Cardiology Flashcards
1
Q
Describe the fetal circulation?
A
1) Blood entering fetus through ombilical vein is conducted via the ductus venosus into the IVC bypassing the hepatic circulation
2) Highly oxygenated blood reaches the heart via the IVC and is directed through the foramen ovale (and pumped into the aorta to supply the head and body)
3) deoxygenated blood from the SVC passes through the RA and to the RV (through the main PA) and to the patent ductus arteriosus
2
Q
What happens to baby physiology when the infant takes a breath?
A
Decrease in resistance of pulmonary vasculature
Increase left atrial pressure vs right atrial pressure
3
Q
What causes closure of a ductus?
A
Increased O2 from respiration
Decrease in prostaglandins from placental seperation
4
Q
What helps to close the PDA?
A
Indomethacin
5
Q
What supplies the SA and AV node?
A
Usually the RCA
Infarct may cause nodal dysfunction
6
Q
What is the percentage of right dominant?
A
85% of the PDA arises from the RCA
7
Q
What is the percentage of left dominant?
A
8%, the PDA arises from the LCx
8
Q
what does it mean to be codominent?
A
The PDA arises from both the LCx and the RCA
9
Q
What is the most posterior part of the heart?
A
The left atrium
Enlargement can cause dysphagia (due to compression of the esophagus, or hoarseness due to left recurrent nerve (a branch of the vagus)
10
Q
What are the three layers of the pericardium?
A
1) Fibrous pericardium
2) Parietal layer of the serous pericardium
3) Visceral layer of the serous pericardium
11
Q
How to define the CO?
A
Stroke volume X heart rate
12
Q
What is Fick principal?
A
CO = rate of O2 consumption / arterial O2 content-venous O2 content
13
Q
What is the MAP?
A
The mean arterial pressure is CO X total periphereal resistance
14
Q
What are the componenets of the MAP?
A
2/3 diastolic pressure + 1/3 systolic pressure
15
Q
what is the pulse pressure?
A
systolic pressure-diastolic pressure
16
Q
What is the SV (stroke volume)?
A
end-diastolic volume -end-systolic volume
17
Q
what affects the stroke volume?
A
1) Contractility
2) Increase in preload
3) Decrease in afterload
18
Q
What factors increase the contractility?
A
1) Catecholamines (increase Ca into the sarcoplasmic reticulum
2) Increase the preload
3) Decrease the afterload
4) Increase the intracellular Ca
5) Decrease the Na
6) Digitalis blocks the Na/K pump
19
Q
How to estimate the preload?
A
By the EDV
20
Q
How to approximate the afterload?
A
MAP
21
Q
What is the ejection fraction?
A
EF = SV/EDV
22
Q
what are the components of the heart sounds?
A
S1: mitral and tricuspid valve closure (loudest over the mitral)
S2: aortic and pulmonary valve closure (upper left)
S3 rapid ventricular filling phase (increase filling pressures mitral regurgitation and HF), can be normal in young patients
S4: Atrial kick (best heard at the apex with the patient in left lateral decubitus), consider abnormal at all ages
23
Q
What are the components of the JVP?
A
a wave: atrial contraction
C wave: RV contraction (closed tricuspid valve against the bulging atrium)
x descent: atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction
v wave: Increased right atrial pressure due to filling
y descent: RA emptying into the RV
24
Q
Normal splitting
Wide splitting
Fixed splitting
Paradoxical splitting
A
Normal: P2 splits because of the drop in intrathoracic pressure with increase in venous return
S1–A2-P2
Wide Splitting: S1–A2–P2 (delay of Rv emptying) due to pulmonary stenosis and right bundle branch block
Fixed splitting: S1–A2–P2 (due to ASF and left to right shunting)
Paradoxical splitting: S1–P2-A2 (NOTE the P2 is before the A2, that is due to conditions when there is delay in the closure of the aortic valve (like aortic stenosis)
25
What type of murmure is aortic area?
Systolic murmure: Aortic stenosis
| Flow murmure: aortic sclerosis
26
What types of mumure in the pulmonic area?
Systolic ejection murmure
| Pulmonary stenosis
27
What type of murmure in the tricuspid area?
