Cardiovascular Flashcards
(45 cards)
1
Q
What is used to treat primary (essential) hypertension?
A
- Thiazide diuretics
- ACE inhibitors
- ARBs
- Ca2+ channel blockers (dihydropyridines)
2
Q
What is used to treat hypertension w/ heart failure?
A
- Diuretics
- ACE inhibitors/ARBs
- β-blockers (compensated heart failure)
- used cautiously in decompensated heart failure
- contraindicated in cardiogenic shock
- Aldosterone antagonists
3
Q
What is used to treat hypertension w/ diabetes mellitus?
A
- ACE inhibitors/ARBs
- protective against diabetic nephropathy
- Ca2+ channel blockers
- Thiazide diuretics
- β-blockers
4
Q
What is used to treat hypertension in pregnancy?
A
- Hydralazine
- Labetalol
- Methyldopa
- Nifedipine
5
Q
Which Ca2+ channel blocker is used to treat subarachnoid hemorrhage?
A
Nifedipine - prevents cerebral vasospasm
6
Q
Which Ca2+ is used to treat hypertensive urgency/emergency?
A
Clevidipine
7
Q
Which nitrate has the highest oral bioavailability?
A
isosorbide mononitrate
8
Q
What HTN drug can cause cyanide toxicity?
A
Nitroprusside
9
Q
Which anti-arrythmic drugs can lead to heart failure?
A
Negative inotropes:
- Ca2+ blockers (especially non-dihydopyridines)
- β-blockers
10
Q
What increases stroke volume?
A
SV CAP
- Increase contractility, prelodad
- Decrease afterload
11
Q
How do calculate MAP?
A
- MAP = CO x total peripheral resistance (TPR)
- MAP = 2/3 diastolic pressure + 1/3 systolic pressure
12
Q
What is the physiology of normal splitting?
A
Inspiration ⇒ ↓ intrathoracic pressure ⇒ ↑ venous return ⇒ ↑ RV filling ⇒ ↑ RV stroke volume ⇒ ↑RV ejection time ⇒ delayed closure of pulmonic valve
- ↓ pulmonary impedance ( ↑ capacity of pulmonary circulation) also occurs which contirbutes to delayed closure of the pulmonary valve
13
Q
Causes of:
- Wide splitting
- Fixed splitting
- Paradoxical splitting
A
-
Wide splitting (conditions that delay RV filling)
- pulmonic stenosis, RBBB
-
Fixed splitting (pulmonic closure is greatly delayed)
- ASD (L to R shunt ⇒ ↑ RA & RV volumes ⇒ ↑ flow thru pulmonic valve)
-
Paradoxical splitting (delay in aortic valve closure)
- aortic stenosis, LBBB (P2 occurs before delayed A2)
14
Q
Bedside maneuvers:
Inspiration
A
↑ intensity of right heart sounds
15
Q
Bedside maneuvers:
Hand grip
A
- ↑ intensity of MR, AR, VSD murmurs
- ↓ intensity hypertrophic cardiomyopathy murmurs
- MVP: later onset of click/murmur
16
Q
Bedside maneuvers:
Valsava (phase II), standing up (↓ preload)
A
↓ intensity of most murmurs (including AS)
↑ intensity hypertrophic cardiomyopathy murmur
MVP: early onset of click/murmur
17
Q
Bedside maneuver:
Rapid squatting (↑ venous return, ↑ preload)
A
- ↓ intensity hypertrophic cardiomyopathy murmur
- ↑ intensity of AS murmur
- MVP: later onset of click/murmur
18
Q
Speed of conduction ⇒
A
Purkinje fibers > atria > ventricles > Av node
19
Q
Pacemaker activity ⇒
A
SA node > AV node > Bundle of His/Purkinje fibers
20
Q
List the Right -to -Left Shunts:
A
- Patent Truncus Arteriosus
- Transposition of the Great Vessels
- Triscupid Atresia
- Tetralogy of Fallot
- Total Anomalous Pulmonary Venous Return
21
Q
List the Left-to-Right shunts:
A
- Ventricular Septal Defect
- Atrial Septal Defect
- Patent Ductus Arteriosus
- Eisenmenger Syndrome
22
Q
What are the waves for the jugular venous pulse (JVP)?
A
-
a wave: atrial contraction
- absent in a-fib
-
c wave: RV contraction
- closed tricuspid valve bulging into atrium
-
x descent: atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction
- absent in tricuspid regurgitation
- v wave: inc right atrial pressure due to filling (“villing”) against closed tricuspid valve
- y descent: RA emptying into RV
23
Q
Brugada syndrome
- Inheritance:
- Epidemiology:
- EKG findings:
- Risks:
- Treatment:
A
- Inheritance:
- autosomal dominant
- Epidemiology:
- most common in asian males
- EKG findings:
- pseudo-right bundle branch block and ST elevations in V1-V3
- Risks:
- inc. risk of ventricular tachyarrthymias and SCD
- Treatment:
- implantable cardioverter-defribrillator (ICD)
24
Q
What are the causes of drug-induced prolonged QT?
