold by blocking K channels and prolonging repolarization and refractory period
Relaxes vascular smooth muscle to decrease PVR and increase coronary perfusion
Negative chronotrope
Negative inotrope
Negative dromotrope
Electrical Phase Cardiac Arrest
0-4min
Electrical conduction chaotic with lots of irritable foci
Defibrillation needed
Circulatory Phase Cardiac Arrest
4-10min
Drop in BP without perfusion to heart or brain
CPR needed
Metabolic Phase Cardiac Arrest
> 10 min
Metabolic acidosis kicks in due to anaerobic metabolism
Decreased transport of O2 needed for perfusion
Possible sodium bicarb
Ventricular Fibrillation
Multiple ectopic foci in ventricles at rates up to 500bpm
Rapid and irregular activity rendering ventricles unable to contract in synchronized manner
Loss of heart as a pump
Cardioversion
Place all cardiac cells in depolarized state, allowing dominant pacemaker to proceed