```
Holosytolic murmure (TR) or VSD
Diastolic murmure: Tricuspid stenosis (atrial septal defect)
```
28
Maneuver for heart sounds: Inspiration?
Increase intensity of the right heart sounds
29
Maneuver of the hand grip (increase afterload)?
Increase intensity of MR, AR, VSD
| MVP will have later onset of the click
30
Manuover of Valsalva? (decrease the preload)
1) Decrease the intensity of most murmers
| 2) Increase the intensity of hypertrophic cardiomyopathy
31
Maneouver of rapid squatting (increase venous return, increase preload, increase afterload)
Increase the intensity of AS murmure
MVP (late onset of click andmurmure)
Decrease the intensity of hypertrophic
32
What type pf murmure for aortic stenosis?
Cresecendo-descendo systolic ejection murmure (might have a click)
Pulsus parvus et tardus (weak pulse with a delayed peak)
33
What is the mitral/tricuspid regrugitation mumure?
S1--------S2
1) Holosystolic high pitched blowing murmure
2) Mitra area (loudest at apex and radiates toward the axilla)
3) Tricuspid: loudest in tricuspid area and radiates to the sternal border (RV dilatation)
34
What are characteristics of mitral valve prolapse?
S1 MC(clicK)------S2
Late systolic crescendo murmure with midsystolic click due to sudden tensing of the chordae tendinea
35
What is the murmure for VSD?
Holosystolic (Harsh sounding) Loudest in the tricuspid area
S1-------------S2
36
What does the diastolic murmure of aortic regurgitation sound like?
S1 S2--------- (early diastolic decrescendo murmure) Can have head bobbing when chronic
Wide pulse pressure
37
What does the murmure for mitral stenosis sound like?
S1 S2 OS-------
OS= opening snap
This is due to the abrupt halt in leaflet motion in diastole
Often second to rheumatic fever
38
What is the murmure of PDA?
S1------S1------
Continous machine like murmure
Loudest at S2
39
what are the phases of myocardial action potential?
Phase O: Rapid upstroke and depolarization
Phase 1: Initial repolarization (voltage Na channels open)
Phase 2: Plateau Ca 2+ influx through gated Ca channels with K efflux
Phase 3 Rapid repolarization, massice K efflux due to opening of voltage gated slow K+ channels
Phase 4: resting potential, high K permeability through K+ channels.
40
What are some differences between cardiac muscle action potential and skeletal muscle?
1) Cardiac muscle action potential which has a plateau (due to Ca2+ influx and K influx)
2) Cardiac muscle requires constant Ca 2+ influx from ECF
3) Cardiac myocytes are electrically coupled to each other by their gap junctions
41
What are the phases of the pacemaker action potential?
```
Phase O: upstroke and opening of the voltage gated Ca 2+ channels
Phase 3 (no phase 1 and 2): Inactivation of Ca2+ channels and increased activation of K+ channels allowing K+ efflux
Phase 4:slow spontaneous diastolic depolarization due to If channels (mixed Na/K inward current)
```
42
What are the conduction pathways?
SA to atria to AV node to bundle of HIS to right and left sided bundle branches to purkinje fibers to the ventricles (left bundle branch divides to the left anterior and posterior fascicles
43
What is the function of the SA node?
Pacemaker inherent dominence with the slow phase of the upstroke
44
What are the pacemaker rates (fastest to slowest)
SA> AV> Bundle of His )Purkinje/ventricles
45
What does the P wave of EKG correspond to?
Atrial repolarization
46
What does the PR interval?
Time from start of atrial depolzarization to start of ventricular depolarization (normally less then
47
what is the QRS complexe?
Ventricular depolarization
48
What is the QT interval?
Ventricular deploarization (mechanical contraction of the ventricles)
49
What is the T wave?
Ventricular repolarization (inversion might indicate recent MI)
50
what is a J point?
Junction between the end of the QRS and start of the ST segment
51
What is the ST segment?
Isoelectric, ventricle depolarization (U wave) prominent in hypokalemiz and bradycardia
52
What are torsades de points?
Polymorphic ventricular tachycardia (shifting sinusoidal form) Can progress to ventricular fibrillation
Long QT syndrome will predispose
Caused by decreased K and Mg levels
53
What drugs cause torsades de points?