(hint: Anti-“ABCDE”)
A
- Anti-Arrhythmics (class IA, III)
- AntiBiotics (e.g. macrolides)
- Anti “C“ychotics (e.g. haloperidol)
- AntiDepressants (e.g. TCAs)
- AntiEmetics (e.g. ondansetron)
25
What is the most common type of ventricular pre-excitation syndrome?
Wolf-Parkinson-White syndrome
26
What is the lab indicator for heart failure?
**BNP**
* released by **ventricular myocytes** in response to inc. tension
* longer 1/2 life than ANP
* very good negative predictive value
27
How do organs react to hypoxia?
* hypoxia in pulmonary vasculature ⇒ **vasoconstriction**
* so only well-ventilated areas are perfused
* hypoxia in other organs ⇒ vasodilation
28
* Aortic arch ⇒
* Carotid sinus ⇒
* Baroreceptors ⇒
* Chemoreceptors ⇒
* Aortic arch ⇒ transmits via vagus nerve (CN 10) to solitary nucleus of medulla (**responds to Δ BP**)
* Carotid sinus (at carotid bifurcation) ⇒ transmits via glossopharyngeal nerve to solitary nucleus of medulla (**responds to Δ BP**)
* Baroreceptors ⇒ respond to **stretch** (see page 286 of first aid)
* Chemoreceptors ⇒
* Peripheral: respond to Δ PO2, PCO2, and pH of blood
* Central: respond to Δ in interstitial brain pH and PCO2 and are influenced by PaCO2
29
* What is Cushing reaction?
* What contributes to this reaction?
* **Cushing reaction:** HTN, bradycardia, respiratory depression
* **Baroreceptors:**
* ↑ intracranial pressure constricts arterioles ⇒ cerebral ischemia ⇒ **↑ pCO2 and ↓ pH** ⇒ central reflex sympathetic ↑ in perfusion pressure (HTN) ⇒ **↑ stretch** ⇒ peripheral reflex baroreceptor induced **bradycardia**
30
In mitral stenosis, what happens to the PCWP?
**PCWP \> LV diastolic pressure**
31
Causes of edema:
1. capillary pressure
2. plasma proteins
3. capillary permeability
4. interstitial fluid colloid osmotic pressure
1. **↑ capillary pressure**
* e.g. HF
2. **↓ plasma proteins**
* e.g. nephrotic syndrome, liver failure
3. **↑ capillary permeability**
* e.g. toxins, infections,, burns
4. **↑ interstitial fluid colloid osmotic pressure**
* e.g. lymphatic blockage
32
What are the signs of hyperlipidemia?
1. **Xanthomas:**
* Plaques or nodules composed of **lipid-laden histiocytes in skin**, especially on **eyelids** (xanthalasma)
2. **Tendinous xanthoma**
* lipid deposits in **tendon**, especially **Achilles**
3. **Corneal arcus**
* lipid deposits in **cornea**
* common in **elderly** (arcus senilis)
* appears earlier in life in **hypercholesterolemia**
33
Define **arteriosclerosis**:
hardening of arteries, w/ **arterial wall thickening** and **loss of elasticity**
Two types:
1. Arteriolosclerosis
2. Monckeberg (medial calcific stenosis)
34
Arteriolosclerosis vs. Monckeberg (medial calcific sclerosis)
1. **Arteriolosclerosis**
* **Common**
* affects **small arteries and arterioles**
* Two types:
* **hyaline** → _thickening of vessel walls in essential HTN and diabetes_
* **hyperplastic** → **"onion skinning"** in severe HTN w/ _proliferation of smooth muscle_
2. **Monckeberg (medial calcific sclerosis)**
* Uncommon
* affects **medium-sized arteries**
* **calcification of elastic lamina** of arteries → vasular stiffening **w/o obstruction**
* **"pipestem"** appearance on x-ray
* **does not obstruct blood flow; intima not invloved**
35
Define **atherosclerosis**:
Disease of **elastic arteries, large and medium-sized muscular arteries**
* form of arteriosclerosis caused by **buildup of cholesterol plaques**
* **very common**
36
**Evolution of MI**
* Commonly occluded arteries:
* Symptoms:
* **0 - 4 hours**
* **4 - 24 hours**
* **1 - 3 days**
* **3 - 14 days**
* **2 weeks - several months**
* Commonly occluded arteries: **LAD \> RCA \> circumflex**
* Symptoms: diaphoresis, n/v, severe retrosternal pain, pain in lt. arm and/or jaw, SOB, fatigue
* **0 - 4 hours:** (none)
* arrhythmia, HF, cardiogenic shock
* **4 - 24 hours:** (early coagulative necrosis, wavy fibers, neutrophils appear, reperfusion injury)
* arrhythmia, HF, cardiogenic shock
* **1 - 3 days:** (extensive coagulative necrosis, acute inflammation w/ neutrophils)
* postinfarct fibrinous **pericarditis**
* **3 - 14 days:** (macrophages and granulation tissue)