```
Anti arrythmic (Class I1, III)
Antibiotics (Macrolides)
Antipyschotics (haldol)
Antidepreseents (TCA)
Antiemetics (Ondansetron)
```
54
What are the congenitial long QT syndromes?
Inherited disorders of myocardial repolarization
| Typically due to ion channel defects (increase risk of sudden death)
55
What are the types of congential QT syndrome?
Romano-Ward syndrome: autosomal dominent (pure cardiac phenotype, no deafness)
Jervell and Lange Nielsen syndrome: Autosomal recessive (sensorineural deafness)
56
Brugada syndrome?
Automsomal dominent
Common in Asian males
Pseudo right bundle branch block with ST elevations in V1-V3
Prevent SCD with ICD
57
What is wolf-parkinson white syndrome?
Preventricular excitation syndrome
Abnormal fast accessory conduction pathways
Ventricles depolarize quickly
Can have SVNRT
58
What is atrial fibrillation?
Chaotic baseline, no discret P waves (irregular, irregular)
59
What is atrial flutter?
Rapid back to back depolarization (sawtooth appearance with flutter waves)
Treat like Afib (abalation is the definitive treatment)
60
what is ventricular fibrillation?
Erratic rhythm with no identifiable waves
| Fatal without CPR or defibrillation
61
what is a first degree block?
PR interval more then 200 msec
62
What is a second degree block?
Mobitztype I : lengthening of PR inteval until a beat is dropped (assymptomatic)
Mobitz Type 2:Dropped beats that are not preceeded by a change in the length of the PR interval
May progress to 3rd degree block (often need pacemaker)
63
What is a 3rd degree block?
Atria and ventricules beat independently of one another.
| The atrial rate is usually faster then the ventricular rate
64
What is the Atrial Natriuretic peptide?
Released from atrial myocytes to increase the blood volume and the pressure
Acts as cGMP
Causes vasodilation and decrease Na 2+ absorption
65
What is a B-type (brain natriuretic peptide)?
Released from the ventricular myocytes in response to increse in tension
BNP is used to diagnose heart failure
66
What are the receptors for BP?
Aortic arch to the vagus nerve to respond to increase and decrease in the BP
Carotid sinus (dilated region at carotid bifurcation) transmits via glossopharyngeal nerve
67
How do baraoreceptors react to hypotension?
1) Decrease arterial pressure, decrease stretch
2) Leads to decrease efferent parasympathetic stimulation (vasoconstriction)
3) Can cause increase in HR and contractility
68
How does the carotid massage work?
Increase in pressure of the carotid
Increase the stretch
Decrease the heart rate
69
What is Cushings's reaction triad?
Hypertension, bradycardia and respiratory depression
Causes increase in intracranial pressure (constricts arterioles) causing cerebral ischemia
Increase the pCO2
Decrease the Ph
70
How do the chemoreceptors work?
1) Periphereal-carotid and aortic bodies stimulate by decreasing PO2
71
How are chemorecpetors (central) stimulated?
changes in pH and PCO2 of the brain (DOES NOT RESPOND DIRECTLY TO PO2)
72
What are the normal cardiac pressures?
PWCP is estimation of the left capillary wedge pressure
73
What happens to the wedge pressure in mitral stenosis?
PCWP is higher then LV end diastolic pressure
74
What autoregulates the blood flow of the heart?
NO, CO2 and decreased O2
75
What autoregulates blood flow to the brain?
CO2 and PH
76
What autoregulates the kidneys?
Myogenic and tubuloglomerular feedback
77
What autoregulates the lungs?
Hypoxia causes vasoconstriction
78
What autoregulates skeletal muscles?
Lactate
Adenosine
K+, H+ and Co 2
79
What autoregulates the skin?
Sympathetic stimulation (usually temperature control)
80
What are the starling factors for the capillary fluid exchange?
Capillary pressure pushes fluid out of the capillary
Interstitial fluid pressure: pushes fluid into capillary
Plasma oncotic prressure: pulls fluid into the capillary
Interstitial fluid colloid osmotic pressure (pulls fluid out of the capillary)
81
How is edema caused?
Increased capillary pressure
Decrease in plasma proteins
Increase in capillary permeability
Increase in interstitial fluid and colloid osmotic pressure
82
What is the long term consequences of VSD?
May lead to LV overload and heart failure
83
What is the atrial septal defect cause?
Most common is ostium secondum
| Will have increased O2 saturation in the RA, RV, and the pulmonary artery
84
How to maintain the PDA?
PGE
| Low O2 tension
85
What are treatments to try and close the PDA?
Endomethacin
86
What happens with chronic left to right shunt?
1) VSD, ASD and PDA
2) Increased in pulmonary blood flow
3) Remodelling of pulmonary vasculature
4) Pulmonary HTN
5) Leads to cyanosis and clubbing
87
What are some problems associated with coarctation of the aorta?
1) Associated with a bicuspid valve
2) Turner's syndrome
3) Other heart defects
4) Will have HTN in extemties and weak, delayed pulses in the lower extremities
5) With age will have intercoastal arteries that enlage, and notched appearence on X ray
88
What are complications associated with a coarctation?
Heart failure
Cerebral hemorrhage
Aortic rupture
Endocarditis
89
What congenital cardiac defects are asssociated with ETOH?
VSD, PDA, ASD, tetralogy of fallot
90
Heart defects associated with congenital rubella?
PDA
Pulmonary artery stenosis
Septal defects
91
Defects associated with down's syndrome?
AVSD
VSD
ASD
92
Heart defects associated with diabetic mother?
Transposition of the great vessels
93
Defects associated with Marfan's disease?
MVP
Thoracis aortic aneurysms
Dissected aorta
Aortic regurgitation
94
Defects associated with lithium exposure?
Ebstein's anomaly
95
Defect associated with Turner's syndrome?
Bicuspid aortic valve
| Coarctation of the aorta
96
Defect associated with Williams syndrome?
Supravalvular aortic stenosis
97
Defect associated with 22q11 syndrome?
Truncus arteriosus
| Tetralogy of fallot
98
What is hypertension?
BP more then 140 mmHg
| Bp > 90 mmhg
99
what are risk factors for hypertension?
```
Increased age
Diabetes
Physical inactivity
Too much salt
Too much ETOH
Family history
African American
```
100
What is the most common type of hypertension?
Essential HTN associated with increased CO or increased total periphereal resistance
101
What are the other type of HTN?
```
Renovascular disease and muscular dysplasia (10%)
And hyperaldosteron (usually found in younger women)
```
102
What is categorized as a hypertensive urgency?
180/120, can lead to acute end organ damage
103
What is categorized as a hypertensive emergency?
```
Severe HTN with evidence of end organ damage
Encephalopathy
Stroke
Retinal damage
Exudates
Papilledema
```
104
What does HTN predispose to?
```
CAD
LVH
HF
aortic dissection
Aneurysm
Stroke
Chronic kidney disease
Hypertensive nephropathy
Retinopathy
```
105
What are signs of hyperlipidemia?
Xanthomas: nodules or lipd-laden histocytes in the skin (especially on the eyelids)
Tendinous xanthomas: lipid deposirs on the tendon (usually the Achilles)
Corneal Arcus: lipid deposit in the cornea
106
What are the signs of arteriosclerosis?
Hardening of the arteries
107
What are the two types of arteriosclerosis?
Hyperplastic (onion skinning) if have severe hypertnesion
Hyaline (thickening of the vessel walls in essential hypertension) or diabetes
108
What are monckeberg sclerosis (medial calcific sclerosis)
Medium sized arteries are affected
Vascular stiffening without obstruction
Pipestem appearance on x-ray
109
what are the common sites of atherosclerosis?
aabdominal aorta (most common) > coronary artery > poplitel artery > carotid artery
110
What are the modifiable factors?
Smoking
HTN
Hyperlipidemia
Diabetes
Sex
Age
Family history
111
What is the process of the formation?
endothelial cell dysfunction to macrophages to foam cell formation to fatty streaks to smooth muscle migration to proliferation and extracellular matrix deposition and formation of fibrous plaques and atheromas
112
Risk factors for abdominal aneurysm?
Tobacco use
Age
Male sex
113
What are risk factors for thoracic aortic aneurysms?