* **Free-wall rupture** → tamponade; papillary muscle rupture → mitral regurgitation; interventricular septal rupture due to macrophage-mediated structural degradation
* **LV pseudoaneurysm** (risk of rupture)
* **2 weeks - several months:** (complete contracted scar)
* **Dressler syndrome**, HF, arrythmias, **true ventricular aneurysm** (risk of mural thrombus)
37
Causes of **dilated cardiomyopathy:**
| (hint: **ABCCCD**)
* **A**lcohol abuse
* wet **B**eriberi
* **C**ocksakie B virus myocarditis
* chronic **C**ocaine use
* **C**hagas disease
* **D**oxorubicin/**D**aunorubicin
* Other causes: hemochromatosis, sarcoidosis, peripartum cardiomyopathy (pregnant women)
38
Findings in HF:
* Systolic dysfunction:
* Diastolic dysfunction:
**Heart failure:** dyspnea, orthopnea, fatigue; rales, JVD, pitting edema
* **Systolic dysfunction:**
* **reduced EF, ↑ EDV ⇒ ↓ contractility** often 2/2 ischemia/MI or dilated cardiomyopathy
* **Diastolic dysfunction:**
* **preserved EF, normal EDV** ⇒ **↓ compliance** often 2/2 myocardial hypertrophy
39
Right HF most often results from ....
Isolated right HF is usually due to ....
Right HF most often results from **left HF**
Isolated right HF is usually due to **cor pulmonale**
40
List the **vasculitides:**
1. **Large vessel vasculitis**
2. **Medium vessel vasculitis**
3. **Small vessel vasculitis**
1. **Large vessel vasculitis**
* Temporal arteritis
* Takayasu arteritis
2. **Medium vessel vasculitis**
* Polyarteritis nodosa
* Kawasaki disease
* Buerger disease (thromboangitis obliterans)
3. **Small vessel vasculitis**
* Granulomatosis w/ polyangitis (Wegener)
* Microscopic polyangitis
* Eosinophilic granulomatosis w/ polyangitis (Churg-Strauss)
* Henoch-Schönlein purpura
41
**Temporal (giant cell) arteritis**
* Epidemiology:
* Presentation:
* Pathology:
* Treatment:
* Epidemiology:
* elderly females
* Presentation:
* **unilateral headache,** **jaw claudication,**
* may lead to _opthalmic artery occlusion_ → _blindness_
* associated with _polymyalgia rheumatica_
* Pathology:
* affects **branches of carotid artery**
* focal granulomatous inflammation
* ↑ ESR
* Treatment:
* **high dose steroids prior to temporal artery biopsy** to prevent blindness
42
**Takayasu disease**
* Epidemiology:
* Presentation:
* Pathology:
* Treatment:
* Epidemiology:
* **asian females \< 40** yrs old
* Presentation:
* **"Pulseless disease"** (weak UE pulses), fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances
* Pathology:
* Granulomatous thickening and narrowing of **aortic arch** **and proximal great vessels**
* ↑ ESR
* Treatment:
* corticosteroids
43
**\*Polyarteritis nodosa**
* Epidemiology:
* Presentation:
* Pathology:
* Treatment:
* Epidemiology:
* **young adults**
* **Hepatitis B (+)** in 30% of patients
* Presentation:
* fever, weight loss, malaise, headache
* **GI:** abdominal pain, melena
* HTN, _neurologic dysfunction_, _cutaneous eruptions_, _renal damage_
* Pathology: **Type III Hypersensitivity**
* **renal and visceral vessels** _not pulmonary vessels_
* **immune complex mediated**
* **transmural inflammation of arterial wall w/fibrinoid necrosis**
* **innumerable renal microaneurysms and spasm on arteriogram**
* Treatment:
* corticosteroids, _cyclophosphamide_
44
**Kawasaki disease**
* Epidemiology:
* Presentation:
* Pathology:
* Treatment:
* Epidemiology:
* **Asian children \< 4 yrs old**
* Presentation: **CRASH** and **burn**
* **C**onjuctival injection, **R**ash (polymorphous → desquamating), **A**denopathy (cervical), **S**trawberry tongue (oral mucositis), **H**and/foot changes (edema, erythema), **fever**
* Pathology:
* may develop _coronary artery aneurysms_
* Treatment:
* **IV Ig** and **aspirin**
45
**Beurger disease (thromboangitis obliterans)**
* Epidemiology:
* Presentation:
* Pathology:
* Treatment:
* Epidemiology:
* **heavy smokers, males \< 40 yrs old**
* Presentation:
* **intermittent claudication** → gangrene, autoamputation of digits, superficial nodular phlebitis
* **Raynuad phenomenon** often present
* Pathology:
* **segmental thrombosing vasculitis**
* Treatment:
* **smoking cessation**