```
Cystic medial degeneration
Hypertension
Bicuspid aortic valve
Connective tissue disease
Can be associated with syphlis
```
114
What are traumatic rupture of the aorta?
Trauma or deceleration injury
| Aortic isthmus
115
What is variant, prinzmetal angina?
Due to coronary spasm
Can have transient ST elevation on ECG
Triggered by tobacco, cocaine, and triptophans
Treatmant Calcium blockers
116
What causes unstab;e angina?
Thrombosis of the coronary artery with ST depression or T wave inversion of ECG but no increase in biomarkers
117
What is coronary steal syndrome?
Distal to stenosis, vessels are maximally dilated at baseling
When you give vasodilators, it shunts blood to well perfused areas.
Can have decreased flow and ischemia in poststenotic regions
118
What are the causes of sudden cardiac death?
```
Death within 1 hour of symptoms
Usually arrythmia VF
Associated with CAD within 70% of cases
Cardiomyopathy
Long QT
Burgada
```
119
What are characteristics of ST MI?
Transmural
Full thickness of the myocardial wall
ST elevation of ECG and Q waves
120
What are NON ST segment MI (NSTEMI)?
Subendocardial infarcts
Subendocardium (inner 1/3) in areas
ST depression
121
What are the most commonly occluded coronary arteries?
LAD > RCA > circumflex
122
What is seen 0-24 after infarct? (microscopy and CX)
Coagulative necrosis, edema, hemorrahe
Can have reperfusion injury with free radicals
Cx: Ventricular arrythmias and cardiogenic shock
123
What is seen 1-3 after infarct? (mico and CX)
Coaguative necrosis
| Postinfarction fibrinous pericarditis
124
What is seen 3-14 after infarct (micro and CX)
Free wall rupture
Tamponade (papillary muscle rupture)
Acute MR
LV pseudoaneurysm with risk to rupture
125
What is seen 2 weeks to several months?
```
Contracted scar complete
Dressler syndrome
HF
Arrythmias
True ventricular aneurysm
Risk of mural thrombus
```
126
In first 6 hours, after MI, what is gold standard?
EKG
127
When do trops rise?
4 hours (peak at 24 hours)
128
When do CK MB rise?
```
6 hours (peak at 16-24 hours)
Most useful in diagnosing reinfarction following an acute MI (and return to normal after 48 hours)
```
129
Where is CK-MB found?
Predominantly in the myocardium but some from skeletal
130
What are the ECG infarct location?
```
LAD: V1 to V2
Distal LAD V3 to V4
Anterolateral LAD or CX: V5 to V6
Lateral I to aVL
Inferior RCA: II, III and aVF
PosterioR PDA V7-V9, ST depression in V1 to V3 and tall R wave
```
131
What are the most common cardiomyopathy?
90% is idiopathic or familial
132
What are other etiologies of cardiomyopathies?
```
Beriberi
Coxsackie
Chronic cocaine use
Chagas disease
Doxrubin toxicity
Hemochromacytosis
Sarcoidosis
Peripartum
```
133
Dilated cardiomyopathy, is it eccentric or concentric hypertrophy?
eccentric
134
How should dilated cadiomyopathy be treated?
```
Na restriction
ACE inhibition
B Blockers
diuretics
Digoxin
ICD
Heart transplant
```
135
What are causes of hypertrophic cardiomyopathy?
70% is familial and autosomal (usually B chain myosin)
136
How to treat hypertrophic cardiomyopathy?
Cessation of athletics
B blocker of C blocker
ICD
137
How does obstuctive hypertrophic cardiomyopathy work?
Assymmetric septal hypertrophy
Have systolic anterior motion of the mitral valve
Outflow obstruction
Syncope
138
What are causes of restrictive/infiltrative cardiomyopathy?
```
Sarccoidosis
Postradiation fribosis
Endocardial fibroelastosis
Loeffler syndrome (eosinophils)
```
139
Restrictive cardiomyopathy ECK?
Have low voltage EKG (despite thick myocardium)
140
what are signs of left heart failure?
1) Orthopnea (shortness of breath when supine)
2) PND: breathless awakening from sleep (due to redistribution of blood)
3) Pulmonary edema: increased pulmonary venous distention and transudation of fluid
141
What are signs of right heart failure?
Hepatomegaly: increased CV and can lead to cirrhosis
JVP distended
Peripheral edema due to fluid transudation
142
What are the characteristics of hypovolemic shock?
Decreased PCWP
Decreased CO
Increased SVR
Treatement with IV fluid
143
What are characteristics of cardiogenic shock?
Increased PCWP
Decreased CO
Increased SVR
Treatement with inotropes
144
What are characteristics of distributive shock?
Decreased PCWP
Decreased CO
Decreased SVR
145
what is the most common valve involved in endocarditis?
Mitral valve
146
What is the endocarditis of prosthetic valves?
S. Epidermis
147
Which bug is associated with colon cancer endocarditis?
S. Bovis *gallolyticus*
148
What causes Rheumatic fever?
B hemolytic strep
149
Which heart valves are most often affected in Rheumatic fever?
Mitral > aortic > tricuspid
150
What are the early lesions of rheumatic fever?
Mitral regurgitation
151
what are the criteria for the rhuematic fever?
Joint pain, migratory
Nodules on the skin
Erythema
Sydenham chorea
152
What are causes of acute pericarditis?
```
Inflammation
Neoplasia
Autoimmune
Viral
Infection
SLE
```
153
What is pulsus paradoxus?
```
Decrease in amplitude BP > 10 mmHG during inspiration
Seen in cardiac tamponade
asthma
Sleep apnea
Pericarditis
Croup
```
154
What are consequences of syhilitic heart disease?
Disrupts the vasa vasorum of the aorta causing dilatation of the aorta
Can lead to the aneurysm of the ascending aorta and insufficiency
155
What are the most common cardiac tumors?
Most common is metastasis
| Myxomas are primary tumor (90% are in the atria)
156
What are most common tumor in children?
Rhabdomyomas
157
What is Kussmaul's sign?
High JVD
Inspiration leads to neagtive intrathoracic pressure that is not transmitted to the heart, and imparied filling of the right ventricle.
158
What are the large vessel vascultis (epi and path)?
1) Giant cell : elderly female, and unilateral temporal artery
Focal granulomatous inflammation, increased ESR
Usually the branches of the carotid
2)Takayasu arteritis: Asian females less then 40 years old
(weak extremity pulses, fever, night sweats, arthritis, myalgias, skin nodules)
PAth: granulomatous thickening and narrowing of the aortic arch
Treat with corticosteroids
159
what are medium vasculitis with path characteristics?
1) Polyarteritis nodosa: Young adult, Hep B, presents with abdominal pain, melena
HTN, neurological dysfunction and renal damage
Transmural inflammation with renal microaneurysms
Treat with corticosteroids
2) Kawasaki disease: Asian children less then 4 years old. Conjunctival infection, with rash, and adenopathy.
Strawberry tongue and hand-foot changes
Can develope coronary aneurysm
3) Buerger disease: heavy smokers
160
What are examples of small vessel vasculitis?
```
1) Granulomatosis with polyangiitis
Triad of Focal
a) necrotizing vasculitis
b) Necrotizing granulomas
c)Necrotizing glomerulonephritis
d) PR3-ANCA, c-ANCA
```
2) Microscopic polyangiitis
Necrotizing vasculitis involving the lungs, kidney and skin
No granulomas
MPO-ANCA
3)Eosinophilic granulomatosis polyangitis (Churg-Strauss)
Granulomatous, necrotizing vasculitis with eosinophilia
MPO-ANCA/p-ANCA
Increased IgE level
4) Henoch-Schonlein purpura: most commonly childhood vasculitis (following URI)
```
Triad:
Skin (papable purpura)
Arthalgias
Abdominal Pain
Vasculitis secondary to IgA (associated with IgA nephropathy)
```
161
What are the treatments for HTN?
1) Primary: Thiazide diuretics,ACE, angiotensin II receptor blockers, Calcium channel blockers
2) HTN with heart failure: diuretics, ACE, ARB, B blockers (if stable)
3) HTN with DM: Ace/ARB, CA +blockers, thiazide, diuretics
4) HTN with pregnancy: Hydralazine, labetalol, methyldopa
162
What conditions are dihydropyridines used to treat? (calcium channel blocker)
HTN, Angina, Raynauds
163
What conditions are nimodipine used to treat?
Cerebral vasospasm (subarachnoid hemorrage)
164
what are the conditions used to treat clevidipine?
HTN emergency
165
What are conditions treated with non-dihydropyridine?
HTN, angina, atrial fibrillation/flutter
166
What are the adverse effects of non-dihydropyridine?
Cardiac depression, AV block, hyperprolactemia, constipation
167
What is the mechanism of Hydralazine? Clincal use, adverse effects?
```
Increase cAMP (increase smooth muscle relaxation)
Vasodilates arterioles > veins (afterload reduction)
```
Clinical use: Severe HTN, HF due to organic nitrate (safe during pregnancy)
Can lead to compensatory tachycardia (contra-indicated in angina/CAD) fluid retention, headache, lupus
168
what are the drugs used in HTN emergency?
1) Nitroprusside: short acting cGMP (direct release of NO) can use with cyanide toxicity
2) Fenoldopam: Dopamine receptor agonist: coronary, periphereal, renal and splanic vasodilation
3) Nitrates: vasodilates by NO in vascular smooth muscle, dilates the veins more then arteries and decreases the preload
Clinical uses: reflex tachycardia, B blockers, HTN, flushng, headaches, can have tolerace that developes.
169
Mechanism and use of Ranolazine?
1) Inhibits the late phase of sodium current, reducinf diastolic wall tension and oxygen consumption
Clinical use: angina refractory to other medical
Adverse effects: Constipation, dizziness, headache, nausea, QT prolongation.
170
what are 4 types of lipid lowering agents?
1) HMG-CoA reductase inhibitors (lovastatin, pravastatin), decrease LDL, increase LDL, decrease triglycerides
Adverse effects: Heptatoxicity
Decreases mortality in CAD patients
2) Bile acid resins (Cholestryramine, colestipol, colesevelam) decrease LDL, HDL higher
Prevents intestinal reasoption of bile acids. Liver must use cholesterol to make more
Adverse effect: decrease absorption of other drugs and fat soluable vitamins
3) Ezetimibe: decrease LDL, prevent cholesterol absorption at small intestine
4) Fibrates: decrease LDL, increase HDL, decrease triglycerides
Cause myopathy, cholesterol and gallstones
5) Niacin: decrease LDL, increase LDL, decrease triglycerides
inhibits lipolysis (hormone sensitive
171
What are cardiac glycosides?
Digoxin
Inhibits Na/K ATP ase
Increase Ca + for positive inotropy
Uses:
Increase contractility
Decrease atrial fibrillation
Can lead to hyperkalemia (poor prognosis)
Antidote: Normalize K, Cardiac pacer, digibind
172
What are the classes of anti-arrythmics? What are the adverse effects?
1) Sodium channel blocker, used for atrial and ventricular arrythmias
Examples: Quinidine, procanamide
Adverse effects: Cinchonism, Heat failure, torsades, QT interval
2) Decrease the action potential duration (lidocaine, mexileTine)
Clinically used within ventricular arrythmias
Venticular arrythmias
Can cause CNS depression
3) Class IC (flecanide, propafenone)
Medication: prolongs the ERP in AV node and accessory bypass tracts
Last resort in refractory VT
Can be proarrythmic especially post MI
Contra-indicated in structural and ishchemic heart disease
4) Class II (B blockers) Metroprolol, esmolol, timolol
Decrease the SA and the AV node activity
Uses:SVT and rate control for afib and atrial flutter
Adverse effects: metroprolol causes dyslipidemia
Propranolol can have vasospasm.
5) Class III (Potassium channel blocker) amiodarone and sotalol.
1) Use with afib, aflutter
2) Sideffects of amio: fiborisis, heptatoxicity, corneal deposits, grey skin
Need to check the PFT, LFT, TFT
6) Calcium Channel Blockers
Verapamil , diltiazem
Uses: prevents nodal arrythmias, and rate control in afib
Adverse effects include: flushing, edema, etc.
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What type of anti-arrythmic is adenosine?
Potassium out of the cell, hyperpolarizing.
Very short acting
Effective in torsades de pointes and digoxin toxicity
